FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Ahn, AC
Gow, BJ
Martinsen, OG
Zhao, M
Grodzinsky, AJ
Baikie, ID
AF Ahn, Andrew C.
Gow, Brian J.
Martinsen, Orjan G.
Zhao, Min
Grodzinsky, Alan J.
Baikie, Iain D.
TI Applying the Kelvin probe to biological tissues: Theoretical and
computational analyses
SO PHYSICAL REVIEW E
LA English
DT Article
ID CAPACITANCE; MICROSCOPY; MONOLAYERS; CORROSION; CELLS
AB The Kelvin probe measures surface electrical potential without making physical contact with the specimen. It relies on capacitive coupling between an oscillating metal tip that is normal to a specimen's surface. Kelvin probes have been increasingly used to study surface and electrical properties of metals and semiconductors and are capable of detecting material surface potentials with submillivolt resolution at a micrometer spatial scale. Its capability for measuring electrical potential without being confounded by electrode-specimen contact makes extending its use towards biological materials particularly appealing. However, the theoretical basis for applying the Kelvin probe to dielectric or partially conductive materials such as biological tissue has not been evaluated and remains unclear. This study develops the theoretical basis underlying Kelvin probe measurements in five theoretical materials: highly conductive, conductive dielectric with rapid charge relaxation, conductive dielectric with slow charge relaxation, perfect dielectric, and tissue with a bulk serial resistance. These theoretically derived equations are then computationally analyzed using parameters from both theoretical specimens and actual biomaterials-including wet skin, dry skin, cerebrospinal fluid, and tendon. Based on these analyses, a Kelvin probe performs in two distinct ways depending on the charge relaxation rates of the sample: The specimen is treated either as a perfect dielectric or as highly conductive material. Because of their rapid relaxation rate and increased permittivity biomaterials behave similarly to highly conductive materials, such as metal, when evaluated by the Kelvin probe. These results indicate that the Kelvin probe can be readily applied to studying the surface potential of biological tissue.
C1 [Ahn, Andrew C.; Gow, Brian J.] Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Martinsen, Orjan G.] Univ Oslo, Dept Phys, NO-0316 Oslo, Norway.
[Martinsen, Orjan G.] Oslo Univ Hosp, Rikshosp, Dept Biomed & Clin Engn, NO-0027 Oslo, Norway.
[Zhao, Min] UC Davis Sch Med, Dermatol & Ophthalmol Res Inst Regenerat Cures, Sacramento, CA 95817 USA.
[Zhao, Min] Univ Aberdeen, Sch Med Sci, Aberdeen AB25 2ZD, Scotland.
[Grodzinsky, Alan J.] MIT, Ctr Biomed Engn, Cambridge, MA 02139 USA.
[Baikie, Iain D.] KP Technol Ltd, Wick KW1 5LE, Scotland.
RP Ahn, AC (reprint author), Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, 149 13th St, Charlestown, MA 02129 USA.
EM aahn1@partners.org
RI Martinsen, Orjan/M-4459-2014
OI Martinsen, Orjan/0000-0003-1632-4352
FU National Center for Complementary Alternative Medicine (NCCAM)
[R21AT005249, P30AT005895]
FX This research was supported by Grants No. R21AT005249 and No.
P30AT005895 of the National Center for Complementary Alternative
Medicine (NCCAM).
NR 21
TC 1
Z9 1
U1 1
U2 15
PU AMER PHYSICAL SOC
PI COLLEGE PK
PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA
SN 2470-0045
EI 2470-0053
J9 PHYS REV E
JI Phys. Rev. E
PD JUN 1
PY 2012
VL 85
IS 6
AR 061901
DI 10.1103/PhysRevE.85.061901
PN 1
PG 13
WC Physics, Fluids & Plasmas; Physics, Mathematical
SC Physics
GA 951BG
UT WOS:000304695000009
PM 23005121
ER
PT J
AU Myaskovsky, L
Doebler, DA
Posluszny, DM
Dew, MA
Unruh, M
Crowley-Matoka, M
Switzer, GE
Dabbs, AD
Chang, CCH
DiMartini, AF
Shapiro, R
Tan, HK
AF Myaskovsky, Larissa
Doebler, Donna Almario
Posluszny, Donna M.
Dew, Mary Amanda
Unruh, Mark
Crowley-Matoka, Megan
Switzer, Galen E.
Dabbs, Annette DeVito
Chang, Chung-Chou H.
DiMartini, Andrea F.
Shapiro, Ron
Tan, Henkie
TI Rates and correlates of health maintenance behaviors after living kidney
donation
SO PROGRESS IN TRANSPLANTATION
LA English
DT Article
ID QUALITY-OF-LIFE; TERM-FOLLOW-UP; DONOR NEPHRECTOMY; TRANSPLANTATION;
OUTCOMES; CONSEQUENCES; DISEASE; IMPACT
AB Context and Objective-Donating a kidney may provide an opportunity for donors to reevaluate their health maintenance behaviors (eg, regular exercise, smoking cessation, medical checkups). Although the effect of donation on donors' health, quality of life, and financial outcomes has received growing attention, no studies have examined whether donation is related to changes in health maintenance behaviors. The study aims were to (I) describe and compare kidney donors' health maintenance behaviors before and after donation, and (2) determine the correlates of health maintenance behaviors after donation.
Design, Setting, Participants and Measures-We conducted a telephone-interview study with 85 randomly selected laparoscopic kidney donors in a major US transplant center to assess health behaviors before and after donation, postdonation characteristics (eg, quality of life, postsurgical pain), and demographics.
Results-Sample demographics included a median age of 48 years; 55% were female, 82% were white, 71% were married, and 52% were college graduates. Few health behaviors changed significantly from before to after donation. Only the rate of medical checkups increased after donation (P<.001). Logistic regression was used to examine the association of demographics and postdonation characteristics with postdonation health maintenance behaviors, after adjusting for predonation behavior. Older age, higher income, less postsurgical pain, and better physical functioning were associated with more exercise after donation. Longer time since donation was associated with a higher prevalence of obesity.
Conclusions-These results may help identify donors who are at greater risk for poor health maintenance behaviors after donation and suggest areas of health behavior that should be the focus of education sessions before donation. (Progress in Transplantation. 2012;22:147-154) (C) 2012 NATCO, The Organization for Transplant Professionals doi: http://dx.doi.org/10.7182/pit2012287
C1 [Myaskovsky, Larissa] VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA 15206 USA.
[Myaskovsky, Larissa; Doebler, Donna Almario; Posluszny, Donna M.; Dew, Mary Amanda; Unruh, Mark; Switzer, Galen E.; Dabbs, Annette DeVito; Chang, Chung-Chou H.; DiMartini, Andrea F.; Shapiro, Ron; Tan, Henkie] Univ Pittsburgh, Pittsburgh, PA USA.
[Crowley-Matoka, Megan] Northwestern Univ, Evanston, IL USA.
RP Myaskovsky, L (reprint author), VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, 7180 Highland Dr,151C-H, Pittsburgh, PA 15206 USA.
EM larissa.myaskovsky@va.gov
FU UPMC Starzl Transplant Institute [XNV 72-069]; VA Health Services
Research and Development Division [IIR 06-220]
FX Funding for this project was provided by grant XNV 72-069 from the UPMC
Starzl Transplant Institute and grant IIR 06-220 from the VA Health
Services Research and Development Division.
NR 41
TC 4
Z9 4
U1 0
U2 1
PU INNOVISION COMMUNICATIONS
PI ALISO VIEJO
PA 101 COLUMBIA, ALISO VIEJO, CA 92656 USA
SN 1526-9248
J9 PROG TRANSPLANT
JI Prog. Transplant.
PD JUN
PY 2012
VL 22
IS 2
BP 147
EP 154
DI 10.7182/pit2012287
PG 8
WC Surgery; Transplantation
SC Surgery; Transplantation
GA 956NA
UT WOS:000305095200006
PM 22878071
ER
PT J
AU Greenfield, BL
Venner, KL
Kelly, JF
Slaymaker, V
Bryan, AD
AF Greenfield, Brenna L.
Venner, Kamilla L.
Kelly, John F.
Slaymaker, Valerie
Bryan, Angela D.
TI The Impact of Depression on Abstinence Self-Efficacy and Substance Use
Outcomes Among Emerging Adults in Residential Treatment
SO PSYCHOLOGY OF ADDICTIVE BEHAVIORS
LA English
DT Article
DE emerging adults; substance use disorder; residential treatment;
abstinence self-efficacy; major depressive disorder
ID RANDOMIZED CONTROLLED-TRIAL; DRUG-USE CONSEQUENCES; USE DISORDERS;
RETEST RELIABILITY; RELAPSE PREVENTION; ALCOHOL-USE; DRINKING;
PREDICTORS; PREVALENCE; MECHANISMS
AB A large proportion of emerging adults treated for substance use disorder (SUD) present with symptoms of negative affect and major depressive disorder (MDD). However, little is known regarding how these comorbidities influence important mechanisms of treatment response, such as increases in abstinence self-efficacy (ASE). This study tested the degree to which MDD and/or depressive symptoms interacted with during-treatment changes in ASE and examined these variables' relation to outcome at 3 months' posttreatment. Participants (N = 302; 74% male) completed measures at intake, midtreatment, end-of-treatment, and at 3-month follow-up. ASE was measured with the Alcohol and Drug Use Self-Efficacy (ADUSE) scale; depressive symptoms were assessed with the Brief Symptom Inventory 18 (BSI 18) Depression scale; and current MDD diagnoses were deduced from the Structured Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV). Random coefficient regression analyses focused on during-treatment changes in ASE, with BSI 18 scores and MDD diagnosis included as moderators. At intake, individuals with MDD or high levels of depressive symptoms had significantly lower ASE, particularly in negative affect situations. No evidence for moderation was found: ASE significantly increased during treatment regardless of MDD status. There was a main effect of BSI 18 Depression scores: those with lower BSI 18 scores had lower ASE scores at each time point. MOD and BSI 18 Depression did not predict 3-month outcome, but similar to previous findings ASE did predict abstinence status at 3 months. Treatment-seeking emerging adults with MDD merit particular clinical attention because of their lower reported self-efficacy throughout treatment.
C1 [Greenfield, Brenna L.; Venner, Kamilla L.; Bryan, Angela D.] Univ New Mexico, Ctr Alcoholism Substance Abuse & Addict, Albuquerque, NM 87106 USA.
[Greenfield, Brenna L.; Venner, Kamilla L.; Bryan, Angela D.] Univ New Mexico, Dept Psychol, Albuquerque, NM 87106 USA.
[Kelly, John F.] Massachusetts Gen Hosp, Dept Psychiat, Ctr Addict Med, Boston, MA 02114 USA.
[Slaymaker, Valerie] Hazelden Fdn, Hazelden Grad Sch Addict Studies, Ctr City, MN USA.
RP Greenfield, BL (reprint author), Univ New Mexico, Ctr Alcoholism Substance Abuse & Addict, 2650 Yale SE,MSC11-6280, Albuquerque, NM 87106 USA.
EM brenna@unm.edu
FU NIAAA NIH HHS [1R21AA018185-01A, R21 AA018185, R21 AA018185-01A2]
NR 52
TC 13
Z9 14
U1 6
U2 15
PU EDUCATIONAL PUBLISHING FOUNDATION-AMERICAN PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST, NE, WASHINGTON, DC 20002-4242 USA
SN 0893-164X
EI 1939-1501
J9 PSYCHOL ADDICT BEHAV
JI Psychol. Addict. Behav.
PD JUN
PY 2012
VL 26
IS 2
BP 246
EP 254
DI 10.1037/a0026917
PG 9
WC Substance Abuse; Psychology, Multidisciplinary
SC Substance Abuse; Psychology
GA 956NX
UT WOS:000305097500008
PM 22288980
ER
PT J
AU Mattson, RE
O'Farrell, TJ
Lofgreen, AM
Cunningham, K
Murphy, CM
AF Mattson, Richard E.
O'Farrell, Timothy J.
Lofgreen, Ashton M.
Cunningham, Karlene
Murphy, Christopher M.
TI The Role of Illicit Substance Use in a Conceptual Model of Intimate
Partner Violence in Men Undergoing Treatment for Alcoholism
SO PSYCHOLOGY OF ADDICTIVE BEHAVIORS
LA English
DT Article
DE violence; intimate partners; substance use; substance abuse; drugs
ID DRUG-USE; PHYSICAL AGGRESSION; DYADIC ADJUSTMENT; STRUCTURAL MODELS;
EARLY MARRIAGE; ABUSE; MEDIATION; COEFFICIENT; STATISTICS; VALIDATION
AB Illicit substance use (ISU) predicts intimate partner violence (IPV) above and beyond alcohol use and other known IPV correlates. Stuart and colleagues (2008) provided evidence for a theoretical framework by which ISU contributes both directly and indirectly to IPV. We sought to replicate and extend their findings using data from 181 married or cohabiting heterosexual couples in which the male had recently begun a substance abuse treatment program and met criteria for alcohol dependence (97%) or abuse (3%). Using SEM, we found that (a) Stuart et al.'s model provided a good fit to the data; (b) men's cocaine use and women's sedative use emerged as particularly relevant to their respective perpetration of IPV; (c) a positive association between men's antisociality and physical aggression was mediated by increased stimulant use; and (d) the specific pattern of IPV predicted by women's sedative use differed across levels of aggression severity. These findings not only highlight the direct role of ISU in relationship aggression, but also support a larger theory-driven model comprising various proximal and distal precursors of IPV.
C1 [Mattson, Richard E.; Lofgreen, Ashton M.; Cunningham, Karlene] Auburn Univ, Dept Psychol, Auburn, AL 36849 USA.
[O'Farrell, Timothy J.] VA Boston Hlth Care Syst, Dept Psychiat, Families & Addict Program, Boston, MA USA.
[O'Farrell, Timothy J.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Murphy, Christopher M.] Univ Maryland Baltimore Cty, Dept Psychol, Baltimore, MD 21228 USA.
RP O'Farrell, TJ (reprint author), VA Boston, VAMC 116B1,940 Belmont St, Brockton, MA 02301 USA.
EM timothy_ofarrell@hms.harvard.edu
FU NIAAA NIH HHS [R01 AA010796, R01 AA010796-04]
NR 67
TC 17
Z9 17
U1 1
U2 6
PU EDUCATIONAL PUBLISHING FOUNDATION-AMERICAN PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST, NE, WASHINGTON, DC 20002-4242 USA
SN 0893-164X
EI 1939-1501
J9 PSYCHOL ADDICT BEHAV
JI Psychol. Addict. Behav.
PD JUN
PY 2012
VL 26
IS 2
BP 255
EP 264
DI 10.1037/a0025030
PG 10
WC Substance Abuse; Psychology, Multidisciplinary
SC Substance Abuse; Psychology
GA 956NX
UT WOS:000305097500009
PM 21875168
ER
PT J
AU Green, KE
Feinstein, BA
AF Green, Kelly E.
Feinstein, Brian A.
TI Substance Use in Lesbian, Gay, and Bisexual Populations: An Update on
Empirical Research and Implications for Treatment
SO PSYCHOLOGY OF ADDICTIVE BEHAVIORS
LA English
DT Article
DE substance use; lesbian; gay; bisexual; review; treatment
ID CLUB DRUG-USE; ALCOHOL-RELATED PROBLEMS; HOMOSEXUALLY ACTIVE MEN;
NEW-YORK-CITY; SEXUAL ORIENTATION; ABUSE TREATMENT; RISK BEHAVIORS; USE
DISORDERS; COLLEGE-STUDENTS; RANDOMIZED-TRIAL
AB Historically, substance use problems were thought to be more prevalent in lesbian, gay, and bisexual (LGB) populations, and correcting skewed perceptions about substance abuse among LGB individuals is critically important. This review provides an update on empirical evidence on LGB substance use patterns and treatment outcome, with specific focus on clinical implications of findings. Compared to earlier studies, the recent research included in this review has used more sophisticated methodologies and more representative samples, and also has investigated multiple dimensions of sexual orientation in relation to substance use patterns. Findings from recent research suggest that lesbians and bisexual women are at greater risk for alcohol and drug use disorders and related problems, and that gay and bisexual men are at greater risk for illicit drug use and related problems. Several sociocultural factors have emerged as correlates of substance use patterns in LGB populations (e.g., affiliation with gay culture, HIV status), and several demographic characteristics (e.g., female, older age) do not appear to be as robust of protective factors against substance abuse for LGB individuals compared to heterosexual populations. Bisexual identity and/or behavior in particular seem to be related to increased risk for substance abuse. In terms of treatment outcome, limitations of extant research prevent conclusions about the relative impact of LGB-specific interventions, and further research that includes women and uses more equivalent comparison interventions is needed. Clinical implications of research findings are discussed for case identification, selection of treatment goals (e.g., moderation vs. abstinence), targets for intervention, and specific treatment modalities.
C1 [Green, Kelly E.] VA Boston Healthcare Syst, Psychol Serv, Brockton, MA 02310 USA.
[Green, Kelly E.] Harvard Univ, Sch Med, Dept Psychiat, Cambridge, MA 02138 USA.
[Feinstein, Brian A.] SUNY Stony Brook, Dept Psychol, Stony Brook, NY USA.
RP Green, KE (reprint author), VA Boston Healthcare Syst, Psychol Serv 116B, 940 Belmont St, Brockton, MA 02310 USA.
EM Kelly.Green3@va.gov
FU NIAAA NIH HHS [T32 AA007569, T32 AA007569-05, T32 AA07569]
NR 68
TC 49
Z9 49
U1 5
U2 21
PU EDUCATIONAL PUBLISHING FOUNDATION-AMERICAN PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST, NE, WASHINGTON, DC 20002-4242 USA
SN 0893-164X
J9 PSYCHOL ADDICT BEHAV
JI Psychol. Addict. Behav.
PD JUN
PY 2012
VL 26
IS 2
BP 265
EP 278
DI 10.1037/a0025424
PG 14
WC Substance Abuse; Psychology, Multidisciplinary
SC Substance Abuse; Psychology
GA 956NX
UT WOS:000305097500010
PM 22061339
ER
PT J
AU Carmody, TP
Delucchi, K
Simon, JA
Duncan, CL
Solkowitz, SN
Huggins, J
Lee, SK
Hall, SM
AF Carmody, Timothy P.
Delucchi, Kevin
Simon, Joel A.
Duncan, Carol L.
Solkowitz, Sharon N.
Huggins, Joy
Lee, Sharon K.
Hall, Sharon M.
TI Expectancies Regarding the Interaction Between Smoking and Substance Use
in Alcohol-Dependent Smokers in Early Recovery
SO PSYCHOLOGY OF ADDICTIVE BEHAVIORS
LA English
DT Article
DE smoking cessation; tobacco use; nicotine dependence; alcohol dependence;
expectancies
ID ADDICTION SEVERITY INDEX; FAGERSTROM TOLERANCE QUESTIONNAIRE; NICOTINE
DEPENDENCE; ABUSE TREATMENT; CESSATION INTERVENTIONS; ABSTINENCE;
DISORDERS; TOBACCO; METAANALYSIS; INDIVIDUALS
AB The purpose of this study was to investigate expectancies regarding the interaction between cigarette smoking and use of alcohol among alcohol-dependent smokers in early recovery, using the Nicotine and Other Substances Interaction Expectancies Questionnaire (NOSIE). Participants were 162 veterans, 97% male, with a mean age of 50 years, enrolled in a clinical trial aimed at determining the efficacy of an intensive smoking cessation intervention versus usual care. At baseline, participants were assessed on measures of smoking behavior, abstinence thoughts about alcohol and tobacco use, symptoms of depression, and smoking-substance use interaction expectancies. In addition, biologically verified abstinence from tobacco and alcohol was assessed at 26 weeks. Participants reported that they expected smoking to have less of an impact on substance use than substance use has on smoking (p < .001). Severity of depressive symptoms was significantly associated with the expectancy that smoking provides a way of coping with the urge to use other substances (p < .01). The expectation that smoking increases substance urges/use was predictive of prospectively measured and biologically verified abstinence from smoking at 26 weeks (p < .03). The results add to our knowledge of smoking-substance use interaction expectancies among alcohol-dependent smokers in early recovery and will inform the development of more effective counseling interventions for concurrent alcohol and tobacco use disorders.
C1 [Carmody, Timothy P.; Simon, Joel A.; Duncan, Carol L.; Solkowitz, Sharon N.; Huggins, Joy; Lee, Sharon K.] San Francisco VA Med Ctr, Mental Hlth Serv, San Francisco, CA USA.
[Delucchi, Kevin; Hall, Sharon M.] Univ Calif San Francisco, Treatment Res Ctr, Dept Psychiat, San Francisco, CA 94143 USA.
RP Carmody, TP (reprint author), Vet Affairs Med Ctr, Mental Hlth Serv 116B, 4150 Clement St, San Francisco, CA 94121 USA.
EM timothy.carmody@va.gov
FU NIDA NIH HHS [P50 DA09253, P50 DA009253-09, P50 DA009253]
NR 36
TC 8
Z9 8
U1 1
U2 4
PU EDUCATIONAL PUBLISHING FOUNDATION-AMERICAN PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST, NE, WASHINGTON, DC 20002-4242 USA
SN 0893-164X
J9 PSYCHOL ADDICT BEHAV
JI Psychol. Addict. Behav.
PD JUN
PY 2012
VL 26
IS 2
BP 358
EP 363
DI 10.1037/a0024424
PG 6
WC Substance Abuse; Psychology, Multidisciplinary
SC Substance Abuse; Psychology
GA 956NX
UT WOS:000305097500021
PM 21707127
ER
PT J
AU Hess, DR
AF Hess, Dean R.
TI The Growing Role of Noninvasive Ventilation in Patients Requiring
Prolonged Mechanical Ventilation
SO RESPIRATORY CARE
LA English
DT Article; Proceedings Paper
CT 49th Respiratory Care Journal Conference on Chronically Critically Ill
Patient
CY SEP 09-10, 2011
CL St Petersburg, FL
SP Amer Resp Care Fdn
DE amyotrophic lateral sclerosis; bi-level pressure ventilation; chronic
obstructive pulmonary disease; cystic fibrosis; Duchenne muscular
dystrophy; noninvasive ventilation; obesity hypoventilation syndrome;
restrictive thoracic disorder
ID POSITIVE-PRESSURE VENTILATION; OBESITY-HYPOVENTILATION SYNDROME;
OBSTRUCTIVE PULMONARY-DISEASE; DUCHENNE MUSCULAR-DYSTROPHY; CHRONIC
RESPIRATORY-FAILURE; STABLE HYPERCAPNIC COPD; RANDOMIZED CROSSOVER
TRIAL; PROPORTIONAL ASSIST VENTILATION; AMYOTROPHIC-LATERAL-SCLEROSIS;
NOCTURNAL NASAL VENTILATION
AB For many patients with chronic respiratory failure requiring ventilator support, noninvasive ventilation (NIV) is preferable to invasive support by tracheostomy. Currently available evidence does not support the use of nocturnal NIV in unselected patients with stable COPD. Several European studies have reported benefit for high intensity NIV, in which setting of inspiratory pressure and respiratory rate are selected to achieve normocapnia. There have also been studies reporting benefit for the use of NIV as an adjunct to exercise training. NIV may be useful as an adjunct to airway clearance techniques in patients with cystic fibrosis. Accumulating evidence supports the use of NIV in patients with obesity hypoventilation syndrome. There is considerable observational evidence supporting the use of NIV in patients with chronic respiratory failure related to neuromuscular disease, and one randomized controlled trial reported that the use of NIV was life-prolonging in patients with amyotrophic lateral sclerosis. A variety of interfaces can be used to provide NIV in patients with stable chronic respiratory failure. The mouthpiece is an interface that is unique in this patient population, and has been used with success in patients with neuromuscular disease. Bi-level pressure ventilators are commonly used for NIV, although there are now a new generation of intermediate ventilators that are portable, have a long battery life, and can be used for NIV and invasive applications. Pressure support ventilation, pressure controlled ventilation, and volume controlled ventilation have been used successfully for chronic applications of NIV. New modes have recently become available, but their benefits await evidence to support their widespread use. The success of NIV in a given patient population depends on selection of an appropriate patient, selection of an appropriate interface, selection of an appropriate ventilator and ventilator settings, the skills of the clinician, the motivation of the patient, and the support of the family.
C1 [Hess, Dean R.] Massachusetts Gen Hosp, Dept Resp Care, Boston, MA 02114 USA.
[Hess, Dean R.] Harvard Univ, Sch Med, Dept Anesthesia, Boston, MA 02115 USA.
RP Hess, DR (reprint author), Massachusetts Gen Hosp, Dept Resp Care, Ellison 401,55 Fruit St, Boston, MA 02114 USA.
EM dhess@partners.org
NR 192
TC 16
Z9 17
U1 0
U2 7
PU DAEDALUS ENTERPRISES INC
PI IRVING
PA 9425 N MAC ARTHUR BLVD, STE 100, IRVING, TX 75063-4706 USA
SN 0020-1324
J9 RESP CARE
JI Respir. Care
PD JUN
PY 2012
VL 57
IS 6
BP 900
EP 920
DI 10.4187/respcare.01692
PG 21
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 955UY
UT WOS:000305047600006
PM 22663966
ER
PT J
AU Atwood, CW
AF Atwood, Charles W., Jr.
TI "The Times They Are A Changin:" Home Diagnosis of Sleep Apnea Has
Arrived Commentary on Rosen et al. A multisite randomized trial of
portable sleep studies and positive airway pressure autotitration versus
laboratory-based polysomnography for the diagnosis and treatment of
obstructive sleep apnea: The HomePAP Study. SLEEP 2012;35:757-767
SO SLEEP
LA English
DT Editorial Material
ID OUTCOMES
C1 [Atwood, Charles W., Jr.] Univ Pittsburgh, Div Pulm Allergy & Crit Care Med, Med Ctr, UPMC Sleep Med Ctr, Pittsburgh, PA 15213 USA.
[Atwood, Charles W., Jr.] VA Pittsburgh Healthcare Syst, Pulm Sect, Pittsburgh, PA USA.
[Atwood, Charles W., Jr.] VA Pittsburgh Healthcare Syst, Sleep Disorders Program, Pittsburgh, PA USA.
RP Atwood, CW (reprint author), Univ Pittsburgh, Div Pulm Allergy & Crit Care Med, Med Ctr, UPMC Sleep Med Ctr, 3459 5th Ave,NW628 MUH, Pittsburgh, PA 15213 USA.
EM atwoodcw@upmc.edu
NR 8
TC 2
Z9 2
U1 0
U2 0
PU AMER ACAD SLEEP MEDICINE
PI WESTCHESTER
PA ONE WESTBROOK CORPORATE CTR, STE 920, WESTCHESTER, IL 60154 USA
SN 0161-8105
J9 SLEEP
JI Sleep
PD JUN 1
PY 2012
VL 35
IS 6
BP 735
EP 736
DI 10.5665/sleep.1848
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 952CM
UT WOS:000304767300003
PM 22654184
ER
PT J
AU Kim, Y
Bolortuya, Y
Chen, LC
Basheer, R
McCarley, RW
Strecker, RE
AF Kim, Youngsoo
Bolortuya, Yunren
Chen, Lichao
Basheer, Radhika
McCarley, Robert W.
Strecker, Robert E.
TI Decoupling of Sleepiness from Sleep Time and Intensity during Chronic
Sleep Restriction: Evidence for a Role of the Adenosine System
SO SLEEP
LA English
DT Article
DE Chronic sleep restriction; rat; allostasis; sleep latency; adenosine;
receptor
ID HOMEOSTATIC REGULATION; DOSE-RESPONSE; A(1) RECEPTOR; RISK-FACTOR;
DEPRIVATION; RATS; BRAIN; RECOVERY; DURATION; MICE
AB Study Objective: Sleep responses to chronic sleep restriction (CSR) might be very different from those observed after short-term total sleep deprivation. For example, after sleep restriction continues for several consecutive days, animals no longer express compensatory increases in daily sleep time and sleep intensity. However, it is unknown if these allostatic, or adaptive, sleep responses to CSR are paralleled by behavioral and neurochemical measures of sleepiness.
Design: This study was designed to investigate CSR-induced changes in (1) sleep time and intensity as a measure of electrophysiological sleepiness, (2) sleep latency as a measure of behavioral sleepiness, and (3) brain adenosine A1 (A1R) and A2a receptor (A2aR) mRNA levels as a putative neurochemical correlate of sleepiness.
Subjects: Male Sprague-Dawley rats
Interventions: A 5-day sleep restriction (SR) protocol consisting of 18-h sleep deprivation and 6-h sleep opportunity each day.
Measurement and Results: Unlike the first SR day, rats did not sleep longer or deeper on days 2 through 5, even though they exhibited significant elevations of behavioral sleepiness throughout all 5 SR days. For all SR days and recovery day 1, A1R mRNA in the basal forebrain was maintained at elevated levels, whereas A2aR mRNA in the frontal cortex was maintained at reduced levels.
Conclusion: CSR leads to a decoupling of sleepiness from sleep time and sleep intensity, suggesting that there are at least two different sleep regulatory systems: one mediating sleepiness (homeostatic) and the other mediating sleep time/intensity (allostatic). The time course of changes observed in adenosine receptor mRNA levels suggests that the basal forebrain and cortical adenosine system might mediate sleepiness rather than sleep time or intensity.
C1 [Kim, Youngsoo] VA Boston Healthcare Syst, Res Serv, Brockton, MA 02301 USA.
Harvard Univ, Sch Med, Dept Psychiat, Res Serv, Brockton, MA 02301 USA.
RP Kim, Y (reprint author), VA Boston Healthcare Syst, Res Serv, 151-C,940 Belmont St, Brockton, MA 02301 USA.
EM youngsoo_kim@hms.harvard.edu
RI McCarley, Robert/N-5562-2014
OI McCarley, Robert/0000-0001-5705-7495
FU Department of Veterans Affairs Medical Research Service [T32 HL07901,
R37 MH039683, P50 HL060292, HL095491]
FX We thank Ritchie E. Brown and Michael A. Christie for helpful
discussions. This research was supported by: Department of Veterans
Affairs Medical Research Service Award (RES), T32 HL07901 (YK), R37
MH039683 (RWM & RES), P50 HL060292 (RES & RWM), HL095491 (RWM & RES).
NR 36
TC 21
Z9 21
U1 2
U2 7
PU AMER ACAD SLEEP MEDICINE
PI WESTCHESTER
PA ONE WESTBROOK CORPORATE CTR, STE 920, WESTCHESTER, IL 60154 USA
SN 0161-8105
J9 SLEEP
JI Sleep
PD JUN 1
PY 2012
VL 35
IS 6
BP 861
EP 869
DI 10.5665/sleep.1890
PG 9
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 952CM
UT WOS:000304767300024
PM 22654205
ER
PT J
AU Biering-Sorensen, F
Krassioukov, A
Alexander, MS
Donovan, W
Karlsson, AK
Mueller, G
Perkash, I
Sheel, AW
Wecht, J
Schilero, GJ
AF Biering-Sorensen, F.
Krassioukov, A.
Alexander, M. S.
Donovan, W.
Karlsson, A-K
Mueller, G.
Perkash, I.
Sheel, A. William
Wecht, J.
Schilero, G. J.
TI International Spinal Cord Injury Pulmonary Function Basic Data Set
SO SPINAL CORD
LA English
DT Article
DE spinal cord injury; international data set; pulmonary function;
pneumonia; sleep apnea; ventilator
ID FORCED VITAL CAPACITY; MORTALITY; SLEEP; DEATH; FEV1; FVC
AB Objectives: To develop the International Spinal Cord Injury (SCI) Pulmonary Function Basic Data Set within the framework of the International SCI Data Sets in order to facilitate consistent collection and reporting of basic bronchopulmonary findings in the SCI population.
Setting: International.
Methods: The SCI Pulmonary Function Data Set was developed by an international working group. The initial data set document was revised on the basis of suggestions from members of the Executive Committee of the International SCI Standards and Data Sets, the International Spinal Cord Society (ISCoS) Executive and Scientific Committees, American Spinal Injury Association (ASIA) Board, other interested organizations and societies and individual reviewers. In addition, the data set was posted for 2 months on ISCoS and ASIA websites for comments.
Results: The final International SCI Pulmonary Function Data Set contains questions on the pulmonary conditions diagnosed before spinal cord lesion, if available, to be obtained only once; smoking history; pulmonary complications and conditions after the spinal cord lesion, which may be collected at any time. These data include information on pneumonia, asthma, chronic obstructive pulmonary disease and sleep apnea. Current utilization of ventilator assistance including mechanical ventilation, diaphragmatic pacing, phrenic nerve stimulation and Bi-level positive airway pressure can be reported, as well as results from pulmonary function testing includes: forced vital capacity, forced expiratory volume in one second and peak expiratory flow. The complete instructions for data collection and the data sheet itself are freely available on the website of ISCoS (http://www.iscos.org.uk). Spinal Cord (2012) 50, 418-421; doi:10.1038/sc.2011.183; published online 24 January 2012
C1 [Biering-Sorensen, F.] Rigshosp, Clin Spinal Cord Injuries, Ctr Neurosci, DK-2100 Copenhagen, Denmark.
[Biering-Sorensen, F.] Univ Copenhagen, DK-2100 Copenhagen O, Denmark.
[Krassioukov, A.; Sheel, A. William] Univ British Columbia, ICORD, Vancouver, BC V5Z 1M9, Canada.
[Krassioukov, A.; Sheel, A. William] Vancouver Coastal Hlth, Vancouver, BC, Canada.
[Alexander, M. S.] Renown Rehabil Hosp, Reno, NV USA.
[Donovan, W.] Univ Texas Hlth Sci Ctr, Baylor Coll Med, Houston, TX USA.
[Karlsson, A-K] Sahlgrens Univ Hosp, Gothenburg, Sweden.
[Mueller, G.] Swiss Parapleg Ctr, Clin Trial Unit, Nottwil, Switzerland.
[Perkash, I.] Stanford Univ, Palo Alto, CA 94304 USA.
[Perkash, I.] Vet Adm Palo Alto, Palo Alto, CA USA.
[Wecht, J.; Schilero, G. J.] James J Peters Vet Affairs Med Ctr, Bronx, NY USA.
[Wecht, J.; Schilero, G. J.] Mt Sinai Sch Med, New York, NY USA.
RP Biering-Sorensen, F (reprint author), RIGSHOSP TH2091, Clin Spinal Cord Injuries, Ctr Neurosci, 9 Blegdamsvej, DK-2100 Copenhagen O, Denmark.
EM finbs@rh.dk
FU Coloplast A/S, Denmark
FX Coloplast A/S, Denmark has supported the work with this Data Set with an
unconditional grant. We are thankful for comments and suggestions
received from Lawrence Vogel, Susan Charlifue, Gordana Savic and Michael
DeVivo.
NR 15
TC 10
Z9 10
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1362-4393
J9 SPINAL CORD
JI Spinal Cord
PD JUN
PY 2012
VL 50
IS 6
BP 418
EP 421
DI 10.1038/sc.2011.183
PG 4
WC Clinical Neurology; Rehabilitation
SC Neurosciences & Neurology; Rehabilitation
GA 951LC
UT WOS:000304721100005
PM 22270192
ER
PT J
AU Lubitz, CC
Nagarkatti, SS
Faquin, WC
Samir, AE
Hassan, MC
Barbesino, G
Ross, DS
Randolph, GW
Gaz, RD
Stephen, AE
Hodin, RA
Daniels, GH
Parangi, S
AF Lubitz, Carrie C.
Nagarkatti, Sushruta S.
Faquin, William C.
Samir, Anthony E.
Hassan, Maria C.
Barbesino, Giuseppe
Ross, Douglas S.
Randolph, Gregory W.
Gaz, Randall D.
Stephen, Antonia E.
Hodin, Richard A.
Daniels, Gilbert H.
Parangi, Sareh
TI Diagnostic Yield of Nondiagnostic Thyroid Nodules Is Not Altered by
Timing of Repeat Biopsy
SO THYROID
LA English
DT Article
ID FINE-NEEDLE-ASPIRATION; MANAGEMENT
AB Background: Guidelines from the National Cancer Institute Thyroid Fine Needle Aspiration State of the Science Conference recommend a repeat fine-needle aspiration biopsy (FNAB) after 3 months for thyroid nodules with a nondiagnostic (ND) result. Our aims were to assess which factors influenced their clinical management and to determine if the timing of the repeat FNAB affects the diagnostic yield.
Methods: A retrospective institutional review of 298 patients from 1/2006 to 12/2007 with an ND FNAB was performed. The factors influencing the next step in management, including age, gender, history of radiation, presence of Hashimoto's thyroiditis, thyroid-stimulating hormone levels, and ultrasound characteristics, were evaluated. The effect of the time of the repeat FNABs on their diagnostic yield was assessed.
Results: Of the 298 patients in our cohort, 9% were referred directly for surgery, 76% had a repeat FNAB, and 15% were observed. Tumor size was the only independent variable correlated with treatment strategy after a ND FNAB. There was not a significant difference in diagnostic yields between repeat FNABs performed earlier than 3 months compared to those preformed later (p=0.58).
Conclusion: The timing of repeat FNAB for an initial ND FNAB does not affect diagnostic yield of the repeat FNAB.
C1 [Lubitz, Carrie C.; Nagarkatti, Sushruta S.; Hassan, Maria C.; Randolph, Gregory W.; Gaz, Randall D.; Stephen, Antonia E.; Hodin, Richard A.; Parangi, Sareh] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Surg,Endocrine Surg Unit, Boston, MA 02114 USA.
[Faquin, William C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol, Boston, MA 02114 USA.
[Samir, Anthony E.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA 02114 USA.
[Barbesino, Giuseppe; Ross, Douglas S.; Daniels, Gilbert H.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med,Thyroid Unit, Boston, MA 02114 USA.
RP Lubitz, CC (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Surg,Endocrine Surg Unit, 55 Fruit St,Yawkey 7B, Boston, MA 02114 USA.
EM clubitz@partners.org
OI Samir, Anthony/0000-0002-7801-8724
FU NCI NIH HHS [R01 CA149738]
NR 11
TC 19
Z9 19
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
J9 THYROID
JI Thyroid
PD JUN
PY 2012
VL 22
IS 6
BP 590
EP 594
DI 10.1089/thy.2011.0442
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 955EZ
UT WOS:000305001200006
PM 22667452
ER
PT J
AU Kim, SB
Williams, SB
Cheng, SC
Sanda, MG
Wagner, AA
AF Kim, Sarah B.
Williams, Stephen B.
Cheng, Su-Chun
Sanda, Martin G.
Wagner, Andrew A.
TI Evaluation of Patient-reported Quality-of-life Outcomes After Renal
Surgery
SO UROLOGY
LA English
DT Article
ID RECOVERY EVALUATION CARE; CELL CARCINOMA; PROSTATE-CANCER; HEALTH
SURVEY; VALIDATION; CONVALESCENCE; NEPHRECTOMY; IMPACT; MEN
AB OBJECTIVE To assess the feasibility of 2 patient-reported health-related quality of life (HRQOL) instruments, Convalescence and Recovery Evaluation (CARE), and SF-12, as tools for evaluating HRQOL outcome consequences after renal surgery, and to determine which domains of these HRQOL instruments are most sensitive to HRQOL outcome effects of renal surgery.
METHODS Patients completed CARE and SF-12 preoperatively (baseline) and at 2, 4, 12, and 24 weeks after surgery. Clinical data, patient response rate, HRQOL changes over time, and likelihood of patient return to baseline HRQOL were evaluated.
RESULTS Seventy-one patients were enrolled. Sixty patients completed the baseline and at least 1 follow-up set of questionnaires. The CARE pain, gastrointestinal (GI), and activity domain scores and the SF-12 physical composite score (PCS) were sensitive to changes in HRQOL (all P<.05), whereas other domain subscores of these instruments did not change from presurgical baseline to postsurgical follow-up. Postsurgical HRQOL effects detected by the CARE pain, GI, and activity domains, and SF-12 PCS were most evident at 2 weeks (all P<.001). The CARE composite score demonstrated that 74% and 50% of patients returned to within 90% of baseline 4 weeks after radical and partial nephrectomy, respectively.
CONCLUSION Evaluation of patient-reported HRQOL outcomes after renal surgery is feasible; our findings suggest that the activity, pain, and GI domains of CARE and PCS subscores of the SF-12 are sensitive measures of HRQOL outcome consequences of renal surgery and represent appropriate measures of either care quality or comparative effectiveness analyses of robotic, laparoscopic, and open renal surgery. UROLOGY 79: 1268-1273, 2012. (c) 2012 Elsevier Inc.
C1 [Wagner, Andrew A.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Surg, Boston, MA 02215 USA.
[Wagner, Andrew A.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Div Urol, Boston, MA 02215 USA.
St Joseph Hosp, Ctr Canc Prevent & Treatment, Div Urol Oncol, Orange, CA USA.
Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
RP Wagner, AA (reprint author), Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Surg, 330 Brookline Ave,Rabb 440, Boston, MA 02215 USA.
EM awagner@bidmc.harvard.edu
RI Sanda, Martin/A-6202-2013; Sanda, Martin/B-2023-2015
FU Dana Farber/Harvard Cancer Center: Kidney Cancer SPORE; Kidney Cancer
Association
FX This project was supported by a joint Developmental Award from the Dana
Farber/Harvard Cancer Center: Kidney Cancer SPORE and the Kidney Cancer
Association.
NR 16
TC 6
Z9 6
U1 1
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0090-4295
J9 UROLOGY
JI Urology
PD JUN
PY 2012
VL 79
IS 6
BP 1268
EP 1273
DI 10.1016/j.urology.2012.02.047
PG 6
WC Urology & Nephrology
SC Urology & Nephrology
GA 951KX
UT WOS:000304720600023
PM 22542421
ER
PT J
AU Saboo, SS
Krajewski, KM
Jagannathan, JP
Ramaiya, N
AF Saboo, Sachin S.
Krajewski, Katherine M.
Jagannathan, Jyothi P.
Ramaiya, Nikhil
TI IVC Tumor Thrombus: An Advanced Case of Rare Extraosseous Ewing Sarcoma
of the Adrenal Gland
SO UROLOGY
LA English
DT Editorial Material
AB Extraosseous Ewing sarcoma (ES) of the adrenal gland is a rare, aggressive tumor of young adults, with <10 cases reported. We present the radiological findings of an unusual case of adrenal and renal vein tumor thrombosis extending into the inferior vena cava, secondary to ES of the adrenal gland in a 26-year-old female. UROLOGY 79: e77-e78, 2012. (c) 2012 Elsevier Inc.
C1 [Saboo, Sachin S.] Brigham & Womens Hosp, Dana Farber Canc Inst, Dept Radiol, Boston, MA 02215 USA.
[Saboo, Sachin S.] Harvard Univ, Sch Med, Boston, MA 02215 USA.
RP Saboo, SS (reprint author), Brigham & Womens Hosp, Dana Farber Canc Inst, Dept Radiol, 450 Brookline Ave, Boston, MA 02215 USA.
EM ssaboo@partners.org
NR 5
TC 2
Z9 2
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0090-4295
J9 UROLOGY
JI Urology
PD JUN
PY 2012
VL 79
IS 6
BP E77
EP E78
DI 10.1016/j.urology.2012.03.008
PG 2
WC Urology & Nephrology
SC Urology & Nephrology
GA 951KX
UT WOS:000304720600001
PM 22656426
ER
PT J
AU Todoran, TM
Connors, G
Engelson, BA
Sobieszczyk, PS
Eisenhauer, AC
Kinlay, S
AF Todoran, Thomas M.
Connors, Gerard
Engelson, Brian A.
Sobieszczyk, Piotr S.
Eisenhauer, Andrew C.
Kinlay, Scott
TI Femoral artery percutaneous revascularization for patients with critical
limb ischemia: Outcomes compared to patients with claudication over 2.5
years
SO VASCULAR MEDICINE
LA English
DT Article
DE amputation; angioplasty; atherosclerosis; claudication (see intermittent
claudication); femoral artery; ischemia; leg; longitudinal studies;
outcome assessment (health care); peripheral arterial disease
ID INFRAINGUINAL BYPASS; LOWER-EXTREMITY; INTERVENTIONS; ANGIOPLASTY;
SALVAGE; DISEASE; SURGERY; EVENTS; TRIAL; MULTICENTER
AB Patients with critical limb ischemia have higher rates of death and amputation after revascularization compared to patients with intermittent claudication. However, the differences in patency after percutaneous revascularization of the superficial femoral artery are uncertain and impact the long-term risk of amputation and function in critical limb ischemia. We identified 171 limbs from 136 consecutive patients who had angioplasty and/or stenting for superficial femoral artery stenoses or occlusions from July 2003 through June 2007. Patients were followed for primary and secondary patency, death and amputation up to 2.5 years, and 111 claudicants were retrospectively compared to the 25 patients with critical limb ischemia. Successful percutaneous revascularization occurred in 128 of 142 limbs (90%) with claudication versus 25 of 29 limbs (86%) with critical limb ischemia (p = 0.51). Overall secondary patency at 2.5 years was 91% for claudication and 88% for critical limb ischemia. In Cox proportional hazards models, percutaneous revascularization for critical limb ischemia had similar long-term primary patency (adjusted hazard ratio = 1.1, 95% CI = 0.4, 2.6; p = 0.89) and secondary patency (adjusted hazard ratio = 1.1, 95% CI = 0.2, 6.0; p = 0.95) to revascularization for claudication. Patients with critical limb ischemia had higher mortality and death rates compared to claudicants, with prior statin use associated with less death (p = 0.034) and amputation (p = 0.010), and prior clopidogrel use associated with less amputation (p = 0.034). In conclusion, percutaneous superficial femoral artery revascularization is associated with similar long-term durability in both groups. Intensive treatment of atherosclerosis risk factors and surveillance for restenosis likely contribute to improving the long-term outcomes of both manifestations of peripheral artery disease.
C1 [Kinlay, Scott] VA Boston Healthcare Syst, Intervent Cardiol & Vasc Med, Div Cardiovasc, Boston, MA USA.
[Todoran, Thomas M.] Med Univ S Carolina, Div Cardiovasc, Charleston, SC 29425 USA.
[Connors, Gerard] Princess Alexandra Hosp, Div Cardiovasc, Brisbane, Qld 4102, Australia.
[Connors, Gerard] Greenslopes Hosp, Brisbane, Qld, Australia.
[Connors, Gerard] Univ Queensland, Brisbane, Qld, Australia.
[Engelson, Brian A.; Sobieszczyk, Piotr S.; Eisenhauer, Andrew C.; Kinlay, Scott] Brigham & Womens Hosp, Div Cardiovasc, Intervent & Vasc Med Sect, Boston, MA 02115 USA.
[Engelson, Brian A.; Sobieszczyk, Piotr S.; Eisenhauer, Andrew C.; Kinlay, Scott] Harvard Univ, Sch Med, Boston, MA USA.
RP Kinlay, S (reprint author), VA Boston Healthcare Syst, Intervent Cardiol & Vasc Med, Div Cardiovasc, W Roxbury, MA 02132 USA.
EM Scott.kinlay@va.gov
NR 23
TC 4
Z9 4
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1358-863X
J9 VASC MED
JI Vasc. Med.
PD JUN
PY 2012
VL 17
IS 3
BP 138
EP 144
DI 10.1177/1358863X12440141
PG 7
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 951KR
UT WOS:000304719900002
PM 22496125
ER
PT J
AU Weinberg, I
Giri, J
Calfon, MA
Hawkins, BM
Weinberg, MD
Schainfeld, RM
Jaff, MR
AF Weinberg, Ido
Giri, Jay
Calfon, Marcella A.
Hawkins, Beau M.
Weinberg, Mitchell D.
Schainfeld, Robert M.
Jaff, Michael R.
TI Anatomic correlates of supranormal ankle brachial indices (ABI)
SO VASCULAR MEDICINE
LA English
DT Meeting Abstract
C1 [Weinberg, Ido; Giri, Jay; Calfon, Marcella A.; Hawkins, Beau M.; Weinberg, Mitchell D.; Schainfeld, Robert M.; Jaff, Michael R.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
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 1358-863X
J9 VASC MED
JI Vasc. Med.
PD JUN
PY 2012
VL 17
IS 3
MA 10
BP 200
EP 201
PG 2
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 951KR
UT WOS:000304719900019
ER
PT J
AU Baron, JM
Johnson, SM
Ledford-Kraemer, MR
Hayward, CP
Meijer, P
Van Cott, EM
AF Baron, Jason M.
Johnson, Stephen M.
Ledford-Kraemer, Marlies R.
Hayward, Catherine P.
Meijer, Piet
Van Cott, Elizabeth M.
TI Protein C Assay Performance An Analysis of North American Specialized
Coagulation Laboratory Association Proficiency Testing Results
SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article
DE Protein C; Quality assurance; Hypercoagulability
AB To determine the performance and frequency of protein C reagents currently used by clinical laboratories, we analyzed North American Specialized Coagulation Laboratory Association (NASCOLA) protein C proficiency testing data from 6 surveys conducted in 2009 and 2010 (2009-1 to 2009-3 and 2010-1 to 2010-3). Interlaboratory coefficients of variation (CV) for commonly used reagents on a survey with normal protein C ranged from 8% to 12% for antigenic assays, from 4% to 7% for chromogenic activity assays, and from 7% to 22% for clot-based activity assays. CVs for commonly used reagents on specimens with abnormal protein C ranged from 15% to 24% for antigenic, 4% to 11% for chromogenic, and 10% to 17% for clot-based assays (averaged across 3 surveys). Some reagents were used by relatively few laboratories and therefore additional study may be needed for those reagents. For all commonly used reagents, biases were usually small and often not statistically significant. All assessed reagents were clinically accurate, and were considered acceptable options for a specialized coagulation laboratory.
C1 [Baron, Jason M.; Van Cott, Elizabeth M.] Harvard Univ, Dept Pathol, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA.
[Johnson, Stephen M.] Tufts Med Ctr, Dept Pathol, Boston, MA USA.
[Ledford-Kraemer, Marlies R.] CLOT ED, Islamorada, FL USA.
[Hayward, Catherine P.] McMaster Univ, Dept Pathol & Mol Med, Hamilton, ON, Canada.
[Hayward, Catherine P.] McMaster Univ, Dept Med, Hamilton, ON, Canada.
[Meijer, Piet] ECAT Fdn, Leiden, Netherlands.
RP Van Cott, EM (reprint author), Harvard Univ, Dept Pathol, Massachusetts Gen Hosp, Sch Med, GRJ 235,55 Fruit St, Boston, MA 02114 USA.
OI Hayward, Catherine/0000-0002-2843-0817
NR 8
TC 5
Z9 5
U1 0
U2 0
PU AMER SOC CLINICAL PATHOLOGY
PI CHICAGO
PA 2100 W HARRISON ST, CHICAGO, IL 60612 USA
SN 0002-9173
J9 AM J CLIN PATHOL
JI Am. J. Clin. Pathol.
PD JUN
PY 2012
VL 137
IS 6
BP 909
EP 915
DI 10.1309/AJCP8MWU4QSTCLPU
PG 7
WC Pathology
SC Pathology
GA 949KS
UT WOS:000304575700008
PM 22586050
ER
PT J
AU Sheehy, E
O'Connor, KJ
Luskin, RS
Howard, RJ
Cornell, D
Finn, J
Mone, T
Selck, FW
Delmonico, FL
AF Sheehy, E.
O'Connor, K. J.
Luskin, R. S.
Howard, R. J.
Cornell, D.
Finn, J.
Mone, T.
Selck, F. W.
Delmonico, F. L.
TI Investigating Geographic Variation in Mortality in the Context of Organ
Donation
SO AMERICAN JOURNAL OF TRANSPLANTATION
LA English
DT Article
DE Donation rate; donation service area; organ allocation; organ donation
ID UNITED-STATES; PROCUREMENT; TRANSPLANTATION; PERFORMANCE; DONORS; TRENDS
AB Organ procurement organizations (OPOs) report a nearly fourfold difference in donor availability as measured by eligible deaths per million population (PMP) based on hospital referrals. We analyzed whether mortality data help explain geographic variation in organ supply as measured by the number of eligible deaths for organ donation. Using the 2007 National Center for Health Statistics mortality data, we analyzed deaths occurring in acute care hospitals, aged = 70 years from cerebrovascular accidents and trauma. These deaths were mapped at the county level and compared to eligible deaths reported by OPOs. In 2007, there were 2 428 343 deaths reported in the United States with 42 339 in-hospital deaths = 70 years from cerebrovascular accidents (CVA) or trauma that were correlated with eligible deaths PMP (r2= 0.79.) Analysis revealed a broad range in the death rate across OPOs: trauma deaths: 44118 PMP; deaths from CVA: 34118 PMP; and combined CVA and trauma: 91229 PMP. Mortality data demonstrate that deaths by neurologic criteria of people who are likely to be suitable deceased donors are not evenly distributed across the nation. These deaths are correlated with eligible deaths for organ donation. Regional availability of organs is affected by deaths which should be accounted for in the organ allocation system.
C1 [Sheehy, E.; Luskin, R. S.] New England Organ Bank Inc, Waltham, MA USA.
[O'Connor, K. J.] LifeCtr NW, Bellevue, WA USA.
[Howard, R. J.; Cornell, D.] LifeQuest Organ Recovery Serv, Gainesville, FL USA.
[Finn, J.] Midwest Transplant Network, Westwood, KS USA.
[Mone, T.] OneLegacy, Los Angeles, CA USA.
[Selck, F. W.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Delmonico, F. L.] New England Organ Bank Inc, Boston, MA USA.
[Delmonico, F. L.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Sheehy, E (reprint author), New England Organ Bank Inc, Waltham, MA USA.
EM ellenhsheehy@gmail.com
NR 20
TC 14
Z9 14
U1 1
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1600-6135
J9 AM J TRANSPLANT
JI Am. J. Transplant.
PD JUN
PY 2012
VL 12
IS 6
BP 1598
EP 1602
DI 10.1111/j.1600-6143.2011.03981.x
PG 5
WC Surgery; Transplantation
SC Surgery; Transplantation
GA 948SM
UT WOS:000304522900031
PM 22443186
ER
PT J
AU Sheehan, WJ
Hoffman, EB
Fu, CX
Baxi, SN
Bailey, A
King, EM
Chapman, MD
Lane, JP
Gaffin, JM
Permaul, P
Gold, DR
Phipatanakul, W
AF Sheehan, William J.
Hoffman, Elaine B.
Fu, Chunxia
Baxi, Sachin N.
Bailey, Ann
King, Eva-Maria
Chapman, Martin D.
Lane, Jeffrey P.
Gaffin, Jonathan M.
Permaul, Perdita
Gold, Diane R.
Phipatanakul, Wanda
TI Endotoxin exposure in inner-city schools and homes of children with
asthma
SO ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY
LA English
DT Article
ID DAY-CARE-CENTERS; HOUSE-DUST ENDOTOXIN; ENVIRONMENTAL INTERVENTION;
AGE-CHILDREN; CHILDHOOD; ALLERGEN; WHEEZE; DETERMINANTS; COCKROACH;
SYMPTOMS
AB Background: Endotoxins are stimulators of the immune system and, despite their potential to protect against allergy, have been associated with early wheezing and asthma morbidity.
Objective: To compare inner-city school endotoxin exposure with home endotoxin exposure in children with asthma.
Methods: Students with asthma were recruited from 12 urban elementary schools. Settled and airborne dust samples, linked to enrolled students, were collected from school classrooms, gymnasiums, and cafeterias twice during the academic year. For comparison, settled dust was collected once from the bedrooms of students with asthma.
Results: Two hundred twenty-nine school settled dust samples and 118 bedroom settled dust samples were collected and analyzed for endotoxin. The median endotoxin concentration for school samples was 13.4 EU/mg (range, 0.7-360.7 EU/mg) and for home samples was 7.0 EU/mg (range = LLOD-843.0 EU/mg). The median concentration within each individual school varied from 6.6 EU/mg to 24.0 EU/mg. One hundred four students with asthma had matched classroom and bedroom endotoxin exposure measurements performed in the same season and demonstrated significantly higher concentrations of endotoxin in the students' classrooms (mean log value, 1.13 vs 0.99, P = .04). The median of the classrooms was 12.5 EU/mg compared with their bedrooms, with a median of 7.0 EU/mg. Within the school environment, no significant difference was seen between the fall and spring samples (mean log value 1.14 vs 1.09; P = .35).
Conclusion: Inner-city children with asthma were exposed to higher concentrations of endotoxin in their classrooms as compared with their bedrooms. Further studies are needed to evaluate school endotoxin exposure as a factor in asthma morbidity. (C) 2012 American College of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
C1 [Sheehan, William J.; Baxi, Sachin N.; Phipatanakul, Wanda] Childrens Hosp, Dept Pediat, Div Allergy & Immunol, Boston, MA 02115 USA.
[Sheehan, William J.; Baxi, Sachin N.; Gaffin, Jonathan M.; Permaul, Perdita; Gold, Diane R.; Phipatanakul, Wanda] Harvard Univ, Sch Med, Boston, MA USA.
[Hoffman, Elaine B.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Fu, Chunxia; Bailey, Ann; Gold, Diane R.; Phipatanakul, Wanda] Brigham & Womens Hosp, Channing Lab, Div Resp Epidemiol, Boston, MA 02115 USA.
[King, Eva-Maria; Chapman, Martin D.] Indoor Biotechnol Inc, Charlottesville, VA USA.
[Gaffin, Jonathan M.] Childrens Hosp, Dept Pediat, Div Pulmonol, Boston, MA 02115 USA.
[Permaul, Perdita] Massachusetts Gen Hosp, Div Pediat Allergy & Immunol, Boston, MA 02114 USA.
RP Phipatanakul, W (reprint author), Childrens Hosp, Dept Pediat, Div Allergy & Immunol, 300 Longwood Ave, Boston, MA 02115 USA.
EM wanda.phipatanakul@childrens.harvard.edu
FU Foundation of ACAAI; NIH [R01 AI 073964, R01 AI 073964-02S1]; Harvard
Catalyst Catalyst \ The Harvard Clinical and Translational Science
Center (NIH) [UL1 RR 025758]; Harvard University; [T32-AI-007512]
FX Foundation of ACAAI, Young Faculty Support Award (Dr. Phipatanakul) NIH
Grants: R01 AI 073964 and R01 AI 073964-02S1. Dr. Sheehan received
partial support from T32-AI-007512. This work was conducted with support
from Harvard Catalyst Catalyst vertical bar The Harvard Clinical and
Translational Science Center (NIH Award #UL1 RR 025758 and financial
contributions from Harvard University and its affiliated academic health
care centers). The content is solely the responsibility of the authors
and does not necessarily represent the official views of Harvard
Catalyst, Harvard University and its affiliated academic health care
centers, the National Center for Research Resources, or the National
Institutes of Health.
NR 31
TC 23
Z9 23
U1 3
U2 14
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1081-1206
J9 ANN ALLERG ASTHMA IM
JI Ann. Allergy Asthma Immunol.
PD JUN
PY 2012
VL 108
IS 6
BP 418
EP 422
DI 10.1016/j.anai.2012.04.003
PG 5
WC Allergy; Immunology
SC Allergy; Immunology
GA 948SC
UT WOS:000304521900008
PM 22626594
ER
PT J
AU Kradin, RL
Sheldon, TA
Nielsen, P
Selig, M
Hunt, J
AF Kradin, Richard L.
Sheldon, Thomas A.
Nielsen, Petur
Selig, Martin
Hunt, Jennifer
TI Malacoplakia of the tongue complicating the site of irradiation for
squamous cell carcinoma with review of the literature
SO ANNALS OF DIAGNOSTIC PATHOLOGY
LA English
DT Review
DE Malacoplakia; Gram-negative bacilli; Tongue; Infection; Macrophage
ID MALAKOPLAKIA; PATHOGENESIS
AB Malacoplakia is a benign and uncommon inflammatory response that develops most frequently in the genitourinary tract but has been reported at other sites. We report the case of 67-year-old man who presented with a lesion at the base of the tongue 7 months after chemoradiation for biopsy-proven invasive squamous cell carcinoma of the tongue. The lesion showed intense avidity by positron emission tomography and was biopsied with the putative clinical diagnosis of recurrent malignancy. Histologically, the lesion showed the characteristics of malacoplakia as well as abundant intracellular gram-negative bacilli. Ultrastructural analysis revealed giant lysosomes, intracytoplasmic calcific concretions (Michaelis-Gutman bodies), and partially digested gram-negative bacilli within vacuolated lysosomes of macrophages. To our knowledge, this is the seventh reported case of malacoplakia of the tongue and the first to develop at the site of prior radiation treatment of a carcinoma. The clinical features of this case, a review of previously reported cases, and a consideration of pathogenesis are presented. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Kradin, Richard L.; Nielsen, Petur; Selig, Martin; Hunt, Jennifer] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Kradin, Richard L.; Nielsen, Petur; Selig, Martin; Hunt, Jennifer] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Kradin, Richard L.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Sheldon, Thomas A.] Concord Hosp, Payson Ctr Canc Care, Concord, NH 03301 USA.
RP Kradin, RL (reprint author), Massachusetts Gen Hosp, Dept Pathol, Warren 253, Boston, MA 02114 USA.
EM rkradin@partners.org
NR 15
TC 2
Z9 2
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1092-9134
J9 ANN DIAGN PATHOL
JI Ann. Diagn. Pathol.
PD JUN
PY 2012
VL 16
IS 3
BP 214
EP 218
DI 10.1016/j.anndiagpath.2011.02.001
PG 5
WC Pathology
SC Pathology
GA 948GE
UT WOS:000304490800009
PM 21530340
ER
PT J
AU Zaman, K
Thurlimann, B
Huober, J
Schonenberger, A
Pagani, O
Luthi, J
Simcock, M
Giobbie-Hurder, A
Berthod, G
Genton, C
Brauchli, P
Aebi, S
AF Zaman, K.
Thuerlimann, B.
Huober, J.
Schoenenberger, A.
Pagani, O.
Luethi, J.
Simcock, M.
Giobbie-Hurder, A.
Berthod, G.
Genton, C.
Brauchli, P.
Aebi, S.
CA Swiss Grp Clinical Canc Res SAKK
TI Bone mineral density in breast cancer patients treated with adjuvant
letrozole, tamoxifen, or sequences of letrozole and tamoxifen in the BIG
1-98 study (SAKK 21/07)
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE aromatase inhibitors; BIG 1-98; bone; breast cancer; endocrine therapy;
tamoxifen
ID QUALITY-OF-LIFE; POSTMENOPAUSAL WOMEN; AROMATASE INHIBITOR;
RANDOMIZED-TRIAL; ANASTROZOLE; FRACTURES; OSTEOPOROSIS; COMBINATION;
EXEMESTANE; THERAPY
AB Background: The risk of osteoporosis and fracture influences the selection of adjuvant endocrine therapy. We analyzed bone mineral density (BMD) in Swiss patients of the Breast International Group (BIG) 1-98 trial [treatment arms: A, tamoxifen (T) for 5 years; B, letrozole (L) for 5 years; C, 2 years of T followed by 3 years of L; D, 2 years of L followed by 3 years of T].
Patients and methods: Dual-energy X-ray absorptiometry (DXA) results were retrospectively collected. Patients without DXA served as control group. Repeated measures models using covariance structures allowing for different times between DXA were used to estimate changes in BMD. Prospectively defined covariates were considered as fixed effects in the multivariable models.
Results: Two hundred and sixty-one of 546 patients had one or more DXA with 577 lumbar and 550 hip measurements. Weight, height, prior hormone replacement therapy, and hysterectomy were positively correlated with BMD; the correlation was negative for letrozole arms (B/C/D versus A), known osteoporosis, time on trial, age, chemotherapy, and smoking. Treatment did not influence the occurrence of osteoporosis (T score < -2.5 standard deviation).
Conclusions: All aromatase inhibitor regimens reduced BMD. The sequential schedules were as detrimental for bone density as L monotherapy.
C1 [Zaman, K.; Berthod, G.] Univ Hosp, CePO, Breast Ctr, Lausanne, Switzerland.
[Thuerlimann, B.; Huober, J.] Kantonsspital, Breast Ctr, St Gallen, Switzerland.
[Schoenenberger, A.] Kantonsspital, Dept Oncol, Aarau, Switzerland.
[Pagani, O.] Osped Italiano, Oncol Inst So Switzerland, Lugano, Switzerland.
[Luethi, J.] Hosp Thun, Dept Oncol, Bern, Switzerland.
[Simcock, M.; Genton, C.; Brauchli, P.] SAKK Coordinating Ctr, Bern, Switzerland.
[Giobbie-Hurder, A.] Dana Farber Canc Inst, Ctr Stat, Int Breast Canc Study Grp, Boston, MA 02115 USA.
[Aebi, S.] Univ Hosp, Div Med Oncol, Bern, Switzerland.
RP Zaman, K (reprint author), Univ Hosp CHUV, Multidisciplinary Ctr Oncol, 46 Rue Bugnon, CH-1011 Lausanne, Switzerland.
EM Khalil.Zaman@chuv.ch
RI Aebi, Stefan/F-2004-2010
OI Aebi, Stefan/0000-0002-3383-9449
FU State Secretariat for Education and Research (SER); Novartis
Switzerland; Novartis
FX State Secretariat for Education and Research (SER); Novartis
Switzerland.; The following authors have declared conflict of
interest-BT: stock of Novartis, travel grant for educational activities
from Novartis, and honorarium from Astrazeneca for educational
activities; JH: advisory relationship with Novartis and Astrazeneca and
honorarium from Novartis and Astrazeneca. The following authors have
declared no conflict of interest: KZ, AS, OP, JL, MS, AG-H, GB, CG, PB,
and SA.
NR 39
TC 11
Z9 11
U1 1
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD JUN
PY 2012
VL 23
IS 6
BP 1474
EP +
DI 10.1093/annonc/mdr448
PG 8
WC Oncology
SC Oncology
GA 948WO
UT WOS:000304534000016
PM 22003243
ER
PT J
AU Heng, DY
MacKenzie, MJ
Vaishampayan, UN
Bjarnason, GA
Knox, JJ
Tan, MH
Wood, L
Wang, Y
Kollmannsberger, C
North, S
Donskov, F
Rini, BI
Choueiri, TK
AF Heng, D. Y.
MacKenzie, M. J.
Vaishampayan, U. N.
Bjarnason, G. A.
Knox, J. J.
Tan, M. H.
Wood, L.
Wang, Y.
Kollmannsberger, C.
North, S.
Donskov, F.
Rini, B. I.
Choueiri, T. K.
TI Primary anti-vascular endothelial growth factor (VEGF)-refractory
metastatic renal cell carcinoma: clinical characteristics, risk factors,
and subsequent therapy
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE primary refractory; renal cell carcinoma; VEGF; mTOR
ID PHASE-III TRIAL; DOUBLE-BLIND; SORAFENIB; SUNITINIB
AB Background: A subset of patients treated with initial anti-vascular endothelial growth factor (VEGF) therapy exhibit progressive disease (PD) as the best response per RECIST criteria.
Methods: Data from patients with metastatic renal cell carcinoma (mRCC) treated with anti-VEGF therapy were collected through the International mRCC Database Consortium from 12 centers.
Results: One thousand and fifty-six assessable patients received initial VEGF inhibitors and 272 (26%) of these patients had PD as best response. Initial treatment included sunitinib (n = 203), sorafenib (n = 51), or bevacizumab (n = 18). Six percent of patients were at favorable risk, 55% at intermediate risk, and 39% at poor risk. On multivariable analysis, predictors of PD were Karnofsky performance status < 80% [odds ratio (OR) = 2.3, P < 0.0001], diagnosis to treatment < 1 year (OR = 2.1, P < 0.0001), neutrophilia (OR = 1.9, P = 0.0021), thrombocytosis (OR = 1.7, P = 0.0068), and anemia (OR = 1.6, P = 0.0058). Median progression-free survival (PFS) in patients with PD versus without PD was 2.4 versus 11 months (P < 0.0001) and overall survival (OS) was 6.8 versus 29 months (P < 0.0001), respectively. One hundred and eight (40%) VEGF-refractory patients proceeded to receive further systemic therapies. Response rate, PFS, and OS for subsequent therapy were 9%, 2.5 months, and 7.4 months, respectively, with no statistical differences between patients who received VEGF versus mammalian target of rapamycin (mTOR) inhibitors.
Conclusions: Primary anti-VEGF-refractory mRCC patients have a dismal prognosis. Second-line anti-mTOR and anti-VEGF agents produce similar outcomes.
C1 [Heng, D. Y.; Wang, Y.] Univ Calgary, Dept Med Oncol, Tom Baker Canc Ctr, Alberta Hlth Serv Canc Care, Calgary, AB T2N 4N2, Canada.
[MacKenzie, M. J.] London Reg Hlth Sci Ctr, Dept Oncol, London, ON, Canada.
[Vaishampayan, U. N.] Karmanos Canc Inst, Dept Oncol, Detroit, MI USA.
[Bjarnason, G. A.] Sunnybrook Odette Canc Ctr, Dept Oncol, Toronto, ON, Canada.
[Knox, J. J.] Princess Margaret Hosp, Dept Med Oncol, Toronto, ON M4X 1K9, Canada.
[Tan, M. H.] Natl Canc Ctr, Inst Bioengn & Nanotechnol, Dept Oncol, Singapore, Singapore.
[Wood, L.] Queen Elizabeth 2 Hlth Sci Ctr, Dept Oncol, Halifax, NS, Canada.
[Kollmannsberger, C.] BC Canc Agcy, Dept Oncol, Vancouver, BC, Canada.
[North, S.] Univ Alberta, Dept Oncol, Alberta Hlth Serv Canc Care, Cross Canc Inst, Edmonton, AB, Canada.
[Donskov, F.] Aarhus Univ Hosp, Dept Oncol, DK-8000 Aarhus, Denmark.
[Rini, B. I.] Cleveland Clin Taussig Canc Inst, Dept Solid Tumor Oncol, Cleveland, OH USA.
[Choueiri, T. K.] Brigham & Womens Hosp, Dana Farber Canc Inst, Kidney Canc Ctr, Boston, MA 02115 USA.
[Choueiri, T. K.] Harvard Univ, Sch Med, Boston, MA USA.
RP Heng, DY (reprint author), Univ Calgary, Dept Med Oncol, Tom Baker Canc Ctr, Alberta Hlth Serv Canc Care, 1331-29th St NW, Calgary, AB T2N 4N2, Canada.
EM daniel.heng@albertahealthservices.ca
OI Bjarnason, Georg Arnold/0000-0001-6903-5357; Donskov,
Frede/0000-0002-8449-863X
FU Pfizer; Novartis; Bayer
FX DYH, JJK, GAB, CK, SN have received consulting honoraria from Pfizer and
Novartis. JK, FD, GB, BR, TC have received research funding from Pfizer
and Novartis. JK has received research funding from Bayer. This project
received no direct or indirect industry or pharmaceutical company
funding. The other authors declare no conflicts of interest.
NR 20
TC 52
Z9 55
U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD JUN
PY 2012
VL 23
IS 6
BP 1549
EP +
DI 10.1093/annonc/mdr533
PG 7
WC Oncology
SC Oncology
GA 948WO
UT WOS:000304534000028
PM 22056973
ER
PT J
AU Said, SM
Ashikhmina, E
Greason, KL
Suri, RM
Park, SJ
Daly, RC
Burkhart, HM
Dearani, JA
Sundt, TM
Schaff, HV
AF Said, Sameh M.
Ashikhmina, Elena
Greason, Kevin L.
Suri, Rakesh M.
Park, Soon J.
Daly, Richard C.
Burkhart, Harold M.
Dearani, Joseph A.
Sundt, Thoralf M., III
Schaff, Hartzell V.
TI Do Pericardial Bioprostheses Improve Outcome of Elderly Patients
Undergoing Aortic Valve Replacement?
SO ANNALS OF THORACIC SURGERY
LA English
DT Article
ID PORCINE; BOVINE; DURABILITY; PERIMOUNT; SIZE
AB Background. Pericardial bioprostheses have favorable echocardiographic hemodynamics in the aortic position compared with porcine valves; however, there are few data comparing clinical outcomes. Our objective was to assess the late results of the two valve types.
Methods. We reviewed 2,979 patients aged 65 years or older undergoing aortic valve replacement with pericardial (n = 1,976) or porcine (n = 1,003) prostheses between January 1993 and December 2007. The most common pericardial prostheses were Carpentier-Edwards Perimount and Mitroflow, and the most common porcine valves were Medtronic Mosaic, Carpentier-Edwards, Hancock modified orifice, and St. Jude Biocor. Follow-up extended to a maximum of 16 years (mean, 5.2 +/- 3.5 years).
Results. Survival at 5, 10 and 12 years was, respectively, 68%, 33%, and 21% overall, was 68%, 30%, and 16% for patients with pericardial bioprosthesis, and was 69%, 38% and 27% for the porcine group. In a multivariate model, long-term survival was reduced in patients with diabetes, renal failure, prior myocardial infarction, congestive heart failure, and older age, but late survival was not higher in the pericardial valve group. Overall freedom from reoperation was 96%, 92%, and 90% at 5, 10, and 12 years, and freedom from explant was 98%, 96%, and 94% during the same period. The reason for explant was structural valve deterioration in 50 patients (2%).
Conclusions. Despite the better hemodynamic performance documented in prior investigations, pericardial valves do not confer any survival advantage over porcine valves in patients aged 65 years or older undergoing aortic valve replacement. (Ann Thorac Surg 2012;93:1868-75) (C) 2012 by The Society of Thoracic Surgeons
C1 [Said, Sameh M.] Mayo Clin, Div Cardiovasc Surg, Rochester, MN 55905 USA.
Massachusetts Gen Hosp, Div Cardiac Surg, Boston, MA 02114 USA.
Brigham & Womens Hosp, Div Anesthesia, Boston, MA 02115 USA.
RP Said, SM (reprint author), Mayo Clin, Div Cardiovasc Surg, 200 1st St SW, Rochester, MN 55905 USA.
EM schaft@mayo.edu
OI Schaff, Hartzell/0000-0003-0994-027X
NR 17
TC 11
Z9 11
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-4975
J9 ANN THORAC SURG
JI Ann. Thorac. Surg.
PD JUN
PY 2012
VL 93
IS 6
BP 1868
EP 1875
DI 10.1016/j.athoracsur.2012.01.061
PG 8
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 947VG
UT WOS:000304460000026
PM 22440366
ER
PT J
AU Cervera, R
Bakaeen, FG
Cornwell, LD
Wang, XL
Coselli, JS
LeMaire, SA
Chu, D
AF Cervera, Roberto
Bakaeen, Faisal G.
Cornwell, Lorraine D.
Wang, Xing Li
Coselli, Joseph S.
LeMaire, Scott A.
Chu, Danny
TI Impact of Functional Status on Survival After Coronary Artery Bypass
Grafting in a Veteran Population
SO ANNALS OF THORACIC SURGERY
LA English
DT Article
ID AORTIC-VALVE-REPLACEMENT; HIGH-RISK PATIENTS; CARDIAC-SURGERY; LATE
MORTALITY; FRAILTY; OLDER; OUTCOMES; AGE; DISEASE; INDEX
AB Background. Although functional impairment has been shown to be an adverse outcome of frailty, little is known of its effect on patients after cardiac operations. We aimed to assess the effect of limited functional status on long-term survival after coronary artery bypass grafting (CABG).
Methods. We reviewed prospectively gathered data from 1,503 consecutive patients who underwent isolated CABG between 1997 and 2009. We compared the outcomes of 318 patients with limited functional status and 1,185 patients without any functional impairment. The mean follow-up period was 65 months (range, 1 to 157 months). We assessed the relationship between functional status impairment and long-term survival by Cox regression analysis adjusted for confounding factors.
Results. Functionally impaired patients were slightly older (63 +/- 9 vs 62 +/- 8 years, p = 0.05) and had more risk factors for adverse outcomes than patients who were functionally unimpaired. After adjustment for potential confounding variables by multivariate logistic regression analysis, preoperative limited functional status was not an independent predictor (odds ratio [95% confidence interval]) of 30-day mortality (1.4 [0.3 to 5.8], p = 0.67) or major adverse cardiac events (1.3 [0.5 to 3.3], p = 0.71), nor was it predictive of reduced long-term survival (10-year hazard ratio 1.0 [0.7 to 1.4], p = 0.85).
Conclusions. Limited functional status was not an independent risk factor for early postoperative complications or death. Long-term survival in patients whose functional status was impaired before they underwent CABG was similar to that of patients who were functionally independent.
C1 [Chu, Danny] Baylor Coll Med, Texas Heart Inst, Michael E DeBakey Vet Affairs Med Ctr, Div Cardiothorac Surg, Houston, TX 77030 USA.
Baylor Coll Med, Michael E DeBakey Dept Surg, Div Cardiothorac Surg, Houston, TX 77030 USA.
St Lukes Episcopal Hosp, Texas Heart Inst, Div Cardiovasc Surg, Houston, TX USA.
RP Chu, D (reprint author), Baylor Coll Med, Texas Heart Inst, Michael E DeBakey Vet Affairs Med Ctr, Div Cardiothorac Surg, 2002 Holcombe Blvd,OCL 112, Houston, TX 77030 USA.
EM dchu@bcm.edu
NR 21
TC 6
Z9 6
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-4975
J9 ANN THORAC SURG
JI Ann. Thorac. Surg.
PD JUN
PY 2012
VL 93
IS 6
BP 1950
EP 1955
DI 10.1016/j.athoracsur.2012.02.071
PG 6
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 947VG
UT WOS:000304460000038
PM 22560262
ER
PT J
AU Carrick, R
Ge, L
Lee, LC
Zhang, ZH
Mishra, R
Axel, L
Guccione, JM
Grossi, EA
Ratcliffe, MB
AF Carrick, Richard
Ge, Liang
Lee, Lik Chuan
Zhang, Zhihong
Mishra, Rakesh
Axel, Leon
Guccione, Julius M.
Grossi, Eugene A.
Ratcliffe, Mark B.
TI Patient-Specific Finite Element-Based Analysis of Ventricular Myofiber
Stress After Coapsys: Importance of Residual Stress
SO ANNALS OF THORACIC SURGERY
LA English
DT Article
ID ISCHEMIC MITRAL REGURGITATION; VOLUME REDUCTION SURGERY; DILATED
CARDIOMYOPATHY; PAPILLARY-MUSCLE; REPAIR TECHNIQUE; ANNULOPLASTY; VALVE;
MODEL
AB Background. We sought to determine regional myofiber stress after Coapsys device (Myocor, Inc, Maple Grove, MN) implantation using a finite element model of the left ventricle (LV). Chronic ischemic mitral regurgitation is caused by LV remodeling after posterolateral myocardial infarction. The Coapsys device consists of a single trans-LV chord placed below the mitral valve such that when tensioned it alters LV shape and decreases chronic ischemic mitral regurgitation.
Methods. Finite element models of the LV were based on magnetic resonance images obtained before (preoperatively) and after (postoperatively) coronary artery bypass grafting with Coapsys implantation in a single patient. To determine the effect of Coapsys and LV before stress, virtual Coapsys was performed on the preoperative model. Diastolic and systolic material variables in the preoperative, postoperative, and virtual Coapsys models were adjusted so that model LV volume agreed with magnetic resonance imaging data. Chronic ischemic mitral regurgitation was abolished in the postoperative models. In each case, myofiber stress and pump function were calculated.
Results. Both postoperative and virtual Coapsys models shifted end-systolic and end-diastolic pressure-volume relationships to the left. As a consequence and because chronic ischemic mitral regurgitation was reduced after Coapsys, pump function was unchanged. Coapsys decreased myofiber stress at end-diastole and end-systole in both the remote and infarct regions of the myocardium. However, knowledge of Coapsys and LV prestress was necessary for accurate calculation of LV myofiber stress, especially in the remote zone.
Conclusions. Coapsys decreases myofiber stress at end-diastole and end-systole. The improvement in myofiber stress may contribute to the long-term effect of Coapsys on LV remodeling.
C1 Univ Vermont, Coll Med, Burlington, VT USA.
Univ Calif San Francisco, Dept Surg, San Francisco, CA USA.
Univ Calif San Francisco, Dept Bioengn, San Francisco, CA 94143 USA.
Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
Vet Affairs Med Ctr, San Francisco, CA 94121 USA.
NYU, Dept Cardiothorac Surg, New York, NY USA.
NYU, Dept Radiol, New York, NY 10016 USA.
New York Harbor Vet Affairs Med Ctr, New York, NY USA.
RP Ratcliffe, MB (reprint author), San Francisco VA Med Ctr, Surg Serv 112, 4150 Clement St, San Francisco, CA 94121 USA.
EM mark.ratclifte@va.gov
OI GROSSI, eugene/0000-0002-2066-7035; Axel, Leon/0000-0003-0608-4690
FU NIH [R01-HL084431, R01-HL077921, R01-HL086400]; University of Vermont
FX This study was supported by NIH grants R01-HL084431 (M.B.R.),
R01-HL077921 (J.M.G.), and R01-HL086400 (J.M.G.). RC. was supported by a
Summer Research Fellowship from the University of Vermont. This support
is gratefully acknowledged.
NR 30
TC 14
Z9 14
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-4975
J9 ANN THORAC SURG
JI Ann. Thorac. Surg.
PD JUN
PY 2012
VL 93
IS 6
BP 1964
EP 1971
DI 10.1016/j.athoracsur.2012.03.001
PG 8
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 947VG
UT WOS:000304460000040
PM 22560323
ER
PT J
AU Jernigan, MG
Press, EG
Nguyen, MH
Clancy, CJ
Shields, RK
AF Jernigan, Meredith G.
Press, Ellen G.
Nguyen, M. Hong
Clancy, Cornelius J.
Shields, Ryan K.
TI The Combination of Doripenem and Colistin Is Bactericidal and
Synergistic against Colistin-Resistant, Carbapenemase-Producing
Klebsiella pneumoniae
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID RISK-FACTORS; INFECTION; OUTCOMES; PHARMACOKINETICS; ACQUISITION;
PREDICTORS; MORTALITY; IMPACT
AB We tested two-drug combinations of doripenem, colistin, gentamicin, and doxycycline against 12 carbapenemase-producing Klebsiella pneumoniae (KPC) isolates by time-kill. The combination of doripenem and colistin reduced the starting inocula by 2 logs for each isolate (range, 2.02 to 6.01 log(10)) and was bactericidal and synergistic against 75 and 50%, respectively. Among colistin- and pan-drug-resistant isolates, synergy was identified in 60 and 67%, respectively. All other combinations were inferior. We are currently evaluating the combination of doripenem and colistin as a frontline therapy for KPC infection.
C1 [Press, Ellen G.; Nguyen, M. Hong; Clancy, Cornelius J.; Shields, Ryan K.] Univ Pittsburgh, Dept Med, Pittsburgh, PA 15260 USA.
[Jernigan, Meredith G.] Univ Pittsburgh, Dept Pharm & Therapeut, Pittsburgh, PA USA.
[Clancy, Cornelius J.] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
RP Clancy, CJ (reprint author), Univ Pittsburgh, Dept Med, Pittsburgh, PA 15260 USA.
EM cjc76@pitt.edu
FU National Center for Research Resources [KL2 RR024154]
FX The project described was supported by award number KL2 RR024154 from
the National Center for Research Resources to R.K.S.
NR 24
TC 37
Z9 43
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD JUN
PY 2012
VL 56
IS 6
BP 3395
EP 3398
DI 10.1128/AAC.06364-11
PG 4
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA 947LZ
UT WOS:000304432800082
PM 22430958
ER
PT J
AU Roemer, FW
Kwoh, CK
Hannon, MJ
Green, SM
Jakicic, JM
Boudreau, R
Crema, MD
Moore, CE
Guermazi, A
AF Roemer, Frank W.
Kwoh, C. Kent
Hannon, Michael J.
Green, Stephanie M.
Jakicic, John M.
Boudreau, Robert
Crema, Michel D.
Moore, Carolyn E.
Guermazi, Ali
TI Risk factors for magnetic resonance imaging-detected patellofemoral and
tibiofemoral cartilage loss during a six-month period: The Joints On
Glucosamine study
SO ARTHRITIS AND RHEUMATISM
LA English
DT Article
ID SYMPTOMATIC KNEE OSTEOARTHRITIS; RADIOGRAPHIC OSTEOARTHRITIS; DISEASE
PROGRESSION; MULTICENTER OSTEOARTHRITIS; MENISCAL EXTRUSION;
NATURAL-HISTORY; ASSOCIATION; FRAMINGHAM; SYNOVITIS; VOLUME
AB Objective To assess several baseline risk factors that may predict patellofemoral and tibiofemoral cartilage loss during a 6-month period. Methods For 177 subjects with chronic knee pain, 3T magnetic resonance imaging (MRI) of both knees was performed at baseline and followup. Knees were semiquantitatively assessed, evaluating cartilage morphology, subchondral bone marrow lesions, meniscal morphology/extrusion, synovitis, and effusion. Age, sex, and body mass index (BMI), bone marrow lesions, meniscal damage/extrusion, synovitis, effusion, and prevalent cartilage damage in the same subregion were evaluated as possible risk factors for cartilage loss. Logistic regression models were applied to predict cartilage loss. Models were adjusted for age, sex, treatment, and BMI. Results Seventy-nine subregions (1.6%) showed incident or worsening cartilage damage at followup. None of the demographic risk factors was predictive of future cartilage loss. Predictors of patellofemoral cartilage loss were effusion, with an adjusted odds ratio (OR) of 3.5 (95% confidence interval [95% CI] 1.39.4), and prevalent cartilage damage in the same subregion with an adjusted OR of 4.3 (95% CI 1.314.1). Risk factors for tibiofemoral cartilage loss were baseline meniscal extrusion (adjusted OR 3.6 [95% CI 1.310.1]), prevalent bone marrow lesions (adjusted OR 4.7 [95% CI 1.119.5]), and prevalent cartilage damage (adjusted OR 15.3 [95% CI 4.947.4]). Conclusion Cartilage loss over 6 months is rare, but may be detected semiquantitatively by 3T MRI and is most commonly observed in knees with Kellgren/Lawrence grade 3. Predictors of patellofemoral cartilage loss were effusion and prevalent cartilage damage in the same subregion. Predictors of tibiofemoral cartilage loss were prevalent cartilage damage, bone marrow lesions, and meniscal extrusion.
C1 [Roemer, Frank W.] Boston Univ, Med Ctr, Dept Radiol, Quantitat Imaging Ctr, Boston, MA 02118 USA.
[Roemer, Frank W.] Klinikum Augsburg, Augsburg, Germany.
[Kwoh, C. Kent; Hannon, Michael J.; Green, Stephanie M.; Jakicic, John M.; Boudreau, Robert] Univ Pittsburgh, Pittsburgh, PA USA.
[Kwoh, C. Kent] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Crema, Michel D.] Inst Diagnost Imaging, Ribeirao Preto, Brazil.
[Crema, Michel D.] Univ Sao Paulo, BR-14049 Ribeirao Preto, Brazil.
[Moore, Carolyn E.] Texas Womans Univ, Houston, TX USA.
RP Roemer, FW (reprint author), Boston Univ, Med Ctr, Dept Radiol, Quantitat Imaging Ctr, FGH Bldg,3rd Floor,820 Harrison Ave, Boston, MA 02118 USA.
EM froemer@bu.edu
OI Boudreau, Robert/0000-0003-0162-5187
FU Beverage Institute for Health & Wellness, the Coca Cola Company;
Multidisciplinary Clinical Research Center for Musculoskeletal and Skin
Diseases at the University of Pittsburgh (NIH/National Institute of
Arthritis and Musculoskeletal and Skin Diseases) [P60]; Beverage
Institute for Health Wellness; Jenny Craig; Alere Wellbeing; Facet
Solutions; Genzyme; Stryker; Merck Serono; AstraZeneca; General Electric
Healthcare
FX The Joints On Glucosamine study is funded by a grant from the Beverage
Institute for Health & Wellness, the Coca Cola Company. The statistical
analysis was partially supported by the Multidisciplinary Clinical
Research Center for Musculoskeletal and Skin Diseases at the University
of Pittsburgh (NIH/National Institute of Arthritis and Musculoskeletal
and Skin Diseases P60 grant).; Drs. Roemer and Guermazi own stock or
stock options in Boston Imaging Core Lab; Dr. Roemer is vice president
and Dr. Guermazi is president of Boston Imaging Core Lab. Dr. Kwoh has
received a research grant from the Beverage Institute for Health &
Wellness. Dr. Jakicic has received consulting fees, speaking fees,
and/or honoraria from Jenny Craig and Alere Wellbeing (less than $10,000
each). Dr. Crema owns stock or stock options in Boston Imaging Core Lab.
Dr. Guermazi has received consulting fees, speaking fees, and/or
honoraria from Facet Solutions, Genzyme, and Stryker (less than $10,000
each) and from Merck Serono and AstraZeneca (more than $10,000 each) and
has received a research grant from General Electric Healthcare.
NR 51
TC 29
Z9 29
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD JUN
PY 2012
VL 64
IS 6
BP 1888
EP 1898
DI 10.1002/art.34353
PG 11
WC Rheumatology
SC Rheumatology
GA 948SE
UT WOS:000304522100022
PM 22213129
ER
PT J
AU Washington, S
Caughey, AB
Cheng, YW
Bryant, AS
AF Washington, Sierra
Caughey, Aaron B.
Cheng, Yvonne W.
Bryant, Allison S.
TI Racial and Ethnic Differences in Indication for Primary Cesarean
Delivery at Term: Experience at One U.S. Institution
SO BIRTH-ISSUES IN PERINATAL CARE
LA English
DT Article
DE cesarean delivery; disparity; race and ethnicity
ID HEALTH-CARE BENEFICIARIES; US MILITARY HOSPITALS; BREECH PRESENTATION;
SECTION DELIVERY; RATES; RISK; RACE; POPULATION; CALIFORNIA; PREMIUMS
AB Background Black and Latina women in the United States are known to undergo cesarean delivery at a higher rate than other women. We sought to explore the role of medical indications for cesarean delivery as a potential explanation for these differences. Methods A retrospective cohort study was conducted of 11,034 primiparas delivering at term at the University of California, San Francisco, between 1990 and 2008. We used multivariable analyses to evaluate racial and ethnic differences in risks of, and indications for, cesarean delivery. Results The overall rate of cesarean delivery in our cohort was 21.9 percent. Black and Latina women were at significantly higher odds of undergoing cesarean delivery than white women (adjusted odds ratio or AOR: 1.54; 95% CI: 1.30, 1.83, and 1.21; 95% CI: 1.03, 1.43, respectively). Black women were at significantly higher odds of undergoing cesarean delivery for nonreassuring fetal heart tracings than white women (AOR: 2.19; 95% CI: 1.55, 3.09), and black women (AOR: 1.55; 95% CI: 1.21, 1.98), Latina women (AOR: 1.48; 95% CI: 1.19, 1.85), and Asian women (AOR: 1.47; 95% CI: 1.22, 1.85) were at significantly higher odds of undergoing cesarean delivery for failure to progress. Black, Latina, and Asian women were at significantly lower odds of undergoing cesarean delivery for malpresentation than white women (AOR: 0.56; 95% CI: 0.34, 0.89, 0.66; 95% CI: 0.44, 0.98, and 0.55; 95% CI: 0.40, 0.76, respectively). Conclusions Racial and ethnic differences exist in specific indications for cesarean delivery among primiparas. Clarifying the possible reasons for increased cesareans for nonreassuring fetal heart tracing in black women, in particular, may help to decrease excess cesarean deliveries in this racial and ethnic group. (BIRTH 39:2 June 2012)
C1 [Washington, Sierra; Caughey, Aaron B.; Cheng, Yvonne W.; Bryant, Allison S.] Massachusetts Gen Hosp, Dept Obstet & Gynecol, Boston, MA 02114 USA.
[Caughey, Aaron B.] Oregon Hlth & Sci Univ, Dept Obstet & Gynecol, Portland, OR 97201 USA.
[Cheng, Yvonne W.] Univ Calif San Francisco, Dept Obstet Gynecol & Reprod Sci, San Francisco, CA USA.
[Bryant, Allison S.] Massachusetts Gen Hosp, Vincent Dept Obstet & Gynecol, Boston, MA 02114 USA.
[Washington, Sierra] Indiana Univ, Dept Obstet & Gynecol, Indianapolis, IN USA.
RP Bryant, AS (reprint author), Massachusetts Gen Hosp, Dept Obstet & Gynecol, 55 Fruit St,Founders 4, Boston, MA 02114 USA.
FU National Institutes of Health (NIH/NCRR/OD UCSF-CTSI), Washington, DC
[KL2 RR024130]; Robert Wood Johnson Foundation, Princeton, New Jersey,
United States of America [RWJF-63524, RWJF-61535]
FX Funding for this publication was supported by grants from the National
Institutes of Health (NIH/NCRR/OD UCSF-CTSI Grant No. KL2 RR024130),
Washington, DC, and from the Amos Medical Faculty Development Award of
the Robert Wood Johnson Foundation (Grant No. RWJF-63524), Princeton,
New Jersey, United States of America, to Dr Allison Bryant. Dr Aaron
Caughey is supported by the Robert Wood Johnson Foundation as a
Physician Faculty Scholar (Grant No. RWJF-61535), Princeton, New Jersey,
United States of America.
NR 37
TC 15
Z9 15
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0730-7659
J9 BIRTH-ISS PERINAT C
JI Birth-Issue Perinat. Care
PD JUN
PY 2012
VL 39
IS 2
BP 128
EP 134
PG 7
WC Nursing; Obstetrics & Gynecology; Pediatrics
SC Nursing; Obstetrics & Gynecology; Pediatrics
GA 949SY
UT WOS:000304597400006
PM 23281861
ER
PT J
AU Wu, AHB
Lorizio, W
Tchu, S
Lynch, K
Gerona, R
Ji, WY
Ruan, WM
Ruddy, KJ
Desantis, SD
Burstein, HJ
Ziv, E
AF Wu, Alan H. B.
Lorizio, Wendy
Tchu, Simone
Lynch, Kara
Gerona, Roy
Ji, Wuyang
Ruan, Weiming
Ruddy, Kathryn J.
Desantis, Stephen D.
Burstein, Harold J.
Ziv, Elad
TI Estimation of tamoxifen metabolite concentrations in the blood of breast
cancer patients through CYP2D6 genotype activity score
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Breast cancer; Tamoxifen; Endoxifen; Genotype; Activity score; CYP2D6
ID THERAPY; WOMEN; PHARMACOGENOMICS; POLYMORPHISMS; PERFORMANCE; EXPOSURE;
OUTCOMES; IMPACT
AB Tamoxifen, a prodrug used for adjuvant breast cancer therapy, requires conversion to the active metabolite endoxifen through CYP 2D6. We aimed to construct an algorithm to predict endoxifen concentrations based on a patient's CYP 2D6 genotype, demographic factors, and co-medication use. Eighty-eight women enrolled in the UCSF TamGen II study and 81 women enrolled in a prospective study at Dana-Farber Cancer Institute were included in this analysis. All the women had been on tamoxifen for at least 3 months before blood collection. Demographic information included the patient's age, race/ethnicity, body mass index (where available), and self-reported and measured medications and herbals that affect 2D6 activity. DNA was extracted and genotyped for 2D6 (Amplichip, Roche Diagnostics). An activity score was calculated based on genotypes and adjusted for use of medications known to inhibit 2D6. Serum was tested for tamoxifen and metabolite concentrations and for the presence of drugs by liquid chromatography/mass spectrometry. Univariate and multivariate regression analysis were computed for age, body mass index, ethnicity, and adjusted activity score to predict tamoxifen metabolite concentrations in the training data-set of UCSF patients, and the resulting algorithm was validated in the Dana-Farber patients. For the training set, the correlation coefficient (r (2)) for log endoxifen and N-desmethyltamoxifen:endoxifen ratio to activity score, age, and race, were 0.520 and 0.659, respectively; 0.324 and 0.567 for the validation; and 0.396 and 0.615 for both the datasets combined. An algorithm that incorporates genotype and demographic variables can be used to predict endoxifen concentrations for women on tamoxifen therapy. If endoxifen levels are confirmed to be predictive of tamoxifen benefit, then this algorithm may be helpful to determine which women warrant endoxifen testing.
C1 [Wu, Alan H. B.; Tchu, Simone; Lynch, Kara; Gerona, Roy; Ji, Wuyang; Ruan, Weiming] San Francisco Gen Hosp, Dept Lab Med, San Francisco, CA 94110 USA.
[Lorizio, Wendy; Ziv, Elad] Univ Calif San Francisco, Div Gen Internal Med, San Francisco, CA 94143 USA.
[Ruddy, Kathryn J.; Desantis, Stephen D.; Burstein, Harold J.] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Wu, AHB (reprint author), San Francisco Gen Hosp, Dept Lab Med, 1001 Potrero Ave,Room 2M27, San Francisco, CA 94110 USA.
EM wualan@labmed2.ucsf.edu; wlorizio@medicine.ucsf.edu;
Simone.Tchu@ucsf.edu; kara.lynch@ucsf.edu; Roy.Gerona@ucsf.edu;
jiwuyang5@gmail.com; weiming0603@gmail.com; kruddy@partners.org;
Stephen_Desantis@dfci.harvard.edu; hal_burstein@dfci.harvard.edu;
elad.ziv@ucsf.edu
RI Ziv, Elad/L-5396-2014
FU NCI NIH HHS [R01 CA120120]
NR 23
TC 10
Z9 10
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD JUN
PY 2012
VL 133
IS 2
BP 677
EP 683
DI 10.1007/s10549-012-1963-2
PG 7
WC Oncology
SC Oncology
GA 949XJ
UT WOS:000304610600026
PM 22294487
ER
PT J
AU Metcalfe, KA
Mian, N
Enmore, M
Poll, A
Llacuachaqui, M
Nanda, S
Sun, P
Hughes, KS
Narod, SA
AF Metcalfe, Kelly A.
Mian, Nida
Enmore, Melissa
Poll, Aletta
Llacuachaqui, Marcia
Nanda, Sonia
Sun, Ping
Hughes, Kevin S.
Narod, Steven A.
TI Long-term follow-up of Jewish women with a BRCA1 and BRCA2 mutation who
underwent population genetic screening
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE BRCA1; BRCA2; Breast cancer Genetic testing; Jewish
ID HEREDITARY BREAST-CANCER; PROPHYLACTIC SURGERY; FOUNDER MUTATIONS;
OVARIAN-CANCER; INCREASED RISK; EVENT SCALE; IMPACT; DISTRESS; CARRIERS;
SURVEILLANCE
AB There are two mutations in BRCA1 and one in BRCA2, which are present in up to 2.5% of Jewish women. Population genetic testing for Jewish women has been proposed; however, it is unclear how this would impact the uptake of cancer prevention options and psychosocial functioning in women with a positive result. Two thousand and eighty unselected Jewish women were tested for the Jewish BRCA mutations, and 1.1% were positive. Cancer-related distress was measured before testing, and at 1 and 2 years post-testing. Information on uptake of cancer risk reduction options was collected at 2 years. Breast and ovarian cancer risks were estimated using BRCAPRO. Within 2 years of receiving a positive result, 11.1% of women had prophylactic mastectomy, and 89.5% had a prophylactic oophorectomy. The mean breast cancer risk was estimated to be 37.2% at time of testing, compared to 20.9% at 2 years post-testing. The mean ovarian cancer risk was estimated to be 24.5% at time of testing, compared to 7.5% at 2 years following testing. Distress decreased between 1 and 2 years for women with prophylactic mastectomy and oophorectomy (P = 0.02), and for women with prophylactic oophorectomy only (P = 0.04) but not for those with neither surgery. The majority of Jewish women with a BRCA mutation identified through a population screening elected prophylactic oophorectomy, but a few had a prophylactic mastectomy. Uptake of either surgery resulted in decreased distress. Provision of population BRCA testing resulted in reduced risks of breast and ovarian cancers in women with a mutation.
C1 [Metcalfe, Kelly A.; Mian, Nida; Enmore, Melissa; Poll, Aletta; Llacuachaqui, Marcia; Nanda, Sonia; Sun, Ping; Narod, Steven A.] Womens Coll Res Inst, Toronto, ON M5G 1N8, Canada.
[Metcalfe, Kelly A.] Univ Toronto, Lawrence S Bloomberg Fac Nursing, Toronto, ON, Canada.
[Hughes, Kevin S.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Narod, Steven A.] Univ Toronto, Dalla Lana Sch Publ Hlth, Toronto, ON, Canada.
RP Narod, SA (reprint author), Womens Coll Res Inst, 790 Bay St, Toronto, ON M5G 1N8, Canada.
EM Steven.narod@wchospital.ca
OI Hughes, Kevin/0000-0003-4084-6484
NR 23
TC 23
Z9 23
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD JUN
PY 2012
VL 133
IS 2
BP 735
EP 740
DI 10.1007/s10549-011-1941-0
PG 6
WC Oncology
SC Oncology
GA 949XJ
UT WOS:000304610600032
PM 22240989
ER
PT J
AU Kimball, AB
AF Kimball, A. B.
TI A new era in skin care: the omics revolution
SO BRITISH JOURNAL OF DERMATOLOGY
LA English
DT Editorial Material
C1 [Kimball, A. B.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Kimball, A. B.] Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA.
RP Kimball, AB (reprint author), Harvard Univ, Sch Med, Boston, MA 02114 USA.
EM harvardskinstudies@partners.org
NR 7
TC 0
Z9 0
U1 1
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-0963
J9 BRIT J DERMATOL
JI Br. J. Dermatol.
PD JUN
PY 2012
VL 166
SU 2
SI SI
DI 10.1111/j.1365-2133.2012.10858.x
PG 2
WC Dermatology
SC Dermatology
GA 953VJ
UT WOS:000304901000001
ER
PT J
AU Reardon, DA
Conrad, CA
Cloughesy, T
Prados, MD
Friedman, HS
Aldape, KD
Mischel, P
Xia, J
DiLea, C
Huang, J
Mietlowski, W
Dugan, M
Chen, W
Yung, WKA
AF Reardon, David A.
Conrad, Charles A.
Cloughesy, Timothy
Prados, Michael D.
Friedman, Henry S.
Aldape, Kenneth D.
Mischel, Paul
Xia, Jane
DiLea, CliVord
Huang, Jerry
Mietlowski, William
Dugan, Margaret
Chen, Wei
Yung, W. K. Alfred
TI Phase I study of AEE788, a novel multitarget inhibitor of ErbB- and
VEGF-receptor-family tyrosine kinases, in recurrent glioblastoma
patients
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE Glioblastoma; Tyrosine kinase inhibitor; Epidermal growth factor
receptor; Vascular endothelial growth factor receptor; RAD001
ID EPIDERMAL-GROWTH-FACTOR; BEVACIZUMAB PLUS IRINOTECAN; CONFERS ENHANCED
TUMORIGENICITY; NUDE-MOUSE MODEL; MALIGNANT GLIOMA; TARGETED THERAPY;
REDUCES GROWTH; BRAIN-TUMORS; TRIAL; EXPRESSION
AB Vascular endothelial growth factor receptor (VEGFR) and epidermal growth factor receptor (EGFR) play a significant role in glioblastoma angiogenesis and proliferation, making tyrosine kinase (TK) receptors logical targets for treatment. We evaluated AEE788, a reversible TK inhibitor that inhibits EGFR and VEGFR, in recurrent glioblastoma patients.
In this dose-escalation, phase I study, patients with recurrent glioblastoma received AEE788 once daily in 28-day cycles in stratified subgroups: those receiving (1) non-enzyme-inducing anticonvulsants drugs or no anticonvulsants (Group A) and (2) enzyme-inducing anticonvulsant drugs (Group B). A dose-expansion phase stratified patients by surgical eligibility. Primary objectives were to determine dose-limiting toxicity (DLT) and maximum tolerated dose; secondary objectives included evaluating (1) safety/tolerability, (2) pharmacokinetics, and (3) preliminary antitumor activity.
Sixty-four glioblastoma patients were enrolled. Two Group A patients experienced DLTs (proteinuria and stomatitis) at 550 mg; 550 mg was, therefore, the highest dose evaluated and dose limiting. One Group B patient receiving 800 mg experienced a DLT (diarrhea). The initially recommended dose for dose-expansion phase for Group A was 400 mg; additional patients received 250 mg to assess the hepatotoxicity. Most frequently reported adverse events (AEs) included diarrhea and rash. Serious AEs, most commonly grade 3/4 liver function test elevations, were responsible for treatment discontinuation in 17% of patients. AEE788 concentrations were reduced by EIACD. The best overall response was stable disease (17%).
Continuous, once-daily AEE788 was associated with unacceptable toxicity and minimal activity for the treatment of recurrent glioblastoma. The study was, therefore, discontinued prematurely.
C1 [Reardon, David A.] Dana Farber Canc Inst, Ctr Neurooncol, Boston, MA 02215 USA.
[Conrad, Charles A.; Aldape, Kenneth D.; Yung, W. K. Alfred] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Cloughesy, Timothy; Mischel, Paul; Chen, Wei] Univ Calif Los Angeles, Los Angeles, CA USA.
[Prados, Michael D.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Friedman, Henry S.] Duke Univ, Med Ctr, Preston Robert Tisch Brain Tumor Ctr, Durham, NC 27710 USA.
[Xia, Jane; DiLea, CliVord; Huang, Jerry; Mietlowski, William; Dugan, Margaret] Novartis Pharmaceut, E Hanover, NJ USA.
RP Reardon, DA (reprint author), Dana Farber Canc Inst, Ctr Neurooncol, 450 Brookline Ave,SW 460F, Boston, MA 02215 USA.
EM David_Reardon@DFCI.harvard.edu
FU NCATS NIH HHS [UL1 TR000124]
NR 45
TC 22
Z9 22
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD JUN
PY 2012
VL 69
IS 6
BP 1507
EP 1518
DI 10.1007/s00280-012-1854-6
PG 12
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 950BB
UT WOS:000304622600013
PM 22392572
ER
PT J
AU De Costa, AMA
Schuyler, CA
Walker, DD
Young, MRI
AF De Costa, Anna-Maria A.
Schuyler, Corinne A.
Walker, David D.
Young, M. Rita I.
TI Characterization of the evolution of immune phenotype during the
development and progression of squamous cell carcinoma of the head and
neck
SO CANCER IMMUNOLOGY IMMUNOTHERAPY
LA English
DT Article
DE HNSCC; Premalignant; Immunoediting; Th1/Tc1 cells; Th17 cells
ID T-CELLS; PD-1 EXPRESSION; TH17 CELLS; CANCER; MODEL; DYSFUNCTION; MICE;
INFLAMMATION; LYMPHOCYTES; INTERFERON
AB While studies have indicated that squamous cell carcinoma of the head and neck (HNSCC) is associated with immune suppression, these studies did not analyze the immune response at the dysplastic stage. The present study utilized a mouse model of 4-nitroquinoline 1-oxide-induced oral carcinogenesis to examine the alterations in immune phenotype at the premalignant and malignant stages of HNSCC. Cervical lymph nodes of HNSCC-bearing mice were found to contain a greater number of cells, including a greater number of conventional (Tconv) and regulatory (Treg) T cells, compared to cervical lymph nodes of control and premalignant lesion-bearing mice, though the Tconv cells appear to be less proliferative and the Treg cells appear to be less suppressive at the HNSCC stage. Premalignant lesion-bearing mouse lymph nodes consist of a greater percentage of Tconv cells expressing markers for activation, memory, and exhaustion compared to both control and HNSCC-bearing mice. Also, lymph nodes' cells from both premalignant lesion-bearing and HNSCC-bearing mice include increased levels of Th1, Tc1, and Th17 cells, with no differences in levels of Th2 cells, compared to control mice. The data show that while there is the expected increase in immunosuppressive Tregs in lymph nodes when HNSCC is present, there is also an unexpected increase in immune populations usually associated with a beneficial antitumor response, including Tconv cells and Th1 and Tc1 cells. In addition, the results demonstrate that the premalignant stage of HNSCC development is associated with a robust immune response involving an increase in inflammatory Th1, Tc1, and Th17 cells.
C1 [De Costa, Anna-Maria A.; Schuyler, Corinne A.; Young, M. Rita I.] Ralph H Johnson Vet Affairs Med Ctr, Res Serv 151, Charleston, SC 29401 USA.
[De Costa, Anna-Maria A.; Walker, David D.; Young, M. Rita I.] Med Univ S Carolina, Dept Otolaryngol Head & Neck Surg, Charleston, SC 29401 USA.
[De Costa, Anna-Maria A.; Young, M. Rita I.] Med Univ S Carolina, Dept Med, Charleston, SC 29401 USA.
RP Young, MRI (reprint author), Ralph H Johnson Vet Affairs Med Ctr, Res Serv 151, Charleston, SC 29401 USA.
EM rita.young@va.gov
FU Medical Research Service of the Department of Veterans Affairs; National
Institutes of Health [RO1 CA128837, RO1 DE018268]
FX This work was supported by the Medical Research Service of the
Department of Veterans Affairs and by grants RO1 CA128837 and RO1
DE018268 from the National Institutes of Health to MRIY.
NR 37
TC 11
Z9 11
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-7004
J9 CANCER IMMUNOL IMMUN
JI Cancer Immunol. Immunother.
PD JUN
PY 2012
VL 61
IS 6
BP 927
EP 939
DI 10.1007/s00262-011-1154-8
PG 13
WC Oncology; Immunology
SC Oncology; Immunology
GA 950AU
UT WOS:000304621900017
PM 22116344
ER
PT J
AU Carrithers, MD
AF Carrithers, Michael D.
TI Current Immunotherapy of Multiple Sclerosis and Future Challenges:
Relevance of Immune-Mediated Repair
SO CURRENT PHARMACEUTICAL BIOTECHNOLOGY
LA English
DT Review
DE Brain; demyelination; immune surveillance; innate immunity; interferon;
lymphocyte; natalizumab
ID PLACEBO-CONTROLLED TRIAL; PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY;
CENTRAL-NERVOUS-SYSTEM; CONTROLLED PHASE IIB; DOUBLE-BLIND; T-CELLS;
GLATIRAMER ACETATE; INTERFERON-BETA; IN-VITRO; INTRAMUSCULAR INTERFERON
AB Multiple sclerosis is the most common chronic inflammatory disease of the central nervous system and can cause severe neurological disability. Current immune therapy with beta-interferons, glatiramer acetate, immune suppressives, or selective adhesion molecule inhibitors can reduce the frequency and severity of acute attacks in a majority of patients but have little effect on the progressive phase of the disease. Patients who require aggressive immune therapy are also at risk for the development of potentially fatal opportunistic infections. Here current and emerging immune therapy options are discussed, and immune-mediated strategies to preserve normal immune surveillance and mediate tissue repair are proposed.
C1 [Carrithers, Michael D.] Univ Wisconsin, Dept Neurol, Madison, WI 53706 USA.
[Carrithers, Michael D.] William S Middleton Mem Vet Adm Med Ctr, Neurol Serv, Madison, WI USA.
RP Carrithers, MD (reprint author), Univ Wisconsin, Dept Neurol, 1300 Univ Ave, Madison, WI 53706 USA.
EM carrithers@neurology.wisc.edu
NR 96
TC 3
Z9 3
U1 1
U2 6
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1389-2010
J9 CURR PHARM BIOTECHNO
JI Curr. Pharm. Biotechnol.
PD JUN
PY 2012
VL 13
IS 8
BP 1409
EP 1417
PG 9
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 949SQ
UT WOS:000304596600005
PM 22339217
ER
PT J
AU Ibrahimi, OA
Kilmer, SL
AF Ibrahimi, Omar A.
Kilmer, Suzanne L.
TI Long-Term Clinical Evaluation of a 800-nm Long-Pulsed Diode Laser with a
Large Spot Size and Vacuum-Assisted Suction for Hair Removal
SO DERMATOLOGIC SURGERY
LA English
DT Article
ID MODE RUBY-LASER; FOLLOW-UP; REDUCTION; ALEXANDRITE; DAMAGE; TRIAL;
LIGHT; NM
AB Background The long-pulsed diode (800810-nm) laser is one of the most commonly used and effective lasers for hair removal. Limitations of currently available devices include a small treatment spot size, treatment-associated pain, and the need for skin cooling. Objective To evaluate the long-term hair reduction capabilities of a long-pulsed diode laser with a large spot size and vacuum assisted suction. Methods Thirty-five subjects were enrolled in a prospective, self-controlled, single-center study of axillary hair removal. The study consisted of three treatments using a long-pulsed diode laser with a large spot size and vacuum-assisted suction at 4- to 6-week intervals with follow-up visits 6 and 15 months after the last treatment. Hair clearance was quantified using macro hair-count photographs taken at baseline and at 6- and 15-month follow-up visits. Changes in hair thickness and color, levels of treatment-associated pain, and adverse events were additional study endpoints. Results There was statistically significant hair clearance at the 6 (54%) and 15-month (42%) follow-up visits. Remaining hairs were thinner and lighter at the 15-month follow-up visit, and the majority of subjects reported feeling up to mild to moderate pain during treatment without the use of pretreatment anesthesia or skin cooling. Conclusions A long-pulsed diode laser with a large spot size and vacuum-assisted suction is safe and effective for long-term hair removal. This is the largest prospective study to evaluate long-term hair removal and the first to quantify decreases in hair thickness and darkness with treatment.
C1 [Ibrahimi, Omar A.] Univ Connecticut, Ctr Hlth, Dept Dermatol, Farmington, CT 06032 USA.
[Ibrahimi, Omar A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Wellman Ctr Photomed, Boston, MA USA.
[Kilmer, Suzanne L.] Laser & Skin Surg Ctr No Calif, Sacramento, CA USA.
RP Ibrahimi, OA (reprint author), Univ Connecticut, Ctr Hlth, Dept Dermatol, 21 South Rd,2nd Floor, Farmington, CT 06032 USA.
EM omar.ibrahimi@gmail.com
NR 16
TC 5
Z9 5
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1076-0512
J9 DERMATOL SURG
JI Dermatol. Surg.
PD JUN
PY 2012
VL 38
IS 6
BP 912
EP 917
DI 10.1111/j.1524-4725.2012.02380.x
PG 6
WC Dermatology; Surgery
SC Dermatology; Surgery
GA 948UK
UT WOS:000304528100013
PM 22455549
ER
PT J
AU Barrett, LF
AF Barrett, Lisa Feldman
TI Emotions Are Real
SO EMOTION
LA English
DT Article
DE emotion; affect; social construction; conceptual acts
ID BILATERAL AMYGDALA DAMAGE; DEEP BRAIN-STIMULATION; HUNTINGTONS-DISEASE;
BASIC EMOTIONS; PREFRONTAL CORTEX; NATURAL KINDS; PSYCHOLOGICAL
CONSTRUCTION; EXPRESSION RECOGNITION; HIPPOCAMPAL-FORMATION; IMPAIRED
RECOGNITION
AB It is obvious that emotions are real, but the question is what kind of "real" are they? In this article, I outline a theoretical approach where emotions are a part of social reality. I propose that physical changes (in the face, voice, and body, or neural circuits for behavioral adaptations like freezing, fleeing, or fighting) transform into an emotion when those changes take on psychological functions that they cannot perform by their physical nature alone. This requires socially shared conceptual knowledge that perceivers use to create meaning from these physical changes (as well as the circuitry that supports this meaning making). My claim is that emotions are, at the same time, socially constructed and biologically evident. Only when we understand all the elements that construct emotional episodes, in social, psychological, and biological terms, will we understand the nature of emotion.
C1 [Barrett, Lisa Feldman] Northeastern Univ, Dept Psychol, Boston, MA 02115 USA.
[Barrett, Lisa Feldman] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Psychiat, Cambridge, MA 02138 USA.
[Barrett, Lisa Feldman] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, Cambridge, MA 02138 USA.
RP Barrett, LF (reprint author), Northeastern Univ, Dept Psychol, Boston, MA 02115 USA.
EM l.barrett@neu.edu
FU NIH HHS [DP1OD003312]
NR 148
TC 66
Z9 67
U1 7
U2 56
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 1528-3542
J9 EMOTION
JI Emotion
PD JUN
PY 2012
VL 12
IS 3
BP 413
EP 429
DI 10.1037/a0027555
PG 17
WC Psychology, Experimental
SC Psychology
GA 948OO
UT WOS:000304512700001
PM 22642358
ER
PT J
AU Campos, SM
Dizon, DS
AF Campos, Susana M.
Dizon, Don S.
TI Antimitotic Inhibitors
SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Microtubule-targeting agents; Microtubule resistance; Epothilones;
Eribulin; Cabazitaxel; Aurora kinase inhibitors; PLK inhibitors; KSP
inhibitors
ID METASTATIC BREAST-CANCER; ADVANCED SOLID TUMORS; RESISTANT
PROSTATE-CANCER; MICROTUBULE-STABILIZING AGENTS;
GYNECOLOGIC-ONCOLOGY-GROUP; PRIMARY PERITONEAL CANCER; PHASE-II TRIAL;
IXABEPILONE PLUS CAPECITABINE; ALBUMIN-BOUND PACLITAXEL; TUBULIN-BINDING
AGENTS
AB Of the agents available in the treatment of both solid and hematologic cancers, microtubule-targeted agents are among the most widely used and exploiting other mechanisms involving the microtubule and its role in mitosis is an area of continued interest. This review will focus on novel microtubule-targeted agents, both recently approved (eg, ixabepilone and eribulin) and in later-stage clinical trials, and kinase inhibitors that aim to directly inhibit the mitotic spindle, such as the aurora kinase, pololike kinase, and kinsein-spindle protein inhibitors.
C1 [Dizon, Don S.] Brown Univ, Warren Alpert Med Sch, Program Womens Oncol, Women & Infants Hosp, Providence, RI 02905 USA.
[Campos, Susana M.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Program Gynecol Oncol,Dept Med Oncol, Boston, MA 02215 USA.
RP Dizon, DS (reprint author), Brown Univ, Warren Alpert Med Sch, Program Womens Oncol, Women & Infants Hosp, 101 Dudley St, Providence, RI 02905 USA.
EM ddizon@wihri.org
NR 143
TC 9
Z9 9
U1 0
U2 8
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-8588
EI 1558-1977
J9 HEMATOL ONCOL CLIN N
JI Hematol. Oncol. Clin. North Am.
PD JUN
PY 2012
VL 26
IS 3
BP 607
EP +
DI 10.1016/j.hoc.2012.01.007
PG 24
WC Oncology; Hematology
SC Oncology; Hematology
GA 949JF
UT WOS:000304571800009
PM 22520982
ER
PT J
AU Lee, W
Nelson, R
Akmal, Y
Mailey, B
McKenzie, S
Artinyan, A
Ashing-Giwa, KT
Chen, YJ
Garcia-Aguilar, J
Kim, J
AF Lee, Wendy
Nelson, Rebecca
Akmal, Yasir
Mailey, Brian
McKenzie, Shaun
Artinyan, Avo
Ashing-Giwa, Kimlin Tam
Chen, Yi-Jen
Garcia-Aguilar, Julio
Kim, Joseph
TI Racial and ethnic disparities in outcomes with radiation therapy for
rectal adenocarcinoma
SO INTERNATIONAL JOURNAL OF COLORECTAL DISEASE
LA English
DT Article
DE Rectal cancer; Radiation; Neoadjuvant; Disparities
ID PATHOLOGICAL COMPLETE RESPONSE; COLORECTAL-CANCER TREATMENTS;
PREOPERATIVE CHEMORADIATION; SOCIOECONOMIC-STATUS; PREDICTIVE FACTORS;
ADJUVANT THERAPY; SURVIVAL; CHEMORADIOTHERAPY; RADIOTHERAPY;
CAPECITABINE
AB Race/ethnicity may modify cancer outcomes and manifest as survival disparities for patients with rectal cancer. Our objective was to determine whether disparate rectal cancer outcomes result from variable efficacy of radiation therapy for major racial/ethnic groups.
The Los Angeles County Cancer Surveillance Program (CSP) identified patients with rectal adenocarcinoma between the years 1988 and 2006. Patients who underwent curative-intent surgery were grouped by race/ethnicity and by receipt (yes vs. no) and timing (neoadjuvant vs. adjuvant) of radiation therapy. The impact of receipt and timing of radiation therapy on overall survival was then assessed.
Of 4,961 patients in CSP, 2,229 (45%) received radiation therapy. Overall, there was no difference in survival among patients according to receipt of radiation therapy. We then examined the radiation cohort, wherein 919 (41%) and 1,310 (59%) patients received neoadjuvant or adjuvant radiation, respectively. Overall, patients who received neoadjuvant compared to adjuvant radiation had improved survival (median survival (MS), 9.4 vs. 6.8 years, respectively; p < 0.001). Among those patients who received neoadjuvant radiation, whites, Hispanics, and Asians had significantly longer survival than blacks (MS, 10.4, 10.4, and 10.4 vs. 4.4 years, respectively; p = 0.003). On multivariate analysis, race/ethnicity was an independent predictor of survival (p = 0.001).
To our knowledge, this is the first study examining the efficacy of radiation therapy for racial/ethnic groups with rectal cancer. Disparate outcomes were observed for the administration of radiation therapy for select racial/ethnic groups. The reasons for these disparities in outcomes should be investigated to better optimize radiation therapy for patients with rectal cancer.
C1 [Lee, Wendy; Akmal, Yasir; Mailey, Brian; Garcia-Aguilar, Julio; Kim, Joseph] City Hope Comprehens Canc Ctr, Dept Surg, Duarte, CA 91010 USA.
[Nelson, Rebecca] City Hope Comprehens Canc Ctr, Dept Biostat, Duarte, CA 91010 USA.
[McKenzie, Shaun] Univ Kentucky, Sch Med, Dept Surg, Lexington, KY 40536 USA.
[Ashing-Giwa, Kimlin Tam] City Hope Comprehens Canc Ctr, Dept Populat Sci, Duarte, CA 91010 USA.
[Chen, Yi-Jen] City Hope Comprehens Canc Ctr, Dept Radiat Oncol, Duarte, CA 91010 USA.
[Artinyan, Avo] Baylor Coll Med, Michael E DeBakey Vet Affairs Med Ctr, Michael E DeBakey Dept Surg, Houston, TX 77030 USA.
[Artinyan, Avo] Baylor Coll Med, Michael E DeBakey Vet Affairs Med Ctr, Res Ctr Excellence, Houston, TX 77030 USA.
[Artinyan, Avo] Baylor Coll Med, Michael E DeBakey Vet Affairs Med Ctr, Houston Hlth Serv, Houston, TX 77030 USA.
RP Kim, J (reprint author), City Hope Comprehens Canc Ctr, Dept Surg, 1500 E Duarte Rd, Duarte, CA 91010 USA.
EM jokim@coh.org
RI Nelson, Rebecca/C-4438-2014
NR 32
TC 4
Z9 4
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0179-1958
J9 INT J COLORECTAL DIS
JI Int. J. Colorectal Dis.
PD JUN
PY 2012
VL 27
IS 6
BP 737
EP 749
DI 10.1007/s00384-011-1378-2
PG 13
WC Gastroenterology & Hepatology; Surgery
SC Gastroenterology & Hepatology; Surgery
GA 947VQ
UT WOS:000304461400007
PM 22159751
ER
PT J
AU Mureithi, MW
Poole, D
Naranbhai, V
Reddy, S
Mkhwanazi, NP
Sibeko, S
Werner, L
Karim, QA
Karim, SA
Ndung'u, T
Altfeld, M
AF Mureithi, Marianne W.
Poole, Danielle
Naranbhai, Vivek
Reddy, Shabashini
Mkhwanazi, Nompumelelo P.
Sibeko, Sengeziwe
Werner, Lise
Karim, Quarraisha Abdool
Karim, Salim Abdool
Ndung'u, Thumbi
Altfeld, Marcus
CA CAPRISA 004 Trial Grp
TI Preservation HIV-1-Specific IFN gamma+CD4+T-Cell Responses in
Breakthrough Infections After Exposure to Tenofovir Gel in the CAPRISA
004 Microbicide Trial
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE HIV-1; vaginal microbicide; tenofovir; HIV-1-specific CD4+T-cell help
ID ACUTE HIV-1 INFECTION; T-CELL RESPONSES; DENDRITIC CELLS; CD4(+);
VACCINE
AB The Centre for the AIDS Program of Research in South Africa 004 trial demonstrated reduction of sexual HIV-1 acquisition in women using a vaginal microbicide containing tenofovir. A better understanding of the consequences of antiretroviral-containing microbicides for immune responses in individuals with intercurrent HIV-1 infection is needed for future trials combining the use of microbicides with HIV-1 vaccines. Investigation of immune responses in women who acquired HIV-1 although using tenofovir gel showed significantly higher (P = 0.01) Gag-specific IFN gamma+ CD4+ T-cell responses. The use of tenofovir-containing gel around the time of infection can modulate HIV-1 immunity, and these immunological changes need to be considered in future trials combining vaccines and microbicides.
C1 [Altfeld, Marcus] Harvard Univ, Sch Med, Ragon Inst Massachusetts Gen Hosp MIT & Harvard, Charlestown, MA 02129 USA.
[Mureithi, Marianne W.; Poole, Danielle; Naranbhai, Vivek; Reddy, Shabashini; Mkhwanazi, Nompumelelo P.; Ndung'u, Thumbi; Altfeld, Marcus] Univ KwaZulu Natal, Doris Duke Med Res Inst, HIV Pathogenesis Program, Durban, South Africa.
[Mureithi, Marianne W.; Poole, Danielle; Naranbhai, Vivek; Reddy, Shabashini; Mkhwanazi, Nompumelelo P.; Ndung'u, Thumbi; Altfeld, Marcus] Univ KwaZulu Natal, Nelson R Mandela Sch Med, KwaZulu Natal Res Inst TB & HIV KRITH, Durban, South Africa.
[Naranbhai, Vivek; Sibeko, Sengeziwe; Werner, Lise; Karim, Quarraisha Abdool; Karim, Salim Abdool] Univ KwaZulu Natal, Ctr AIDS Program Res S Africa CAPRISA, Durban, South Africa.
[Karim, Quarraisha Abdool; Karim, Salim Abdool] Columbia Univ, Dept Epidemiol, New York, NY USA.
RP Altfeld, M (reprint author), Harvard Univ, Sch Med, Ragon Inst Massachusetts Gen Hosp MIT & Harvard, 149 13th St, Charlestown, MA 02129 USA.
EM maltfeld@partners.org
RI Abdool Karim, Salim Safurdeen/N-5947-2013
OI Abdool Karim, Salim Safurdeen/0000-0002-4986-2133
FU KwaZulu-Natal Research Institute for TB and HIV (K-RITH); Doris Duke
Charitable Foundation; United States Agency for International
Development (USAID); FHI360 [USAID] [GPO-A-00-05-00022-00, 132119];
Technology Innovation Agency (LIFElab) of the South African government's
Department of Science Technology; CONRAD, Eastern Virginia Medical
School [USAID] [GP00-08-00005-00, PPA-09-046]; National Institutes of
Health Office of the Director, Fogarty International Center [R24
TW007988]
FX Supported through the KwaZulu-Natal Research Institute for TB and HIV
(K-RITH) and by a grant from the Doris Duke Charitable Foundation to MA.
The parent trial (CAPRISA 004) was supported by the United States Agency
for International Development (USAID), FHI360 [USAID co-operative
agreement # GPO-A-00-05-00022-00, contract # 132119], and the Technology
Innovation Agency (LIFElab) of the South African government's Department
of Science & Technology. Tenofovir was provided by Gilead Sciences and
the gel was manufactured and supplied for the CAPRISA 004 trial by
CONRAD. The current studies are part of the CAPRISA TRAPS (Tenofovir gel
Research for AIDS Prevention Science) Program, which is funded by
CONRAD, Eastern Virginia Medical School [USAID co-operative grant #
GP00-08-00005-00, subproject agreement # PPA-09-046]. The views
expressed by the authors do not necessarily reflect the views of USAID,
Gilead Sciences, Eastern Virginia Medical School or CONRAD.; The authors
Q. A. K. and S. S. A. K. are coinventors with investigators from Gilead
Sciences on two pending patents on tenofovir gel. The authors S. S. A.
K. once received $2500 for serving on an Advisory Panel on PrEP for
Merck. M. A. once received $1500 as a CME Honorarium from Gilead
Science. M. W. M. was supported by the National Institutes of Health
Office of the Director, Fogarty International Center, through the
International Clinical Research Fellows Program at Vanderbilt (R24
TW007988).
NR 22
TC 8
Z9 8
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD JUN 1
PY 2012
VL 60
IS 2
BP 124
EP 127
DI 10.1097/QAI.0b013e31824f53a9
PG 4
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 947NL
UT WOS:000304436600012
PM 22362152
ER
PT J
AU Mosam, A
Shaik, F
Uldrick, TS
Esterhuizen, T
Friedland, GH
Scadden, DT
Aboobaker, J
Coovadia, HM
AF Mosam, Anisa
Shaik, Fahmida
Uldrick, Thomas S.
Esterhuizen, Tonya
Friedland, Gerald H.
Scadden, David T.
Aboobaker, Jamila
Coovadia, Hoosen M.
TI A Randomized Controlled Trial of Highly Active Antiretroviral Therapy
Versus Highly Active Antiretroviral Therapy and Chemotherapy in
Therapy-Naive Patients With HIV-Associated Kaposi Sarcoma in South
Africa
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE Kaposi sarcoma; AIDS; HIV; highly active antiretroviral therapy; South
Africa
ID PEGYLATED-LIPOSOMAL DOXORUBICIN; QUALITY-OF-LIFE; MULTICENTRIC CASTLEMAN
DISEASE; CLINICAL-TRIALS; IMMUNE RECONSTITUTION; INFLAMMATORY SYNDROME;
AIDS; HERPESVIRUS; INDIVIDUALS; REPLICATION
AB Background: The optimal approach to HIV-associated Kaposi sarcoma (HIV-KS) in sub-Saharan Africa is unknown. With large-scale rollout of highly active antiretroviral therapy (HAART) in South Africa, we hypothesized that survival in HIV-KS would improve and administration of chemotherapy in addition to HAART would be feasible and improve KS-specific outcomes.
Methods: We conducted a randomized, controlled, open-label trial with intention-to-treat analysis. Treatment-naive patients from King Edward VIII Hospital, Durban, South Africa, a public-sector tertiary referral center, with HIV-KS, but no symptomatic visceral disease or fungating lesions requiring urgent chemotherapy, were randomized to HAART alone or HAART and chemotherapy (CXT). HAART arm received stavudine, lamivudine, and nevirapine (Triomune; CXT arm received Triomune plus bleomycin, doxorubicin, and vincristine every 3 weeks. When bleomycin, doxorubicin, and vincristine were not available, oral etoposide (50-100 mg for 1-21 days of a 28-day cycle) was substituted. Primary outcome was overall KS response using AIDS Clinical Trial Group criteria 12 months after HAART initiation. Secondary comparisons included time to response, progression-free survival, overall survival, adverse events, HIV control, CD4 reconstitution, adherence, and quality of life.
Results: Fifty-nine subjects were randomized to HAART and 53 to CXT; 12-month overall KS response was 39% in the HAART arm and 66% in the CXT arm (difference, 27%; 95% confidence interval, 9%-43%; P = 0.005). At 12 months, 77% were alive (no survival difference between arms; P = 0.49), 82% had HIV viral load <50 copies per milliliter without difference between the arms (P = 0.47); CD4 counts and quality-of-life measures improved in all patients.
Conclusions: HAART with chemotherapy produced higher overall KS response over 12 months, whereas HAART alone provided similar improvement in survival and select measures of morbidity. In Africa, with high prevalence of HIV and human herpes virus-8 and limited resources, HAART alone provides important benefit in patients with HIV-KS.
C1 [Mosam, Anisa] Univ KwaZulu Natal, Nelson R Mandela Sch Med, Dept Dermatol, ZA-4013 Durban, South Africa.
[Shaik, Fahmida; Uldrick, Thomas S.] Univ KwaZulu Natal, CAPRISA, ZA-4013 Durban, South Africa.
[Uldrick, Thomas S.] Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA.
[Esterhuizen, Tonya] Univ KwaZulu Natal, Dept Bioeth, ZA-4013 Durban, South Africa.
[Friedland, Gerald H.] Yale Univ, Dept Internal Med, Infect Dis Sect, Friedland AIDS Program, New Haven, CT USA.
[Scadden, David T.] Harvard Univ, Massachusetts Gen Hosp, Ctr Canc, Sch Med, Boston, MA 02114 USA.
[Scadden, David T.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, AIDS Res Ctr, Boston, MA USA.
[Coovadia, Hoosen M.] Univ Witwatersrand, Johannesburg, South Africa.
RP Mosam, A (reprint author), Univ KwaZulu Natal, Nelson R Mandela Sch Med, Dept Dermatol, Rm 327 3rd Floor Med Sch,Private Bag X 7, ZA-4013 Durban, South Africa.
EM mosama@ukzn.ac.za
FU National Research Foundation [GUN 2054349]; National Cancer Institute
AIDS Malignancy Consortium, an AIDS Community Research Initiative of
America [14]; Fogarty International Center, National Institutes of
Health [D43TW00231]; Irene Diamond Fund; Doris Duke Charitable
Foundation
FX Supported by the National Research Foundation Thuthuka Grant GUN
2054349, National Cancer Institute AIDS Malignancy Consortium Grant
Supplement 14, an AIDS Community Research Initiative of America Grant,
and a Training Supplement to the Columbia University-Southern African
Fogarty AIDS International Training and Research Programme, Fogarty
International Center, National Institutes of Health (grant #
D43TW00231), and the Irene Diamond Fund and Doris Duke Charitable
Foundation. Triomune donated by Cipla-Medpro.
NR 35
TC 37
Z9 38
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD JUN 1
PY 2012
VL 60
IS 2
BP 150
EP 157
DI 10.1097/QAI.0b013e318251aedd
PG 8
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 947NL
UT WOS:000304436600016
PM 22395672
ER
PT J
AU Vazquez, GH
Tondo, L
Mazzarini, L
Gonda, X
AF Vazquez, Gustavo H.
Tondo, Leonardo
Mazzarini, Lorenzo
Gonda, Xenia
TI Affective temperaments in general population: A review and combined
analysis from national studies
SO JOURNAL OF AFFECTIVE DISORDERS
LA English
DT Review
DE Affective temperament; Gender differences; General population;
Nonclinical population; TEMPS-A
ID A BUENOS-AIRES; TEMPS-A; PSYCHOMETRIC VALIDATION; INTERNAL CONSISTENCY;
BEHAVIORAL-GENETICS; SAN-DIEGO; QUESTIONNAIRE; PERSONALITY; TRAITS;
ENDOPHENOTYPE
AB Background: The aim of this study was to investigate the characteristics of affective temperaments in general non-clinical population in different countries
Method: We performed a detailed search of published studies (one unpublished) investigating affective temperaments in non-clinical populations by administering the Temperament Evaluation of Memphis, Paris and San Diego Auto-questionnaire (TEMPS-A) in its 110-items version. We have included a total of six studies published from different countries (Argentina, Germany, Hungary, Korea. Lebanon, and Portugal) and one unpublished with preliminary data from Spain. We analyzed the combined data from the collected studies.
Results: We found significant gender differences, with men scoring higher in irritable and hyperthymic, and women in anxious, depressive and cyclothymic temperaments. Age had a significant effect in women with depressive temperament. Correlations among temperament scores have shown positive associations between depressive and anxious, and cyclothymic and irritable.
Conclusions: There was a similarity in gender differences and the association between different affective temperaments. Our results indicate that affective temperaments show both universal and distinctive characteristics.
Limitation: The sample populations in different countries were not homogeneous for age and socio-economic composition. In the Korean study of Kang et al. the version of the TEMPS was not validated. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Vazquez, Gustavo H.] Univ Palermo, Dept Neurosci, RA-1425 Buenos Aires, DF, Argentina.
[Vazquez, Gustavo H.; Tondo, Leonardo] Harvard Univ, Sch Med, Dept Psychiat, Int Consortium Bipolar Disorders Res, Boston, MA 02115 USA.
[Vazquez, Gustavo H.; Tondo, Leonardo] Harvard Univ, Sch Med, Neurosci Program, Boston, MA 02115 USA.
[Vazquez, Gustavo H.; Tondo, Leonardo] Massachusetts Gen Hosp, McLean Div, Belmont, MA USA.
[Tondo, Leonardo] Lucio Bini Mood Disorder Ctr, Cagliari, Sardinia, Italy.
[Mazzarini, Lorenzo] Univ Roma La Sapienza, Sch Med 2, St Andrea Hosp, Dept Neurosci,Unit Psychiat, Rome, Italy.
[Mazzarini, Lorenzo] Suore Hosp Sacred Heart Jesus, Dept Neuropsychiat, Viterbo, Italy.
[Gonda, Xenia] Semmelweis Univ, Dept Clin & Theoret Mental Hlth, Kutvolgyi Clin Ctr, Budapest, Hungary.
[Gonda, Xenia] Semmelweis Univ, Dept Pharmacol & Pharmacotherapy, Budapest, Hungary.
RP Vazquez, GH (reprint author), Univ Palermo, Dept Neurosci, Mario Bravo 1259, RA-1425 Buenos Aires, DF, Argentina.
EM gvazquez@palermo.edu
NR 27
TC 23
Z9 23
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0327
J9 J AFFECT DISORDERS
JI J. Affect. Disord.
PD JUN
PY 2012
VL 139
IS 1
BP 18
EP 22
DI 10.1016/j.jad.2011.06.032
PG 5
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 948GC
UT WOS:000304490600003
PM 21774989
ER
PT J
AU Dip, PV
Saw, WG
Roessle, M
Marshansky, V
Gruber, G
AF Dip, Phat Vinh
Saw, Wuan Geok
Roessle, Manfred
Marshansky, Vladimir
Grueber, Gerhard
TI Solution structure of subunit a, a (104-363), of the Saccharomyces
cerevisiae V-ATPase and the importance of its C-terminus in structure
formation
SO JOURNAL OF BIOENERGETICS AND BIOMEMBRANES
LA English
DT Article
DE Vacuolar ATPase; V1VO ATPase; V-1 ATPase; Vph1p; Subunit a; Cytohesin-2;
Small angle X-ray scattering
ID ELECTRON-MICROSCOPY; VACUOLAR ATPASE; 3-DIMENSIONAL STRUCTURE; SOLUTION
SCATTERING; EXCHANGE FACTOR; DOMAIN; ARNO; A2-SUBUNIT; PROTEINS
AB The 95 kDa subunit a of eukaryotic V-ATPases consists of a C-terminal, ion-translocating part and an N-terminal cytosolic domain. The latter's N-terminal domain (similar to 40 kDa) is described to bind in an acidification-dependent manner with cytohesin-2 (ARNO), giving the V-ATPase the putative function as pH-sensing receptor. Recently, the solution structure of the very N-terminal segment of the cytosolic N-terminal domain has been solved. Here we produced the N-terminal truncated form SCa (104-363) of the N-terminal domain (SCa (1-363)) of the Saccharomyces cerevisiae V-ATPase and determined its low resolution solution structure, derived from SAXS data. SCa (104-363) shows an extended S-like conformation with a width of about 3.88 nm and a length of 11.4 nm. The structure has been superimposed into the 3D reconstruction of the related A(1)A(O) ATP synthase from Pyrococcus furiosus, revealing that the SCa (104-363) fits well into the density of the collar structure of the enzyme complex. To understand the importance of the C-terminus of the protein SCa (1-363), and to determine the localization of the N- and C-termini in SCa (104-363), the C-terminal truncated form SCa (106-324) was produced and analyzed by SAXS. Comparison of the SCa (104-363) and SCa (106-324) shapes showed that the additional loop region in SCa (104-363) consists of the C-terminal residues. Whereas SCa (104-363) is monomeric in solution, SCa (106-324) forms a dimer, indicating the importance of the very C-terminus in structure formation. Finally, the solution structure of SCa (104-363) and SCa (106-324) will be discussed in terms of the topological arrangement of subunit a and cytoheisn-2 in V-ATPases.
C1 [Dip, Phat Vinh; Saw, Wuan Geok; Grueber, Gerhard] Nanyang Technol Univ, Sch Biol Sci, Singapore 637551, Singapore.
[Roessle, Manfred] DESY, EMBL, Hamburg Outstn, D-22603 Hamburg, Germany.
[Marshansky, Vladimir] Harvard Univ, Sch Med, Dept Med, Boston, MA 02114 USA.
[Marshansky, Vladimir] Massachusetts Gen Hosp, Simches Res Ctr, Div Nephrol, Boston, MA 02114 USA.
[Marshansky, Vladimir] Massachusetts Gen Hosp, Program Membrane Biol, Ctr Syst Biol, Boston, MA 02114 USA.
RP Gruber, G (reprint author), Nanyang Technol Univ, Sch Biol Sci, 60 Nanyang Dr, Singapore 637551, Singapore.
EM ggrueber@ntu.edu.sg
OI Dip, Phat Vinh/0000-0002-1535-9644
FU A*STAR BMRC [09/1/22/19/609]
FX We thank Dr. S.M. Malathy Sony for her support in SAXS data analysis and
art. Phat Vinh Dip is grateful to receive the Singapore International
Graduate Award (SINGA). This research was supported by A*STAR BMRC
(09/1/22/19/609).
NR 29
TC 6
Z9 6
U1 1
U2 3
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0145-479X
J9 J BIOENERG BIOMEMBR
JI J. Bioenerg. Biomembr.
PD JUN
PY 2012
VL 44
IS 3
BP 341
EP 350
DI 10.1007/s10863-012-9442-3
PG 10
WC Biophysics; Cell Biology
SC Biophysics; Cell Biology
GA 949YG
UT WOS:000304613700006
PM 22562380
ER
PT J
AU Mamon, HJ
AF Mamon, Harvey J.
TI Long-Term Follow-Up of a Paradigm-Changing Study: The Paradigm Still
Holds
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Editorial Material
ID RECTAL-CANCER; PREOPERATIVE RADIOTHERAPY; CHEMORADIATION THERAPY;
NONOPERATIVE TREATMENT; PATHOLOGICAL RESPONSE; GASTRIC-CARCINOMA; PLUS
RADIOTHERAPY; CHEMORADIOTHERAPY; TRIAL; SURVIVAL
C1 Brigham & Womens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Mamon, HJ (reprint author), Brigham & Womens Hosp, Dana Farber Canc Inst, 75 Francis St, Boston, MA 02115 USA.
NR 24
TC 2
Z9 2
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD JUN 1
PY 2012
VL 30
IS 16
BP 1901
EP 1903
DI 10.1200/JCO.2012.41.8863
PG 3
WC Oncology
SC Oncology
GA 949SS
UT WOS:000304596800005
PM 22529256
ER
PT J
AU Jakubowiak, AJ
Benson, DM
Bensinger, W
Siegel, DSD
Zimmerman, TM
Mohrbacher, A
Richardson, PG
Afar, DEH
Singhal, AK
Anderson, KC
AF Jakubowiak, Andrzej J.
Benson, Don M.
Bensinger, William
Siegel, David S. D.
Zimmerman, Todd M.
Mohrbacher, Ann
Richardson, Paul G.
Afar, Daniel E. H.
Singhal, Anil K.
Anderson, Kenneth C.
TI Phase I Trial of Anti-CS1 Monoclonal Antibody Elotuzumab in Combination
With Bortezomib in the Treatment of Relapsed/Refractory Multiple Myeloma
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID THERAPY
AB Purpose
To evaluate the maximum-tolerated dose (MTD), safety, and efficacy of elotuzumab in combination with bortezomib in patients with relapsed or relapsed and refractory multiple myeloma (MM).
Patients and Methods
Elotuzumab (2.5, 5.0, 10, or 20 mg/kg intravenously [IV]) and bortezomib (1.3 mg/m(2) IV) were administered on days 1 and 11 and days 1, 4, 8, and 11, respectively, in 21-day cycles by using a 3 + 3 dose-escalation design. Patients with stable disease or better after four cycles could continue treatment until disease progression or unexpected toxicity. Responses were assessed during each cycle by using European Group for Blood and Marrow Transplantation (EBMT) criteria.
Results
Twenty-eight patients with a median of two prior therapies were enrolled; three patients each received 2.5, 5.0, and 10 mg/kg of elotuzumab and 19 received 20 mg/kg (six during dose escalation and 13 during an expansion phase). No dose-limiting toxicities were observed during cycle 1 of the dose-escalation phase, and the MTD was not reached up to the maximum planned dose of 20 mg/kg. The most frequent grade 3 to 4 adverse events (AEs) were lymphopenia (25%) and fatigue (14%). Two elotuzumab-related serious AEs of chest pain and gastroenteritis occurred in one patient. An objective response (a partial response or better) was observed in 13 (48%) of 27 evaluable patients and in two (67%) of three patients refractory to bortezomib. Median time to progression was 9.46 months.
Conclusion
The combination of elotuzumab and bortezomib was generally well-tolerated and showed encouraging activity in patients with relapsed/refractory MM.
C1 [Jakubowiak, Andrzej J.] Univ Chicago, Med Ctr, Hematol Oncol Sect, Chicago, IL 60637 USA.
[Jakubowiak, Andrzej J.] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Jakubowiak, Andrzej J.; Benson, Don M.; Richardson, Paul G.; Anderson, Kenneth C.] Multiple Myeloma Res Consortium, Norwalk, CT USA.
[Benson, Don M.] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
[Bensinger, William] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Siegel, David S. D.] Hackensack Univ, Med Ctr, Hackensack, NJ USA.
[Mohrbacher, Ann] Univ So Calif, Keck Sch Med, Los Angeles, CA 90033 USA.
[Afar, Daniel E. H.; Singhal, Anil K.] Abbott Biotherapeut, Redwood City, CA USA.
[Richardson, Paul G.; Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Jakubowiak, AJ (reprint author), Univ Chicago, Med Ctr, Hematol Oncol Sect, 5841 S Maryland Ave,MC 2115, Chicago, IL 60637 USA.
EM ajakubowiak@medicine.bsd.uchicago.edu
FU PDL BioPharma; Millennium Pharmaceuticals; Abbott Biotherapeutics
FX William Bensinger, PDL BioPharma; David S. D. Siegel, Millennium
Pharmaceuticals; Supported by Abbott Biotherapeutics.
NR 16
TC 101
Z9 101
U1 0
U2 3
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD JUN 1
PY 2012
VL 30
IS 16
BP 1960
EP 1965
DI 10.1200/JCO.2011.37.7069
PG 6
WC Oncology
SC Oncology
GA 949SS
UT WOS:000304596800017
PM 22291084
ER
PT J
AU Fisch, MJ
Lee, JW
Weiss, M
Wagner, LI
Chang, VT
Cella, D
Manola, JB
Minasian, LM
McCaskill-Stevens, W
Mendoza, TR
Cleeland, CS
AF Fisch, Michael J.
Lee, Ju-Whei
Weiss, Matthias
Wagner, Lynne I.
Chang, Victor T.
Cella, David
Manola, Judith B.
Minasian, Lori M.
McCaskill-Stevens, Worta
Mendoza, Tito R.
Cleeland, Charles S.
TI Prospective, Observational Study of Pain and Analgesic Prescribing in
Medical Oncology Outpatients With Breast, Colorectal, Lung, or Prostate
Cancer
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID RACIAL-DIFFERENCES; PREVALENCE; MANAGEMENT; CARE; COMMUNICATION;
PERCEPTIONS; VALIDATION; PHYSICIANS; ATTITUDES; RELIEF
AB Purpose
Pain is prevalent among patients with cancer, yet pain management patterns in outpatient oncology are poorly understood.
Patients and Methods
A total of 3,123 ambulatory patients with invasive cancer of the breast, prostate, colon/rectum, or lung were enrolled onto this prospective study regardless of phase of care or stage of disease. At initial assessment and 4 to 5 weeks later, patients completed a 25-item measure of pain, functional interference, and other symptoms. Providers recorded analgesic prescribing. The pain management index was calculated to assess treatment adequacy.
Results
Of the 3,023 patients we identified to be at risk for pain, 2,026 (67%) reported having pain or requiring analgesics at initial assessment; of these 2,026 patients, 670 (33%) were receiving inadequate analgesic prescribing. We found no difference in treatment adequacy between the initial and follow-up visits. Multivariable analysis revealed that the odds of a non-Hispanic white patient having inadequate pain treatment were approximately half those of a minority patient after adjusting for other explanatory variables (odds ratio, 0.51; 95% CI, 0.37 to 0.70; P = .002). Other significant predictors of inadequate pain treatment were having a good performance status, being treated at a minority treatment site, and having nonadvanced disease without concurrent treatment.
Conclusion
Most outpatients with common solid tumors must confront issues related to pain and the use of analgesics. There is significant disparity in pain treatment adequacy, with the odds of undertreatment twice as high for minority patients. These findings persist over 1 month of follow-up, highlighting the complexity of these problems.
C1 [Fisch, Michael J.] Univ Texas MD Anderson Canc Ctr, Dept Gen Oncol, Houston, TX 77030 USA.
[Lee, Ju-Whei; Manola, Judith B.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Weiss, Matthias] Marshfield Clin Fdn Med Res & Educ, Marshfield, WI USA.
[Wagner, Lynne I.; Cella, David] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Chang, Victor T.] New Jersey Hlth Care Syst, Dept Vet Affairs, E Orange, NJ USA.
[Chang, Victor T.] Univ Med & Dent New Jersey, Newark, NJ 07103 USA.
[Minasian, Lori M.; McCaskill-Stevens, Worta] NCI, Bethesda, MD 20892 USA.
RP Fisch, MJ (reprint author), Univ Texas MD Anderson Canc Ctr, Dept Gen Oncol, Unit 410,1515 Holcombe Blvd, Houston, TX 77030 USA.
EM mfisch@mdanderson.org
FU Public Health Service [CA37604, CA23318, CA026582, CA17145]; National
Cancer Institute, National Institutes of Health; Department of Health
and Human Services
FX Supported in part by Public Health Service Grants No. CA37604, CA23318,
CA026582, and CA17145 and grants from the National Cancer Institute,
National Institutes of Health, and the Department of Health and Human
Services.
NR 29
TC 89
Z9 91
U1 4
U2 17
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD JUN 1
PY 2012
VL 30
IS 16
BP 1980
EP 1988
DI 10.1200/JCO.2011.39.2381
PG 9
WC Oncology
SC Oncology
GA 949SS
UT WOS:000304596800020
PM 22508819
ER
PT J
AU Ignatiadis, M
Singhal, SK
Desmedt, C
Haibe-Kains, B
Criscitiello, C
Andre, F
Loi, S
Piccart, M
Michiels, S
Sotiriou, C
AF Ignatiadis, Michail
Singhal, Sandeep K.
Desmedt, Christine
Haibe-Kains, Benjamin
Criscitiello, Carmen
Andre, Fabrice
Loi, Sherene
Piccart, Martine
Michiels, Stefan
Sotiriou, Christos
TI Gene Modules and Response to Neoadjuvant Chemotherapy in Breast Cancer
Subtypes: A Pooled Analysis
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID EXPRESSION PROFILES; PREOPERATIVE CHEMOTHERAPY; MOLECULAR SUBTYPES;
TARGETED THERAPIES; IMMUNE-RESPONSE; PHASE-3 TRIAL; MUTANT-CELLS;
PROGNOSIS; SIGNATURE; SURVIVAL
AB Purpose
To investigate the association between chemotherapy response and gene expression modules describing important biologic processes and druggable oncogenic pathways in breast cancer (BC) subtypes.
Patients and Methods
We searched for publicly available gene expression studies evaluating anthracycline with or without taxane-based neoadjuvant chemotherapy and identified eight studies with 996 patients. We computed 17 gene modules and calculated odds ratios (ORs) for pathologic complete response (pCR) for one-unit increases in scaled modules with and without adjustment for clinicopathologic characteristics. Added predictive accuracy was evaluated using the area under the receiver operating characteristic curve (AUC) and integrated discrimination index (IDI). We used the false discovery rate (FDR) to adjust for multiple testing.
Results
High immune module scores were associated with increased pCR probability in all BC subtypes. High module scores of chromosomal instability, phosphatase and tensin homolog (PTEN) loss, and E2F3 transcription factor were associated with increased pCR probability in estrogen receptor (ER) -negative/human epidermal growth factor receptor 2 (HER2) -negative and ER-positive/HER2-negative but not in HER2-positive tumors (interactions between HER2 and each of these modules for their association with pCR: P < .05; FDR, 0.17; trend for interaction between HER2 and PTEN). High values of insulin-like growth factor 1 activation module were associated with increased pCR probability only in ER-positive/HER2-negative tumors (interaction between insulin-like growth factor 1 and ER: P = .002; FDR, 0.03). When adding the immune module to clinicopathologic characteristics, we observed substantial increases in predictive accuracy for pCR in the HER2-positive subtype (IDI, 0.093; P = .004; increase in AUC from 0.760 to 0.836).
Conclusion
Different processes and pathways are associated with pCR in different BC subtypes.
C1 [Ignatiadis, Michail] Univ Libre Brussels, Inst Jules Bordet, Dept Med Oncol, B-1000 Brussels, Belgium.
[Haibe-Kains, Benjamin] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Haibe-Kains, Benjamin] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Andre, Fabrice] Univ Paris 11, Inst Gustave Roussy, Paris, France.
RP Ignatiadis, M (reprint author), Univ Libre Brussels, Inst Jules Bordet, Dept Med Oncol, 121 Blvd Waterloo, B-1000 Brussels, Belgium.
EM michail.ignatiadis@bordet.be
RI Loi, Sherene/H-1979-2016; Haibe-Kains, Benjamin/D-3702-2011; Michiels,
Stefan/L-1516-2013
OI Loi, Sherene/0000-0001-6137-9171; Desmedt,
Christine/0000-0002-5223-5579; Haibe-Kains,
Benjamin/0000-0002-7684-0079; Michiels, Stefan/0000-0002-6963-2968
FU Breast Cancer Research Foundation; Fonds de la Recherche Scientifique;
MEDIC Foundation; la Fondation Luxembourgeoise contre le Cancer; Les
Amis de l'Institut Bordet; Greek Ministry of Education, Lifelong
Learning & Religious Affairs [266]
FX Supported in part by grants from the Breast Cancer Research Foundation,
Fonds de la Recherche Scientifique, MEDIC Foundation, la Fondation
Luxembourgeoise contre le Cancer and "Les Amis de l'Institut Bordet" (M.
I., C. S.) and by the Greek Operational Program "Education & Lifelong
Learning" ESPA-THALIS #266 of the Greek Ministry of Education, Lifelong
Learning & Religious Affairs (M.I.).
NR 58
TC 113
Z9 116
U1 0
U2 6
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD JUN 1
PY 2012
VL 30
IS 16
BP 1996
EP 2004
DI 10.1200/JCO.2011.39.5624
PG 9
WC Oncology
SC Oncology
GA 949SS
UT WOS:000304596800022
PM 22508827
ER
PT J
AU Anesi, GL
Levine, D
Attar, EC
Fathi, AT
AF Anesi, George L.
Levine, Danielle
Attar, Eyal C.
Fathi, Amir T.
TI Bilateral Ear Swelling and Erythema After Chemotherapy: A Case of Ara-C
Ears
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID LEUKEMIA; THERAPY
C1 [Anesi, George L.; Levine, Danielle; Attar, Eyal C.; Fathi, Amir T.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Anesi, GL (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 4
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD JUN 1
PY 2012
VL 30
IS 16
BP E146
EP E146
DI 10.1200/JCO.2011.39.5970
PG 1
WC Oncology
SC Oncology
GA 949SS
UT WOS:000304596800001
PM 22508815
ER
PT J
AU Fiore, C
Bailey, D
Conlon, N
Wu, XQ
Martin, N
Fiorentino, M
Finn, S
Fall, K
Andersson, SO
Andren, O
Loda, M
Flavin, R
AF Fiore, Christopher
Bailey, Dyane
Conlon, Niamh
Wu, Xiaoqiu
Martin, Neil
Fiorentino, Michelangelo
Finn, Stephen
Fall, Katja
Andersson, Swen-Olof
Andren, Ove
Loda, Massimo
Flavin, Richard
TI Utility of multispectral imaging in automated quantitative scoring of
immunohistochemistry
SO JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article
ID PTEN TUMOR-SUPPRESSOR; PROSTATE-CANCER; ALPHA-CATENIN; INTEROBSERVER
REPRODUCIBILITY; RECEPTOR EXPRESSION; TISSUE MICROARRAY;
BREAST-CARCINOMA; GROWTH; CELLS; OVEREXPRESSION
AB Background Automated scanning devices and image analysis software provide a means to overcome the limitations of manual semiquantitative scoring of immunohistochemistry. Common drawbacks to automated imaging systems include an inability to classify tissue type and an inability to segregate cytoplasmic and nuclear staining.
Methods Immunohistochemistry for the membranous marker a-catenin, the cytoplasmic marker stathmin and the nuclear marker Ki-67 was performed on tissue microarrays (TMA) of archival formalin-fixed paraffin-embedded tissue comprising 471 (alpha-catenin and stathmin) and 511 (Ki-67) cases of prostate adenocarcinoma. These TMA were quantitatively analysed using two commercially available automated image analysers, the Ariol SL-50 system and the Nuance system from CRi. Both systems use brightfield microscopy for automated, unbiased and standardised quantification of immunohistochemistry, while the Nuance system has spectral deconvolution capabilities.
Results Overall concordance between scores from both systems was excellent (r=0.90; 0.83-0.95). The software associated with the multispectral imager allowed accurate automated classification of tissue type into epithelial glandular structures and stroma, and a single-step segmentation of staining into cytoplasmic or nuclear compartments allowing independent evaluation of these areas. The Nuance system, however, was not able to distinguish reliably between tumour and non-tumour tissue. In addition, variance in the labour and time required for analysis between the two systems was also noted.
Conclusion Despite limitations, this study suggests some beneficial role for the use of a multispectral imaging system in automated analysis of immunohistochemistry.
C1 [Conlon, Niamh; Finn, Stephen; Flavin, Richard] St James Hosp, Dept Pathol, Trinity Coll, Dublin 8, Ireland.
[Fiore, Christopher; Bailey, Dyane; Wu, Xiaoqiu; Fiorentino, Michelangelo; Finn, Stephen; Loda, Massimo; Flavin, Richard] Dana Farber Canc Inst, Ctr Mol Oncol Pathol, Boston, MA 02115 USA.
[Fiore, Christopher; Bailey, Dyane; Wu, Xiaoqiu; Fiorentino, Michelangelo; Finn, Stephen; Loda, Massimo; Flavin, Richard] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Martin, Neil] Harvard Radiat Oncol Program, Dept Radiat Oncol, Boston, MA USA.
[Fiorentino, Michelangelo] St Orsola Marcello Malpighi Hosp, Pathol Unit, Addarii Inst, Bologna, Italy.
[Fall, Katja] Univ Orebro, Sch Hlth & Med Sci, Orebro, Sweden.
[Fall, Katja; Andersson, Swen-Olof; Andren, Ove] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
RP Flavin, R (reprint author), St James Hosp, Dept Pathol, Trinity Coll, Jamess St, Dublin 8, Ireland.
EM flavinrichard@gmail.com
RI Martin, Neil/E-2193-2014;
OI Martin, Neil/0000-0002-8164-8516; Finn, Stephen/0000-0002-8628-5814;
Fall, Katja/0000-0002-3649-2639
FU Prostate Cancer Foundation; National Cancer Institute [RO1CA131945,
PO1CA89021, P50 CA90381]; Linda and Arthur Gelb Center for Translational
Research; Dana Farber Cancer Institute-Novartis
FX ML is supported by the Prostate Cancer Foundation, the National Cancer
Institute (RO1CA131945, PO1CA89021 and P50 CA90381), the Linda and
Arthur Gelb Center for Translational Research and a gift from Nuclea
Biomarkers to the Jimmy Fund and the Loda laboratory. ML is also the
recipient of a grant from the Dana Farber Cancer Institute-Novartis Drug
Development Program.
NR 30
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U1 0
U2 9
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0021-9746
J9 J CLIN PATHOL
JI J. Clin. Pathol.
PD JUN
PY 2012
VL 65
IS 6
BP 496
EP 502
DI 10.1136/jclinpath-2012-200734
PG 7
WC Pathology
SC Pathology
GA 949XE
UT WOS:000304609900003
PM 22447914
ER
PT J
AU So, C
Kirby, KA
Mehta, K
Hoffman, RM
Powell, AA
Freedland, SJ
Sirovich, B
Yano, EM
Walter, LC
AF So, Cynthia
Kirby, Katharine A.
Mehta, Kala
Hoffman, Richard M.
Powell, Adam A.
Freedland, Stephen J.
Sirovich, Brenda
Yano, Elizabeth M.
Walter, Louise C.
TI Medical Center Characteristics Associated with PSA Screening in Elderly
Veterans with Limited Life Expectancy
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE PSA screening; regional variation; elderly; life expectancy
ID PRIMARY-CARE PHYSICIANS; ANTIGEN TEST USE; PROSTATE-CANCER;
COLORECTAL-CANCER; UNITED-STATES; DECISION-MAKING; MEN; OLDER;
DETERMINANTS; COMORBIDITY
AB Although guidelines recommend against prostate-specific antigen (PSA) screening in elderly men with limited life expectancy, screening is common.
We sought to identify medical center characteristics associated with screening in this population.
We conducted a prospective study of 622,262 screen-eligible men aged 70+ seen at 104 VA medical centers in 2003.
Primary outcome was the percentage of men at each center who received PSA screening in 2003, based on VA data and Medicare claims. Men were stratified into life expectancy groups ranging from favorable (age 70-79 with Charlson score = 0) to limited (age 85+ with Charlson score a parts per thousand yen1 or age 70+ with Charlson score a parts per thousand yen4). Medical center characteristics were obtained from the 1999-2000 VA Survey of Primary Care Practices and publicly available VA data sources.
Among 123,223 (20%) men with limited life expectancy, 45% received PSA screening in 2003. Across 104 VAs, the PSA screening rate among men with limited life expectancy ranged from 25-79% (median 43%). Higher screening was associated with the following center characteristics: no academic affiliation (50% vs. 43%, adjusted RR = 1.14, 95% CI 1.04-1.25), a ratio of midlevel providers to physicians a parts per thousand yen3:4 (55% vs. 45%, adjusted RR = 1.20, 95% CI 1.09-1.32) and location in the South (49% vs. 39% in the West, adjusted RR = 1.25, 95% CI 1.12-1.40). Use of incentives and high scores on performance measures were not independently associated with screening. Within centers, the percentages of men screened with limited and favorable life expectancies were highly correlated (r = 0.90).
Substantial practice variation exists for PSA screening in older men with limited life expectancy across VAs. The high center-specific correlation of screening among men with limited and favorable life expectancies indicates that PSA screening is poorly targeted according to life expectancy.
C1 [So, Cynthia] Univ Calif San Francisco, Sch Med, San Francisco, CA USA.
[Kirby, Katharine A.; Mehta, Kala; Walter, Louise C.] San Francisco VA Med Ctr, Div Geriatr, San Francisco, CA USA.
[Hoffman, Richard M.] New Mexico VA Hlth Care Syst, Albuquerque, NM USA.
[Hoffman, Richard M.] Univ New Mexico, Dept Med, Albuquerque, NM 87131 USA.
[Powell, Adam A.] Minneapolis VA Hlth Care Syst, Ctr Chron Dis Outcomes Res, Minneapolis, MN USA.
[Powell, Adam A.] Univ Minnesota, Dept Med, Minneapolis, MN 55455 USA.
[Freedland, Stephen J.] Duke Univ, Durham VA Med Ctr, Durham, NC USA.
[Freedland, Stephen J.] Duke Univ, Duke Prostate Ctr, Durham, NC USA.
[Sirovich, Brenda] White River Junct VA, Windsor, VT USA.
[Yano, Elizabeth M.] UCLA Sch Publ Hlth, VA Greater Los Angeles Hlth Syst, VA HSR&D Ctr Study Healthcare Provider Behav, Los Angeles, CA USA.
[Yano, Elizabeth M.] UCLA Sch Publ Hlth, Dept Hlth Serv, Los Angeles, CA USA.
RP Walter, LC (reprint author), VA Med Ctr 181G, 4150 Clement St, San Francisco, CA 94121 USA.
EM Louise.Walter@ucsf.edu
FU National Cancer Institute at the National Institutes of Health [R01
CA134425]; American Federation for Aging Research; National Institute on
Aging [K-01AG025444]; New Mexico VA Health Care System; White River
Junction VA; VA HSRD [05-195]
FX This work was supported by the National Cancer Institute at the National
Institutes of Health (grant number R01 CA134425) to [LW, RH, AP, and
SF]; the Medical Student Training in Aging Research Program at the
American Federation for Aging Research to [CS]; the National Institute
on Aging (grant number K-01AG025444) to [KM]; the New Mexico VA Health
Care System to [RH]; the White River Junction VA to [BS]; and the VA
HSR&D Research Career Development Award (Project #05-195) to [EY].
NR 46
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U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD JUN
PY 2012
VL 27
IS 6
BP 653
EP 660
DI 10.1007/s11606-011-1945-9
PG 8
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 947BZ
UT WOS:000304402900009
PM 22180196
ER
PT J
AU Pandhi, N
DeVoe, JE
Schumacher, JR
Bartels, C
Thorpe, CT
Thorpe, JM
Smith, MA
AF Pandhi, Nancy
DeVoe, Jennifer E.
Schumacher, Jessica R.
Bartels, Christie
Thorpe, Carolyn T.
Thorpe, Joshua M.
Smith, Maureen A.
TI Number of First-Contact Access Components Required to Improve Preventive
Service Receipt in Primary Care Homes
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE patient-centered medical home; preventive medicine; access to care;
continuity of care; primary care; health care utilization; aging
ID INFLUENZA VACCINATION; SCREENING MAMMOGRAPHY; METAANALYSIS; MORTALITY;
ADULTS; CONTINUITY; COMMUNITY; DEATHS; US
AB A fundamental aim of primary care redesign and the patient-centered medical home is improving access to care. Patients who report having a usual site of care and usual provider are more likely to receive preventive services, but less is known about the influence of specific components of first-contact access (e.g., availability of appointments, advice by telephone) on preventive services receipt.
To examine the relationship between number of first-contact access components and receipt of recommended preventive services.
Secondary survey data analysis.
Five thousand five hundred and seven insured adults who had continuity with a usual primary care physician and participated in the 2003-2006 round of the Wisconsin Longitudinal Survey.
Using multivariable logistic regression, we calculated adjusted risk ratios, adjusted predicted probabilities and 95% confidence intervals for each preventive service.
Experiencing more first-contact access components was significantly associated with a higher rate of receiving cholesterol tests, flu shots and prostate exams but not mammography. There was variation in the number of components needed (between two and seven) to achieve a significant difference.
Having an increasing number of first-access components in a primary care office may improve preventive services receipt, and more components may be required for those services requiring greater provider contact (e.g., prostate exam) versus those that require less (e.g., mammography). In primary care redesign, the largest gains in preventive services receipt likely will come with redesign of multiple components simultaneously. While our study is a necessary step towards broadly understanding the relationship between first-contact access and preventive service receipt, other important questions remain. Certain components may drive greater improvements in the receipt of different services, and the effect of some of these components may depend on individual patient characteristics. Further research is critical for understanding redesign strategies that may optimize preventive service delivery.
C1 [Pandhi, Nancy; Smith, Maureen A.] Univ Wisconsin Madison, Dept Family Med, Madison, WI USA.
[Pandhi, Nancy; Smith, Maureen A.] Univ Wisconsin Madison, Dept Populat Hlth Sci, Madison, WI USA.
[DeVoe, Jennifer E.] Oregon Hlth & Sci Univ, Dept Family Med, Portland, OR 97201 USA.
[Schumacher, Jessica R.] Univ Florida Gainesville, Dept Hlth Serv Res Management & Policy, Gainesville, FL USA.
[Bartels, Christie] Univ Wisconsin, Dept Med, Rheumatol Sect, Sch Med & Publ Hlth, Madison, WI USA.
[Thorpe, Carolyn T.; Thorpe, Joshua M.] Vet Affairs Pittsburgh Healthcare Syst, Hlth Serv Res & Dev, Pittsburgh, PA USA.
[Thorpe, Carolyn T.; Thorpe, Joshua M.] Univ Pittsburgh, Sch Pharm, Dept Pharm & Therapeut, Pittsburgh, PA 15261 USA.
[Pandhi, Nancy; Schumacher, Jessica R.; Bartels, Christie; Thorpe, Carolyn T.; Thorpe, Joshua M.; Smith, Maureen A.] Univ Wisconsin, Hlth Innovat Program, Sch Med & Publ Hlth, Dept Populat Hlth Sci, Madison, WI USA.
[Smith, Maureen A.] Univ Wisconsin, Dept Surg, Sch Med & Publ Hlth Madison, Madison, WI 53706 USA.
RP Pandhi, N (reprint author), 800 Univ Bay Dr,Box 9445, Madison, WI 53705 USA.
EM nancy.pandhi@fammed.wisc.edu
RI Thorpe, Joshua/C-1188-2013
FU University of Wisconsin Institute for Clinical and Translational
Research (UW ICTR); NIH [1 UL1 RR025011]; National Institute on Aging [l
K08 AG029527, R01 AG09775, R01 AG033285]; Agency for Healthcare Research
and Quality (AHRQ) [K08 HS16181]; University of Wisconsin Carbone Cancer
Center (UWCCC) from the National Cancer Institute [P30 CA014520]; Vilas
Estate Trust; National Science Foundation; Spencer Foundation; Graduate
School of the University of Wisconsin-Madison; UW School of Medicine and
Public Health
FX This project was supported by the Health Innovation Program and the
Community-Academic Partnerships core of the University of Wisconsin
Institute for Clinical and Translational Research (UW ICTR) funded
through an NIH Clinical and Translational Science Award (CTSA), grant
number 1 UL1 RR025011. In addition, Nancy Pandhi is supported by a
National Institute on Aging Mentored Clinical Scientist Research Career
Development Award, grant number l K08 AG029527. Dr. DeVoe's time on this
project was supported by grant number K08 HS16181 from the Agency for
Healthcare Research and Quality (AHRQ). This project was also supported
by the University of Wisconsin Carbone Cancer Center (UWCCC) Support
Grant from the National Cancer Institute, grant number P30 CA014520.
Additional support was provided by the UW School of Medicine and Public
Health from the Wisconsin Partnership Program. This research uses data
from the Wisconsin Longitudinal Study of the University of
Wisconsin-Madison. Since 1991, the WLS has been supported principally by
the National Institute on Aging (R01 AG09775, R01 AG033285), with
additional support from the Vilas Estate Trust, the National Science
Foundation, the Spencer Foundation, and the Graduate School of the
University of Wisconsin-Madison. A public use file of data from the
Wisconsin Longitudinal Study is available from the Wisconsin
Longitudinal Study, University of Wisconsin-Madison, 1180 Observatory
Drive, Madison, Wisconsin, 53706 and at
http://www.ssc.wisc.edu/wlsresearch/data/. The view expressed in this
article are those of the authors and do not necessarily reflect the
position or policy of the Department of Veterans Affairs or the United
States government.
NR 37
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PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD JUN
PY 2012
VL 27
IS 6
BP 677
EP 684
DI 10.1007/s11606-011-1955-7
PG 8
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 947BZ
UT WOS:000304402900012
PM 22215269
ER
PT J
AU Chen, B
Covinsky, KE
Cenzer, IS
Adler, N
Williams, BA
AF Chen, Bonnie
Covinsky, Kenneth E.
Cenzer, Irena Stijacic
Adler, Nancy
Williams, Brie A.
TI Subjective Social Status and Functional Decline in Older Adults
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE health disparities; functional decline; geriatrics; socioeconomic
status; determinants of health
ID SELF-RATED HEALTH; SOCIOECONOMIC-STATUS; UNITED-STATES; WHITEHALL-II;
LIFE-COURSE; MORTALITY; INEQUALITIES; AMERICANS; POSITION; OUTCOMES
AB It is unknown whether subjective assessment of social status predicts health outcomes in older adults.
To describe the relationship between subjective social status and functional decline in older adults.
Longitudinal cohort study.
The Health and Retirement Study, a nationally representative survey of community-dwelling older adults (2004-2008).
Two thousand five hundred and twenty-three community-dwelling older adults.
Self-report of social status (SSS), categorized into three groups, reported by participants who marked a 10-rung ladder to represent where they stand in society. Four-year functional decline (new difficulty in any of five activities of daily living, mobility decline and/or death)
Mean age was 64; 46% were male, 85% were white. At baseline, lower SSS was associated with being younger, unmarried, of nonwhite race/ethnicity, higher rates of chronic medical conditions and ADL impairment (P < 0.01). Over 4 years, 50% in the lowest SSS group declined in function, compared to the middle and highest groups (28% and 26%), P-trend < 0.001. Those in the lowest rungs of SSS were at increased risk of 4-year functional decline (unadjusted RR = 1.91, CI 1.-9-2.46). The relationship between a subjective belief that one is worse off than others and functional decline persisted after serial adjustment for demographics, objective SES measures, and baseline health and functional status (RR 1.36, CI 1.08-1.73).
In older adults, the belief that one is in the lowest rungs of social status is a measure of socioeconomic distress and of significant risk for functional decline. These findings suggest that self-report of low subjective social status may give clinicians additional information about which older adults are at high risk for future functional decline.
C1 [Covinsky, Kenneth E.; Cenzer, Irena Stijacic; Williams, Brie A.] Univ Calif San Francisco, Dept Med, Div Geriatr, San Francisco, CA 94143 USA.
[Covinsky, Kenneth E.; Williams, Brie A.] Hlth Serv Res & Dev Res Enhancement Award Program, San Francisco VA Med Ctr, San Francisco, CA USA.
[Adler, Nancy] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA.
[Adler, Nancy] Univ Calif San Francisco, Dept Pediat, San Francisco, CA USA.
[Adler, Nancy] Univ Calif San Francisco, Ctr Hlth & Commun, San Francisco, CA 94143 USA.
RP Williams, BA (reprint author), Univ Calif San Francisco, Dept Med, Div Geriatr, San Francisco, CA 94143 USA.
EM brie.williams@ucsf.edu
FU Brookdale Leadership in Aging Fellowship; National Institute on Aging
[K23AG033102, R01 AG028481, K24 AG029812]; UCSF Hartford Foundation
Center of Excellence; Program for the Aging Century; MacArthur
Foundation Research Network on Socioeconomic Status and Health; Veterans
Affairs Medical Center, San Francisco, California
FX Dr. Williams was funded by the Brookdale Leadership in Aging Fellowship,
the National Institute on Aging (K23AG033102), the UCSF Hartford
Foundation Center of Excellence Physician-Scholar Award and the Program
for the Aging Century. Dr. Covinsky was supported by the National
Institute on Aging (R01 AG028481and K24 AG029812). The R01 was
administered by the Northern California Institute for Research and
Education, and with resources of the San Francisco Veterans Affairs
Medical Center. Dr. Adler received support from the MacArthur Foundation
Research Network on Socioeconomic Status and Health. These funding
sources had no role in the design and conduct of the study; collection,
management, analysis, and interpretation of the data; or preparation,
review, or approval of the manuscript. This work was supported with
resources of the Veterans Affairs Medical Center, San Francisco,
California. Drs. Williams and Covinsky are employees of the Department
of Veterans Affairs. The opinions expressed in this manuscript may not
represent those of the VA.
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PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD JUN
PY 2012
VL 27
IS 6
BP 693
EP 699
DI 10.1007/s11606-011-1963-7
PG 7
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 947BZ
UT WOS:000304402900014
PM 22215272
ER
PT J
AU Dinh, TA
Alperin, P
Walter, LC
Smith, R
AF Dinh, Tuan A.
Alperin, Peter
Walter, Louise C.
Smith, Robert
TI Impact of Comorbidity on Colorectal Cancer Screening Cost-Effectiveness
Study in Diabetic Populations
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Review
DE colorectal cancer screening; cost-effectiveness analysis; health care
modeling; comorbidity; optimal screening cessation; individualized
guidelines
ID SERVICES TASK-FORCE; FECAL OCCULT BLOOD; ADJUSTED LIFE-YEAR;
UNITED-STATES; PHYSICAL-ACTIVITY; AMERICAN-COLLEGE; WOMENS HEALTH; EQ-5D
INDEX; RISK; COLONOSCOPY
AB Although comorbidity has been shown to affect the benefits and risks of colorectal cancer (CRC) screening, it has not been accounted for in prior cost-effectiveness analyses of CRC screening.
To evaluate the impact of diagnosis of diabetes mellitus, a highly prevalent comorbidity in U.S. adults aged 50 and older, on health and economic outcomes of CRC screening.
Cost-effectiveness analysis using an integrated modeling framework.
Derived from basic and epidemiologic studies, clinical trials, cancer registries, and a colonoscopy database.
U.S. 50-year-old population.
Lifetime.
Costs are based on Medicare reimbursement rates.
Colonoscopy screening at ten-year intervals, beginning at age 50, and discontinued after age 50, 60, 70, 80 or death.
Health outcomes and cost effectiveness.
Diabetes diagnosis significantly affects cost-effectiveness of CRC screening. For the same CRC screening strategy, a person without diabetes at age 50 gained on average 0.07-0.13 life years more than a person diagnosed with diabetes at age 50 or younger. For a population of 1,000 patients diagnosed with diabetes at baseline, increasing stop age from 70 years to 80 years increased quality-adjusted life years (QALYs) gained by 0.3, with an incremental cost-effectiveness ratio of $206,671/QALY. The corresponding figures for 1,000 patients without diabetes are 2.3 QALYs and $46,957/QALY.
Cost-effectiveness results are sensitive to cost of colonoscopy and adherence to colonoscopy screening.
Results depend on accuracy of model assumptions.
Benefits of CRC screening differ substantially for patients with and without diabetes. Screening for CRC in patients diagnosed with diabetes at age 50 or younger is not cost-effective beyond age 70. Screening recommendations should be individualized based on the presence of comorbidities.
C1 [Dinh, Tuan A.; Alperin, Peter] Archimedes Inc, San Francisco, CA 94105 USA.
[Walter, Louise C.] San Francisco VA Med Ctr, Div Geriatr, San Francisco, CA USA.
[Walter, Louise C.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Smith, Robert] Amer Canc Soc, Canc Control Dept, Atlanta, GA 30329 USA.
RP Dinh, TA (reprint author), Archimedes Inc, 201 Mission St,29th Floor, San Francisco, CA 94105 USA.
EM tuan.dinh@archimedesmodel.com
FU National Cancer Institute [1R01CA134425]
FX The authors declare no conflict of interest. This study was carried out
by Archimedes in collaboration with Drs. Smith and Walter. Dr. Walter is
supported by a grant 1R01CA134425 from the National Cancer Institute.
NR 68
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U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD JUN
PY 2012
VL 27
IS 6
BP 730
EP 738
DI 10.1007/s11606-011-1972-6
PG 9
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 947BZ
UT WOS:000304402900018
PM 22237663
ER
PT J
AU Vick, A
Kraemer, RR
Morris, JL
Willett, LL
Centor, RM
Estrada, CA
Rodriguez, JM
AF Vick, Amanda
Kraemer, Ryan R.
Morris, Jason L.
Willett, Lisa L.
Centor, Robert M.
Estrada, Carlos A.
Rodriguez, J. Martin
TI A 60-Year-Old Woman with Chorea and Weight Loss
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Editorial Material
DE diagnostic reasoning; clinical problem solving; dual process theory;
illness scripts; chorea; paraneoplastic syndrome
ID STRATEGIES; MODEL
C1 [Vick, Amanda; Kraemer, Ryan R.; Morris, Jason L.; Willett, Lisa L.; Centor, Robert M.; Estrada, Carlos A.; Rodriguez, J. Martin] Univ Alabama Birmingham, Birmingham, AL 35294 USA.
[Kraemer, Ryan R.; Morris, Jason L.; Centor, Robert M.; Estrada, Carlos A.] Birmingham Vet Affairs Med Ctr, Birmingham, AL USA.
[Estrada, Carlos A.] Vet Affairs Natl Qual Scholars Program, Birmingham, AL USA.
RP Rodriguez, JM (reprint author), Univ Alabama Birmingham, THT 229 1530 3rd Ave S, Birmingham, AL 35294 USA.
EM mrodri2@uab.edu
NR 11
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U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD JUN
PY 2012
VL 27
IS 6
BP 747
EP 751
DI 10.1007/s11606-011-1928-x
PG 5
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 947BZ
UT WOS:000304402900021
PM 22143453
ER
PT J
AU Baffy, G
Brunt, EM
Caldwell, SH
AF Baffy, Gyoergy
Brunt, Elizabeth M.
Caldwell, Stephen H.
TI Hepatocellular carcinoma in non-alcoholic fatty liver disease: An
emerging menace
SO JOURNAL OF HEPATOLOGY
LA English
DT Review
DE Non-alcoholic fatty liver disease; Hepatocellular carcinoma;
Hepatocarcinogenesis; Cancer surveillance
ID POPULATION-BASED COHORT; TNF-ALPHA PRODUCTION; TERM-FOLLOW-UP;
INSULIN-RESISTANCE; HEPATITIS-C; DIABETIC-PATIENTS; RISK-FACTORS;
CRYPTOGENIC CIRRHOSIS; METABOLIC SYNDROME; VIRAL-HEPATITIS
AB Hepatocellular carcinoma (HCC) is a common cancer worldwide that primarily develops in cirrhosis resulting from chronic infection by hepatitis B virus and hepatitis C virus, alcoholic injury, and to a lesser extent from genetically determined disorders such as hemochromatosis. HCC has recently been linked to non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of obesity and related metabolic disorders such as diabetes. This association is alarming due to the globally high prevalence of these conditions and may contribute to the rising incidence of HCC witnessed in many industrialized countries. There is also evidence that NAFLD acts synergistically with other risk factors of HCC such as chronic hepatitis C and alcoholic liver injury. Moreover, HCC may complicate non-cirrhotic NAFLD with mild or absent fibrosis, greatly expanding the population potentially at higher risk. Major systemic and liver-specific molecular mechanisms involved include insulin resistance and hyperinsulinemia, increased TNF signaling pathways, and alterations in cellular lipid metabolism. These provide new targets for prevention, early recognition, and effective treatment of HCC associated with NAFLD. Indeed, both metformin and PPAR gamma agonists have been associated with lower risk and improved prognosis of HCC. This review summarizes current evidence as it pertains to the epidemiology, pathogenesis, and prevention of NAFLD-associated HCC. Published by Elsevier B.V. on behalf of the European Association for the Study of the Liver.
C1 [Baffy, Gyoergy] Harvard Univ, Sch Med, VA Boston Healthcare Syst, Gastroenterol Sect, Boston, MA 02130 USA.
[Baffy, Gyoergy] Harvard Univ, Sch Med, Brigham & Womens Hosp, Boston, MA 02130 USA.
[Brunt, Elizabeth M.] Washington Univ, Dept Pathol & Immunol, St Louis, MO USA.
[Caldwell, Stephen H.] Univ Virginia Hlth Syst, Digest Hlth Ctr Excellence, Div Gastroenterol & Hepatol, Charlottesville, VA USA.
RP Baffy, G (reprint author), Harvard Univ, Sch Med, VA Boston Healthcare Syst, Gastroenterol Sect, 150 S Huntington Ave,Room 6A-46, Boston, MA 02130 USA.
EM gbaffy@partners.org
NR 115
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U1 5
U2 55
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
EI 1600-0641
J9 J HEPATOL
JI J. Hepatol.
PD JUN
PY 2012
VL 56
IS 6
BP 1384
EP 1391
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 948OK
UT WOS:000304512300026
PM 22326465
ER
PT J
AU Edlow, BL
Takahashi, E
Wu, ON
Benner, T
Dai, GP
Bu, LH
Grant, PE
Greer, DM
Greenberg, SM
Kinney, HC
Folkerth, RD
AF Edlow, Brian L.
Takahashi, Emi
Wu, Ona
Benner, Thomas
Dai, Guangping
Bu, Lihong
Grant, Patricia Ellen
Greer, David M.
Greenberg, Steven M.
Kinney, Hannah C.
Folkerth, Rebecca D.
TI Neuroanatomic Connectivity of the Human Ascending Arousal System
Critical to Consciousness and Its Disorders
SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
LA English
DT Article
DE Arousal; Ascending reticular activating system (ARAS); Brainstem;
Consciousness; High angular resolution diffusion imaging (HARDI);
Neuroanatomy; Tractography
ID TRAUMATIC BRAIN-INJURY; STATE FREE PRECESSION; INTRALAMINAR THALAMIC
NUCLEI; PERSISTENT VEGETATIVE STATE; DIFFUSION-TENSOR; WHITE-MATTER;
RETICULAR-FORMATION; CEREBRAL-CORTEX; MRI DATA; TRACTOGRAPHY
AB The ascending reticular activating system (ARAS) mediates arousal, an essential component of human consciousness. Lesions of the ARAS cause coma, the most severe disorder of consciousness. Because of current methodological limitations, including of postmortem tissue analysis, the neuroanatomic connectivity of the human ARAS is poorly understood. We applied the advanced imaging technique of high angular resolution diffusion imaging (HARDI) to elucidate the structural connectivity of the ARAS in 3 adult human brains, 2 of which were imaged postmortem. High angular resolution diffusion imaging tractography identified the ARAS connectivity previously described in animals and also revealed novel human pathways connecting the brainstem to the thalamus, the hypothalamus, and the basal forebrain. Each pathway contained different distributions of fiber tracts from known neurotransmitter-specific ARAS nuclei in the brainstem. The histologically guided tractography findings reported here provide initial evidence for human-specific pathways of the ARAS. The unique composition of neurotransmitter-specific fiber tracts within each ARAS pathway suggests structural specializations that subserve the different functional characteristics of human arousal. This ARAS connectivity analysis provides proof of principle that HARDI tractography may affect the study of human consciousness and its disorders, including in neuropathologic studies of patients dying in coma and the persistent vegetative state.
C1 [Edlow, Brian L.] Brigham & Womens Hosp, Dept Neurol, Boston, MA 02115 USA.
[Folkerth, Rebecca D.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Takahashi, Emi; Grant, Patricia Ellen] Harvard Univ, Sch Med, Childrens Hosp Boston, Div Newborn Med, Boston, MA USA.
[Takahashi, Emi; Grant, Patricia Ellen] Harvard Univ, Sch Med, Childrens Hosp Boston, Fetal Neonatal Neuroimaging & Dev Sci Ctr, Boston, MA USA.
[Bu, Lihong] Harvard Univ, Sch Med, Childrens Hosp Boston, FM Kirby Neurobiol Ctr, Boston, MA USA.
[Grant, Patricia Ellen] Harvard Univ, Sch Med, Dept Radiol, Childrens Hosp Boston, Boston, MA 02115 USA.
[Kinney, Hannah C.; Folkerth, Rebecca D.] Harvard Univ, Sch Med, Dept Pathol, Childrens Hosp Boston, Boston, MA 02115 USA.
[Edlow, Brian L.; Greer, David M.; Greenberg, Steven M.] Harvard Univ, Sch Med, Dept Neurol, J Philip Kistler Stroke Res Ctr,Massachusetts Gen, Boston, MA 02115 USA.
[Wu, Ona] Harvard Univ, Sch Med, Dept Radiol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Edlow, Brian L.; Takahashi, Emi; Wu, Ona; Benner, Thomas; Dai, Guangping; Grant, Patricia Ellen] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA USA.
[Greer, David M.] Yale Univ, Sch Med, Dept Neurol, Yale New Haven Hosp, New Haven, CT 06510 USA.
RP Edlow, BL (reprint author), Brigham & Womens Hosp, Dept Neurol, 75 Francis St, Boston, MA 02115 USA.
EM bedlow@partners.org
FU National Institutes of Health [R25 NS065743, R01 HD20991, R21 HD069001,
P41 RR14075]; Center for Integration of Medicine & Innovative
Technology; Neuropathology Division, Department of Pathology, Brigham
and Women's Hospital, Boston, MA; National Center for Research Resources
[1S10RR016811-01]
FX This work was supported by grants from the National Institutes of Health
(R25 NS065743 [B. L. E.], R01 HD20991 [H. C. K.], R21 HD069001 [E. T.],
and P41 RR14075 [Athinoula A. Martinos Center for Biomedical Imaging])
and by the Center for Integration of Medicine & Innovative Technology,
and by the Neuropathology Division, Department of Pathology, Brigham and
Women's Hospital, Boston, MA. This work also involved the use of
instrumentation supported by the National Center for Research Resources
(1S10RR016811-01).
NR 80
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U1 3
U2 13
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-3069
J9 J NEUROPATH EXP NEUR
JI J. Neuropathol. Exp. Neurol.
PD JUN
PY 2012
VL 71
IS 6
BP 531
EP 546
DI 10.1097/NEN.0b013e3182588293
PG 16
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 949QB
UT WOS:000304589600006
PM 22592840
ER
PT J
AU William, C
Andermann, M
Goldey, G
Roumis, D
Reid, RC
Shatz, C
Albers, M
Frosch, M
Hyman, B
AF William, Christopher
Andermann, Mark
Goldey, Glenn
Roumis, Demetris
Reid, R. Clay
Shatz, Carla
Albers, Mark
Frosch, Matthew
Hyman, Bradley
TI Early Visual System Synaptic Plasticity Defects in Alzheimer Disease
Model Transgenic Mice
SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
LA English
DT Meeting Abstract
CT 88th Annual Meeting of the American-Association-of-Neuropathologists
CY JUN 21-24, 2012
CL Chicago, IL
SP Amer Assoc Neuropathol
C1 [William, Christopher; Frosch, Matthew] Massachusetts Gen Hosp, Neuropathol Serv, Boston, MA 02114 USA.
[Andermann, Mark; Goldey, Glenn; Roumis, Demetris; Reid, R. Clay] Harvard Univ, Sch Med, Dept Neurobiol, Boston, MA 02115 USA.
[Shatz, Carla] Stanford Univ, Stanford, CA 94305 USA.
[Albers, Mark; Hyman, Bradley] MGH, MassGen Inst Neurodegenerat Dis, 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 0022-3069
J9 J NEUROPATH EXP NEUR
JI J. Neuropathol. Exp. Neurol.
PD JUN
PY 2012
VL 71
IS 6
MA 14
BP 550
EP 551
PG 2
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 949QB
UT WOS:000304589600021
ER
PT J
AU McGuone, D
Stemmer-Rachamimov, A
Stone, J
Deshpande, V
AF McGuone, Declan
Stemmer-Rachamimov, Anat
Stone, John
Deshpande, Vikram
TI Lymphoplasmacytic Hypophysitis: An IgG4-related Disease?
SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
LA English
DT Meeting Abstract
CT 88th Annual Meeting of the American-Association-of-Neuropathologists
CY JUN 21-24, 2012
CL Chicago, IL
SP Amer Assoc Neuropathol
C1 [McGuone, Declan; Stemmer-Rachamimov, Anat; Stone, John; Deshpande, Vikram] Harvard Univ, Massachusetts Gen Hosp, Boston, MA 02115 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 0022-3069
J9 J NEUROPATH EXP NEUR
JI J. Neuropathol. Exp. Neurol.
PD JUN
PY 2012
VL 71
IS 6
MA 37
BP 557
EP 557
PG 1
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 949QB
UT WOS:000304589600044
ER
PT J
AU Auluck, P
Lindquist, S
AF Auluck, Pavan
Lindquist, Susan
TI Cytoprotective chemical screens in a yeast model for
alpha-synucleinopathies
SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
LA English
DT Meeting Abstract
CT 88th Annual Meeting of the American-Association-of-Neuropathologists
CY JUN 21-24, 2012
CL Chicago, IL
SP Amer Assoc Neuropathol
C1 [Auluck, Pavan] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Lindquist, Susan] MIT, Cambridge, MA 02139 USA.
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 0022-3069
J9 J NEUROPATH EXP NEUR
JI J. Neuropathol. Exp. Neurol.
PD JUN
PY 2012
VL 71
IS 6
MA 70
BP 566
EP 566
PG 1
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 949QB
UT WOS:000304589600077
ER
PT J
AU Auluck, P
Lindquist, S
AF Auluck, Pavan
Lindquist, Susan
TI Retrograde Trafficking Defects Enhance alpha-Synuclein Toxicity in a
Yeast Model
SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
LA English
DT Meeting Abstract
CT 88th Annual Meeting of the American-Association-of-Neuropathologists
CY JUN 21-24, 2012
CL Chicago, IL
SP Amer Assoc Neuropathol
C1 [Auluck, Pavan] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Lindquist, Susan] MIT, Cambridge, MA 02139 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-3069
J9 J NEUROPATH EXP NEUR
JI J. Neuropathol. Exp. Neurol.
PD JUN
PY 2012
VL 71
IS 6
MA 74
BP 567
EP 567
PG 1
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 949QB
UT WOS:000304589600081
ER
PT J
AU Suva, M
Rheinbay, E
Chi, A
Louis, D
Bernstein, B
AF Suva, Mario
Rheinbay, Esther
Chi, Andrew
Louis, David
Bernstein, Bradley
TI Chromatin Landscape Analysis to Identify the Core Transcriptional
Regulatory Network of Glioblastoma Cancer Stem Cells
SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
LA English
DT Meeting Abstract
CT 88th Annual Meeting of the American-Association-of-Neuropathologists
CY JUN 21-24, 2012
CL Chicago, IL
SP Amer Assoc Neuropathol
C1 [Suva, Mario; Rheinbay, Esther; Louis, David; Bernstein, Bradley] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Chi, Andrew] Massachusetts Gen Hosp, Dept Neurol, 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 0022-3069
J9 J NEUROPATH EXP NEUR
JI J. Neuropathol. Exp. Neurol.
PD JUN
PY 2012
VL 71
IS 6
MA 115
BP 578
EP 579
PG 2
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 949QB
UT WOS:000304589600122
ER
PT J
AU Ciarlini, P
Wood, B
Klein, J
Lyons, J
Milner, D
Philips, R
Schutten, M
Henrich, T
Johnson, J
Gabuzda, D
De Girolami, U
Folkerth, R
AF Ciarlini, Pedro
Wood, Brian
Klein, Joshua
Lyons, Jennifer
Milner, Danny
Philips, Richard
Schutten, Martin
Henrich, Timothy
Johnson, Jennifer
Gabuzda, Dana
De Girolami, Umberto
Folkerth, Rebecca
TI Biopsy Pathology of HIV-2 Encephalitis: Case Report
SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
LA English
DT Meeting Abstract
CT 88th Annual Meeting of the American-Association-of-Neuropathologists
CY JUN 21-24, 2012
CL Chicago, IL
SP Amer Assoc Neuropathol
C1 [Ciarlini, Pedro; Milner, Danny; De Girolami, Umberto; Folkerth, Rebecca] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Wood, Brian; Henrich, Timothy; Johnson, Jennifer] Brigham & Womens Hosp, Div Infect Dis, Boston, MA 02115 USA.
[Klein, Joshua; Lyons, Jennifer; Philips, Richard] Brigham & Womens Hosp, Dept Neurol, Boston, MA 02115 USA.
[Klein, Joshua] Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA.
[Schutten, Martin] Erasmus MC, Dept Virol, Rotterdam, Netherlands.
[Gabuzda, Dana] Dana Farber Canc Inst, Boston, MA USA.
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 0022-3069
J9 J NEUROPATH EXP NEUR
JI J. Neuropathol. Exp. Neurol.
PD JUN
PY 2012
VL 71
IS 6
MA 130
BP 583
EP 583
PG 1
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 949QB
UT WOS:000304589600137
ER
PT J
AU McGuone, D
Kimchi, E
Neilan, A
Robbins, G
Frosch, M
Hedley-Whyte, ET
AF McGuone, Declan
Kimchi, Eyal
Neilan, Anne
Robbins, Gregory
Frosch, Matthew
Hedley-Whyte, E. Tessa
TI Rabies Encephalitis of Bat-strain Type in a 63 Year Old Man: Failure of
the Milwaukee Protocol
SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
LA English
DT Meeting Abstract
CT 88th Annual Meeting of the American-Association-of-Neuropathologists
CY JUN 21-24, 2012
CL Chicago, IL
SP Amer Assoc Neuropathol
C1 [McGuone, Declan; Kimchi, Eyal; Neilan, Anne; Robbins, Gregory; Frosch, Matthew; Hedley-Whyte, E. Tessa] Harvard Univ, Massachusetts Gen Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-3069
J9 J NEUROPATH EXP NEUR
JI J. Neuropathol. Exp. Neurol.
PD JUN
PY 2012
VL 71
IS 6
MA 135
BP 584
EP 584
PG 1
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 949QB
UT WOS:000304589600142
ER
PT J
AU Ghetti, B
Brashear, A
Hagen, M
Sweadner, K
AF Ghetti, Bernardino
Brashear, Allison
Hagen, Matthew
Sweadner, Kathleen
TI Rapid Onset Dystonia-Parkinsonism Associated with the I758S ATP1A3
Mutation: A Neuropathologic Study of Two Affected Siblings
SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
LA English
DT Meeting Abstract
CT 88th Annual Meeting of the American-Association-of-Neuropathologists
CY JUN 21-24, 2012
CL Chicago, IL
SP Amer Assoc Neuropathol
C1 [Ghetti, Bernardino] Indiana Univ, Bloomington, IN 47405 USA.
[Brashear, Allison] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Hagen, Matthew] Univ Cincinnati, Cincinnati, OH 45221 USA.
[Sweadner, Kathleen] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RI Brashear, Allison/G-3853-2015
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 0022-3069
J9 J NEUROPATH EXP NEUR
JI J. Neuropathol. Exp. Neurol.
PD JUN
PY 2012
VL 71
IS 6
MA 166
BP 592
EP 593
PG 2
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 949QB
UT WOS:000304589600173
ER
PT J
AU Hulten, EA
Bittencourt, MS
Ghoshhajra, B
Blankstein, R
AF Hulten, Edward A.
Bittencourt, Marcio Sommer
Ghoshhajra, Brian
Blankstein, Ron
TI Stress CT perfusion: Coupling coronary anatomy with physiology
SO JOURNAL OF NUCLEAR CARDIOLOGY
LA English
DT Article
DE Computed tomography (CT); coronary artery disease; ischemia; myocardial;
vasodilator stress
ID COMPUTED-TOMOGRAPHY ANGIOGRAPHY; FRACTIONAL FLOW RESERVE; DUAL-SOURCE
CT; MYOCARDIAL-PERFUSION; ARTERY-DISEASE; DIAGNOSTIC PERFORMANCE;
PROGNOSTIC VALUE; MAGNETIC-RESONANCE; CARDIAC RISK; SPECT
AB While multiple different imaging tests can be used to evaluate patients with known or suspected coronary artery disease (CAD), each of them is designed to evaluate either coronary anatomy or physiology. Recently, it has been recognized that cardiac CT can be used to evaluate stress and rest myocardial perfusion in addition to its capabilities to image the coronary arteries, thus allowing for the simultaneous evaluation of the anatomical burden and physiological significance of CAD in a single exam. In this review, the strengths and the limitations of imaging coronary anatomy and myocardial perfusion will be discussed. Next, key technical aspects of how to perform and interpret CT perfusion imaging will be summarized while providing an update of the most recent data in this emerging field. Finally, future directions and opportunities for further research will be discussed.
C1 [Hulten, Edward A.; Bittencourt, Marcio Sommer; Blankstein, Ron] Brigham & Womens Hosp, Noninvas Cardiovasc Imaging Program, Div Cardiovasc, Dept Med, Boston, MA 02115 USA.
[Hulten, Edward A.; Bittencourt, Marcio Sommer; Blankstein, Ron] Brigham & Womens Hosp, Noninvas Cardiovasc Imaging Program, Div Cardiovasc, Dept Radiol, Boston, MA 02115 USA.
[Blankstein, Ron] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Ghoshhajra, Brian] Massachusetts Gen Hosp, Dept Radiol, Cardiac MR PET CT Program, Boston, MA 02114 USA.
RP Blankstein, R (reprint author), Brigham & Womens Hosp, Noninvas Cardiovasc Imaging Program, Div Cardiovasc, Dept Med, 75 Francis St, Boston, MA 02115 USA.
EM rblankstein@partners.org
RI Ghoshhajra, Brian/J-2114-2016; Bittencourt, Marcio/C-1444-2011;
OI Ghoshhajra, Brian/0000-0002-3865-3432; Bittencourt,
Marcio/0000-0002-3711-1754; Hulten, Edward/0000-0001-9281-0032
NR 57
TC 13
Z9 13
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1071-3581
J9 J NUCL CARDIOL
JI J. Nucl. Cardiol.
PD JUN
PY 2012
VL 19
IS 3
BP 588
EP 600
DI 10.1007/s12350-012-9546-5
PG 13
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA 947BO
UT WOS:000304401800023
PM 22456969
ER
PT J
AU Kwon, JY
Campbell, JT
Myerson, MS
AF Kwon, John Y.
Campbell, John T.
Myerson, Mark S.
TI Posterior Tibial Tendon Tear After 4-Cortex Syndesmotic Screw Fixation:
A Case Report and Literature Review
SO JOURNAL OF ORTHOPAEDIC TRAUMA
LA English
DT Article
DE posterior tibial tendon tear; four cortice syndesmotic screw fixation;
syndesmotic screw fixation
ID CLOSED ANKLE FRACTURE; RUPTURE; REMOVAL; DISLOCATION
AB We describe a previously unreported problem of a patient who underwent errant 4-cortex syndesmotic screw fixation with resultant posterior tibial tendon tear necessitating removal of hardware and repair of a tendon tear.
C1 [Kwon, John Y.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Orthopaed Surg, Boston, MA 02114 USA.
[Campbell, John T.; Myerson, Mark S.] Inst Foot & Ankle Reconstruct Mercy, Baltimore, MD USA.
RP Kwon, JY (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Orthopaed Surg, 55 Fruit St, Boston, MA 02114 USA.
EM johnkwonmd@gmail.com
NR 15
TC 2
Z9 2
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0890-5339
J9 J ORTHOP TRAUMA
JI J. Orthop. Trauma
PD JUN
PY 2012
VL 26
IS 6
BP E66
EP E69
DI 10.1097/BOT.0b013e31821e127f
PG 4
WC Orthopedics; Sport Sciences
SC Orthopedics; Sport Sciences
GA 947FO
UT WOS:000304414300007
PM 21849910
ER
PT J
AU Makino, CL
AF Makino, Clint L.
TI Easy does it when bleaching isolated mouse rods
SO JOURNAL OF PHYSIOLOGY-LONDON
LA English
DT Editorial Material
C1 [Makino, Clint L.] Massachusetts Eye & Ear Infirm, Dept Ophthalmol, Boston, MA 02114 USA.
[Makino, Clint L.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Makino, CL (reprint author), Massachusetts Eye & Ear Infirm, Dept Ophthalmol, 243 Charles St, Boston, MA 02114 USA.
EM cmakino@meei.harvard.edu
OI Makino, Clint/0000-0002-6005-9069
NR 4
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3751
J9 J PHYSIOL-LONDON
JI J. Physiol.-London
PD JUN
PY 2012
VL 590
IS 11
BP 2551
EP 2552
DI 10.1113/jphysiol.2012.233643
PG 2
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA 950OZ
UT WOS:000304659900006
PM 22787167
ER
PT J
AU Spina, JL
McIntyre, CL
Pulcini, JA
AF Spina, Jennifer L.
McIntyre, C. Lynne
Pulcini, Joyce A.
TI An Intervention to Increase High School Students' Compliance With
Carrying Auto-Injectable Epinephrine: A MASNRN Study
SO JOURNAL OF SCHOOL NURSING
LA English
DT Article
DE allergies; adolescents; evidence-based practice; epinephrine
ID ALLERGIC REACTIONS; FOOD ALLERGY; ANAPHYLACTIC REACTIONS; UNITED-STATES;
CHILDREN
AB Adolescents with life-threatening allergies are at a greater risk for a fatal anaphylactic event since only about half of them carry unexpired epinephrine available for emergency use. The aim of this study was to test the effectiveness of school nurse interventions that consisted of either routine or periodic checks during the school year for the availability of unexpired auto-injectable epinephrine. Seventy-seven students from 11 Massachusetts high schools participated in this study. Descriptive and chi-square (chi(2)) statistics as well as the Fisher's exact test were used to analyze data. Findings suggest that while periodic checks for the availability of epinephrine throughout the school year do not increase the likelihood that students will have epinephrine available, those students who do carry their epinephrine are more likely to have unexpired medication with periodic reminders during the school year.
C1 [Spina, Jennifer L.] Massachusetts Gen Hosp Boys & Girls Clubs Boston, Lynn, MA 01904 USA.
[McIntyre, C. Lynne] DotWell, Evaluat & Planning, Dorchester, MA USA.
[Pulcini, Joyce A.] Boston Coll, Connell Sch Nursing, Boston, MA USA.
RP Spina, JL (reprint author), Massachusetts Gen Hosp Boys & Girls Clubs Boston, 22 Maplewood Rd, Lynn, MA 01904 USA.
EM jenniferspina@comcast.net
FU NASN (National Association of School Nurses)
FX The author(s) disclosed receipt of the following financial support for
the research, authorship, and/or publication of this article: The
author(s) received a NASN (National Association of School Nurses)
Research Award to conduct this research study.
NR 27
TC 6
Z9 6
U1 2
U2 6
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1059-8405
J9 J SCH NURS
JI J. Sch. Nurs.
PD JUN
PY 2012
VL 28
IS 3
BP 230
EP 237
DI 10.1177/1059840511431459
PG 8
WC Nursing
SC Nursing
GA 951DL
UT WOS:000304700900010
PM 22217467
ER
PT J
AU Bober, S
Falk, S
Patendaude, A
AF Bober, Sharon
Falk, Sandy
Patendaude, Andrea
TI THE HIGH COST OF RISK REDUCTION: SEXUAL DYSFUNCTION IN YOUNG BRCA1/2
MUTATION CARRIERS AFTER PROPHYLACTIC OOPHORECTOMY AND NEXT STEPS FOR
ADDRESSING INTERVENTION
SO JOURNAL OF SEXUAL MEDICINE
LA English
DT Meeting Abstract
C1 [Bober, Sharon] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Bober, Sharon; Falk, Sandy; Patendaude, Andrea] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1743-6095
J9 J SEX MED
JI J. Sex. Med.
PD JUN
PY 2012
VL 9
SU 3
SI SI
BP 178
EP 178
PG 1
WC Urology & Nephrology
SC Urology & Nephrology
GA 950PH
UT WOS:000304660700050
ER
PT J
AU Meissner, TB
Li, A
Kobayashi, KS
AF Meissner, Torsten B.
Li, Amy
Kobayashi, Koichi S.
TI NLRC5: a newly discovered MHC class I transactivator (CITA)
SO MICROBES AND INFECTION
LA English
DT Review
DE MHC class I; NLR proteins; CIITA
ID COMPLEX CLASS-II; BARE LYMPHOCYTE SYNDROME; FAMILY-MEMBER NLRC5;
GTP-BINDING DOMAIN; MICE LACKING; IFN-GAMMA; TRANSCRIPTIONAL REGULATION;
ANTIGEN PRESENTATION; NATURAL-KILLER; PYRIN DOMAIN
AB Major histocompatibility complex (MHC) class I and class II are crucial for the function of the human adaptive immune system. An NLR protein, CIITA (MHC class II transactivator), is a master regulator of MHC class 11 gene expression as well as of some of the genes involved in MHC class II antigen presentation. It has recently been discovered that another member of the NI:.,R protein family, NLRC5, transcriptionally activates MHC class I genes, and thus acts as "CITA" (MHC class I transactivator), a counterpart to CIITA. In addition to MHC class I genes, NLRC5 can induce the expression of beta 2M, TAP1 and LMP2, essential components of MHC class I antigen presentation. These findings indicate that NLRC5 and CIITA are transcriptional regulators that orchestrate the concerted expression of critical components in the MHC class I and MHC class 11 pathways, respectively. (C) 2011 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
C1 [Meissner, Torsten B.; Li, Amy; Kobayashi, Koichi S.] Harvard Univ, Sch Med, Dept Canc Immunol & AIDS, Dana Farber Canc Inst, Boston, MA 02215 USA.
[Meissner, Torsten B.; Kobayashi, Koichi S.] Harvard Univ, Sch Med, Dept Microbiol & Immunobiol, Boston, MA 02215 USA.
RP Kobayashi, KS (reprint author), Harvard Univ, Sch Med, Dept Canc Immunol & AIDS, Dana Farber Canc Inst, Dana 1420A,450 Brookline Ave, Boston, MA 02215 USA.
EM Koichi_Kobayashi@dfci.harvard.edu
FU NIH; Crohn's and Colitis Foundation of America; Cancer Research
Institute; Claudia Adams Barr Award; EMBO
FX This work was supported by grants from the NIH and the Crohn's and
Colitis Foundation of America (K.S.K.). K.S.K. is a recipient of the
Investigator Award from the Cancer Research Institute and the Claudia
Adams Barr Award and T.B.M has been a recipient of the EMBO Long Term
fellowship. The authors have no conflicting financial interests.
NR 67
TC 20
Z9 24
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1286-4579
J9 MICROBES INFECT
JI Microbes Infect.
PD JUN
PY 2012
VL 14
IS 6
BP 477
EP 484
DI 10.1016/j.micinf.2011.12.007
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 948RI
UT WOS:000304519900001
PM 22209772
ER
PT J
AU Zorick, T
Lee, B
Mandelkern, MA
Fong, T
Robertson, C
Ghahremani, DG
Brown, AK
Sumerel, B
London, ED
AF Zorick, T.
Lee, B.
Mandelkern, M. A.
Fong, T.
Robertson, C.
Ghahremani, D. G.
Brown, A. K.
Sumerel, B.
London, E. D.
TI Low striatal dopamine receptor availability linked to caloric intake
during abstinence from chronic methamphetamine abuse
SO MOLECULAR PSYCHIATRY
LA English
DT Letter
ID FOOD
C1 [Zorick, T.; Lee, B.; Fong, T.; Ghahremani, D. G.; Brown, A. K.; Sumerel, B.; London, E. D.] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA.
[Zorick, T.] Greater Los Angeles Vet Adm Healthcare Syst, Dept Psychiat, Los Angeles, CA USA.
[Mandelkern, M. A.] Univ Calif Irvine, Dept Phys, Irvine, CA 92717 USA.
[Robertson, C.; London, E. D.] Univ Calif Los Angeles, Dept Mol & Med Pharmacol, Los Angeles, CA 90024 USA.
[London, E. D.] Univ Calif Los Angeles, Brain Res Inst, Los Angeles, CA 90024 USA.
RP Zorick, T (reprint author), Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA.
EM elondon@mednet.ucla.edu
FU NCRR NIH HHS [M01 RR000865, MO1 RR00865]; NIDA NIH HHS [R01 DA020726,
P20 DA022539, R01 DA015179]
NR 9
TC 4
Z9 4
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD JUN
PY 2012
VL 17
IS 6
BP 569
EP 571
DI 10.1038/mp.2011.137
PG 4
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA 947TU
UT WOS:000304454700002
PM 22024765
ER
PT J
AU Varma, D
Chandrasekaran, S
Sundin, LJR
Reidy, KT
Wan, XH
Chasse, DAD
Nevis, KR
DeLuca, JG
Salmon, ED
Cook, JG
AF Varma, Dileep
Chandrasekaran, Srikripa
Sundin, Lynsie J. R.
Reidy, Karen T.
Wan, Xiaohu
Chasse, Dawn A. D.
Nevis, Kathleen R.
DeLuca, Jennifer G.
Salmon, E. D.
Cook, Jeanette Gowen
TI Recruitment of the human Cdt1 replication licensing protein by the loop
domain of Hec1 is required for stable kinetochore-microtubule attachment
SO NATURE CELL BIOLOGY
LA English
DT Article
ID DNA-REPLICATION; CHROMOSOME SEGREGATION; LIVING CELLS; MITOSIS;
CHECKPOINT; INITIATION; GEMININ; COMPLEX; DYNEIN; ORC6
AB Cdt1, a protein critical for replication origin licensing in G1 phase, is degraded during S phase but re-accumulates in G2 phase. We now demonstrate that human Cdt1 has a separable essential mitotic function. Cdtl localizes to kinetochores during mitosis through interaction with the Hec1 component of the Ndc80 complex. G2-specific depletion of Cdtl arrests cells in late prometaphase owing to abnormally unstable kinetochore-microtubule (kMT) attachments and Mad1-dependent spindle-assembly-checkpoint activity. Cdtl binds a unique loop extending from the rod domain of Hec1 that we show is also required for kMT attachment. Mutation of the loop domain prevents Cdtl kinetochore localization and arrests cells in prometaphase. Super-resolution fluorescence microscopy indicates that Cdtl binding to the Hec1 loop domain promotes a microtubule-dependent conformational change in the Ndc80 complex in vivo. These results support the conclusion that Cdtl binding to Hec1 is essential for an extended Ndc80 configuration and stable kMT attachment.
C1 [Varma, Dileep; Wan, Xiaohu; Salmon, E. D.] Univ N Carolina, Dept Biol, Chapel Hill, NC 27599 USA.
[Chandrasekaran, Srikripa; Cook, Jeanette Gowen] Univ N Carolina, Dept Biochem & Biophys, Chapel Hill, NC 27599 USA.
[Sundin, Lynsie J. R.; DeLuca, Jennifer G.] Colorado State Univ, Dept Biochem & Mol Biol, Ft Collins, CO 80523 USA.
[Reidy, Karen T.; Cook, Jeanette Gowen] Univ N Carolina, Curriculum Genet & Mol Biol, Chapel Hill, NC 27599 USA.
[Chasse, Dawn A. D.] Duke Univ, Med Ctr, Duke Inst Genome Sci & Policy, Durham, NC 27710 USA.
[Nevis, Kathleen R.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Charlestown, MA 02129 USA.
RP Salmon, ED (reprint author), Univ N Carolina, Dept Biol, CB 3280, Chapel Hill, NC 27599 USA.
EM tsalmon@email.unc.edu; jean_cook@med.unc.edu
OI Cook, Jeanette/0000-0003-0849-7405
FU NIH [K01 CA094907, GM083024, GM24364, GM088371]; Pew Scholars Program in
the Biomedical Sciences
FX We thank A. Desai for providing Krill, Nsl1, Dsn1 and Spindly
antibodies, A. Musacchio (Max Planck Institute of Molecular Physiology,
Dortmund, Germany) for anti-Mad1, Zwint1 and ZW10 antibodies, B.
Stillman (Cold Spring Harbor Laboratory, New York, USA) for anti-Orc6
antibody, S. Taylor (University of Manchester, UK) for anti-Bub1 and
BubR1 antibodies, T. Stukenberg (University of Virginia at
Charlottesville, Virginia, USA) for anti-Spc24 antibody, T. Yen (Fox
Chase Cancer Center, Philadelphia, Pennsylvania, USA) for anti-CENP-E
antibody and I. Cheeseman (Whitehead Institute of Biomedical Research
and MIT, Cambridge, Massachusetts, USA) for anti-Ska3 antibody. We are
grateful to A. Desai (University of California San Diego, La Jolla, CA,
USA), D. Cheerambathur, T. Stukenberg, K. Slep and T. Maresca for
helpful discussions and to J. Mick for generating Hec1 constructs. We
would also like to thank other members of the Salmon, Cook, A. Desai and
J. Nevins laboratories for their support during this project. J.G.C. was
supported by NIH K01 CA094907 and NIH GM083024, E.D.S. was supported by
NIH GM24364 and J.G.D. was supported by NIH GM088371 and a grant from
the Pew Scholars Program in the Biomedical Sciences.
NR 43
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U1 0
U2 8
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1465-7392
J9 NAT CELL BIOL
JI Nat. Cell Biol.
PD JUN
PY 2012
VL 14
IS 6
BP 593
EP +
DI 10.1038/ncb2489
PG 22
WC Cell Biology
SC Cell Biology
GA 949TW
UT WOS:000304599900009
PM 22581055
ER
PT J
AU Kiezun, A
Garimella, K
Do, R
Stitziel, NO
Neale, BM
McLaren, PJ
Gupta, N
Sklar, P
Sullivan, PF
Moran, JL
Hultman, CM
Lichtenstein, P
Magnusson, P
Lehner, T
Shugart, YY
Price, AL
de Bakker, PIW
Purcell, SM
Sunyaev, SR
AF Kiezun, Adam
Garimella, Kiran
Do, Ron
Stitziel, Nathan O.
Neale, Benjamin M.
McLaren, Paul J.
Gupta, Namrata
Sklar, Pamela
Sullivan, Patrick F.
Moran, Jennifer L.
Hultman, Christina M.
Lichtenstein, Paul
Magnusson, Patrik
Lehner, Thomas
Shugart, Yin Yao
Price, Alkes L.
de Bakker, Paul I. W.
Purcell, Shaun M.
Sunyaev, Shamil R.
TI Exome sequencing and the genetic basis of complex traits
SO NATURE GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; SINGLE-NUCLEOTIDE POLYMORPHISMS; ALLELE
FREQUENCY-SPECTRUM; RARE VARIANTS; POPULATION-STRUCTURE; PROTEIN
FUNCTION; COMMON DISEASES; PLASMA-LEVELS; MUTATIONS; SELECTION
C1 [Kiezun, Adam; McLaren, Paul J.; de Bakker, Paul I. W.; Sunyaev, Shamil R.] Harvard Univ, Sch Med, Dept Med, Div Genet,Brigham & Womens Hosp, Boston, MA 02114 USA.
[Kiezun, Adam; Garimella, Kiran; Do, Ron; Stitziel, Nathan O.; Neale, Benjamin M.; McLaren, Paul J.; Gupta, Namrata; Moran, Jennifer L.; Price, Alkes L.; de Bakker, Paul I. W.; Sunyaev, Shamil R.] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Do, Ron; Neale, Benjamin M.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Stitziel, Nathan O.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Cardiovasc Med, Boston, MA 02115 USA.
[Neale, Benjamin M.; Purcell, Shaun M.] Massachusetts Gen Hosp, Analyt & Translat Genet Unit, Boston, MA 02114 USA.
[Sklar, Pamela] Mt Sinai Sch Med, Dept Psychiat, Friedman Brain Inst, New York, NY USA.
[Sklar, Pamela] Mt Sinai Sch Med, Inst Genom & Multiscale Biol, New York, NY USA.
[Sullivan, Patrick F.] Univ N Carolina, Sch Med, Dept Genet, Chapel Hill, NC USA.
[Hultman, Christina M.; Lichtenstein, Paul; Magnusson, Patrik] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Shugart, Yin Yao] NIMH, Div Neurosci & Basic Behav Sci, Bethesda, MD 20892 USA.
[Price, Alkes L.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Price, Alkes L.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[de Bakker, Paul I. W.] Univ Med Ctr Utrecht, Dept Med Genet, Utrecht, Netherlands.
[de Bakker, Paul I. W.] Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands.
RP Sunyaev, SR (reprint author), Harvard Univ, Sch Med, Dept Med, Div Genet,Brigham & Womens Hosp, Boston, MA 02114 USA.
EM ssunyaev@rics.bwh.harvard.edu
RI de Bakker, Paul/B-8730-2009; Magnusson, Patrik/C-4458-2017;
OI de Bakker, Paul/0000-0001-7735-7858; lichtenstein,
paul/0000-0003-3037-5287; Stitziel, Nathan/0000-0002-4963-8211; Moran,
Jennifer/0000-0002-5664-4716
FU US National Institutes of Health (NIH) [5R01 MH084676]; Collaboration
for AIDS Vaccine Discovery of the Bill and Melinda Gates Foundation; NIH
[AI069474, AI069428, AI69467, AI069415, Al32782, AI27661, AI25859,
AI28568, AI30914, AI069495, AI069471, AI069532, AI069452, AI069450,
AI069556]; Herman Foundation; Stanley Medical Research Institute;
National Institute of Mental Health (NIMH) [1R01MH089208-01]; Canadian
Institutes of Health Research
FX The authors are grateful to S. Pollack for assistance with EIGENSOFT.
This work was made possible, in part, by the US National Institutes of
Health (NIH; grant 5R01 MH084676) and, in part, by the International HIV
Controllers Study, supported by the Collaboration for AIDS Vaccine
Discovery of the Bill and Melinda Gates Foundation (to P.I.W.d.B.), and
the AIDS Clinical Trials Group, supported by the NIH (grants AI069513,
AI34835, AI069432, AI069423, AI069477, AI069501, AI069474, AI069428,
AI69467, AI069415, Al32782, AI27661, AI25859, AI28568, AI30914,
AI069495, AI069471, AI069532, AI069452, AI069450, AI069556, AI069484,
AI069472, AI34853, AI069465, AI069511, AI38844, AI069424, AI069434,
AI46370, AI68634, AI069502, AI069419, AI068636, RR024975 and AI077505).
Sequencing of the SCZ control individuals was funded by the NIH (grant
RC2MH089905), the Herman Foundation and the Stanley Medical Research
Institute. N.O.S. was supported, in part, by an NIH Training Grant
(T32-HL07604-25; Division of Cardiovascular Medicine, Brigham and
Women's Hospital). B.M.N. was supported by a National Institute of
Mental Health (NIMH) grant (1R01MH089208-01). R. D. is supported by a
Canadian Institutes of Health Research Banting Postdoctoral Fellowship.
The views expressed in this paper do not necessarily represent the views
of the NIMH, NIH, Department of Health and Human Services (HHS) or the
US government.
NR 97
TC 195
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U1 1
U2 35
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD JUN
PY 2012
VL 44
IS 6
BP 623
EP 630
DI 10.1038/ng.2303
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 949BT
UT WOS:000304551100006
PM 22641211
ER
PT J
AU Pasaniuc, B
Rohland, N
McLaren, PJ
Garimella, K
Zaitlen, N
Li, H
Gupta, N
Neale, BM
Daly, MJ
Sklar, P
Sullivan, PF
Bergen, S
Moran, JL
Hultman, CM
Lichtenstein, P
Magnusson, P
Purcell, SM
Haas, DW
Liang, LM
Sunyaev, S
Patterson, N
de Bakker, PIW
Reich, D
Price, AL
AF Pasaniuc, Bogdan
Rohland, Nadin
McLaren, Paul J.
Garimella, Kiran
Zaitlen, Noah
Li, Heng
Gupta, Namrata
Neale, Benjamin M.
Daly, Mark J.
Sklar, Pamela
Sullivan, Patrick F.
Bergen, Sarah
Moran, Jennifer L.
Hultman, Christina M.
Lichtenstein, Paul
Magnusson, Patrik
Purcell, Shaun M.
Haas, David W.
Liang, Liming
Sunyaev, Shamil
Patterson, Nick
de Bakker, Paul I. W.
Reich, David
Price, Alkes L.
TI Extremely low-coverage sequencing and imputation increases power for
genome-wide association studies
SO NATURE GENETICS
LA English
DT Article
ID GENOTYPE; POPULATION; SCHIZOPHRENIA; FRAMEWORK; LINKAGE; MODELS
AB Genome-wide association studies (GWAS) have proven to be a powerful method to identify common genetic variants contributing to susceptibility to common diseases. Here, we show that extremely low-coverage sequencing (0.1-0.5x) captures almost as much of the common (>5%) and low-frequency (1-5%) variation across the genome as SNP arrays. As an empirical demonstration, we show that genome-wide SNP genotypes can be inferred at a mean r(2) of 0.71 using off-target data (0.24x average coverage) in a whole-exome study of 909 samples. Using both simulated and real exome-sequencing data sets, we show that association statistics obtained using extremely low-coverage sequencing data attain similar P values at known associated variants as data from genotyping arrays, without an excess of false positives. Within the context of reductions in sample preparation and sequencing costs, funds invested in extremely low-coverage sequencing can yield several times the effective sample size of GWAS based on SNP array data and a commensurate increase in statistical power.
C1 [Pasaniuc, Bogdan; Zaitlen, Noah; Liang, Liming; Price, Alkes L.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Pasaniuc, Bogdan; Zaitlen, Noah; Liang, Liming; Price, Alkes L.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Pasaniuc, Bogdan; Rohland, Nadin; McLaren, Paul J.; Garimella, Kiran; Zaitlen, Noah; Li, Heng; Gupta, Namrata; Neale, Benjamin M.; Daly, Mark J.; Bergen, Sarah; Moran, Jennifer L.; Purcell, Shaun M.; Liang, Liming; Sunyaev, Shamil; Patterson, Nick; de Bakker, Paul I. W.; Reich, David; Price, Alkes L.] Broad Inst Harvard & Massachusetts Inst Technol M, Cambridge, MA USA.
[Rohland, Nadin; Reich, David] Harvard Univ, Sch Med, Dept Genet, Boston, MA USA.
[McLaren, Paul J.; Sunyaev, Shamil; de Bakker, Paul I. W.] Brigham & Womens Hosp, Div Genet, Boston, MA 02115 USA.
[Neale, Benjamin M.; Daly, Mark J.; Purcell, Shaun M.] Massachusetts Gen Hosp, Analyt & Translat Genet Unit, Boston, MA 02114 USA.
[Sklar, Pamela] Mt Sinai Sch Med, Friedman Brain Inst, Dept Psychiat, New York, NY USA.
[Sklar, Pamela] Mt Sinai Sch Med, Inst Genom & Multiscale Biol, New York, NY USA.
[Sullivan, Patrick F.] Univ N Carolina, Sch Med, Dept Genet, Chapel Hill, NC USA.
[Hultman, Christina M.; Lichtenstein, Paul; Magnusson, Patrik] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Haas, David W.] Vanderbilt Univ, Sch Med, Nashville, TN 37212 USA.
[de Bakker, Paul I. W.] Univ Med Ctr Utrecht, Dept Med Genet, Utrecht, Netherlands.
[de Bakker, Paul I. W.] Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands.
RP Pasaniuc, B (reprint author), Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
EM bpasaniu@hsph.harvard.edu; reich@genetics.med.harvard.edu;
aprice@hsph.harvard.edu
RI Pasaniuc, Bogdan/E-9310-2012; Bergen, Sarah/I-8313-2012; Li,
Heng/D-9344-2011; de Bakker, Paul/B-8730-2009; Magnusson,
Patrik/C-4458-2017
OI Bergen, Sarah/0000-0002-5888-0034; lichtenstein,
paul/0000-0003-3037-5287; Moran, Jennifer/0000-0002-5664-4716; Li,
Heng/0000-0003-4874-2874; de Bakker, Paul/0000-0001-7735-7858;
FU US National Institutes of Health (NIH) [R01 HG006399, R01 MH084676]; NIH
[P-30-AI060354, AI069513, AI34835, AI069432, AI069423, AI069477,
AI069501, AI069474, AI069428, AI69467, AI069415, Al32782, AI27661,
AI25859, AI28568, AI30914, AI069495, AI069471, AI069532, AI069452,
AI069450]; NIMH [5RC2MH089905]; Sylvan Herman Foundation; Stanley
Medical Research Institute
FX We would like to acknowledge the ARRA Autism Sequencing Consortium
(AASC) principal investigators for use of the autism data sets,
including E. Boerwinkle, J.D. Buxbaum, E. H. Cook Jr., M.J. Daly
(communicating principal investigator), B. Devlin, R. Gibbs, K. Roeder,
A. Sabo, G. D. Schellenberg and J.S. Sutcliffe. We thank T. Lehner, A.
Felsenfeld and P. Bender for their support and contribution to the AASC
project and to the generation of AUT sequencing data. This research was
supported by US National Institutes of Health (NIH) grants (R01 HG006399
to B. P., N.P., D. R. and A. L. P. and R01 MH084676 to S. S.). The IHCS
acknowledges generous support from the Mark and Lisa Schwartz Foundation
and the Collaboration for AIDS Vaccine Discovery of the Bill and Melinda
Gates Foundation. The IHCS was also supported in part by NIH grants
(P-30-AI060354 to the Harvard University Center for AIDS Research,
AI069513, AI34835, AI069432, AI069423, AI069477, AI069501, AI069474,
AI069428, AI69467, AI069415, Al32782, AI27661, AI25859, AI28568,
AI30914, AI069495, AI069471, AI069532, AI069452, AI069450, AI069556,
AI069484, AI069472, AI34853, AI069465, AI069511, AI38844, AI069424,
AI069434, AI46370, AI68634, AI069502, AI069419, AI068636 and RR024975 to
the AIDS Clinical Trials Group and AI077505 to D. W. H.). Data
generation for the NIMH controls was directly supported by NIH grants
(R01MH089208, R01 MH089025, R01 MH089004 and R01 MH089482). SCZ data
generation was supported by an NIMH grant (5RC2MH089905; P. S. and S. M.
P.) and by the Sylvan Herman Foundation and the Stanley Medical Research
Institute (a gift to the Stanley Center for Psychiatric Research).
NR 29
TC 83
Z9 86
U1 1
U2 29
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 JUN
PY 2012
VL 44
IS 6
BP 631
EP U41
DI 10.1038/ng.2283
PG 6
WC Genetics & Heredity
SC Genetics & Heredity
GA 949BT
UT WOS:000304551100007
PM 22610117
ER
PT J
AU Laurie, CC
Laurie, CA
Rice, K
Doheny, KF
Zelnick, LR
McHugh, CP
Ling, H
Hetrick, KN
Pugh, EW
Amos, C
Wei, QY
Wang, LE
Lee, JE
Barnes, KC
Hansel, NN
Mathias, R
Daley, D
Beaty, TH
Scott, AF
Ruczinski, I
Scharpf, RB
Bierut, LJ
Hartz, SM
Landi, MT
Freedman, ND
Goldin, LR
Ginsburg, D
Li, J
Desch, KC
Strom, SS
Blot, WJ
Signorello, LB
Ingles, SA
Chanock, SJ
Berndt, SI
Le Marchand, L
Henderson, BE
Monroe, KR
Heit, JA
de Andrade, M
Armasu, SM
Regnier, C
Lowe, WL
Hayes, MG
Marazita, ML
Feingold, E
Murray, JC
Melbye, M
Feenstra, B
Kang, JH
Wiggs, JL
Jarvik, GP
McDavid, AN
Seshan, VE
Mirel, DB
Crenshaw, A
Sharopova, N
Wise, A
Shen, J
Crosslin, DR
Levine, DM
Zheng, XW
Udren, JI
Bennett, S
Nelson, SC
Gogarten, SM
Conomos, MP
Heagerty, P
Manolio, T
Pasquale, LR
Haiman, CA
Caporaso, N
Weir, BS
AF Laurie, Cathy C.
Laurie, Cecelia A.
Rice, Kenneth
Doheny, Kimberly F.
Zelnick, Leila R.
McHugh, Caitlin P.
Ling, Hua
Hetrick, Kurt N.
Pugh, Elizabeth W.
Amos, Chris
Wei, Qingyi
Wang, Li-E
Lee, Jeffrey E.
Barnes, Kathleen C.
Hansel, Nadia N.
Mathias, Rasika
Daley, Denise
Beaty, Terri H.
Scott, Alan F.
Ruczinski, Ingo
Scharpf, Rob B.
Bierut, Laura J.
Hartz, Sarah M.
Landi, Maria Teresa
Freedman, Neal D.
Goldin, Lynn R.
Ginsburg, David
Li, Jun
Desch, Karl C.
Strom, Sara S.
Blot, William J.
Signorello, Lisa B.
Ingles, Sue A.
Chanock, Stephen J.
Berndt, Sonja I.
Le Marchand, Loic
Henderson, Brian E.
Monroe, Kristine R.
Heit, John A.
de Andrade, Mariza
Armasu, Sebastian M.
Regnier, Cynthia
Lowe, William L.
Hayes, M. Geoffrey
Marazita, Mary L.
Feingold, Eleanor
Murray, Jeffrey C.
Melbye, Mads
Feenstra, Bjarke
Kang, Jae H.
Wiggs, Janey L.
Jarvik, Gail P.
McDavid, Andrew N.
Seshan, Venkatraman E.
Mirel, Daniel B.
Crenshaw, Andrew
Sharopova, Nataliya
Wise, Anastasia
Shen, Jess
Crosslin, David R.
Levine, David M.
Zheng, Xiuwen
Udren, Jenna I.
Bennett, Siiri
Nelson, Sarah C.
Gogarten, Stephanie M.
Conomos, Matthew P.
Heagerty, Patrick
Manolio, Teri
Pasquale, Louis R.
Haiman, Christopher A.
Caporaso, Neil
Weir, Bruce S.
TI Detectable clonal mosaicism from birth to old age and its relationship
to cancer
SO NATURE GENETICS
LA English
DT Article
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; COPY-NUMBER VARIATION; POLYMORPHISM ARRAY
ANALYSIS; B-CELL LYMPHOCYTOSIS; STEM-CELLS; GENOME; MALIGNANCIES;
ASSOCIATION; GENE; POPULATIONS
AB We detected clonal mosaicism for large chromosomal anomalies (duplications, deletions and uniparental disomy) using SNP microarray data from over 50,000 subjects recruited for genome-wide association studies. This detection method requires a relatively high frequency of cells with the same abnormal karyotype (>5-10%; presumably of clonal origin) in the presence of normal cells. The frequency of detectable clonal mosaicism in peripheral blood is low (<0.5%) from birth until 50 years of age, after which it rapidly rises to 2-3% in the elderly. Many of the mosaic anomalies are characteristic of those found in hematological cancers and identify common deleted regions with genes previously associated with these cancers. Although only 3% of subjects with detectable clonal mosaicism had any record of hematological cancer before DNA sampling, those without a previous diagnosis have an estimated tenfold higher risk of a subsequent hematological cancer (95% confidence interval = 6-18).
C1 [Laurie, Cathy C.; Laurie, Cecelia A.; Rice, Kenneth; Zelnick, Leila R.; McHugh, Caitlin P.; Shen, Jess; Crosslin, David R.; Levine, David M.; Zheng, Xiuwen; Udren, Jenna I.; Bennett, Siiri; Nelson, Sarah C.; Gogarten, Stephanie M.; Conomos, Matthew P.; Heagerty, Patrick; Weir, Bruce S.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Doheny, Kimberly F.; Ling, Hua; Hetrick, Kurt N.; Pugh, Elizabeth W.] Johns Hopkins Univ, Ctr Inherited Dis Res, Baltimore, MD USA.
[Amos, Chris; Wei, Qingyi; Wang, Li-E] Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Div Canc Prevent & Populat Sci, Houston, TX 77030 USA.
[Lee, Jeffrey E.] Univ Texas MD Anderson Canc Ctr, Dept Surg Oncol, Div Surg, Houston, TX 77030 USA.
[Barnes, Kathleen C.; Hansel, Nadia N.; Mathias, Rasika] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
[Daley, Denise] Univ British Columbia, Dept Med, Vancouver, BC, Canada.
[Beaty, Terri H.] Johns Hopkins Univ, Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA.
[Scott, Alan F.] Johns Hopkins Univ, Sch Med, Inst Med Genet, Baltimore, MD USA.
[Ruczinski, Ingo] Johns Hopkins Univ, Dept Biostat, Baltimore, MD 21205 USA.
[Scharpf, Rob B.] Johns Hopkins Univ, Dept Oncol, Baltimore, MD USA.
[Bierut, Laura J.; Hartz, Sarah M.] Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA.
[Landi, Maria Teresa; Freedman, Neal D.; Goldin, Lynn R.; Chanock, Stephen J.; Berndt, Sonja I.; Caporaso, Neil] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Ginsburg, David] Univ Michigan, Howard Hughes Med Inst, Ann Arbor, MI 48109 USA.
[Ginsburg, David] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Li, Jun] Univ Michigan, Dept Human Genet, Ann Arbor, MI 48109 USA.
[Desch, Karl C.] Univ Michigan, Dept Pediat & Communicable Dis, Ann Arbor, MI 48109 USA.
[Blot, William J.; Signorello, Lisa B.] Vanderbilt Univ, Dept Med, Vanderbilt Epidemiol Ctr, Div Epidemiol, Nashville, TN USA.
[Ingles, Sue A.; Henderson, Brian E.; Monroe, Kristine R.; Haiman, Christopher A.] Univ So Calif, Keck Sch Med, Norris Comprehens Canc Ctr, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Le Marchand, Loic] Univ Hawaii, Canc Res Ctr, Program Epidemiol, Honolulu, HI 96813 USA.
[Heit, John A.] Mayo Clin, Dept Internal Med, Rochester, MN USA.
[de Andrade, Mariza; Armasu, Sebastian M.] Mayo Clin, Div Biomed Stat & Informat, Dept Hlth Sci Res, Rochester, MN USA.
[Regnier, Cynthia] Mayo Clin, Div Nephrol & Hypertens, Rochester, MN USA.
[Regnier, Cynthia] Mayo Clin, Mayo Hyperoxaluria Ctr, Rochester, MN USA.
[Lowe, William L.; Hayes, M. Geoffrey] Northwestern Univ, Div Endocrinol Metab & Mol Med, Chicago, IL 60611 USA.
[Marazita, Mary L.] Univ Pittsburgh, Sch Dent Med, Dept Oral Biol, Ctr Craniofacial & Dent Genet, Pittsburgh, PA USA.
[Feingold, Eleanor] Univ Pittsburgh, Dept Human Genet, Pittsburgh, PA USA.
[Murray, Jeffrey C.] Univ Iowa, Dept Pediat, Iowa City, IA 52242 USA.
[Melbye, Mads; Feenstra, Bjarke] Statens Serum Inst, Dept Epidemiol Res, DK-2300 Copenhagen, Denmark.
[Kang, Jae H.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Wiggs, Janey L.; Pasquale, Louis R.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol, Boston, MA USA.
[Jarvik, Gail P.] Univ Washington, Div Med Genet, Seattle, WA 98195 USA.
[McDavid, Andrew N.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Seshan, Venkatraman E.] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA.
[Mirel, Daniel B.; Crenshaw, Andrew] Broad Inst Harvard & MIT, Cambridge, MA USA.
[Sharopova, Nataliya] Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
[Wise, Anastasia; Manolio, Teri] NHGRI, Off Populat Genom, NIH, Bethesda, MD 20892 USA.
RP Laurie, CC (reprint author), Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
EM cclaurie@u.washington.edu
RI Weir, Bruce/A-2894-2013; Rice, Kenneth/A-4150-2013; Jarvik,
Gail/N-6476-2014; Freedman, Neal/B-9741-2015;
OI Rice, Kenneth/0000-0001-5779-4495; Jarvik, Gail/0000-0002-6710-8708;
Freedman, Neal/0000-0003-0074-1098; Feenstra,
Bjarke/0000-0003-1478-649X; Feingold, Eleanor/0000-0003-2898-6484;
McDavid, Andrew/0000-0002-6581-1213; Zheng, Xiuwen/0000-0002-1390-0708;
Gogarten, Stephanie/0000-0002-7231-9745; Hartz,
Sarah/0000-0002-5429-3799
FU US National Institutes of Health (NIH) Genes, Environment and Health
Initiative (GEI); NIH (NCI) [R29CA70334, R01CA100264, P50CA093459,
U10AA008401, CA63464, CA54281, CA1326792, RC2 CA148085]; NIH
[U01HG004738, HHSN268200782096C, U01HG004726, U01HG004735, U01HG004415,
U01HG004423]; NIH (National Institute Dental and Craniofacial Research
(NIDCR) [U01DE018993]; NIH, National Institute on Alcohol Abuse and
Alcoholism (NIAAA) [U01HG004422]; NIH, National Institute on Drug Abuse
(NIDA) [P01CA089392, R01DA013423, R01DA019963]; NIH (NIDCR)
[U01DE018903, R01DE014899]; NIH, NIH Center for Inherited Disease
Research (CIDR) [HHSN268200-782096C]; NIH, National Eye Institute (NEI)
[U01HG004728, R01EY015473, R01EY015872]; NIH, GENEVA Coordinating Center
[U01 HG004446]; NIG, CIDR [HHSN268200782096C, U01HG004438]; NIH, Broad
Center for Genotyping and Analysis [U01HG04424]; NIH, the National
Library of Medicine; Division of Cancer Epidemiology and Genetics, NCI,
NIH; Research to Prevent Blindness in NYC; Harvard Medical School;
Harvard Glaucoma Center of Excellence; NCI [T32 CA09168]
FX The GENEVA Consortium thanks the subjects and the staff of all GENEVA
studies for their important contributions. We thank the following state
cancer registries for their help: Alaska, Arizona, Arkansas, California,
Colorado, Connecticut, Delaware, Florida, Georgia, Idaho, Illinois,
Indiana, Iowa, Kentucky, Louisiana, Maine, Maryland, Massachusetts,
Michigan, Nebraska, New Hampshire, New Jersey, New York, North Carolina,
North Dakota, Ohio, Oklahoma, Oregon, Pennsylvania, Rhode Island, South
Carolina, Tennessee, Texas, Virginia, Washington and Wyoming. We thank
C. Laird and G. Marti for helpful comments on the manuscript and B.
Wakimoto and D. Gottschling for enlightening discussions. We also thank
K. Jacobs for exchanging ideas and for working with us to estimate
cross-method concordance of mosaic detection using the PLCO/GENEVA Lung
Cancer study. Support for the GENEVA genome-wide association studies was
provided through the US National Institutes of Health (NIH) Genes,
Environment and Health Initiative (GEI). Some studies also received
support from individual NIH Institutes. The grant numbers are: Melanoma
(NCI R29CA70334, R01CA100264 and P50CA093459); Lung Health
(U01HG004738); Cleft Lip/Palate (National Institute Dental and
Craniofacial Research (NIDCR): U01DE018993 and NIH contract:
HHSN268200782096C); Addiction (U01HG004422, National Institute on
Alcohol Abuse and Alcoholism (NIAAA): U10AA008401, National Cancer
Institute (NCI): P01CA089392, National Institute on Drug Abuse (NIDA):
R01DA013423 and R01DA019963); Lung Cancer (Z01CP010200); Blood Clotting
(R37 HL 039693); Prostate Cancer (U01HG004726, NCI: CA63464, CA54281,
CA1326792 and RC2 CA148085); Venous Thromboembolism (U01HG004735); Birth
Weight (U01HG004415); Dental Caries (NIDCR: U01DE018903 and R01DE014899,
NIH Center for Inherited Disease Research (CIDR) contract:
HHSN268200-782096C); Prematurity (U01HG004423); Glaucoma (U01HG004728,
National Eye Institute (NEI): R01EY015473 and R01EY015872); GENEVA
Coordinating Center (U01 HG004446); CIDR (U01HG004438 and
HHSN268200782096C); Broad Center for Genotyping and Analysis
(U01HG04424); the Intramural Research Program of the NIH, the National
Library of Medicine; and the Intramural Research Program of the Division
of Cancer Epidemiology and Genetics, NCI, NIH. L. R. P. was also
supported by a Physician Scientist award from Research to Prevent
Blindness in NYC and an Ophthalmology Scholar Award from Harvard Medical
School and from the Harvard Glaucoma Center of Excellence. L.R.Z. was
supported by the NCI (T32 CA09168).
NR 53
TC 161
Z9 161
U1 6
U2 36
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 JUN
PY 2012
VL 44
IS 6
BP 642
EP U58
DI 10.1038/ng.2271
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 949BT
UT WOS:000304551100010
PM 22561516
ER
PT J
AU Jacobs, KB
Yeager, M
Zhou, WY
Wacholder, S
Wang, ZM
Rodriguez-Santiago, B
Hutchinson, A
Deng, X
Liu, CW
Horner, MJ
Cullen, M
Epstein, CG
Burdett, L
Dean, MC
Chatterjee, N
Sampson, J
Chung, CC
Kovaks, J
Gapstur, SM
Stevens, VL
Teras, LT
Gaudet, MM
Albanes, D
Weinstein, SJ
Virtamo, J
Taylor, PR
Freedman, ND
Abnet, CC
Goldstein, AM
Hu, N
Yu, K
Yuan, JM
Liao, LD
Ding, T
Qiao, YL
Gao, YT
Koh, WP
Xiang, YB
Tang, ZZ
Fan, JH
Aldrich, MC
Amos, C
Blot, WJ
Bock, CH
Gillanders, EM
Harris, CC
Haiman, CA
Henderson, BE
Kolonel, LN
Le Marchand, L
McNeill, LH
Rybicki, BA
Schwartz, AG
Signorello, LB
Spitz, MR
Wiencke, JK
Wrensch, M
Wu, XF
Zanetti, KA
Ziegler, RG
Figueroa, JD
Garcia-Closas, M
Malats, N
Marenne, G
Prokunina-Olsson, L
Baris, D
Schwenn, M
Johnson, A
Landi, MT
Goldin, L
Consonni, D
Bertazzi, PA
Rotunno, M
Rajaraman, P
Andersson, U
Freeman, LEB
Berg, CD
Buring, JE
Butler, MA
Carreon, T
Feychting, M
Ahlbom, A
Gaziano, JM
Giles, GG
Hallmans, G
Hankinson, SE
Hartge, P
Henriksson, R
Inskip, PD
Johansen, C
Landgren, A
McKean-Cowdin, R
Michaud, DS
Melin, BS
Peters, U
Ruder, AM
Sesso, HD
Severi, G
Shu, XO
Visvanathan, K
White, E
Wolk, A
Zeleniuch-Jacquotte, A
Zheng, W
Silverman, DT
Kogevinas, M
Gonzalez, JR
Villa, O
Li, DH
Duell, EJ
Risch, HA
Olson, SH
Kooperberg, C
Wolpin, BM
Jiao, L
Hassan, M
Wheeler, W
Arslan, AA
Bueno-de-Mesquita, HB
Fuchs, CS
Gallinger, S
Gross, MD
Holly, EA
Klein, AP
LaCroix, A
Mandelson, MT
Petersen, G
Boutron-Ruault, MC
Bracci, PM
Canzian, F
Chang, K
Cotterchio, M
Giovannucci, EL
Goggins, M
Bolton, JAH
Jenab, M
Khaw, KT
Krogh, V
Kurtz, RC
McWilliams, RR
Mendelsohn, JB
Rabe, KG
Riboli, E
Tjonneland, A
Tobias, GS
Trichopoulos, D
Elena, JW
Yu, H
Amundadottir, L
Stolzenberg-Solomon, RZ
Kraft, P
Schumacher, F
Stram, D
Savage, SA
Mirabello, L
Andrulis, IL
Wunder, JS
Garcia, AP
Sierrasesumaga, L
Barkauskas, DA
Gorlick, RG
Purdue, M
Chow, WH
Moore, LE
Schwartz, KL
Davis, FG
Hsing, AW
Berndt, SI
Black, A
Wentzensen, N
Brinton, LA
Lissowska, J
Peplonska, B
McGlynn, KA
Cook, MB
Graubard, BI
Kratz, CP
Greene, MH
Erickson, RL
Hunter, DJ
Thomas, G
Hoover, RN
Real, FX
Fraumeni, JF
Caporaso, NE
Tucker, M
Rothman, N
Perez-Jurado, LA
Chanock, SJ
AF Jacobs, Kevin B.
Yeager, Meredith
Zhou, Weiyin
Wacholder, Sholom
Wang, Zhaoming
Rodriguez-Santiago, Benjamin
Hutchinson, Amy
Deng, Xiang
Liu, Chenwei
Horner, Marie-Josephe
Cullen, Michael
Epstein, Caroline G.
Burdett, Laurie
Dean, Michael C.
Chatterjee, Nilanjan
Sampson, Joshua
Chung, Charles C.
Kovaks, Joseph
Gapstur, Susan M.
Stevens, Victoria L.
Teras, Lauren T.
Gaudet, Mia M.
Albanes, Demetrius
Weinstein, Stephanie J.
Virtamo, Jarmo
Taylor, Philip R.
Freedman, Neal D.
Abnet, Christian C.
Goldstein, Alisa M.
Hu, Nan
Yu, Kai
Yuan, Jian-Min
Liao, Linda
Ding, Ti
Qiao, You-Lin
Gao, Yu-Tang
Koh, Woon-Puay
Xiang, Yong-Bing
Tang, Ze-Zhong
Fan, Jin-Hu
Aldrich, Melinda C.
Amos, Christopher
Blot, William J.
Bock, Cathryn H.
Gillanders, Elizabeth M.
Harris, Curtis C.
Haiman, Christopher A.
Henderson, Brian E.
Kolonel, Laurence N.
Le Marchand, Loic
McNeill, Lorna H.
Rybicki, Benjamin A.
Schwartz, Ann G.
Signorello, Lisa B.
Spitz, Margaret R.
Wiencke, John K.
Wrensch, Margaret
Wu, Xifeng
Zanetti, Krista A.
Ziegler, Regina G.
Figueroa, Jonine D.
Garcia-Closas, Montserrat
Malats, Nuria
Marenne, Gaelle
Prokunina-Olsson, Ludmila
Baris, Dalsu
Schwenn, Molly
Johnson, Alison
Landi, Maria Teresa
Goldin, Lynn
Consonni, Dario
Bertazzi, Pier Alberto
Rotunno, Melissa
Rajaraman, Preetha
Andersson, Ulrika
Freeman, Laura E. Beane
Berg, Christine D.
Buring, Julie E.
Butler, Mary A.
Carreon, Tania
Feychting, Maria
Ahlbom, Anders
Gaziano, J. Michael
Giles, Graham G.
Hallmans, Goran
Hankinson, Susan E.
Hartge, Patricia
Henriksson, Roger
Inskip, Peter D.
Johansen, Christoffer
Landgren, Annelie
McKean-Cowdin, Roberta
Michaud, Dominique S.
Melin, Beatrice S.
Peters, Ulrike
Ruder, Avima M.
Sesso, Howard D.
Severi, Gianluca
Shu, Xiao-Ou
Visvanathan, Kala
White, Emily
Wolk, Alicja
Zeleniuch-Jacquotte, Anne
Zheng, Wei
Silverman, Debra T.
Kogevinas, Manolis
Gonzalez, Juan R.
Villa, Olaya
Li, Donghui
Duell, Eric J.
Risch, Harvey A.
Olson, Sara H.
Kooperberg, Charles
Wolpin, Brian M.
Jiao, Li
Hassan, Manal
Wheeler, William
Arslan, Alan A.
Bueno-de-Mesquita, H. Bas
Fuchs, Charles S.
Gallinger, Steven
Gross, Myron D.
Holly, Elizabeth A.
Klein, Alison P.
LaCroix, Andrea
Mandelson, Margaret T.
Petersen, Gloria
Boutron-Ruault, Marie-Christine
Bracci, Paige M.
Canzian, Federico
Chang, Kenneth
Cotterchio, Michelle
Giovannucci, Edward L.
Goggins, Michael
Bolton, Judith A. Hoffman
Jenab, Mazda
Khaw, Kay-Tee
Krogh, Vittorio
Kurtz, Robert C.
McWilliams, Robert R.
Mendelsohn, Julie B.
Rabe, Kari G.
Riboli, Elio
Tjonneland, Anne
Tobias, Geoffrey S.
Trichopoulos, Dimitrios
Elena, Joanne W.
Yu, Herbert
Amundadottir, Laufey
Stolzenberg-Solomon, Rachael Z.
Kraft, Peter
Schumacher, Fredrick
Stram, Daniel
Savage, Sharon A.
Mirabello, Lisa
Andrulis, Irene L.
Wunder, Jay S.
Patino Garcia, Ana
Sierrasesumaga, Luis
Barkauskas, Donald A.
Gorlick, Richard G.
Purdue, Mark
Chow, Wong-Ho
Moore, Lee E.
Schwartz, Kendra L.
Davis, Faith G.
Hsing, Ann W.
Berndt, Sonja I.
Black, Amanda
Wentzensen, Nicolas
Brinton, Louise A.
Lissowska, Jolanta
Peplonska, Beata
McGlynn, Katherine A.
Cook, Michael B.
Graubard, Barry I.
Kratz, Christian P.
Greene, Mark H.
Erickson, Ralph L.
Hunter, David J.
Thomas, Gilles
Hoover, Robert N.
Real, Francisco X.
Fraumeni, Joseph F., Jr.
Caporaso, Neil E.
Tucker, Margaret
Rothman, Nathaniel
Perez-Jurado, Luis A.
Chanock, Stephen J.
TI Detectable clonal mosaicism and its relationship to aging and cancer
SO NATURE GENETICS
LA English
DT Article
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; GENOMIC IMBALANCES; MAFFUCCI SYNDROME;
OLLIER DISEASE; MUTATIONS; SUSCEPTIBILITY; ASSOCIATION; ABERRATIONS;
MECHANISMS; ANEUPLOIDY
AB In an analysis of 31,717 cancer cases and 26,136 cancer-free controls from 13 genome-wide association studies, we observed large chromosomal abnormalities in a subset of clones in DNA obtained from blood or buccal samples. We observed mosaic abnormalities, either aneuploidy or copy-neutral loss of heterozygosity, of > 2 Mb in size in autosomes of 517 individuals (0.89%), with abnormal cell proportions of between 7% and 95%. In cancer-free individuals, frequency increased with age, from 0.23% under 50 years to 1.91% between 75 and 79 years (P = 4.8 x 10(-8)). Mosaic abnormalities were more frequent in individuals with solid tumors (0.97% versus 0.74% in cancer-free individuals; odds ratio (OR) = 1.25; P = 0.016), with stronger association with cases who had DNA collected before diagnosis or treatment (OR = 1.45; P = 0.0005). Detectable mosaicism was also more common in individuals for whom DNA was collected at least 1 year before diagnosis with leukemia compared to cancer-free individuals (OR = 35.4; P = 3.8 x 10(-11)). These findings underscore the time-dependent nature of somatic events in the etiology of cancer and potentially other late-onset diseases.
C1 [Jacobs, Kevin B.; Yeager, Meredith; Zhou, Weiyin; Wacholder, Sholom; Wang, Zhaoming; Hutchinson, Amy; Deng, Xiang; Liu, Chenwei; Horner, Marie-Josephe; Cullen, Michael; Epstein, Caroline G.; Burdett, Laurie; Chatterjee, Nilanjan; Sampson, Joshua; Chung, Charles C.; Kovaks, Joseph; Albanes, Demetrius; Weinstein, Stephanie J.; Taylor, Philip R.; Freedman, Neal D.; Abnet, Christian C.; Goldstein, Alisa M.; Hu, Nan; Yu, Kai; Liao, Linda; Ziegler, Regina G.; Figueroa, Jonine D.; Garcia-Closas, Montserrat; Prokunina-Olsson, Ludmila; Baris, Dalsu; Landi, Maria Teresa; Goldin, Lynn; Rotunno, Melissa; Rajaraman, Preetha; Freeman, Laura E. Beane; Hartge, Patricia; Inskip, Peter D.; Landgren, Annelie; Silverman, Debra T.; Mendelsohn, Julie B.; Tobias, Geoffrey S.; Amundadottir, Laufey; Stolzenberg-Solomon, Rachael Z.; Savage, Sharon A.; Mirabello, Lisa; Purdue, Mark; Chow, Wong-Ho; Moore, Lee E.; Hsing, Ann W.; Berndt, Sonja I.; Black, Amanda; Wentzensen, Nicolas; Brinton, Louise A.; McGlynn, Katherine A.; Cook, Michael B.; Graubard, Barry I.; Kratz, Christian P.; Greene, Mark H.; Hoover, Robert N.; Fraumeni, Joseph F., Jr.; Caporaso, Neil E.; Tucker, Margaret; Rothman, Nathaniel; Chanock, Stephen J.] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Jacobs, Kevin B.; Yeager, Meredith; Zhou, Weiyin; Wang, Zhaoming; Hutchinson, Amy; Deng, Xiang; Liu, Chenwei; Cullen, Michael; Burdett, Laurie] NCI, Core Genotyping Facil, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Rodriguez-Santiago, Benjamin; Villa, Olaya; Real, Francisco X.; Perez-Jurado, Luis A.] Univ Pompeu Fabra, Dept Ciencies Expt & Salut, Barcelona, Spain.
[Rodriguez-Santiago, Benjamin; Villa, Olaya; Perez-Jurado, Luis A.] Ctr Invest Biomed Red Enfermedades Raras CIBERER, Barcelona, Spain.
[Rodriguez-Santiago, Benjamin; Villa, Olaya] qGenomics, Quantitat Genom Med Lab, Barcelona, Spain.
[Dean, Michael C.] NCI, Expt Immunol Lab, Ctr Canc Res, Frederick, MD 21701 USA.
[Gapstur, Susan M.; Stevens, Victoria L.; Teras, Lauren T.; Gaudet, Mia M.] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
[Virtamo, Jarmo] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
[Yuan, Jian-Min] Univ Minnesota, Sch Publ Hlth, Dept Epidemiol & Community Hlth, Minneapolis, MN USA.
[Yuan, Jian-Min] Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA.
[Ding, Ti; Tang, Ze-Zhong] Shanxi Canc Hosp, Taiyuan, Peoples R China.
[Qiao, You-Lin; Fan, Jin-Hu] Chinese Acad Med Sci, Dept Epidemiol, Canc Inst Hosp, Beijing 100730, Peoples R China.
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[Wiencke, John K.; Wrensch, Margaret] Univ Calif San Francisco, Dept Neurol Surg, San Francisco, CA USA.
[Garcia-Closas, Montserrat] Inst Canc Res, Div Genet & Epidemiol, London SW3 6JB, England.
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[Johnson, Alison] Vermont Canc Registry, Burlington, VT USA.
[Consonni, Dario; Bertazzi, Pier Alberto] Univ Milan, Dept Occupat & Environm Hlth, Milan, Italy.
[Consonni, Dario; Bertazzi, Pier Alberto] Osped Maggiore Policlin Mangiagalli & Regina Elen, Unit Epidemiol, Fdn Ist Ricevero & Cura Carattere Sci IRCCS, Milan, Italy.
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[Wolk, Alicja] Karolinska Inst, Inst Environm Med, Div Nutr Epidemiol, S-10401 Stockholm, Sweden.
[Zeleniuch-Jacquotte, Anne] NYU, Dept Environm Med, Sch Med, Div Epidemiol, New York, NY 10016 USA.
[Kogevinas, Manolis] Natl Sch Publ Hlth, Athens, Greece.
[Kogevinas, Manolis; Gonzalez, Juan R.] Ctr Res Environm Epidemiol CREAL, Barcelona, Spain.
[Kogevinas, Manolis; Gonzalez, Juan R.] IMIM, Barcelona, Spain.
[Kogevinas, Manolis; Gonzalez, Juan R.] CIBERESP, Barcelona, Spain.
[Li, Donghui; Hassan, Manal] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
[Duell, Eric J.] Inst Invest Biomed Bellvitge IDIBELL, Catalan Inst Oncol ICO, Barcelona, Spain.
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[Bueno-de-Mesquita, H. Bas] Natl Inst Publ Hlth & Environm RIVM, Bilthoven, Netherlands.
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[Krogh, Vittorio] Ist Nazl Tumori, IRCCS, Nutr Epidemiol Unit, I-20133 Milan, Italy.
[Kurtz, Robert C.] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10021 USA.
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[Lissowska, Jolanta] Inst Oncol, Warsaw, Poland.
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[Thomas, Gilles] Univ Lyon 1, Ctr Leon Berard, F-69365 Lyon, France.
[Real, Francisco X.] CNIO, Epithelial Carcinogenesis Grp, Madrid, Spain.
RP Chanock, SJ (reprint author), NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
EM chanocks@mail.nih.gov
RI Consonni, Dario/K-7943-2016; Amundadottir, Laufey/L-7656-2016; Tobias,
Geoffrey/M-4135-2016; Beane Freeman, Laura/C-4468-2015; Kogevinas,
Manolis/C-3918-2017; bertazzi, pietro alberto/D-5039-2017; Tucker,
Margaret/B-4297-2015; Albanes, Demetrius/B-9749-2015; Abnet,
Christian/C-4111-2015; Garcia-Closas, Montserrat /F-3871-2015;
Boutron-Ruault, Marie-Christine/H-3936-2014; Brinton,
Louise/G-7486-2015; Freedman, Neal/B-9741-2015; Malats,
Nuria/H-7041-2015; Perez Jurado, Luis Alberto/M-7706-2015; Real Arribas,
Francisco/H-5275-2015; Savage, Sharon/B-9747-2015; Krogh,
Vittorio/K-2628-2016; Berg , Christine/K-1047-2014; Qiao,
You-Lin/B-4139-2012; Dean, Michael/G-8172-2012; Ruder,
Avima/I-4155-2012; Patino-Garcia, Ana/I-4299-2012; Peplonska,
Beata/F-6004-2010; Aldrich, Melinda/C-7783-2013; Cook,
Michael/A-5641-2009; Gallinger, Steven/E-4575-2013; Andrulis,
Irene/E-7267-2013; Boutron Ruault, Marie-Christine/G-3705-2013; Boutron,
Marie-Christine/K-8168-2013; Michaud, Dominique/I-5231-2014
OI Lissowska, Jolanta/0000-0003-2695-5799; Yuan,
Jian-Min/0000-0002-4620-3108; Giles, Graham/0000-0003-4946-9099;
Zeleniuch-Jacquotte, Anne/0000-0001-9350-1303; Consonni,
Dario/0000-0002-8935-3843; Amundadottir, Laufey/0000-0003-1859-8971;
Tobias, Geoffrey/0000-0002-2878-8253; Beane Freeman,
Laura/0000-0003-1294-4124; bertazzi, pietro alberto/0000-0003-3475-2449;
Duell, Eric J/0000-0001-5256-0163; Rodriguez-Santiago,
Benjamin/0000-0003-1167-3852; Prokunina-Olsson,
Ludmila/0000-0002-9622-2091; Liao, Linda/0000-0002-1923-5294; Abnet,
Christian/0000-0002-3008-7843; Garcia-Closas, Montserrat
/0000-0003-1033-2650; Brinton, Louise/0000-0003-3853-8562; Freedman,
Neal/0000-0003-0074-1098; Malats, Nuria/0000-0003-2538-3784; Real
Arribas, Francisco/0000-0001-9501-498X; Savage,
Sharon/0000-0001-6006-0740; Krogh, Vittorio/0000-0003-0122-8624; Qiao,
You-Lin/0000-0001-6380-0871; Dean, Michael/0000-0003-2234-0631; Ruder,
Avima/0000-0003-0419-6664; Cook, Michael/0000-0002-0533-7302;
FU Intramural Research Program; US National Institutes of Health (NIH), NCI
[HHSN261200800001E]
FX This research was supported by the Intramural Research Program and by
contract number HHSN261200800001E of the US National Institutes of
Health (NIH), NCI. Support for each contributing study is listed in the
Supplementary Note. We thank C. Laurie and B. Weir for constructive
discussion and a comparison of methodology and results for the GENEVA
study. The findings and conclusions in this report are those of the
authors and do not necessarily represent the views of the National
Cancer Institute, the National Institute for Occupational Safety and
Health or the Maryland Cancer Registry.
NR 43
TC 169
Z9 170
U1 2
U2 61
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 JUN
PY 2012
VL 44
IS 6
BP 651
EP U68
DI 10.1038/ng.2270
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA 949BT
UT WOS:000304551100011
PM 22561519
ER
PT J
AU Manning, AK
Hivert, MF
Scott, RA
Grimsby, JL
Bouatia-Naji, N
Chen, H
Rybin, D
Liu, CT
Bielak, LF
Prokopenko, I
Amin, N
Barnes, D
Cadby, G
Hottenga, JJ
Ingelsson, E
Jackson, AU
Johnson, T
Kanoni, S
Ladenvall, C
Lagou, V
Lahti, J
Lecoeur, C
Liu, YM
Martinez-Larrad, MT
Montasser, ME
Navarro, P
Perry, JRB
Rasmussen-Torvik, LJ
Salo, P
Sattar, N
Shungin, D
Strawbridge, RJ
Tanaka, T
van Duijn, CM
An, P
de Andrade, M
Andrews, JS
Aspelund, T
Atalay, M
Aulchenko, Y
Balkau, B
Bandinelli, S
Beckmann, JS
Beilby, JP
Bellis, C
Bergman, RN
Blangero, J
Boban, M
Boehnke, M
Boerwinkle, E
Bonnycastle, LL
Boomsma, DI
Borecki, IB
Boettcher, Y
Bouchard, C
Brunner, E
Budimir, D
Campbell, H
Carlson, O
Chines, PS
Clarke, R
Collins, FS
Corbaton-Anchuelo, A
Couper, D
de Faire, U
Dedoussis, GV
Deloukas, P
Dimitriou, M
Egan, JM
Eiriksdottir, G
Erdos, MR
Eriksson, JG
Eury, E
Ferrucci, L
Ford, I
Forouhi, NG
Fox, CS
Franzosi, MG
Franks, PW
Frayling, TM
Froguel, P
Galan, P
de Geus, E
Gigante, B
Glazer, NL
Goel, A
Groop, L
Gudnason, V
Hallmans, G
Hamsten, A
Hansson, O
Harris, TB
Hayward, C
Heath, S
Hercberg, S
Hicks, AA
Hingorani, A
Hofman, A
Hui, J
Hung, J
Jarvelin, MR
Jhun, MA
Johnson, PCD
Jukema, JW
Jula, A
Kao, WH
Kaprio, J
Kardia, SLR
Keinanen-Kiukaanniemi, S
Kivimaki, M
Kolcic, I
Kovacs, P
Kumari, M
Kuusisto, J
Kyvik, KO
Laakso, M
Lakka, T
Lannfelt, L
Lathrop, GM
Launer, LJ
Leander, K
Li, G
Lind, L
Lindstrom, J
Lobbens, S
Loos, RJF
Luan, JA
Lyssenko, V
Magi, R
Magnusson, PKE
Marmot, M
Meneton, P
Mohlke, KL
Mooser, V
Morken, MA
Miljkovic, I
Narisu, N
O'Connell, J
Ong, KK
Oostra, BA
Palmer, LJ
Palotie, A
Pankow, JS
Peden, JF
Pedersen, NL
Pehlic, M
Peltonen, L
Penninx, B
Pericic, M
Perola, M
Perusse, L
Peyser, PA
Polasek, O
Pramstaller, PP
Province, MA
Raikkonen, K
Rauramaa, R
Rehnberg, E
Rice, K
Rotter, JI
Rudan, I
Ruokonen, A
Saaristo, T
Sabater-Lleal, M
Salomaa, V
Savage, DB
Saxena, R
Schwarz, P
Seedorf, U
Sennblad, B
Serrano-Rios, M
Shuldiner, AR
Sijbrands, EJG
Siscovick, DS
Smit, JH
Small, KS
Smith, NL
Smith, AV
Stancakova, A
Stirrups, K
Stumvoll, M
Sun, YV
Swift, AJ
Toenjes, A
Tuomilehto, J
Trompet, S
Uitterlinden, AG
Uusitupa, M
Vikstrom, M
Vitart, V
Vohl, MC
Voight, BF
Vollenweider, P
Waeber, G
Waterworth, DM
Watkins, H
Wheeler, E
Widen, E
Wild, SH
Willems, SM
Willemsen, G
Wilson, JF
Witteman, JCM
Wright, AF
Yaghootkar, H
Zelenika, D
Zemunik, T
Zgaga, L
Wareham, NJ
McCarthy, MI
Barroso, I
Watanabe, RM
Florez, JC
Dupuis, J
Meigs, JB
Langenberg, C
AF Manning, Alisa K.
Hivert, Marie-France
Scott, Robert A.
Grimsby, Jonna L.
Bouatia-Naji, Nabila
Chen, Han
Rybin, Denis
Liu, Ching-Ti
Bielak, Lawrence F.
Prokopenko, Inga
Amin, Najaf
Barnes, Daniel
Cadby, Gemma
Hottenga, Jouke-Jan
Ingelsson, Erik
Jackson, Anne U.
Johnson, Toby
Kanoni, Stavroula
Ladenvall, Claes
Lagou, Vasiliki
Lahti, Jari
Lecoeur, Cecile
Liu, Yongmei
Martinez-Larrad, Maria Teresa
Montasser, May E.
Navarro, Pau
Perry, John R. B.
Rasmussen-Torvik, Laura J.
Salo, Perttu
Sattar, Naveed
Shungin, Dmitry
Strawbridge, Rona J.
Tanaka, Toshiko
van Duijn, Cornelia M.
An, Ping
de Andrade, Mariza
Andrews, Jeanette S.
Aspelund, Thor
Atalay, Mustafa
Aulchenko, Yurii
Balkau, Beverley
Bandinelli, Stefania
Beckmann, Jacques S.
Beilby, John P.
Bellis, Claire
Bergman, Richard N.
Blangero, John
Boban, Mladen
Boehnke, Michael
Boerwinkle, Eric
Bonnycastle, Lori L.
Boomsma, Dorret I.
Borecki, Ingrid B.
Boettcher, Yvonne
Bouchard, Claude
Brunner, Eric
Budimir, Danijela
Campbell, Harry
Carlson, Olga
Chines, Peter S.
Clarke, Robert
Collins, Francis S.
Corbaton-Anchuelo, Arturo
Couper, David
de Faire, Ulf
Dedoussis, George V.
Deloukas, Panos
Dimitriou, Maria
Egan, Josephine M.
Eiriksdottir, Gudny
Erdos, Michael R.
Eriksson, Johan G.
Eury, Elodie
Ferrucci, Luigi
Ford, Ian
Forouhi, Nita G.
Fox, Caroline S.
Franzosi, Maria Grazia
Franks, Paul W.
Frayling, Timothy M.
Froguel, Philippe
Galan, Pilar
de Geus, Eco
Gigante, Bruna
Glazer, Nicole L.
Goel, Anuj
Groop, Leif
Gudnason, Vilmundur
Hallmans, Goeran
Hamsten, Anders
Hansson, Ola
Harris, Tamara B.
Hayward, Caroline
Heath, Simon
Hercberg, Serge
Hicks, Andrew A.
Hingorani, Aroon
Hofman, Albert
Hui, Jennie
Hung, Joseph
Jarvelin, Marjo-Riitta
Jhun, Min A.
Johnson, Paul C. D.
Jukema, J. Wouter
Jula, Antti
Kao, W. H.
Kaprio, Jaakko
Kardia, Sharon L. R.
Keinanen-Kiukaanniemi, Sirkka
Kivimaki, Mika
Kolcic, Ivana
Kovacs, Peter
Kumari, Meena
Kuusisto, Johanna
Kyvik, Kirsten Ohm
Laakso, Markku
Lakka, Timo
Lannfelt, Lars
Lathrop, G. Mark
Launer, Lenore J.
Leander, Karin
Li, Guo
Lind, Lars
Lindstrom, Jaana
Lobbens, Stephane
Loos, Ruth J. F.
Luan, Jian'an
Lyssenko, Valeriya
Magi, Reedik
Magnusson, Patrik K. E.
Marmot, Michael
Meneton, Pierre
Mohlke, Karen L.
Mooser, Vincent
Morken, Mario A.
Miljkovic, Iva
Narisu, Narisu
O'Connell, Jeff
Ong, Ken K.
Oostra, Ben A.
Palmer, Lyle J.
Palotie, Aarno
Pankow, James S.
Peden, John F.
Pedersen, Nancy L.
Pehlic, Marina
Peltonen, Leena
Penninx, Brenda
Pericic, Marijana
Perola, Markus
Perusse, Louis
Peyser, Patricia A.
Polasek, Ozren
Pramstaller, Peter P.
Province, Michael A.
Raikkonen, Katri
Rauramaa, Rainer
Rehnberg, Emil
Rice, Ken
Rotter, Jerome I.
Rudan, Igor
Ruokonen, Aimo
Saaristo, Timo
Sabater-Lleal, Maria
Salomaa, Veikko
Savage, David B.
Saxena, Richa
Schwarz, Peter
Seedorf, Udo
Sennblad, Bengt
Serrano-Rios, Manuel
Shuldiner, Alan R.
Sijbrands, Eric J. G.
Siscovick, David S.
Smit, Johannes H.
Small, Kerrin S.
Smith, Nicholas L.
Smith, Albert Vernon
Stancakova, Alena
Stirrups, Kathleen
Stumvoll, Michael
Sun, Yan V.
Swift, Amy J.
Toenjes, Anke
Tuomilehto, Jaakko
Trompet, Stella
Uitterlinden, Andre G.
Uusitupa, Matti
Vikstrom, Max
Vitart, Veronique
Vohl, Marie-Claude
Voight, Benjamin F.
Vollenweider, Peter
Waeber, Gerard
Waterworth, Dawn M.
Watkins, Hugh
Wheeler, Eleanor
Widen, Elisabeth
Wild, Sarah H.
Willems, Sara M.
Willemsen, Gonneke
Wilson, James F.
Witteman, Jacqueline C. M.
Wright, Alan F.
Yaghootkar, Hanieh
Zelenika, Diana
Zemunik, Tatijana
Zgaga, Lina
Wareham, Nicholas J.
McCarthy, Mark I.
Barroso, Ines
Watanabe, Richard M.
Florez, Jose C.
Dupuis, Josee
Meigs, James B.
Langenberg, Claudia
CA DIAGRAM Consortium
MUTHER Consortium
TI A genome-wide approach accounting for body mass index identifies genetic
variants influencing fasting glycemic traits and insulin resistance
SO NATURE GENETICS
LA English
DT Article
ID CORONARY-ARTERY-DISEASE; TYPE-2 DIABETES RISK; ASSOCIATION ANALYSIS;
ENVIRONMENT INTERACTION; COMMON VARIANTS; LOCI; OBESITY; SUSCEPTIBILITY;
GLUCOSE; POLYMORPHISM
AB Recent genome-wide association studies have described many loci implicated in type 2 diabetes (T2D) pathophysiology and beta-cell dysfunction but have contributed little to the understanding of the genetic basis of insulin resistance. We hypothesized that genes implicated in insulin resistance pathways might be uncovered by accounting for differences in body mass index (BMI) and potential interactions between BMI and genetic variants. We applied a joint meta-analysis approach to test associations with fasting insulin and glucose on a genome-wide scale. We present six previously unknown loci associated with fasting insulin at P < 5 x 10(-8) in combined discovery and follow-up analyses of 52 studies comprising up to 96,496 non-diabetic individuals. Risk variants were associated with higher triglyceride and lower high-density lipoprotein (HDL) cholesterol levels, suggesting a role for these loci in insulin resistance pathways. The discovery of these loci will aid further characterization of the role of insulin resistance in T2D pathophysiology.
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[Manning, Alisa K.; Chen, Han; Liu, Ching-Ti; Dupuis, Josee] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Manning, Alisa K.; Palotie, Aarno; Saxena, Richa; Voight, Benjamin F.; Florez, Jose C.] Broad Inst MIT & Harvard, Program Med & Populat Genet, Cambridge, MA USA.
[Manning, Alisa K.] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
[Manning, Alisa K.] Harvard Univ, Sch Med, Dept Genet, Boston, MA USA.
[Hivert, Marie-France] Univ Sherbrooke, Dept Med, Sherbrooke, PQ J1K 2R1, Canada.
[Scott, Robert A.; Barnes, Daniel; Forouhi, Nita G.; Loos, Ruth J. F.; Luan, Jian'an; Ong, Ken K.; Wareham, Nicholas J.; Langenberg, Claudia] Addenbrookes Hosp, Inst Metab Sci, Med Res Council MRC Epidemiol Unit, Cambridge, England.
[Grimsby, Jonna L.; Florez, Jose C.; Meigs, James B.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Bouatia-Naji, Nabila; Lecoeur, Cecile; Eury, Elodie; Froguel, Philippe; Lobbens, Stephane] Inst Pasteur, Lille, France.
[Bouatia-Naji, Nabila; Lecoeur, Cecile; Eury, Elodie; Froguel, Philippe; Lobbens, Stephane] Univ Lille Nord France, Lille, France.
[Rybin, Denis] Boston Univ, Data Coordinating Ctr, Boston, MA 02215 USA.
[Bielak, Lawrence F.; Jhun, Min A.; Kardia, Sharon L. R.; Peyser, Patricia A.] Univ Michigan, Dept Epidemiol, Ann Arbor, MI 48109 USA.
[Prokopenko, Inga; Lagou, Vasiliki; Magi, Reedik; McCarthy, Mark I.] Univ Oxford, Oxford Ctr Diabet Endocrinol & Metab, Oxford, England.
[Prokopenko, Inga; Lagou, Vasiliki; Perry, John R. B.; Goel, Anuj; Magi, Reedik; Peden, John F.; Watkins, Hugh; McCarthy, Mark I.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
[Amin, Najaf; van Duijn, Cornelia M.; Aulchenko, Yurii; Hofman, Albert; Uitterlinden, Andre G.; Willems, Sara M.; Witteman, Jacqueline C. M.] Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
[Cadby, Gemma; Palmer, Lyle J.] Ontario Inst Canc Res, Toronto, ON, Canada.
[Cadby, Gemma; Palmer, Lyle J.] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Prosserman Ctr Hlth Res, Toronto, ON M5G 1X5, Canada.
[Hottenga, Jouke-Jan; Boomsma, Dorret I.; de Geus, Eco; Willemsen, Gonneke] Vrije Univ Amsterdam, Dept Biol Psychol, Amsterdam, Netherlands.
[Ingelsson, Erik; Magnusson, Patrik K. E.; Pedersen, Nancy L.; Rehnberg, Emil] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Jackson, Anne U.; Boehnke, Michael] Univ Michigan, Sch Publ Hlth, Dept Biostat, Ann Arbor, MI 48109 USA.
[Jackson, Anne U.; Boehnke, Michael] Univ Michigan, Sch Publ Hlth, Ctr Stat Genet, Ann Arbor, MI 48109 USA.
[Johnson, Toby] Queen Mary Univ London, Barts & London Sch Med & Dent, William Harvey Res Inst, Clin Pharmacol & Genome Ctr, London, England.
[Wheeler, Eleanor; Barroso, Ines] Wellcome Trust Sanger Inst, Metab Dis Grp, Cambridge, England.
[Ladenvall, Claes; Shungin, Dmitry; Franks, Paul W.; Groop, Leif; Hansson, Ola; Lyssenko, Valeriya] Lund Univ, Dept Clin Sci Diabet & Endocrinol, Malmo, Sweden.
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[Lahti, Jari; Raikkonen, Katri] Univ Helsinki, Inst Behav Sci, Helsinki, Finland.
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[Martinez-Larrad, Maria Teresa; Corbaton-Anchuelo, Arturo; Serrano-Rios, Manuel] Inst Invest Sanitaria Hosp Clin San Carlos, Spanish Biomed Res Ctr Diabet & Associated Metab, Madrid, Spain.
[Montasser, May E.; O'Connell, Jeff; Shuldiner, Alan R.] Univ Maryland, Sch Med, Dept Med, Div Endocrinol Diabet & Nutr, Baltimore, MD 21201 USA.
[Navarro, Pau; Hayward, Caroline; Vitart, Veronique; Wright, Alan F.] Univ Edinburgh, MRC Human Genet Unit, MRC Inst Genet & Mol Med IGMM, Edinburgh, Midlothian, Scotland.
[Perry, John R. B.; Frayling, Timothy M.; Yaghootkar, Hanieh] Univ Exeter, Peninsula Coll Med & Dent, Exeter, Devon, England.
[Perry, John R. B.; Small, Kerrin S.] Kings Coll London, Dept Twin Res & Genet Epidemiol, London WC2R 2LS, England.
[Rasmussen-Torvik, Laura J.] Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
[Lindstrom, Jaana; Tuomilehto, Jaakko] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Diabet Prevent Unit, Helsinki, Finland.
[Sattar, Naveed] Univ Glasgow, Inst Cardiovasc & Med Sci, Glasgow, Lanark, Scotland.
[Shungin, Dmitry; Franks, Paul W.] Umea Univ Hosp, Genet Epidemiol & Clin Res Grp, Dept Publ Hlth & Clin Med, S-90185 Umea, Sweden.
[Shungin, Dmitry] Umea Univ, Dept Odontol, Umea, Sweden.
[Strawbridge, Rona J.; Hamsten, Anders; Sabater-Lleal, Maria; Sennblad, Bengt] Karolinska Inst, Atherosclerosis Res Unit, Dept Med Solna, Stockholm, Sweden.
[Ferrucci, Luigi] NIA, Clin Res Branch, Longitudinal Studies Sect, Baltimore, MD 21224 USA.
[van Duijn, Cornelia M.] Netherlands Genom Initiat, Ctr Med Syst Biol, The Hague, Netherlands.
[van Duijn, Cornelia M.; Hofman, Albert; Uitterlinden, Andre G.; Witteman, Jacqueline C. M.] Netherlands Genom Initiat, Netherlands Consortium Hlth Aging, Rotterdam, Netherlands.
[An, Ping; Borecki, Ingrid B.; Province, Michael A.] Washington Univ, Sch Med, Dept Genet, Div Stat Genom, St Louis, MO 63110 USA.
[de Andrade, Mariza] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
[Andrews, Jeanette S.] Wake Forest Sch Med, Div Publ Hlth Sci, Dept Biostat Sci, Winston Salem, NC USA.
[Aspelund, Thor; Eiriksdottir, Gudny; Gudnason, Vilmundur; Smith, Albert Vernon] Iceland Heart Assoc, Kopavogur, Iceland.
[Aspelund, Thor; Gudnason, Vilmundur; Smith, Albert Vernon] Univ Iceland, Reykjavik, Iceland.
[Atalay, Mustafa; Lakka, Timo] Univ Eastern Finland, Inst Biomed Physiol, Kuopio, Finland.
[Balkau, Beverley] INSERM, Ctr Res Epidemiol & Populat Hlth, Ctr Rech Epidemiol & Sante Populat CESP, Villejuif, France.
[Balkau, Beverley] Univ Paris 11, UMRS 1018, Villejuif, France.
[Bandinelli, Stefania] Azienda Sanit Firenze, Geriatr Unit, Florence, Italy.
[Beckmann, Jacques S.] Univ Lausanne, Dept Med Genet, Lausanne, Switzerland.
[Beckmann, Jacques S.] CHU Vaudois, Serv Med Genet, Lausanne, Switzerland.
[Beilby, John P.; Hui, Jennie] Queen Elizabeth II QEII Med Ctr, Dept Mol Genet, PathWest Lab Western Australia, Nedlands, WA, Australia.
[Beilby, John P.; Hui, Jennie] Univ Western Australia, Sch Pathol & Lab Med, Nedlands, WA 6009, Australia.
[Beilby, John P.; Hui, Jennie; Hung, Joseph] QEII Med Ctr, Busselton Populat Med Res Fdn, Nedlands, WA, Australia.
[Bellis, Claire; Blangero, John] Texas Biomed Res Inst, San Antonio, TX USA.
[Bergman, Richard N.; Watanabe, Richard M.] Univ So Calif, Keck Sch Med, Dept Physiol & Biophys, Los Angeles, CA 90033 USA.
[Boban, Mladen; Budimir, Danijela] Univ Split, Dept Pharmacol, Fac Med, Split, Croatia.
[Boerwinkle, Eric] Univ Texas Hlth Sci Ctr Houston, Ctr Human Genet, Houston, TX USA.
[Bonnycastle, Lori L.; Chines, Peter S.; Collins, Francis S.; Erdos, Michael R.; Morken, Mario A.; Narisu, Narisu; Swift, Amy J.] NHGRI, Genome Technol Branch, US NIH, Bethesda, MD 20892 USA.
[Kovacs, Peter] Univ Leipzig, Interdisciplinary Ctr Clin Res, Leipzig, Germany.
[Bouchard, Claude] Pennington Biomed Res Ctr, Baton Rouge, LA USA.
[Brunner, Eric; Kivimaki, Mika; Marmot, Michael] UCL, Dept Epidemiol & Publ Hlth, London, England.
[Campbell, Harry; Rudan, Igor; Wild, Sarah H.; Wilson, James F.; Zgaga, Lina] Univ Edinburgh, Ctr Populat Hlth Sci, Edinburgh, Midlothian, Scotland.
[Carlson, Olga; Egan, Josephine M.] NIA, Clin Invest Lab, Baltimore, MD 21224 USA.
[Clarke, Robert] Univ Oxford, Clin Trial Serv Unit, Oxford, England.
[Couper, David] Univ N Carolina, Dept Biostat, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
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[Dedoussis, George V.; Dimitriou, Maria] Harokopio Univ, Dept Nutr Dietet, Athens, Greece.
[Eriksson, Johan G.] Univ Helsinki, Dept Gen Practice & Primary Hlth Care, Helsinki, Finland.
[Eriksson, Johan G.] Helsinki Univ Cent Hosp, Unit Gen Practice, Helsinki, Finland.
[Eriksson, Johan G.] Folkhalsan Res Ctr, Helsinki, Finland.
[Eriksson, Johan G.] Vaasa Cent Hosp, Vaasa, Finland.
[Ford, Ian; Johnson, Paul C. D.] Univ Glasgow, Robertson Ctr Biostat, Glasgow, Lanark, Scotland.
[Fox, Caroline S.; Dupuis, Josee] NHLBI, Framingham Heart Study, Framingham, MA USA.
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[Franzosi, Maria Grazia] Mario Negri Inst Pharmacol Res, Dept Cardiovasc Res, Milan, Italy.
[Franks, Paul W.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Franks, Paul W.] Univ Paris, Inst Natl Rech Agron, Bobigny, France.
[Froguel, Philippe] Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, London, England.
[Galan, Pilar; Hercberg, Serge] Univ Paris, INSERM, Bobigny, France.
[Glazer, Nicole L.] Boston Univ, Sch Med, Prevent Med & Epidemiol Sect, Dept Med, Boston, MA 02118 USA.
[Glazer, Nicole L.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Goel, Anuj; Peden, John F.] Univ Oxford, Dept Cardiovasc Med, Oxford, England.
[Hallmans, Goeran; Watkins, Hugh] Umea Univ, Dept Publ Hlth & Clin Med, Umea, Sweden.
[Harris, Tamara B.; Launer, Lenore J.] NIA, Intramural Res Program, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Heath, Simon; Lathrop, G. Mark; Zelenika, Diana] Commissariat Energie Atom, Ctr Natl Genotypage, Inst Genom, Evry, France.
[Hicks, Andrew A.; Pramstaller, Peter P.] European Acad Bozen Bolzano EURAC, Inst Med Genet, Bolzano, Italy.
[Hingorani, Aroon; Kumari, Meena] UCL, Dept Epidemiol & Publ Hlth, Genet Epidemiol Grp, London, England.
[Hui, Jennie] Univ Western Australia, Sch Populat Hlth, Nedlands, WA 6009, Australia.
[Hung, Joseph] Univ Western Australia, Sch Med & Pharmacol, Sir Charles Gairdner Hosp, Nedlands, WA 6009, Australia.
[Jarvelin, Marjo-Riitta] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, Dept Epidemiol & Biostat,Fac Med, MRC Hlth Protect Agcy HPA Ctr Environm & Hlth, London, England.
[Keinanen-Kiukaanniemi, Sirkka] Univ Oulu, Inst Hlth Sci, Fac Med, Oulu, Finland.
[Jarvelin, Marjo-Riitta] Univ Oulu, Bioctr Oulu, Oulu, Finland.
[Jarvelin, Marjo-Riitta] Natl Inst Hlth & Welf, Oulu, Finland.
[Jukema, J. Wouter; Trompet, Stella] Leiden Univ, Med Ctr, Dept Cardiol P C5, Leiden, Netherlands.
[Jukema, J. Wouter] Durrer Ctr Cardiogenet Res, Amsterdam, Netherlands.
[Kao, W. H.] Johns Hopkins Sch Publ Hlth, Div Epidemiol, Baltimore, MD USA.
[Kaprio, Jaakko; Palotie, Aarno; Peltonen, Leena; Widen, Elisabeth] Univ Helsinki, Inst Mol Med Finland, Helsinki, Finland.
[Kaprio, Jaakko] Univ Helsinki, Dept Publ Hlth, Hjelt Inst, Helsinki, Finland.
[Keinanen-Kiukaanniemi, Sirkka] Oulu Univ Hosp, Unit Gen Practice, Oulu, Finland.
[Kolcic, Ivana; Polasek, Ozren] Univ Split, Fac Med, Dept Publ Hlth, Split, Croatia.
[Rauramaa, Rainer] Kuopio Univ Hosp, Dept Clin Physiol & Nucl Med, SF-70210 Kuopio, Finland.
[Kuusisto, Johanna; Laakso, Markku; Stancakova, Alena] Univ Eastern Finland, Dept Med, Kuopio, Finland.
[Kyvik, Kirsten Ohm] Univ So Denmark, Inst Reg Hlth Serv Res, Odense, Denmark.
[Kyvik, Kirsten Ohm] Univ So Denmark, Odense Patient Data Explorat Network OPEN, Odense, Denmark.
[Lakka, Timo; Rauramaa, Rainer] Kuopio Res Inst Exercise Med, Kuopio, Finland.
[Lannfelt, Lars] Uppsala Univ, Dept Publ Hlth & Caring Sci, Rudbecklab, Uppsala, Sweden.
[Li, Guo; Siscovick, David S.] Univ Washington, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Lind, Lars] Uppsala Univ, Dept Med Sci, Univ Hosp, Uppsala, Sweden.
[Magi, Reedik] Univ Tartu, Estonian Genome Ctr, EE-50090 Tartu, Estonia.
[Meneton, Pierre] INSERM, Ctr Rech Cordeliers, Paris, France.
[Mohlke, Karen L.] Univ N Carolina, Dept Genet, Chapel Hill, NC USA.
[Mooser, Vincent; Waterworth, Dawn M.] GlaxoSmithKline, Div Genet, Philadelphia, PA USA.
[Miljkovic, Iva] Univ Pittsburgh, Dept Epidemiol, Ctr Aging & Populat Hlth, Pittsburgh, PA 15261 USA.
[Oostra, Ben A.] Erasmus MC, Dept Clin Genet, Rotterdam, Netherlands.
[Palotie, Aarno] Univ Helsinki, Dept Med Genet, Helsinki, Finland.
[Pankow, James S.] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Pehlic, Marina; Zemunik, Tatijana] Univ Split, Dept Biol, Fac Med, Split, Croatia.
[Penninx, Brenda] Leiden Univ, Med Ctr, Dept Psychiat, Leiden, Netherlands.
Univ Groningen, Univ Med Ctr Groningen, Dept Psychiat, Groningen, Netherlands.
[Penninx, Brenda; Smit, Johannes H.] Vrije Univ Amsterdam Med Ctr, Dept Psychiat, Amsterdam, Netherlands.
[Penninx, Brenda] Vrije Univ Amsterdam Med Ctr, Inst Res Extramural Med EMGO Inst Hlth & Care Res, Amsterdam, Netherlands.
[Pericic, Marijana] Inst Anthropol Res, Zagreb, Croatia.
[Perusse, Louis] Univ Laval, Dept Prevent Med, Quebec City, PQ, Canada.
[Rice, Ken] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Rotter, Jerome I.] Cedars Sinai Med Ctr, Inst Med Genet, Los Angeles, CA 90048 USA.
[Rudan, Igor] Univ Split, Ctr Global Hlth, Split, Croatia.
[Ruokonen, Aimo] Univ Oulu, Inst Clin Med, Oulu, Finland.
[Saaristo, Timo] Finnish Diabet Assoc, Tampere, Finland.
[Saaristo, Timo] Pirkanmaa Hosp Dist & Diabet Ctr, Tampere, Finland.
[Savage, David B.; Barroso, Ines] Univ Cambridge, Addenbrookes Hosp, Metab Res Labs, Inst Metab Sci, Cambridge CB2 2QQ, England.
[Saxena, Richa; Florez, Jose C.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Schwarz, Peter] Univ Dresden, Dept Med, Div Prevent & Care Diabet, Dresden, Germany.
[Seedorf, Udo] Univ Munster, Leibniz Inst Arteriosclerosis Res, Munster, Germany.
[Shuldiner, Alan R.] Vet Adm Med Ctr, Geriatr Res & Educ Clin Ctr, Baltimore, MD 21218 USA.
[Sijbrands, Eric J. G.; Uitterlinden, Andre G.] Erasmus MC, Dept Internal Med, Rotterdam, Netherlands.
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[McCarthy, Mark I.] Churchill Hosp, Oxford Natl Inst Hlth Res NIHR Biomed Res Ctr, Oxford OX3 7LJ, England.
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RP Meigs, JB (reprint author), Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
EM jmeigs@partners.org; claudia.langenberg@mrc-epid.cam.ac.uk
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FU British Heart Foundation [RG/07/008/23674]; Chief Scientist Office
[CZB/4/710]; Medical Research Council [G0902037, G0100222, G0701863,
G0900339, G1002084, G19/35, G8802774, MC_PC_U127592696, MC_U106179471,
MC_U106179472, MC_U127561128, MC_U127592696, MC_U137686857,
MC_UP_A100_1003]; NCATS NIH HHS [UL1 TR000124]; NCRR NIH HHS [S10
RR029392]; NHLBI NIH HHS [R01 HL105756]; NIDDK NIH HHS [K24 DK080140,
P30 DK020572, P30 DK063491, R01 DK072193, R01 DK078616]; NIMH NIH HHS
[R37 MH059490]; Wellcome Trust [090532, 091551]
NR 79
TC 236
Z9 240
U1 8
U2 80
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 JUN
PY 2012
VL 44
IS 6
BP 659
EP U81
DI 10.1038/ng.2274
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 949BT
UT WOS:000304551100012
PM 22581228
ER
PT J
AU Ellinor, PT
Lunetta, KL
Albert, CM
Glazer, NL
Ritchie, MD
Smith, AV
Arking, DE
Muller-Nurasyid, M
Krijthe, BP
Lubitz, SA
Bis, JC
Chung, MK
Doerr, M
Ozaki, K
Roberts, JD
Smith, JG
Pfeufer, A
Sinner, MF
Lohman, K
Ding, JZ
Smith, NL
Smith, JD
Rienstra, M
Rice, KM
Van Wagoner, DR
Magnani, JW
Wakili, R
Clauss, S
Rotter, JI
Steinbeck, G
Launer, LJ
Davies, RW
Borkovich, M
Harris, TB
Lin, HH
Volker, U
Volzke, H
Milan, DJ
Hofman, A
Boerwinkle, E
Chen, LY
Soliman, EZ
Voight, BF
Li, G
Chakravarti, A
Kubo, M
Tedrow, UB
Rose, LM
Ridker, PM
Conen, D
Tsunoda, T
Furukawa, T
Sotoodehnia, N
Xu, SY
Kamatani, N
Levy, D
Nakamura, Y
Parvez, B
Mahida, S
Furie, KL
Rosand, J
Muhammad, R
Psaty, BM
Meitinger, T
Perz, S
Wichmann, HE
Witteman, JCM
Kao, WHL
Kathiresan, S
Roden, DM
Uitterlinden, AG
Rivadeneira, F
McKnight, B
Sjogren, M
Newman, AB
Liu, YM
Gollob, MH
Melander, O
Tanaka, T
Stricker, BHC
Felix, SB
Alonso, A
Darbar, D
Barnard, J
Chasman, DI
Heckbert, SR
Benjamin, EJ
Gudnason, V
Kaab, S
AF Ellinor, Patrick T.
Lunetta, Kathryn L.
Albert, Christine M.
Glazer, Nicole L.
Ritchie, Marylyn D.
Smith, Albert V.
Arking, Dan E.
Mueller-Nurasyid, Martina
Krijthe, Bouwe P.
Lubitz, Steven A.
Bis, Joshua C.
Chung, Mina K.
Doerr, Marcus
Ozaki, Kouichi
Roberts, Jason D.
Smith, J. Gustav
Pfeufer, Arne
Sinner, Moritz F.
Lohman, Kurt
Ding, Jingzhong
Smith, Nicholas L.
Smith, Jonathan D.
Rienstra, Michiel
Rice, Kenneth M.
Van Wagoner, David R.
Magnani, Jared W.
Wakili, Reza
Clauss, Sebastian
Rotter, Jerome I.
Steinbeck, Gerhard
Launer, Lenore J.
Davies, Robert W.
Borkovich, Matthew
Harris, Tamara B.
Lin, Honghuang
Voelker, Uwe
Voelzke, Henry
Milan, David J.
Hofman, Albert
Boerwinkle, Eric
Chen, Lin Y.
Soliman, Elsayed Z.
Voight, Benjamin F.
Li, Guo
Chakravarti, Aravinda
Kubo, Michiaki
Tedrow, Usha B.
Rose, Lynda M.
Ridker, Paul M.
Conen, David
Tsunoda, Tatsuhiko
Furukawa, Tetsushi
Sotoodehnia, Nona
Xu, Siyan
Kamatani, Naoyuki
Levy, Daniel
Nakamura, Yusuke
Parvez, Babar
Mahida, Saagar
Furie, Karen L.
Rosand, Jonathan
Muhammad, Raafia
Psaty, Bruce M.
Meitinger, Thomas
Perz, Siegfried
Wichmann, H-Erich
Witteman, Jacqueline C. M.
Kao, W. H. Linda
Kathiresan, Sekar
Roden, Dan M.
Uitterlinden, Andre G.
Rivadeneira, Fernando
McKnight, Barbara
Sjogren, Marketa
Newman, Anne B.
Liu, Yongmei
Gollob, Michael H.
Melander, Olle
Tanaka, Toshihiro
Stricker, Bruno H. Ch
Felix, Stephan B.
Alonso, Alvaro
Darbar, Dawood
Barnard, John
Chasman, Daniel I.
Heckbert, Susan R.
Benjamin, Emelia J.
Gudnason, Vilmundur
Kaeaeb, Stefan
TI Meta-analysis identifies six new susceptibility loci for atrial
fibrillation
SO NATURE GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; CHROMOSOME 4Q25; DILATED CARDIOMYOPATHY;
PACEMAKER CHANNEL; COMMON VARIANTS; PR INTERVAL; CAVEOLIN-1;
REPLICATION; MUTATIONS; PROTEINS
AB Atrial fibrillation is a highly prevalent arrhythmia and a major risk factor for stroke, heart failure and death(1). We conducted a genome-wide association study (GWAS) in individuals of European ancestry, including 6,707 with and 52,426 without atrial fibrillation. Six new atrial fibrillation susceptibility loci were identified and replicated in an additional sample of individuals of European ancestry, including 5,381 subjects with and 10,030 subjects without atrial fibrillation (P < 5 x 10(-8)). Four of the loci identified in Europeans were further replicated in silico in a GWAS of Japanese individuals, including 843 individuals with and 3,350 individuals without atrial fibrillation. The identified loci implicate candidate genes that encode transcription factors related to cardiopulmonary development, cardiac-expressed ion channels and cell signaling molecules.
C1 [Ellinor, Patrick T.; Lubitz, Steven A.; Sinner, Moritz F.; Rienstra, Michiel; Milan, David J.; Mahida, Saagar] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Charlestown, MA 02129 USA.
[Ellinor, Patrick T.; Milan, David J.] Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02114 USA.
[Ellinor, Patrick T.; Rosand, Jonathan] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Ellinor, Patrick T.; Albert, Christine M.; Tedrow, Usha B.; Ridker, Paul M.; Furie, Karen L.; Rosand, Jonathan; Chasman, Daniel I.] Harvard Univ, Sch Med, Boston, MA USA.
[Lunetta, Kathryn L.; Xu, Siyan] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Lunetta, Kathryn L.; Sinner, Moritz F.; Magnani, Jared W.; Levy, Daniel; Benjamin, Emelia J.] NHLBI, Framingham, MA USA.
[Lunetta, Kathryn L.; Sinner, Moritz F.; Magnani, Jared W.; Levy, Daniel; Benjamin, Emelia J.] Boston Univ, Framingham Heart Study, Framingham, MA USA.
[Albert, Christine M.; Lubitz, Steven A.; Tedrow, Usha B.; Rose, Lynda M.; Ridker, Paul M.; Chasman, Daniel I.] Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA.
[Albert, Christine M.; Tedrow, Usha B.; Ridker, Paul M.] Brigham & Womens Hosp, Div Cardiol, Boston, MA 02115 USA.
[Glazer, Nicole L.; Bis, Joshua C.; Smith, Nicholas L.; Li, Guo; Sotoodehnia, Nona; Psaty, Bruce M.; Heckbert, Susan R.] Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA USA.
[Ritchie, Marylyn D.] Penn State Univ, Dept Biochem & Mol Biol, University Pk, PA 16802 USA.
[Smith, Albert V.; Gudnason, Vilmundur] Iceland Heart Assoc Res Inst, Kopavogur, Iceland.
[Smith, Albert V.; Gudnason, Vilmundur] Univ Iceland, Fac Med, Reykjavik, Iceland.
[Arking, Dan E.; Chakravarti, Aravinda] Johns Hopkins Univ, Sch Med, McKusick Nathans Inst Genet Med, Baltimore, MD USA.
[Mueller-Nurasyid, Martina; Sinner, Moritz F.; Wakili, Reza; Clauss, Sebastian; Steinbeck, Gerhard; Kaeaeb, Stefan] Univ Munich, Dept Med 1, Univ Hosp Grosshadern, Munich, Germany.
[Mueller-Nurasyid, Martina] Univ Munich, Inst Med Informat Biometry & Epidemiol, Munich, Germany.
[Mueller-Nurasyid, Martina; Stricker, Bruno H. Ch] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Genet Epidemiol, Neuherberg, Germany.
[Krijthe, Bouwe P.; Hofman, Albert; Witteman, Jacqueline C. M.; Uitterlinden, Andre G.; Rivadeneira, Fernando] Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
[Chung, Mina K.; Smith, Jonathan D.; Van Wagoner, David R.] Cleveland Clin, Dept Cardiovasc Med, Inst Heart & Vasc, Cleveland, OH 44106 USA.
[Chung, Mina K.; Van Wagoner, David R.] Cleveland Clin, Lerner Res Inst, Dept Mol Cardiol, Cleveland, OH 44106 USA.
[Doerr, Marcus; Felix, Stephan B.] Ernst Moritz Arndt Univ Greifswald, Dept Internal Med B, Greifswald, Germany.
[Ozaki, Kouichi; Tanaka, Toshihiro] RIKEN Ctr Genom Med, Lab Cardiovasc Dis, Kanagawa, Japan.
[Roberts, Jason D.; Borkovich, Matthew; Gollob, Michael H.] Univ Ottawa, Inst Heart, Arrhythmia Res Lab, Ottawa, ON, Canada.
[Smith, J. Gustav] Lund Univ, Dept Cardiol, Lund, Sweden.
[Smith, J. Gustav; Voight, Benjamin F.; Kathiresan, Sekar] Broad Inst Harvard & MIT, Cambridge, MA USA.
[Pfeufer, Arne; Meitinger, Thomas] German Res Ctr Environm Hlth, Inst Human Genet, Helmholtz Zentrum Munchen, Neuherberg, Germany.
[Pfeufer, Arne; Meitinger, Thomas] Tech Univ Munich, Klinikum Rechts Isar, Inst Human Genet, D-8000 Munich, Germany.
[Lohman, Kurt] Wake Forest Univ, Bowman Gray Sch Med, Dept Biostat Sci, Winston Salem, NC USA.
[Ding, Jingzhong] Wake Forest Sch Med, Sticht Ctr Aging, Winston Salem, NC USA.
[Smith, Nicholas L.] Dept Vet Affairs Off Res & Dev, Seattle Epidemiol Res & Informat Ctr, Seattle, WA USA.
[Smith, Nicholas L.; Psaty, Bruce M.; Heckbert, Susan R.] Grp Hlth Cooperat Puget Sound, Grp Hlth Res Inst, Seattle, WA USA.
[Smith, Nicholas L.; Psaty, Bruce M.; Heckbert, Susan R.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Smith, Jonathan D.] Cleveland Clin, Dept Cell Biol, Lerner Res Inst, Cleveland, OH 44106 USA.
[Rienstra, Michiel] Univ Groningen, Dept Cardiol, Univ Med Ctr Groningen, Groningen, Netherlands.
[Rice, Kenneth M.; McKnight, Barbara] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Magnani, Jared W.; Lin, Honghuang; Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Med, Cardiol Sect, Boston, MA 02118 USA.
[Rotter, Jerome I.] Cedars Sinai Med Ctr, Inst Med Genet, Los Angeles, CA 90048 USA.
[Launer, Lenore J.; Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, Intramural Res Program, US NIH, Bethesda, MD 20892 USA.
[Davies, Robert W.] Univ Ottawa, Inst Heart, Cardiovasc Res Methods Ctr, Ottawa, ON, Canada.
[Voelker, Uwe] Ernst Moritz Arndt Univ Greifswald, Interfac Inst Genet & Funct Genom, Greifswald, Germany.
[Voelzke, Henry] Ernst Moritz Arndt Univ Greifswald, Inst Community Med, Greifswald, Germany.
[Boerwinkle, Eric] Univ Texas Hlth Sci Ctr Houston, Ctr Human Genet, Houston, TX USA.
[Chen, Lin Y.] Univ Minnesota, Sch Med, Dept Med, Cardiac Arrhythmia Ctr,Cardiovasc Div, Minneapolis, MN 55455 USA.
[Soliman, Elsayed Z.] Wake Forest Univ, Bowman Gray Sch Med, Epidemiol Cardiol Res Ctr EPICARE, Winston Salem, NC USA.
[Kubo, Michiaki] RIKEN Ctr Genom Med, Lab Genotyping Dev, Kanagawa, Japan.
[Conen, David] Univ Basel Hosp, Dept Med, CH-4031 Basel, Switzerland.
[Tsunoda, Tatsuhiko] RIKEN Ctr Genom Med, Lab Med Informat, Kanagawa, Japan.
[Furukawa, Tetsushi] Tokyo Med & Dent Univ, Med Res Inst, Dept Bioinformat Pharmacol, Tokyo, Japan.
[Sotoodehnia, Nona] Univ Washington, Div Cardiol, Seattle, WA 98195 USA.
[Xu, Siyan; Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Kamatani, Naoyuki] RIKEN Ctr Genom Med, Lab Stat Anal, Kanagawa, Japan.
[Nakamura, Yusuke] Univ Tokyo, Inst Med Sci, Ctr Human Genome, Mol Med Lab, Tokyo, Japan.
[Parvez, Babar; Muhammad, Raafia; Roden, Dan M.; Darbar, Dawood] Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37212 USA.
[Furie, Karen L.; Rosand, Jonathan] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Psaty, Bruce M.] Univ Washington, Dept Hlth Serv, Seattle, WA 98195 USA.
[Perz, Siegfried] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Biol & Med Imaging, Neuherberg, Germany.
[Wichmann, H-Erich] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Epidemiol 1, Neuherberg, Germany.
[Wichmann, H-Erich] Univ Munich, Inst Med Informat Biometry & Epidemiol, Chair Epidemiol, Munich, Germany.
[Wichmann, H-Erich] Univ Munich, Klinikum Grosshadern, D-8000 Munich, Germany.
[Kao, W. H. Linda] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA.
[Kao, W. H. Linda] Johns Hopkins Univ, Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD USA.
[Kathiresan, Sekar] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Roden, Dan M.] Vanderbilt Univ, Sch Med, Dept Pharmacol, Nashville, TN 37212 USA.
[Uitterlinden, Andre G.; Rivadeneira, Fernando; Stricker, Bruno H. Ch] Erasmus MC, Dept Internal Med, Rotterdam, Netherlands.
[Sjogren, Marketa; Melander, Olle] Lund Univ, Dept Clin Sci, Malmo, Sweden.
[Newman, Anne B.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA USA.
[Liu, Yongmei] Wake Forest Sch Med, Dept Epidemiol & Prevent, Winston Salem, NC USA.
[Stricker, Bruno H. Ch] Inspectorate Hlth Care, The Hague, Netherlands.
[Stricker, Bruno H. Ch] Erasmus MC, Dept Med Informat, Rotterdam, Netherlands.
[Alonso, Alvaro] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Barnard, John] Cleveland Clin, Dept Quantitat Hlth Sci, Lerner Res Inst, Cleveland, OH 44106 USA.
[Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Med, Prevent Med Sect, Boston, MA 02118 USA.
[Kaeaeb, Stefan] Munich Heart Alliance, Munich, Germany.
RP Ellinor, PT (reprint author), Massachusetts Gen Hosp, Cardiovasc Res Ctr, Charlestown, MA 02129 USA.
EM pellinor@partners.org; skaab@med.uni-muenchen.de
RI Alonso, Alvaro/A-4917-2010; Kaab, Stefan/H-3915-2012; Rice,
Kenneth/A-4150-2013; Pfeufer, Arne/B-6634-2013; Ritchie,
Marylyn/C-1114-2012; Van Wagoner, David/C-6783-2008; Wakili,
Reza/F-1619-2014; Newman, Anne/C-6408-2013; Tsunoda,
Tatsuhiko/K-2061-2014; Darbar, Dawood/C-9079-2015; Gudnason,
Vilmundur/K-6885-2015; Li, Guo/E-5613-2012; Meitinger,
Thomas/O-1318-2015; Rivadeneira, Fernando/O-5385-2015; Tanaka,
Toshihiro/J-9310-2014; Kubo, Michiaki/N-7947-2015; Smith, Albert
Vernon/K-5150-2015;
OI Alonso, Alvaro/0000-0002-2225-8323; Rice, Kenneth/0000-0001-5779-4495;
Van Wagoner, David/0000-0001-8250-9828; Newman,
Anne/0000-0002-0106-1150; Darbar, Dawood/0000-0002-4103-5977; Gudnason,
Vilmundur/0000-0001-5696-0084; Rivadeneira,
Fernando/0000-0001-9435-9441; Tanaka, Toshihiro/0000-0001-6201-9784;
Lunetta, Kathryn/0000-0002-9268-810X; Lin,
Honghuang/0000-0003-3043-3942; Smith, Albert Vernon/0000-0003-1942-5845;
Benjamin, Emelia/0000-0003-4076-2336; Rienstra,
Michiel/0000-0002-2581-070X
FU NCATS NIH HHS [UL1 TR000124]; NHLBI NIH HHS [R01 HL105756, K24 HL105780,
L30 HL097675, R01 HL090620, R01 HL092217, R01 HL092217-04, R01 HL104156,
R21 HL106092, U19 HL065962, U19 HL065962-12]; NIDA NIH HHS [R21
DA027021]
NR 30
TC 232
Z9 239
U1 2
U2 41
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD JUN
PY 2012
VL 44
IS 6
BP 670
EP U88
DI 10.1038/ng.2261
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA 949BT
UT WOS:000304551100013
PM 22544366
ER
PT J
AU Barbieri, CE
Baca, SC
Lawrence, MS
Demichelis, F
Blattner, M
Theurillat, JP
White, TA
Stojanov, P
Van Allen, E
Stransky, N
Nickerson, E
Chae, SS
Boysen, G
Auclair, D
Onofrio, RC
Park, K
Kitabayashi, N
MacDonald, TY
Sheikh, K
Vuong, T
Guiducci, C
Cibulskis, K
Sivachenko, A
Carter, SL
Saksena, G
Voet, D
Hussain, WM
Ramos, AH
Winckler, W
Redman, MC
Ardlie, K
Tewari, AK
Mosquera, JM
Rupp, N
Wild, PJ
Moch, H
Morrissey, C
Nelson, PS
Kantoff, PW
Gabriel, SB
Golub, TR
Meyerson, M
Lander, ES
Getz, G
Rubin, MA
Garraway, LA
AF Barbieri, Christopher E.
Baca, Sylvan C.
Lawrence, Michael S.
Demichelis, Francesca
Blattner, Mirjam
Theurillat, Jean-Philippe
White, Thomas A.
Stojanov, Petar
Van Allen, Eliezer
Stransky, Nicolas
Nickerson, Elizabeth
Chae, Sung-Suk
Boysen, Gunther
Auclair, Daniel
Onofrio, Robert C.
Park, Kyung
Kitabayashi, Naoki
MacDonald, Theresa Y.
Sheikh, Karen
Vuong, Terry
Guiducci, Candace
Cibulskis, Kristian
Sivachenko, Andrey
Carter, Scott L.
Saksena, Gordon
Voet, Douglas
Hussain, Wasay M.
Ramos, Alex H.
Winckler, Wendy
Redman, Michelle C.
Ardlie, Kristin
Tewari, Ashutosh K.
Mosquera, Juan Miguel
Rupp, Niels
Wild, Peter J.
Moch, Holger
Morrissey, Colm
Nelson, Peter S.
Kantoff, Philip W.
Gabriel, Stacey B.
Golub, Todd R.
Meyerson, Matthew
Lander, Eric S.
Getz, Gad
Rubin, Mark A.
Garraway, Levi A.
TI Exome sequencing identifies recurrent SPOP, FOXA1 and MED12 mutations in
prostate cancer
SO NATURE GENETICS
LA English
DT Article
ID ETS GENE FUSIONS; FORKHEAD BOX A1; ANDROGEN RECEPTOR; SUPPRESSOR;
CARCINOMA; PROTEIN; PROGRESSION; EXPRESSION; P27(KIP1); DATABASE
AB Prostate cancer is the second most common cancer in men worldwide and causes over 250,000 deaths each year(1). Overtreatment of indolent disease also results in significant morbidity(2). Common genetic alterations in prostate cancer include losses of NKX3.1 (8p21)(3,4) and PTEN (10q23)(5,6), gains of AR (the androgen receptor gene) 7,8 and fusion of ETS family transcription factor genes with androgen-responsive promoters(9-11). Recurrent somatic base-pair substitutions are believed to be less contributory in prostate tumorigenesis(12,13) but have not been systematically analyzed in large cohorts. Here, we sequenced the exomes of 112 prostate tumor and normal tissue pairs. New recurrent mutations were identified in multiple genes, including MED12 and FOXA1. SPOP was the most frequently mutated gene, with mutations involving the SPOP substrate-binding cleft in 6-15% of tumors across multiple independent cohorts. Prostate cancers with mutant SPOP lacked ETS family gene rearrangements and showed a distinct pattern of genomic alterations. Thus, SPOP mutations may define a new molecular subtype of prostate cancer.
C1 [Barbieri, Christopher E.; Blattner, Mirjam; Chae, Sung-Suk; Boysen, Gunther; Park, Kyung; Kitabayashi, Naoki; MacDonald, Theresa Y.; Sheikh, Karen; Vuong, Terry; Hussain, Wasay M.; Mosquera, Juan Miguel; Rubin, Mark A.] Weill Cornell Med Coll, Dept Pathol & Lab Med, New York, NY USA.
[Barbieri, Christopher E.; Tewari, Ashutosh K.; Rubin, Mark A.] Weill Cornell Med Coll, Dept Urol, New York, NY USA.
[Baca, Sylvan C.; Lawrence, Michael S.; Theurillat, Jean-Philippe; Stojanov, Petar; Van Allen, Eliezer; Stransky, Nicolas; Nickerson, Elizabeth; Auclair, Daniel; Onofrio, Robert C.; Guiducci, Candace; Cibulskis, Kristian; Sivachenko, Andrey; Carter, Scott L.; Saksena, Gordon; Voet, Douglas; Ramos, Alex H.; Winckler, Wendy; Redman, Michelle C.; Ardlie, Kristin; Gabriel, Stacey B.; Golub, Todd R.; Meyerson, Matthew; Lander, Eric S.; Getz, Gad; Garraway, Levi A.] Broad Inst Massachusetts Inst Technol & Harvard, Cambridge, MA USA.
[Baca, Sylvan C.; Ramos, Alex H.; Kantoff, Philip W.; Meyerson, Matthew; Lander, Eric S.; Garraway, Levi A.] Harvard Univ, Sch Med, Boston, MA USA.
[Baca, Sylvan C.; Van Allen, Eliezer; Kantoff, Philip W.; Meyerson, Matthew; Lander, Eric S.; Garraway, Levi A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Demichelis, Francesca; Hussain, Wasay M.] Weill Cornell Med Coll, Inst Computat Biomed, New York, NY USA.
[Demichelis, Francesca] Univ Trento, Ctr Integrat Biol, Trento, Italy.
[White, Thomas A.; Nelson, Peter S.] Fred Hutchinson Canc Res Ctr, Human Biol Div, Seattle, WA 98104 USA.
[Rupp, Niels; Wild, Peter J.; Moch, Holger] Univ Zurich Hosp, Inst Surg Pathol, CH-8091 Zurich, Switzerland.
[Morrissey, Colm; Nelson, Peter S.] Univ Washington, Dept Med, Seattle, WA USA.
[Morrissey, Colm; Nelson, Peter S.] Univ Washington, Dept Urol, Seattle, WA 98195 USA.
[Golub, Todd R.] Howard Hughes Med Inst, Chevy Chase, MD USA.
[Golub, Todd R.] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Golub, Todd R.; Meyerson, Matthew; Garraway, Levi A.] Dana Farber Canc Inst, Ctr Canc Genome Discovery, Boston, MA 02115 USA.
[Lander, Eric S.] MIT, Dept Biol, Cambridge, MA USA.
RP Rubin, MA (reprint author), Weill Cornell Med Coll, Dept Pathol & Lab Med, New York, NY USA.
EM rubinma@med.cornell.edu; levi_garraway@dfci.harvard.edu
RI Meyerson, Matthew/E-7123-2012;
OI Van Allen, Eliezer/0000-0002-0201-4444; Barbieri,
Christopher/0000-0002-0381-1947; Boysen, Gunther/0000-0002-7610-6085;
Rubin, Mark/0000-0002-8321-9950; Demichelis,
Francesca/0000-0002-8266-8631
FU US National Human Genome Research Institute (NHGRI) [U54 HG003067];
Kohlberg Foundation; Starr Cancer Consortium; Prostate Cancer
Foundation; US Department of Defense [PC101020, PC093372];
Dana-Farber/Harvard Cancer Center Prostate Cancer SPORE (US National
Institutes of Health (NIH)) [P50 CA090381]; New Investigator Award
[PC094516]; US National Cancer Institute, Early Detection Research
Network [U01CA111275, NCI EDRN]; US National Cancer Institute [R01
CA125612]; Pacific Northwest Prostate Cancer SPORE [P50CA097186]; Swiss
Science Foundation [PASMP3_134379/1]; US NIH [DP2OD002750]
FX We are grateful for the assistance of members of the Broad Institute
Biological Samples Platform, Genetic Analysis Platform and Genome
Sequencing Platform. We thank S. Banerjee for computational assistance,
R. Kim and R. Leung for their critical contributions to the Weill
Cornell Prostate Cancer Tumor Bank, P. Schraml, S. Dettwiler and M.
Storz for assistance with the University Hospital Zurich cohort and
biobank and the members of the University of Washington Rapid Autopsy
Program. We thank the University of Michigan Prostate Cancer Special
Program of Research Excellence (SPORE) (K. Pienta) for sample
contribution to this study. We are also grateful to the individuals with
prostate cancer and the families who contributed to these studies. This
work was supported by the US National Human Genome Research Institute
(NHGRI) Large Scale Sequencing Program (U54 HG003067 to the Broad
Institute, E. S. L.), the Kohlberg Foundation (L. A. G.), the Starr
Cancer Consortium (M. A. R., F. D. and L. A. G), the Prostate Cancer
Foundation (M. A. R.), US Department of Defense Synergy Awards (PC101020
to F. D., L. A. G. and M. A. R. and PC093372 to T. W. and P.S.N.), the
Dana-Farber/Harvard Cancer Center Prostate Cancer SPORE (US National
Institutes of Health (NIH) P50 CA090381), a New Investigator Award
(PC094516 to F. D.), the US National Cancer Institute, Early Detection
Research Network (U01CA111275 and NCI EDRN to F. D. and M. A. R.), the
US National Cancer Institute (R01 CA125612 to F. D. and M. A. R.), the
Pacific Northwest Prostate Cancer SPORE (P50CA097186 to C. M. and
P.S.N.), the Swiss Science Foundation (PASMP3_134379/1 to J.-P.T.) and a
US NIH Director's New Innovator Award (DP2OD002750 to L. A. G.). S. C.
B. is supported by a Medical Scientist Training Program (MSTP) grant
from the US NIH. C. E. B. is supported by a Prostate Cancer Foundation
Young Investigator Award.
NR 54
TC 467
Z9 477
U1 9
U2 54
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 JUN
PY 2012
VL 44
IS 6
BP 685
EP U107
DI 10.1038/ng.2279
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA 949BT
UT WOS:000304551100016
PM 22610119
ER
PT J
AU Panizzi, JR
Becker-Heck, A
Castleman, VH
Al-Mutairi, DA
Liu, Y
Loges, NT
Pathak, N
Austin-Tse, C
Sheridan, E
Schmidts, M
Olbrich, H
Werner, C
Haffner, K
Hellman, N
Chodhari, R
Gupta, A
Kramer-Zucker, A
Olale, F
Burdine, RD
Schier, AF
O'Callaghan, C
Chung, EMK
Reinhardt, R
Mitchison, HM
King, SM
Omran, H
Drummond, IA
AF Panizzi, Jennifer R.
Becker-Heck, Anita
Castleman, Victoria H.
Al-Mutairi, Dalal A.
Liu, Yan
Loges, Niki T.
Pathak, Narendra
Austin-Tse, Christina
Sheridan, Eamonn
Schmidts, Miriam
Olbrich, Heike
Werner, Claudius
Haeffner, Karsten
Hellman, Nathan
Chodhari, Rahul
Gupta, Amar
Kramer-Zucker, Albrecht
Olale, Felix
Burdine, Rebecca D.
Schier, Alexander F.
O'Callaghan, Christopher
Chung, Eddie M. K.
Reinhardt, Richard
Mitchison, Hannah M.
King, Stephen M.
Omran, Heymut
Drummond, Iain A.
TI CCDC103 mutations cause primary ciliary dyskinesia by disrupting
assembly of ciliary dynein arms
SO NATURE GENETICS
LA English
DT Article
ID RIGHT AXIS FORMATION; ZEBRAFISH PRONEPHROS; PROTEIN; REQUIREMENT;
EXPRESSION; ENCODES; EMBRYOS; GENES
AB Cilia are essential for fertilization, respiratory clearance, cerebrospinal fluid circulation and establishing laterality(1). Cilia motility defects cause primary ciliary dyskinesia (PCD, MIM244400), a disorder affecting 1: 15,000-30,000 births. Cilia motility requires the assembly of multisubunit dynein arms that drive ciliary bending(2). Despite progress in understanding the genetic basis of PCD, mutations remain to be identified for several PCD-linked loci(3). Here we show that the zebrafish cilia paralysis mutant schmalhans (smh(tn222)) encodes the coiled-coil domain containing 103 protein (Ccdc103), a foxj1a-regulated gene product. Screening 146 unrelated PCD families identified individuals in six families with reduced outer dynein arms who carried mutations in CCDC103. Dynein arm assembly in smh mutant zebrafish was rescued by wild-type but not mutant human CCDC103. Chlamydomonas Ccdc103/Pr46b functions as a tightly bound, axoneme-associated protein. These results identify Ccdc103 as a dynein arm attachment factor that causes primary ciliary dyskinesia when mutated.
C1 [Panizzi, Jennifer R.; Liu, Yan; Pathak, Narendra; Hellman, Nathan; Gupta, Amar; Drummond, Iain A.] Massachusetts Gen Hosp, Div Neurol, Charlestown, MA 02129 USA.
[Panizzi, Jennifer R.; Pathak, Narendra; Hellman, Nathan; Drummond, Iain A.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Becker-Heck, Anita] Univ Hosp Freiburg, Dept Pediat, Freiburg, Germany.
[Becker-Heck, Anita; Loges, Niki T.; Olbrich, Heike; Werner, Claudius; Omran, Heymut] Univ Klinikum Munster, Klin & Poliklin Kinder & Jugendmed Allgemeine Pae, Munster, Germany.
[Castleman, Victoria H.] UCL, Mol Med Unit, Inst Child Hlth, London, England.
[Al-Mutairi, Dalal A.; Sheridan, Eamonn] St James Univ Hosp, Leeds Inst Mol Med, Leeds, W Yorkshire, England.
[Al-Mutairi, Dalal A.] Kuwait Univ, Fac Med, Dept Pathol, Kuwait, Kuwait.
[Austin-Tse, Christina] Harvard Univ, Sch Med, Dept Genet, Boston, MA USA.
[Chodhari, Rahul; Chung, Eddie M. K.] UCL, Inst Child Hlth, Gen & Adolescent Paediat Unit, London, England.
[Kramer-Zucker, Albrecht] Univ Hosp Freiburg, Div Renal, Freiburg, Germany.
[Olale, Felix] NYU, Sch Med, Skirball Inst Biomol Med, New York, NY USA.
[Burdine, Rebecca D.] Princeton Univ, Dept Mol Biol, Princeton, NJ 08544 USA.
[Schier, Alexander F.] Harvard Univ, Dept Mol & Cell Biol, Cambridge, MA 02138 USA.
[O'Callaghan, Christopher] Univ Leicester, Dept Infect Immun & Inflammat, Leicester, Leics, England.
[Reinhardt, Richard] Max Planck Inst Plant Breeding Res, Genome Ctr Cologne, Cologne, Germany.
[King, Stephen M.] Univ Connecticut, Ctr Hlth, Dept Mol Microbial & Struct Biol, Farmington, CT USA.
RP Drummond, IA (reprint author), Massachusetts Gen Hosp, Div Neurol, Charlestown, MA 02129 USA.
EM king@neuron.uchc.edu; heymut.omran@ukmuenster.de;
idrummon@receptor.mgh.harvard.edu
RI Schmidts, Miriam/A-3777-2012;
OI Schmidts, Miriam/0000-0002-1714-6749; Austin-Tse,
Christina/0000-0001-6492-6716; Burdine, Rebecca/0000-0001-6620-5015
FU PCD Family Support Group (UK); German patient support group 'Kartagener
Syndrom und Primaere Ciliaere Dyskinesie e.V.'; US National Institutes
of Health [DK053093, GM051293]; National Research Service Award
[F32DK083868]; American Heart Association; Deutsche
Forschungsgemeinschaft (DFG) [DFG Om 6/4, GRK1109, SFB592]; EU; IZKF
[Om2/009/12]; Kindness for Kids grant; Medical Research Council UK;
Wellcome Trust; Fondation Milena Carvajal-ProKartagener
FX We thank the patients and their families for their participation and
acknowledge support from the PCD Family Support Group (UK) and the
German patient support group 'Kartagener Syndrom und Primaere Ciliaere
Dyskinesie e.V.'. We thank R. Mark Gardiner and E. Moya for their help
and involvement in the study. We thank R. Hirst and A. Rutman for
electron microscopy. We thank A. Heer, C. Warmt, D. Nergenau, R. S.
Patel-King and L. Luo for excellent technical assistance. This work was
funded by US National Institutes of Health grants DK053093 (I. A. D.)
and GM051293 (S. M. K.), National Research Service Award fellowship
grant F32DK083868 (J.R.P.), an American Heart Association Established
Investigator Award (A. F. S.), Deutsche Forschungsgemeinschaft (DFG)
grants (DFG Om 6/4, GRK1109 and SFB592), EU grant SYSCILIA, IZKF-project
(Om2/009/12), and Kindness for Kids grant (H. Omran), the Medical
Research Council UK, the Wellcome Trust and the Fondation Milena
Carvajal-ProKartagener.
NR 28
TC 78
Z9 85
U1 2
U2 15
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD JUN
PY 2012
VL 44
IS 6
BP 714
EP U148
DI 10.1038/ng.2277
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 949BT
UT WOS:000304551100022
PM 22581229
ER
PT J
AU Prohaska, R
Sibon, OCM
Rudnicki, DD
Danek, A
Hayflick, SJ
Verhaag, EM
Vonk, JJ
Margolis, RL
Walker, RH
AF Prohaska, Rainer
Sibon, Ody C. M.
Rudnicki, Dobrila D.
Danek, Adrian
Hayflick, Susan J.
Verhaag, Esther M.
Vonk, Jan J.
Margolis, Russell L.
Walker, Ruth H.
TI Brain, blood, and iron: Perspectives on the roles of erythrocytes and
iron in neurodegeneration
SO NEUROBIOLOGY OF DISEASE
LA English
DT Review
DE Neuroacanthocytosis; Neurodegeneration; Iron; NBIA
ID KINASE-ASSOCIATED NEURODEGENERATION; INFANTILE NEUROAXONAL DYSTROPHY;
INDEPENDENT PHOSPHOLIPASE A(2); HALLERVORDEN-SPATZ-SYNDROME;
DISEASE-LIKE 2; DOMINANT CHOREA-ACANTHOCYTOSIS; LIGHT-POLYPEPTIDE GENE;
KELL-NULL PHENOTYPE; MCLEOD-SYNDROME; HUNTINGTONS-DISEASE
AB The terms "neuroacanthocytosis" (NA) and "neurodegeneration with brain iron accumulation" (NBIA) both refer to groups of genetically heterogeneous disorders, classified together due to similarities of their phenotypic or pathological findings. Even collectively, the disorders that comprise these sets are exceedingly rare and challenging to study. The NBIA disorders are defined by their appearance on brain magnetic resonance imaging, with iron deposition in the basal ganglia. Clinical features vary, but most include a movement disorder. New causative genes are being rapidly identified; however, the mechanisms by which mutations cause iron accumulation and neurodegeneration are not well understood. NA syndromes are also characterized by a progressive movement disorder, accompanied by cognitive and psychiatric features, resulting from mutations in a number of genes whose roles are also basically unknown. An overlapping feature of the two groups, NBIA and NA, is the occurrence of acanthocytes, spiky red cells with a poorly-understood membrane dysfunction. In this review we summarise recent developments in this field, specifically insights into cellular mechanisms and from animal models. Cell membrane research may shed light upon the significance of the erythrocyte abnormality, and upon possible connections between the two sets of disorders. Shared pathophysiologic mechanisms may lead to progress in the understanding of other types of neurodegeneration. Published by Elsevier Inc.
C1 [Walker, Ruth H.] James P Peters Vet Affairs Med Ctr, Dept Neurol, Bronx, NY 10468 USA.
[Walker, Ruth H.] Mt Sinai Sch Med, Dept Neurol, New York, NY USA.
[Prohaska, Rainer] Med Univ Vienna, Max F Perutz Labs, Vienna, Austria.
[Sibon, Ody C. M.; Verhaag, Esther M.; Vonk, Jan J.] Univ Groningen, Sect Radiat & Stress Cell Biol, Dept Cell Biol, Univ Med Ctr Groningen, Groningen, Netherlands.
[Rudnicki, Dobrila D.; Margolis, Russell L.] Johns Hopkins Univ, Sch Med, Dept Psychiat, Div Neurobiol,Lab Genet Neurobiol, Baltimore, MD 21205 USA.
[Danek, Adrian] Univ Munich, Neurol Klin & Poliklin, Munich, Germany.
[Hayflick, Susan J.] Oregon Hlth & Sci Univ, Dept Mol & Med Genet, Portland, OR 97201 USA.
[Hayflick, Susan J.] Oregon Hlth & Sci Univ, Dept Pediat & Neurol, Portland, OR 97201 USA.
[Margolis, Russell L.] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA.
[Margolis, Russell L.] Johns Hopkins Univ, Sch Med, Program Cellular & Mol Med, Baltimore, MD USA.
RP Walker, RH (reprint author), James P Peters Vet Affairs Med Ctr, Dept Neurol 127, 130 W Kingsbridge Rd, Bronx, NY 10468 USA.
EM ruth.walker@mssm.edu
RI Danek, Adrian/G-7339-2011
OI Danek, Adrian/0000-0001-8857-5383
FU National Institute of Neurological Diseases and Stroke; Office of Rare
Diseases Research; National Institute of Child Health and Human
Development [1R13NS067922-01]; Movement Disorder Society; Advocacy for
Neuroacanthocytosis Patients (UK); Associazione Italiana Sindromi
Neurodegenerative da Accumulo di Ferro (AISNAF) (Italy); NBIA Disorders
Association (USA); Hoffnungsbaum e.V. (Germany); GlaxoSmithKline;
European Multidisciplinary Initiative on Neuroacanthocytosis (EMINA)
[01GM1003]; RP (FWF) [I 438-B13]; OCMS (ZonMW) [113301162]
FX This article reflects presentations and discussion at a meeting entitled
"Brain, Blood and Iron: Joint International Symposium on
Neuroacanthocytosis and Neurodegeneration with Brain Iron Accumulation"
which was held in Bethesda, MD, USA on Oct 1-2 2010. This meeting was
supported by the National Institute of Neurological Diseases and Stroke;
the Office of Rare Diseases Research, and the National Institute of
Child Health and Human Development [1R13NS067922-01], and also by the
Movement Disorder Society, Advocacy for Neuroacanthocytosis Patients
(UK), Associazione Italiana Sindromi Neurodegenerative da Accumulo di
Ferro (AISNAF) (Italy), NBIA Disorders Association (USA), Hoffnungsbaum
e.V. (Germany) and GlaxoSmithKline. Funding by an ERA-Net E-Rare
project, "European Multidisciplinary Initiative on Neuroacanthocytosis
(EMINA)", is gratefully acknowledged by AD (BMBF/DLR grant 01GM1003), RP
(FWF grant I 438-B13), and OCMS (ZonMW grant 113301162).
NR 228
TC 22
Z9 23
U1 0
U2 11
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0969-9961
EI 1095-953X
J9 NEUROBIOL DIS
JI Neurobiol. Dis.
PD JUN
PY 2012
VL 46
IS 3
BP 607
EP 624
DI 10.1016/j.nbd.2012.03.006
PG 18
WC Neurosciences
SC Neurosciences & Neurology
GA 950DK
UT WOS:000304629300011
PM 22426390
ER
PT J
AU Madan, A
Archambeau, OG
Milsom, VA
Goldman, RL
Borckardt, JJ
Grubaugh, AL
Tuerk, PW
Frueh, BC
AF Madan, Alok
Archambeau, Olga G.
Milsom, Vanessa A.
Goldman, Rachel L.
Borckardt, Jeffery J.
Grubaugh, Anouk L.
Tuerk, Peter W.
Frueh, B. Christopher
TI More Than Black and White: Differences in Predictors of Obesity Among
Native Hawaiian/Pacific Islanders and European Americans
SO OBESITY
LA English
DT Article
ID INTERNATIONAL NEUROPSYCHIATRIC INTERVIEW; DSM-IV; PACIFIC ISLANDERS;
YOUNG-ADULTS; RISK-FACTORS; WEIGHT; HAWAIIANS; DISORDER; MINI
AB Although Native Hawaiians and Pacific Islanders exhibit the highest rates of obesity and associated chronic diseases of any racial/ethnic group, they remain vastly underrepresented in health research. In a cross-sectional survey of college students (N = 402) we examined BMI and health outcomes in an ethno-racially diverse rural sample of Native Hawaiian/Pacific Islanders (25.1%), Asian Americans (39.8%), and European Americans (35.1%). Measures assessed BMI, health status, health behaviors, frequency of exercise, and symptoms of psychiatric disorders (i.e., depression, anxiety, posttraumatic stress, and substance abuse and dependence). Regression analyses revealed that an overall model of five predictors (gender, race, regular exercise, difficulty sleeping, and anxiety) was significantly associated with obesity (P < 0.001) and correctly classified 84.2% of cases. A 30.7% of Native Hawaiians/Pacific Islanders were obese as compared with 9.2% of European Americans and 10.6% of Asian Americans. These findings suggest that Native Hawaiian/Pacific Islanders are at high risk for obesity and associated medical comorbidities, but that regular physical activity may ameliorate this risk. Further, these results support the consideration of Native Hawaiians/Pacific Islanders as a distinct racial/ethnic subgroup separate from other Asian populations.
C1 [Madan, Alok; Goldman, Rachel L.; Borckardt, Jeffery J.; Grubaugh, Anouk L.; Tuerk, Peter W.] Med Univ S Carolina, Dept Psychiat & Behav Sci, Charleston, SC 29425 USA.
[Archambeau, Olga G.; Frueh, B. Christopher] Univ Hawaii, Dept Psychol, Hilo, HI 96720 USA.
[Milsom, Vanessa A.] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA.
[Grubaugh, Anouk L.; Tuerk, Peter W.] Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC USA.
[Frueh, B. Christopher] Menninger Clin, Houston, TX USA.
RP Madan, A (reprint author), Med Univ S Carolina, Dept Psychiat & Behav Sci, 171 Ashley Ave, Charleston, SC 29425 USA.
EM madana@musc.edu
OI Goldman, Rachel/0000-0001-6147-3934
FU National Institute of Mental Health [MH074468]; McNair Foundation
FX This work was partially supported by the grant MH074468 from the
National Institute of Mental Health, and from the McNair Foundation.
Elements of the current work were included in O.G.A.'s master's thesis.
NR 18
TC 5
Z9 5
U1 1
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD JUN
PY 2012
VL 20
IS 6
BP 1325
EP 1328
DI 10.1038/oby.2012.15
PG 4
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 948QO
UT WOS:000304517900034
PM 22286530
ER
PT J
AU Mai, CL
Cote, CJ
AF Mai, Christine L.
Cote, Charles J.
TI A history of pediatric anesthesia: a tale of pioneers and equipment
SO PEDIATRIC ANESTHESIA
LA English
DT Review
DE history; equipment; critical care; developing world; airway devices
equipment; monitors equipment
ID MEASURING CARDIAC-OUTPUT; BISPECTRAL INDEX; PULSE OXIMETRY; CEREBRAL
OXIMETRY; ELECTRICAL VELOCIMETRY; REGIONAL ANESTHESIA; VIDEO
LARYNGOSCOPE; VEIN CANNULATION; LARYNGEAL MASK; CARBON-DIOXIDE
AB The history of pediatric anesthesia is fascinating in terms of how inventive anesthesiologists became over time to address the needs for advances in surgery. We have many pioneers and heroes. We hope you will enjoy this brief overview and that we have not left out any of the early contributors to our speciality. Obviously there is insufficient space to include everyone.
C1 [Mai, Christine L.; Cote, Charles J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Anesthesia Crit Care & Pain Med,MassGen Hosp, Boston, MA 02114 USA.
RP Mai, CL (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Anesthesia Crit Care & Pain Med,MassGen Hosp, Boston, MA 02114 USA.
EM cmai1@partners.org
NR 83
TC 6
Z9 6
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1155-5645
EI 1460-9592
J9 PEDIATR ANESTH
JI Pediatr. Anesth.
PD JUN
PY 2012
VL 22
IS 6
BP 511
EP 520
DI 10.1111/j.1460-9592.2012.03828.x
PG 10
WC Anesthesiology; Pediatrics
SC Anesthesiology; Pediatrics
GA 943PP
UT WOS:000304137100002
PM 22443224
ER
PT J
AU Maples, NJ
Copeland, LA
Zeber, JE
Li, XY
Moore, TA
Dassori, A
Velligan, DI
Miller, AL
AF Maples, Natalie J.
Copeland, Laurel Anne
Zeber, John E.
Li, Xueying
Moore, Troy A.
Dassori, Albana
Velligan, Dawn Irene
Miller, Alexander L.
TI Can Medication Management Coordinators Help Improve Continuity of Care
After Psychiatric Hospitalization?
SO PSYCHIATRIC SERVICES
LA English
DT Article
ID ALGORITHM PROJECT; MENTAL-ILLNESS; RISK-FACTORS; SCHIZOPHRENIA;
REHOSPITALIZATION; PATIENT; IMPLEMENTATION; INDIVIDUALS; STRATEGIES;
DISORDER
AB Objective: This demonstration project examined whether medication management coordinators enhanced continuity of care from inpatient facilities to an outpatient public mental health clinic. Methods: From 2004 to 2008, patients (N=325) hospitalized with schizophrenia or schizoaffeetive or bipolar disorder enrolled in a medication management program before discharge or at their first clinic appointment. Medication management coordinators supplemented existing clinic practices by identifying recently hospitalized patients, providing inpatient and outpatient prescribing clinicians with patients' complete medication history, meeting with patients for six months postdischarge to assess clinical status and provide medication education, and advocating guideline-concordant prescribing. Recently discharged patients (N=345) assigned to a different outpatient clinic within the same agency served as the comparison group. Intent-to-treat, repeated-measures analyses for mixed models compared the groups' number of hospital admissions, hospital days, and medication appointments kept and use of nurse or case manager contact hours and emergency or crisis services during the 12 months before enrollment, the six-month intervention, and the six-month follow-up period. Results: After discharge, individuals enrolled in medication management were more likely than comparison patients to attend outpatient appointments, and they had more medication visits and nurse or case manager treatment hours than the comparison group. Use of hospital and crisis or emergency services by all patients decreased. Almost one-third of patients never attended an outpatient appointment after hospital discharge. Conclusions: Although this program succeeded in improving continuity of care, additional interventions may be required to reduce rehospitalization and crisis care. (Psychiatric Services 63:554-560, 2012; doi: 10.1176/appi.ps.201100264)
C1 [Maples, Natalie J.; Li, Xueying; Moore, Troy A.; Velligan, Dawn Irene; Miller, Alexander L.] UT Hlth Sci Ctr San Antonio, Div Schizophrenia & Related Disorders, Dept Psychiat, San Antonio, TX 78229 USA.
[Copeland, Laurel Anne; Zeber, John E.] Scott & White Healthcare, Ctr Appl Hlth Res, Temple, TX USA.
[Copeland, Laurel Anne; Zeber, John E.] Cent Texas Vet Hlth Care Syst, Temple, TX USA.
[Dassori, Albana] S Texas Vet Hlth Care Syst, San Antonio, TX USA.
RP Maples, NJ (reprint author), UT Hlth Sci Ctr San Antonio, Div Schizophrenia & Related Disorders, Dept Psychiat, 7703 Floyd Curl Dr,MS 7797, San Antonio, TX 78229 USA.
EM maplesn@uthscsa.edu
OI Copeland, Laurel/0000-0002-9478-0209
FU AstraZeneca; U.S. Veterans Health Administration; UT Health Science
Center San Antonio; Scott & White Healthcare; GlaxoSmithKline; Pfizer
FX This demonstration project was funded by AstraZeneca through a grant to
the National Center for Behavioral Health Care Solutions, a 501(c)3
organization affiliated with the Center for Health Care Services.
Additional support was provided by the U.S. Veterans Health
Administration, the UT Health Science Center San Antonio, and Scott &
White Healthcare. The views expressed in this article are those of the
authors and do not necessarily reflect the position or policy of the
U.S. Department of Veterans Affairs or the U.S. government.; Dr. Zeber
received a research grant in 2011-2012 from GlaxoSmithKline as principal
investigator for one site of a multisite study unrelated to this
article. Dr. Velligan is a consultant for or on the advisory boards of
Ortho-McNeil Janssen Pharmaceuticals, Teva Pharmaceuticals, AstraZeneca
Pharmaceuticals, Roche Genentech, Abbott Pharmaceuticals, Lilly
Pharmaceuticals, Pfizer Pharmaceuticals, Bristol-Myers Squibb, Amgen,
and Merck and Shire Pharmaceuticals. Dr. Miller is a member of the data
monitoring committee for Otsuka and was on the advisory board of Myriad
RBM in 2010. He has received investigator-initiated grant funding from
Pfizer. The other authors report no competing interests.
NR 25
TC 4
Z9 4
U1 0
U2 4
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 1075-2730
J9 PSYCHIAT SERV
JI Psychiatr. Serv.
PD JUN
PY 2012
VL 63
IS 6
BP 554
EP 560
DI 10.1176/appi.ps.201100264
PG 7
WC Health Policy & Services; Public, Environmental & Occupational Health;
Psychiatry
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health; Psychiatry
GA 949IE
UT WOS:000304569100007
PM 22476107
ER
PT J
AU Walling, SM
Suvak, MK
Howard, JM
Taft, CT
Murphy, CM
AF Walling, Sherry Muterspaugh
Suvak, Michael K.
Howard, Jamie M.
Taft, Casey T.
Murphy, Christopher M.
TI Race/Ethnicity as a Predictor of Change in Working Alliance During
Cognitive Behavioral Therapy for Intimate Partner Violence Perpetrators
SO PSYCHOTHERAPY
LA English
DT Article
DE working alliance; race; ethnicity; intimate partner violence; group
treatment
ID INDIVIDUAL PSYCHOTHERAPY; HISPANIC COUPLES; REGRESSION; VARIABLES;
CLIENTS; BLACK; WHITE; MEN; ATTENDANCE; PATTERNS
AB Despite evidence that the working alliance (WA) is an important factor in psychotherapy outcome and that race/ethnicity plays an important role in the processes of therapy, few studies have directly examined associations between WA and race/ethnicity. These relationships may be particularly salient for difficult-to-engage populations, such as men participating in treatment for intimate partner violence. The current study examined WA ratings in a sample of 107 male intimate partner violence perpetrators attending a 16-week cognitive-behavioral group program. Approximately 50% of these participants were Caucasian and 50% were members of a racial/ethnic minority group (African American, Asian American, Hispanic, and American Indian). Growth curve modeling was used to assess changes in both therapist and client WA ratings across four time points during therapy. Findings indicated that there was no mean level of change in therapist WA ratings over time. However, clients' WA ratings demonstrated a reliable, steady increase across sessions. A significant interaction between WA and race/ethnicity emerged such that Caucasian participants reported a significant increase in WA over time, whereas members of racial/ethnic minority group did not report a consistent pattern of change. The interaction between client race/ethnicity and WA was also a significant predictor of treatment outcome at 6-month follow-up.
C1 [Walling, Sherry Muterspaugh] Fresno Pacific Univ, Dept Psychol, Fresno, CA 93702 USA.
[Suvak, Michael K.] Suffolk Univ, Dept Psychol, Boston, MA USA.
[Howard, Jamie M.; Taft, Casey T.] VA Boston Healthcare Syst, Natl Ctr PTSD, Boston, MA USA.
[Howard, Jamie M.; Taft, Casey T.] Boston Univ, Sch Med, Boston, MA 02215 USA.
[Murphy, Christopher M.] Univ Maryland, Dept Psychol, College Pk, MD 20742 USA.
RP Walling, SM (reprint author), Fresno Pacific Univ, Dept Psychol, 1717 S Chestnut Ave, Fresno, CA 93702 USA.
EM sherry.walling@fresno.edu
FU NIMH NIH HHS [1R03MH56373, 1F31MH12234]
NR 47
TC 9
Z9 9
U1 1
U2 11
PU AMER PSYCHOLOGICAL ASSOC, DIV PSYCHOTHERAPY
PI CORAL GABLES
PA 1390 SOUTH DIXIE HIGHWAY, STE 2222, CORAL GABLES, FL 33146-2946 USA
SN 0033-3204
J9 PSYCHOTHERAPY
JI Psychotherapy
PD JUN
PY 2012
VL 49
IS 2
BP 180
EP 189
DI 10.1037/a0025751
PG 10
WC Psychology, Clinical
SC Psychology
GA 951TH
UT WOS:000304742400012
PM 22181028
ER
PT J
AU Gellis, LA
AF Gellis, Les A.
TI An Investigation of a Cognitive Refocusing Technique To Improve Sleep
SO PSYCHOTHERAPY
LA English
DT Article
DE insomnia; cognitive therapy; behavior therapy; sleep
ID CHRONIC INSOMNIA; VALIDATION; THOUGHTS; INDEX
AB Developing techniques designed to minimize arousing cognitions during the evening may be important to help improve the treatment of insomnia. This investigation assessed an intervention that focused exclusively on enhancing cognitive refocusing at sleep onset to change the content and style of presleep cognitions in order to improve sleep. Individuals with primary insomnia (N = 10; 90% male, mean age = 49.2, SD = 12.6) attended four weekly individual meetings. Sleep quality (the Pittsburgh Sleep Quality Index), insomnia severity (the Insomnia Severity Index), sleep parameters based on one week of sleep diaries, and arousing thought content, were compared at baseline, posttreatment, and at a 1-month follow-up. Adherence was high, and participants showed good ability to engage in the procedure. Significant improvements in sleep quality, insomnia severity, sleep onset latency, total sleep time, and arousing thought content were revealed. Large effect sizes were observed on the majority of sleep variables at follow-up. Preliminary results were encouraging regarding a technique that targets the refocusing of thoughts during the evening in order to improve sleep. Further study regarding the efficacy of this procedure is warranted.
C1 [Gellis, Les A.] Philadelphia Vet Affairs Med Ctr, Philadelphia, PA USA.
RP Gellis, LA (reprint author), Syracuse Univ, Dept Psychol, 430 Huntington Hall, Syracuse, NY 13244 USA.
EM lesgellis@gmail.com
NR 24
TC 3
Z9 3
U1 1
U2 4
PU AMER PSYCHOLOGICAL ASSOC, DIV PSYCHOTHERAPY
PI CORAL GABLES
PA 1390 SOUTH DIXIE HIGHWAY, STE 2222, CORAL GABLES, FL 33146-2946 USA
SN 0033-3204
J9 PSYCHOTHERAPY
JI Psychotherapy
PD JUN
PY 2012
VL 49
IS 2
BP 251
EP 257
DI 10.1037/a0025746
PG 7
WC Psychology, Clinical
SC Psychology
GA 951TH
UT WOS:000304742400018
PM 22309052
ER
PT J
AU Eisenberg, JD
Harvey, HB
Moore, DA
Gazelle, GS
Pandharipande, PV
AF Eisenberg, Jonathan D.
Harvey, H. Benjamin
Moore, Donald A.
Gazelle, G. Scott
Pandharipande, Pari V.
TI Falling Prey to the Sunk Cost Bias: A Potential Harm of Patient
Radiation Dose Histories
SO RADIOLOGY
LA English
DT Editorial Material
C1 [Eisenberg, Jonathan D.; Gazelle, G. Scott; Pandharipande, Pari V.] Massachusetts Gen Hosp, Inst Technol Assessment, Boston, MA 02114 USA.
[Eisenberg, Jonathan D.; Harvey, H. Benjamin; Gazelle, G. Scott; Pandharipande, Pari V.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Harvey, H. Benjamin; Gazelle, G. Scott; Pandharipande, Pari V.] Harvard Univ, Sch Med, Boston, MA USA.
[Moore, Donald A.] Univ Calif Berkeley, Haas Sch Business, Berkeley, CA 94720 USA.
RP Pandharipande, PV (reprint author), Massachusetts Gen Hosp, Inst Technol Assessment, 101 Merrimac St,10th Floor, Boston, MA 02114 USA.
EM pari@mgh-ita.org
FU NCI NIH HHS [K07CA133097, K07 CA133097]
NR 18
TC 20
Z9 20
U1 0
U2 3
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0033-8419
J9 RADIOLOGY
JI Radiology
PD JUN
PY 2012
VL 263
IS 3
BP 626
EP 628
DI 10.1148/radiol.12112459
PG 3
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 947GK
UT WOS:000304416900002
PM 22623688
ER
PT J
AU Cronin, CG
Prakash, P
Daniels, GH
Boland, GW
Kalra, MK
Halpern, EF
Palmer, EL
Blake, MA
AF Cronin, Carmel G.
Prakash, Priyanka
Daniels, Gilbert H.
Boland, Giles W.
Kalra, Mannudeep K.
Halpern, Elkan F.
Palmer, Edwin L.
Blake, Michael A.
TI Brown Fat at PET/CT: Correlation with Patient Characteristics
SO RADIOLOGY
LA English
DT Article
ID ADIPOSE-TISSUE; MALIGNANT-LYMPHOMA; F-18-FDG PET/CT; USA-FAT;
PREVALENCE; PATTERNS; PITFALLS; CT
AB Purposes: To assess the prevalence of brown fat in patients with cancer, compare demographic characteristics of those with and those without brown fat, and correlate these characteristics with the mean and maximum standardized uptake values of brown fat.
Materials and Methods: This case-control study was institutional review board approved and HIPAA compliant. Informed consent was waived. Reports of 12 195 consecutive positron emission tomography/computed tomography examinations performed in 6867 patients between January 2004 and November 2008 were reviewed for documented fluorodeoxyglucose (FDG) uptake in brown fat (n = 298). Control patients (n = 298) without brown fat were chosen and matched for age, sex, and month and year of examination. Age, sex, weight, body mass index, ethnicity, and examination stage (initial vs restaging) were compared between groups. Paired Student t test, chi(2) test, Pearson correlation coefficient, and analysis of variance were used for statistical analysis.
Results: Uptake of FDG in brown fat was demonstrated in 298 of 6867 (4.33%) patients. Prevalence of brown fat was significantly higher in female (5.9% [211 of 3587]) than in male patients (2.65% [87 of 3280]; P < .001). Those with brown fat had significantly lower body weight (147.5 lb +/- 3.8 vs 168.61 lb +/- 5.0; P < .001) and body mass index (24.3 +/- 0.54 vs 27.6 +/- 0.77; P < .001) than control patients. There was no significant difference in the prevalence of brown fat among ethnic groups. The maximum standardized uptake value of brown fat had a significant inverse correlation with age (r = -0.3, P < .001).
Conclusion: Patients with brown fat were more likely to be female and thinner than those without brown fat. Younger patients were more likely to have higher maximum standardized uptake values of brown fat. (c) RSNA, 2012
C1 [Cronin, Carmel G.; Prakash, Priyanka; Daniels, Gilbert H.; Boland, Giles W.; Kalra, Mannudeep K.; Halpern, Elkan F.; Palmer, Edwin L.; Blake, Michael A.] Massachusetts Gen Hosp, Dept Abdominal Imaging & Intervent Radiol, Boston, MA 02114 USA.
RP Cronin, CG (reprint author), Massachusetts Gen Hosp, Dept Abdominal Imaging & Intervent Radiol, 55 Fruit St,White 270, Boston, MA 02114 USA.
EM cgcronin@partners.org
FU GE Healthcare
FX C.G.C. No potential conflicts of interest to disclose. P.P. No potential
conflicts of interest to disclose. G.D. No potential conflicts of
interest to disclose. G.B. No potential conflicts of interest to
disclose. M.K. Financial activities related to the present article: none
to disclose. Financial activities not related to the present article:
Payment for development of educational presentations and board
membership for GE Healthcare. Institution has grants or grants pending
from GE Healthcare. E.H. Financial activities related to the present
article: none to disclose. Financial activities not related to the
present article: Consultancy with Hologic. E.P. No potential conflicts
of interest to disclose. M.B. Financial activities related to the
present article: none to disclose. Financial activities not related to
the present article: received book editing royalties from Springer
Verlag.
NR 17
TC 19
Z9 21
U1 0
U2 5
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0033-8419
J9 RADIOLOGY
JI Radiology
PD JUN
PY 2012
VL 263
IS 3
BP 836
EP 842
DI 10.1148/radiol.12100683
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 947GK
UT WOS:000304416900026
PM 22623697
ER
PT J
AU Rao, RC
Choudhry, N
Gragoudas, ES
AF Rao, Rajesh C.
Choudhry, Netan
Gragoudas, Evangelos S.
TI Enhanced Depth Imaging Spectral-Domain Optical Coherence Tomography
Findings in Sclerochoroidal Calcification
SO RETINA-THE JOURNAL OF RETINAL AND VITREOUS DISEASES
LA English
DT Editorial Material
DE enhanced depth imaging; optical coherence tomography; sclerochoroidal
calcification
C1 [Choudhry, Netan; Gragoudas, Evangelos S.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol,Retina Serv, Boston, MA 02114 USA.
[Rao, Rajesh C.] Washington Univ, Sch Med, Dept Ophthalmol & Visual Sci, St Louis, MO 63110 USA.
RP Gragoudas, ES (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol,Retina Serv, 243 Charles St, Boston, MA 02114 USA.
EM evangelos_gragoudas@meei.harvard.edu
OI Rao, Rajesh/0000-0002-5776-8366
NR 4
TC 6
Z9 6
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0275-004X
J9 RETINA-J RET VIT DIS
JI Retin.-J. Retin. Vitr. Dis.
PD JUN
PY 2012
VL 32
IS 6
BP 1226
EP 1227
DI 10.1097/IAE.0b013e3182576e50
PG 2
WC Ophthalmology
SC Ophthalmology
GA 948VY
UT WOS:000304532100024
PM 22572772
ER
PT J
AU Rosenbaum, JT
Ku, J
Ali, A
Choi, D
Suhler, EB
AF Rosenbaum, James T.
Ku, Jennifer
Ali, Amro
Choi, Dongseok
Suhler, Eric B.
TI Patients with Retinal Vasculitis Rarely Suffer from Systemic Vasculitis
SO SEMINARS IN ARTHRITIS AND RHEUMATISM
LA English
DT Review
DE retinal vasculitis; vasculitis; Behcet's; granulomatosis with
polyangiitis; polyarteritis nodosa
ID POLYARTERITIS-NODOSA; WEGENERS GRANULOMATOSIS; OCULAR MANIFESTATIONS;
DISEASE; COMPLICATIONS; UVEITIS
AB Objectives: Systemic vasculitis is often mistakenly assumed to be a common cause of retinal vasculitis. We sought to determine the relationship between retinal vasculitis and systemic vasculitis.
Methods: A selected review was performed on 1390 charts of patients attending the uveitis clinic at the Oregon Health and Science University between 1985 and 2010. Included in the review were all patients with diagnoses commonly associated with retinal vasculitis and all patients who were diagnosed with a systemic vasculitis. Retinal vasculitis was identified by perivascular exudates, intraretinal hemorrhage, or cotton wool spots as seen on clinical examination or by vascular occlusion or leakage as identified by fluorescein angiogram.
Results: Two hundred seven or 14.9% of patients with uveitis had retinal vasculitis as a component of the intraocular inflammation. Thirty-five patients had retinal vasculitis that was primary, ie, not associated with a systemic disease, and the dominant manifestation of the uveitis. Fourteen of the patients with retinal vasculitis had Behcet's disease. Only 11 of the 1390 patients with uveitis had a systemic vasculitis. Of these 11, four had retinal vasculitis including 1 secondary to a cytomegalovirus retinitis. Thus, systemic vasculitis was directly responsible for 1.4% or 3 of 207 cases of retinal vasculitis. Nonvasculitic systemic diseases such as sarcoidosis (n = 13), syndromes confined to the eye such as pars planitis (n = 36), and intraocular infections (n = 29) were far more common causes of retinal vasculitis.
Conclusions: Retinal vasculitis is a relatively common feature of uveitis. Patients with retinal vasculitis, however, rarely suffer from 1 of the classical systemic vasculitides. (C) 2012 Elsevier Inc. All rights reserved. Semin Arthritis Rheum 41:859-865
C1 [Rosenbaum, James T.; Ali, Amro; Suhler, Eric B.] Oregon Hlth & Sci Univ, Dept Ophthalmol, Portland, OR 97239 USA.
[Rosenbaum, James T.] Oregon Hlth & Sci Univ, Dept Med, Portland, OR 97239 USA.
[Ku, Jennifer; Choi, Dongseok] Oregon Hlth & Sci Univ, Dept Publ Hlth, Portland, OR 97239 USA.
[Suhler, Eric B.] Portland VA Med Ctr, Portland, OR USA.
RP Rosenbaum, JT (reprint author), Oregon Hlth & Sci Univ, Dept Ophthalmol, 3181 SW Sam Jackson Pk Rd,L467Ad, Portland, OR 97239 USA.
EM rosenbaj@ohsu.edu
FU Research to Prevent Blindness; William C. Kuzell Foundation; Stan and
Madelle Rosenfeld Family Trust; William and Mary Bauman Foundation
FX This work was supported by Research to Prevent Blindness, the William C.
Kuzell Foundation, the Stan and Madelle Rosenfeld Family Trust, and the
William and Mary Bauman Foundation.
NR 24
TC 11
Z9 11
U1 1
U2 4
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0049-0172
J9 SEMIN ARTHRITIS RHEU
JI Semin. Arthritis Rheum.
PD JUN
PY 2012
VL 41
IS 6
BP 859
EP 865
DI 10.1016/j.semarthrit.2011.10.006
PG 7
WC Rheumatology
SC Rheumatology
GA 950XL
UT WOS:000304685100012
PM 22177107
ER
PT J
AU Avigan, D
Rosenblatt, J
Kufe, D
AF Avigan, David
Rosenblatt, Jacalyn
Kufe, Donald
TI Dendritic/Tumor Fusion Cells as Cancer Vaccines
SO SEMINARS IN ONCOLOGY
LA English
DT Review
ID CYTOTOXIC T-LYMPHOCYTES; COLONY-STIMULATING FACTOR; ALLOGENEIC
HEPATOCELLULAR-CARCINOMA; BONE-MARROW-TRANSPLANTATION; ANTIGEN-LOADING
STRATEGIES; AUTOLOGOUS TUMOR-CELLS; ANTITUMOR IMMUNITY;
MULTIPLE-MYELOMA; SUPPRESSOR-CELLS; PERIPHERAL-BLOOD
C1 [Avigan, David; Rosenblatt, Jacalyn] Beth Israel Deaconess Med Ctr, Hematol Malignancies Bone Marrow Transplant Progr, Div Hematol Oncol, Boston, MA 02215 USA.
[Kufe, Donald] Dana Farber Canc Inst, Translat Pharmacol & Early Therapeut Trials Progr, Dept Med Oncol, Boston, MA 02115 USA.
RP Avigan, D (reprint author), Beth Israel Deaconess Med Ctr, Hematol Malignancies Bone Marrow Transplant Progr, Div Hematol Oncol, 330 Brookline Ave,Mailstop KS 121, Boston, MA 02215 USA.
EM davigan@bidmc.harvard.edu
FU NCI NIH HHS [P01 CA078378, P01 CA155258]
NR 99
TC 16
Z9 20
U1 1
U2 18
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0093-7754
J9 SEMIN ONCOL
JI Semin. Oncol.
PD JUN
PY 2012
VL 39
IS 3
BP 287
EP 295
DI 10.1053/j.seminoncol.2012.02.003
PG 9
WC Oncology
SC Oncology
GA 948KW
UT WOS:000304503100006
PM 22595051
ER
PT J
AU Tsai, AC
Bangsberg, DR
Frongillo, EA
Hunt, PW
Muzoora, C
Martin, JN
Weiser, SD
AF Tsai, Alexander C.
Bangsberg, David R.
Frongillo, Edward A.
Hunt, Peter W.
Muzoora, Conrad
Martin, Jeffrey N.
Weiser, Sheri D.
TI Food insecurity, depression and the modifying role of social support
among people living with HIV/AIDS in rural Uganda
SO SOCIAL SCIENCE & MEDICINE
LA English
DT Article
DE AIDS/HIV; International health; Social support; Food; Food insecurity;
Depression; Uganda
ID HIV-INFECTED INDIVIDUALS; ANTIRETROVIRAL THERAPY; MEDICATION ADHERENCE;
HOST-RESISTANCE; POSITIVE WOMEN; MENTAL-HEALTH; BURKINA-FASO; SYMPTOMS;
STRESS; ASSOCIATION
AB Depression is common among people living with HIV/AIDS and contributes to a wide range of worsened HIV-related outcomes, including AIDS-related mortality. Targeting modifiable causes of depression, either through primary or secondary prevention, may reduce suffering as well as improve HIV-related outcomes. Food insecurity is a pervasive source of uncertainty for those living in resource-limited settings, and cross-sectional studies have increasingly recognized it as a critical determinant of poor mental health. Using cohort data from 456 men and women living with HIV/AIDS initiating HIV antiretroviral therapy in rural Uganda, we sought to (a) estimate the association between food insecurity and depression symptom severity, (b) assess the extent to which social support may serve as a buffer against the adverse effects of food insecurity, and (c) determine whether the buffering effects are specific to certain types of social support. Quarterly data were collected by structured interviews and blood draws. The primary outcome was depression symptom severity, measured by a modified Hopkins Symptom Checklist for Depression. The primary explanatory variables were food insecurity, measured with the Household Food Insecurity Access Scale, and social support, measured with a modified version of the Functional Social Support Questionnaire. We found that food insecurity was associated with depression symptom severity among women but not men, and that social support buffered the impacts of food insecurity on depression. We also found that instrumental support had a greater buffering influence than emotional social support. Interventions aimed at improving food security and strengthening instrumental social support may have synergistic beneficial effects on both mental health and HIV outcomes among PLWHA in resource-limited settings. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Tsai, Alexander C.] Harvard Univ, Robert Wood Johnson Hlth & Soc Scholars Program, Cambridge, MA 02138 USA.
[Tsai, Alexander C.; Bangsberg, David R.] Massachusetts Gen Hosp, Ctr Global Hlth, Boston, MA 02114 USA.
[Bangsberg, David R.] Harvard Initiat Global Hlth, Cambridge, MA USA.
[Bangsberg, David R.] Harvard Univ, Sch Med, Boston, MA USA.
[Bangsberg, David R.; Muzoora, Conrad] Mbarara Univ Sci & Technol, Mbarara, Uganda.
[Bangsberg, David R.] Massachusetts Gen Hosp, MIT, Phillip T & Susan M Ragan Inst, Boston, MA 02114 USA.
[Frongillo, Edward A.] Univ S Carolina, Dept Hlth Promot Educ & Behav, Columbia, SC 29208 USA.
[Hunt, Peter W.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Martin, Jeffrey N.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Weiser, Sheri D.] Univ Calif San Francisco, Div HIV AIDS, San Francisco, CA 94143 USA.
[Weiser, Sheri D.] Univ Calif San Francisco, Posit Hlth Program, San Francisco, CA 94143 USA.
RP Tsai, AC (reprint author), Harvard Ctr Populat & Dev Studies, 9 Bow St, Cambridge, MA 02138 USA.
EM atsai@hsph.harvard.edu
RI Nguyen, Giang/D-9027-2016;
OI Tsai, Alexander/0000-0001-6397-7917
FU NIAID NIH HHS [P30 AI027763, P30 AI27763]; NIMH NIH HHS [K23 MH-79713,
K23 MH079713, K23 MH079713-03S1, K23 MH079713-05, K24 MH-087227, K24
MH087227, K24 MH087227-10, MH-79713-03S1, R01 MH-054907, R01 MH054907,
R01 MH054907-17]
NR 89
TC 74
Z9 74
U1 4
U2 51
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0277-9536
J9 SOC SCI MED
JI Soc. Sci. Med.
PD JUN
PY 2012
VL 74
IS 12
BP 2012
EP 2019
DI 10.1016/j.socscimed.2012.02.033
PG 8
WC Public, Environmental & Occupational Health; Social Sciences, Biomedical
SC Public, Environmental & Occupational Health; Biomedical Social Sciences
GA 950IR
UT WOS:000304643300022
PM 22513248
ER
PT J
AU Brouwers, HB
Biffi, A
Ayres, AM
Schwab, K
Cortellini, L
Romero, JM
Rost, NS
Viswanathan, A
Greenberg, SM
Rosand, J
Goldstein, JN
AF Brouwers, H. Bart
Biffi, Alessandro
Ayres, Alison M.
Schwab, Kristin
Cortellini, Lynelle
Romero, Javier M.
Rost, Natalia S.
Viswanathan, Anand
Greenberg, Steven M.
Rosand, Jonathan
Goldstein, Joshua N.
TI Apolipoprotein E Genotype Predicts Hematoma Expansion in Lobar
Intracerebral Hemorrhage
SO STROKE
LA English
DT Article
DE APOE; cerebral amyloid angiopathy; genetics; hematoma expansion;
intracerebral hemorrhage
ID CEREBRAL AMYLOID ANGIOPATHY; ANGIOGRAPHY SPOT SIGN; IDENTIFIES PATIENTS;
HIGHEST RISK; E EPSILON-2; GROWTH; ASSOCIATION; DIAGNOSIS; MORTALITY;
SCORE
AB Background and Purpose-Hematoma volume is the most potent predictor of outcome in spontaneous intracerebral hemorrhage (ICH), and hematoma expansion after hospital presentation occurs in up to 40% of individuals. Among patients with lobar ICH, the apolipoprotein E (APOE) epsilon 2 allele predicts larger hematoma volumes at presentation. We investigated whether the epsilon 2 allele also identifies individuals at increased risk of hematoma expansion.
Methods-We analyzed 510 patients with primary ICH and genetic data available from an ongoing prospective cohort study. Baseline and follow-up CT scans were assessed for ICH location and volume using computer-assisted volumetric methods.
Results-Individuals with lobar ICH who possessed APOE epsilon 2 were at increased risk for hematoma expansion (OR, 2.72; 95% CI, 1.19-6.23; P = 0.009). The highest odds of expansion were in patients who qualified for the diagnosis of cerebral amyloid angiopathy-related ICH and carried the APOE epsilon 2 allele (OR, 6.02; 95% CI, 1.60 -22.58; P = 0.008). There was no effect of epsilon 2 on hematoma expansion in deep ICH and APOE epsilon 4 had no effect on hematoma expansion in lobar or deep ICH.
Conclusions-Possession of APOE epsilon 2 predisposes individuals with lobar ICH to hematoma expansion. This effect is even more pronounced in patients with amyloid angiopathy-related ICH, consistent with the epsilon 2 allele's role in vascular amyloid deposition and vessel fragility. (Stroke. 2012; 43: 1490-1495.)
C1 [Brouwers, H. Bart] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Human Genet Res,Rosand Lab, Boston, MA 02114 USA.
[Brouwers, H. Bart; Biffi, Alessandro; Cortellini, Lynelle; Rost, Natalia S.; Viswanathan, Anand; Rosand, Jonathan; Goldstein, Joshua N.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Neurocrit Care & Emergency Neurol, Boston, MA 02114 USA.
[Brouwers, H. Bart; Biffi, Alessandro; Ayres, Alison M.; Schwab, Kristin; Cortellini, Lynelle; Rost, Natalia S.; Viswanathan, Anand; Greenberg, Steven M.; Rosand, Jonathan; Goldstein, Joshua N.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol,Hemorrhag Stroke Res Grp, Boston, MA 02114 USA.
[Brouwers, H. Bart; Biffi, Alessandro; Ayres, Alison M.; Schwab, Kristin; Cortellini, Lynelle; Rost, Natalia S.; Viswanathan, Anand; Greenberg, Steven M.; Rosand, Jonathan; Goldstein, Joshua N.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, J Philip Kistler Stroke Res Ctr, Boston, MA 02114 USA.
[Romero, Javier M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Serv Neuroradiol, Boston, MA 02114 USA.
[Goldstein, Joshua N.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA 02114 USA.
[Goldstein, Joshua N.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Emergency Med, Boston, MA 02114 USA.
[Biffi, Alessandro; Cortellini, Lynelle; Rost, Natalia S.; Rosand, Jonathan] Broad Inst, Program Med & Populat Genet, Cambridge, MA USA.
RP Brouwers, HB (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Human Genet Res,Rosand Lab, 185 Cambridge St,CPZN 6818, Boston, MA 02114 USA.
EM brouwers@chgr.mgh.harvard.edu
RI Goldstein, Joshua/H-8953-2016;
OI Ayres, Alison/0000-0002-5492-1695
FU National Institutes of Health-National Institute of Neurological
Disorders and Stroke (NIH-NINDS) [R01NS059727, 5K23NS059774,
P50NS051343]; Keane Stroke Genetics Research Fund; Edward and Maybeth
Sonn Research Fund; American Heart Association/Bugher Foundation Centers
for Stroke Prevention Research [0775010N]; National Institutes of Health
(NIH); American Heart Association; National Institute of Neurological
Disorders and Stroke
FX All funding entities had no involvement in study design, data
collection, analysis, and interpretation, writing of the article, or in
the decision to submit for publication. The study was funded by National
Institutes of Health-National Institute of Neurological Disorders and
Stroke (NIH-NINDS) grants R01NS059727, 5K23NS059774, the Keane Stroke
Genetics Research Fund, and the Edward and Maybeth Sonn Research Fund.
Dr Brouwers was supported by the NIH-NINDS Specialized Programs of
Translational Research in Acute Stroke (SPOTRIAS) fellowship grant
P50NS051343. Dr Biffi was supported in part by the American Heart
Association/Bugher Foundation Centers for Stroke Prevention Research
(0775010N).; J.M.R. is on the Imaging Committee of the Desmoteplase in
Acute Ischemic Stroke Trial (DIAS) trial and the advisory board of
Lundbeck Pharmaceuticals. S. M. G. received a research grant from the
National Institutes of Health (NIH); honoraria from Medtronic and
Pfizer; and is a consultant/on the advisory board of Hoffman-La Roche,
Janssen Alzheimer Immunotherapy, and Bristol-Myers Squibb Company. J.R.
received research grants from the NIH and the American Heart
Association. J.N.G. received a research grant from the National
Institute of Neurological Disorders and Stroke and is a consultant/on
the advisory board of CSL Behring.
NR 26
TC 27
Z9 29
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD JUN
PY 2012
VL 43
IS 6
BP 1490
EP +
DI 10.1161/STROKEAHA.111.643262
PG 10
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 948SV
UT WOS:000304523800015
PM 22535266
ER
PT J
AU Allison, SOD
Javitt, MC
Glanc, P
Andreotti, RF
Bennett, GL
Brown, DL
Dubinsky, T
Harisinghani, MG
Harris, RD
Mitchell, DG
Pandharipande, PV
Pannu, HK
Podrasky, AE
Shipp, TD
Siegel, CL
Simpson, L
Wong-You-Cheong, JJ
Zelop, CM
AF Allison, Sandra O. DeJesus
Javitt, Marcia C.
Glanc, Phyllis
Andreotti, Rochelle F.
Bennett, Genevieve L.
Brown, Douglas L.
Dubinsky, Theodore
Harisinghani, Mukesh G.
Harris, Robert D.
Mitchell, Donald G.
Pandharipande, Pari V.
Pannu, Harpreet K.
Podrasky, Ann E.
Shipp, Thomas D.
Siegel, Cary Lynn
Simpson, Lynn
Wong-You-Cheong, Jade J.
Zelop, Carolyn M.
TI ACR Appropriateness Criteria (R) Multiple Gestations
SO ULTRASOUND QUARTERLY
LA English
DT Article
DE appropriateness criteria; twin; triplet; multiple gestations
ID TWIN TRANSFUSION SYNDROME; BIRTH-WEIGHT DISCORDANCE; FETAL WEIGHT;
SONOGRAPHIC PREDICTION; ANTEPARTUM MANAGEMENT; NUCHAL TRANSLUCENCY;
GROWTH DISCORDANCE; TRANSVAGINAL ULTRASONOGRAPHY; CHORIONICITY
DETERMINATION; 1ST-TRIMESTER ULTRASOUND
AB Multiple gestations are high-risk compared with singleton pregnancies. Prematurity and intrauterine growth restrictions are the major sources of morbidity and mortality common to all twin gestations. Monochorionic twins are at a higher risk for twin-twin transfusion, fetal growth restriction, congenital anomalies, vasa previa, velamentous insertion of the umbilical cord and fetal death. Therefore, determination of multiple gestation, amnionicity and chorionicity in the first trimester is important. Follow up examinations to evaluate fetal well-being include assessment of fetal growth and amniotic fluid volume, umbilical artery Doppler, nonstress test and biophysical profile. To date, there is a paucity of literature regarding imaging schedules for follow-up. At the very least, antepartum testing in multiple gestations is recommended in all situations in which surveillance would ordinarily be performed in a singleton pregnancy.
The ACR Appropriateness Criteria (R) are evidence-based guidelines for specific clinical conditions that are reviewed biennially by a multidisciplinary expert panel. The guideline development and review include an extensive analysis of current medical literature from peer reviewed journals and the application of a well-established consensus methodology (modified Delphi) to rate the appropriateness of imaging procedures by the panel. In those instances where evidence is lacking or not definitive, expert opinion may be used to recommend imaging.
C1 [Allison, Sandra O. DeJesus] Georgetown Univ Hosp, Washington, DC 20007 USA.
[Javitt, Marcia C.] Walter Reed Army Med Ctr, Washington, DC 20307 USA.
[Glanc, Phyllis] Sunnybrook Hlth Sci Ctr, Toronto, ON M4N 3M5, Canada.
[Andreotti, Rochelle F.] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
[Bennett, Genevieve L.] NYU, Med Ctr, New York, NY 10016 USA.
[Brown, Douglas L.] Mayo Clin, Rochester, MN USA.
[Dubinsky, Theodore] Univ Washington, Sch Med, Seattle, WA USA.
[Harisinghani, Mukesh G.; Pandharipande, Pari V.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Harris, Robert D.] Dartmouth Hitchcock Med Ctr, Lebanon, NH 03766 USA.
[Mitchell, Donald G.] Thomas Jefferson Univ Hosp, Philadelphia, PA 19107 USA.
[Pannu, Harpreet K.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Podrasky, Ann E.] Baptist Hosp Miami, S Miami Ctr Women & Infants, Miami, FL USA.
[Shipp, Thomas D.] Diagnost Ultrasound Associates, Boston, MA USA.
[Siegel, Cary Lynn] Washington Univ, Med Ctr, Mallinckrodt Inst Radiol, St Louis, MO 63110 USA.
[Simpson, Lynn] Columbia Univ, Amer Coll Obstet & Gynecol, New York, NY USA.
[Wong-You-Cheong, Jade J.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Zelop, Carolyn M.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Boston, MA 02215 USA.
RP Allison, SOD (reprint author), Amer Coll Radiol, Dept Qual & Safety, 1891 PrestonWhite Dr, Reston, VA 20191 USA.
EM sa263@gunet.georgetown.edu
NR 81
TC 4
Z9 4
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0894-8771
J9 ULTRASOUND Q
JI Ultrasound Q.
PD JUN
PY 2012
VL 28
IS 2
BP 149
EP 155
DI 10.1097/RUQ.0b013e31824bfc06
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 948WT
UT WOS:000304534600014
ER
PT J
AU Gupta, S
Singh, AH
Shabbir, A
Hahn, PF
Harris, G
Sahani, D
AF Gupta, Supriya
Singh, Anand H.
Shabbir, Amna
Hahn, Peter F.
Harris, Gordon
Sahani, Dushyant
TI Assessing Renal Parenchymal Volume on Unenhanced CT as a Marker for
Predicting Renal Function in Patients with Chronic Kidney Disease
SO ACADEMIC RADIOLOGY
LA English
DT Article
DE Renal volumetry; split renal function; chronic kidney disease
ID GLOMERULAR-FILTRATION-RATE; RELATIVE LUNG-VOLUME; COMPUTED-TOMOGRAPHY;
LIVER VOLUME; PULMONARY HYPOPLASIA; PLANNING ORGAN; DONORS;
TRANSPLANTATION; ACCURACY; MRI
AB Objectives: To estimate renal volume in chronic kidney disease (CKD) patients using a semiautomated software and compare them with split renal function estimates from radionuclide renogram (RR). We proposed that renal volume from unenhanced computed tomography (CT) scans may serve as surrogate marker for assessing renal function in CKD patients.
Materials and Methods: Unenhanced multidetector CT scans of 26 patients with CKD (estimated glomerular filtration rate [eGFR] <60 mL/kg/body surface area [BSA]) and 10 controls (eGFR >60 mL/kg/BSA) were analyzed to calculate renal volumes using a semiautomated software (AMIRAV5.2.0). Volumes obtained were then correlated with corresponding eGFR and split renal function estimates from RR. Volumes were also compared with those obtained on enhanced scans in 10 cases (five disease group, five controls). Bland-Altman analysis was used to assess agreement between methods.
Results: A moderately positive correlation was found between renal volume obtained on unenhanced CT and eGFR (r = 0.65, P < .0001), whereas a significantly high correlation with split function estimates from RR (r = 0.95, P < .001) was found. Bland-Altman analysis revealed a good agreement between renal volume from CT and renal function from RR (34/36 observations were within 95% CI and there were two outliers). Correlation between volumes obtained from unenhanced and enhanced CT scans was also significant (r = 0.96).
Conclusion: In patients with CKD, renal volume derived from unenhanced CT can possibly serve as a surrogate marker for assessing and monitoring renal function reserves to plan further management.
C1 [Gupta, Supriya; Hahn, Peter F.; Sahani, Dushyant] Massachusetts Gen Hosp, Dept Abdominal & Intervent Radiol, Boston, MA 02114 USA.
[Singh, Anand H.; Harris, Gordon] Massachusetts Gen Hosp, Dept Imaging 3D, Boston, MA 02114 USA.
[Singh, Anand H.] Aga Khan Univ, Karachi, Pakistan.
RP Gupta, S (reprint author), Massachusetts Gen Hosp, Dept Abdominal & Intervent Radiol, 55 Fruit St,White 270, Boston, MA 02114 USA.
EM riya10.in@gmail.com
FU GE Research Foundation
FX D.S. received a grant from GE Research Foundation for this project.
NR 55
TC 6
Z9 7
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1076-6332
J9 ACAD RADIOL
JI Acad. Radiol.
PD JUN
PY 2012
VL 19
IS 6
BP 654
EP 660
DI 10.1016/j.acra.2012.02.006
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 946TZ
UT WOS:000304381700004
PM 22578224
ER
PT J
AU Liapakis, IE
Paschalis, EI
AF Liapakis, Ioannis E.
Paschalis, Eleftherios I.
TI Liposuction and Suspension of the Orbicularis Oculi for the Correction
of Persistent Malar Bags: Description of Technique and Report of a Case
SO AESTHETIC PLASTIC SURGERY
LA English
DT Article
DE Malar bags; Orbicularis oculi suspension; Blepharoplasty; Liposuction
ID COMPOSITE RHYTIDECTOMY; SUBPERIOSTEAL; REJUVENATION; MIDFACE; LIFT;
BLEPHAROPLASTY; DISSECTION; FACELIFT; EYELIDS; MUSCLE
AB The purpose of this study was to present an alternative surgical procedure for the correction of persistent malar bags and to review the literature.
A 45-year-old female patient with persistent malar bags, secondary to previous blepharoplasty, was admitted. Liposuction of the edema and suspension of the orbicularis muscle to the temporal region was performed through a lateral canthal incision.
A successful malar bag removal was demonstrated, exhibiting stable results at the 6-month follow-up.
Persistent malar bags resulting from previous blepharoplasty may be difficult to correct with conventional treatment. The combination of liposuction and suspension of the orbicularis oculi is proposed as an efficient alternative for the correction of persistent malar bags.
C1 [Liapakis, Ioannis E.] OpsisClin Plast & Reconstruct Surg, Iraklion 71304, Crete, Greece.
[Paschalis, Eleftherios I.] Harvard Univ, Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
RP Paschalis, EI (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, 243 Charles St, Boston, MA 02114 USA.
EM eleftherios_paschalis@meei.harvard.edu
OI Paschalis, Eleftherios/0000-0002-4544-4452
NR 27
TC 3
Z9 3
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0364-216X
J9 AESTHET PLAST SURG
JI Aesthet. Plast. Surg.
PD JUN
PY 2012
VL 36
IS 3
BP 546
EP 549
DI 10.1007/s00266-011-9838-1
PG 4
WC Surgery
SC Surgery
GA 944LN
UT WOS:000304203800010
PM 22101985
ER
PT J
AU Lorenzana, SB
Hughes, MD
Grinsztejn, B
Collier, AC
Luz, PM
Freedberg, KA
Wood, R
Levison, JH
Mugyenyi, PN
Salata, R
Wallis, CL
Weinstein, MC
Schooley, RT
Walensky, RP
AF Lorenzana, Sarah B.
Hughes, Michael D.
Grinsztejn, Beatriz
Collier, Ann C.
Luz, Paula Mendes
Freedberg, Kenneth A.
Wood, Robin
Levison, Julie H.
Mugyenyi, Peter N.
Salata, Robert
Wallis, Carole L.
Weinstein, Milton C.
Schooley, Robert T.
Walensky, Rochelle P.
TI Genotype assays and third-line ART in resource-limited settings: a
simulation and cost-effectiveness analysis of a planned clinical trial
SO AIDS
LA English
DT Article
DE A5288; ACTG; antiretroviral therapy; ART; cost-effectiveness; genotype;
HIV; resource-limited setting; third-line ART
ID ACTIVE ANTIRETROVIRAL THERAPY; SOUTH-AFRICA; VIROLOGICAL FAILURE;
DRUG-RESISTANCE; COTE-DIVOIRE; HIV-1-INFECTED PATIENTS; HIV-1 INFECTION;
RISK-FACTORS; ADULTS; PREDICTORS
AB Objectives: To project the clinical and economic outcomes of a genotype assay for selection of third-line antiretroviral therapy (ART) in resource-limited settings, as per the planned international A5288 trial (MULTI-OCTAVE).
Methods: We used the Cost-effectiveness of Preventing AIDS Complications (CEPAC)-International Model to compare three strategies for patients who have failed second-line ART in South Africa: sustained second-line: no genotype assay, all patients remain on second-line ART; A5288: genotype to determine the resistance profile and assign an appropriate regimen; or population-based third-line: no genotype, all patients switch to a potent third-line regimen. Model inputs are from published data in South Africa. Resistance profiles, ART regimens, and efficacy data were those used for trial planning.
Results: Projected life expectancy for sustained second-line, A5288, and population-based third-line are 61.1, 103.8, and 104.2 months. Compared to sustained second-line ($ 12 460), per person lifetime costs increase for the A5288 ($ 39 250) and population-based ($ 44 120) strategies. The incremental cost-effectiveness ratio of A5288, compared to sustained second-line, is $ 7500/year of life saved (YLS), and for population-based third-line, compared to A5288, is $ 154 500/YLS. In the A5288 strategy, very late presentation to care, coupled with lengthy delays to obtain the genotype, dramatically reduces 5-year survival, making the population-based third-line strategy more attractive.
Conclusions: We project that, whereas the public health approach to third-line therapy is unaffordable, genotype assays and third-line ART in resource-limited settings will increase survival and be cost-effective compared to the population-based approach, supporting the value of an efficacy study. (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins
C1 [Freedberg, Kenneth A.; Levison, Julie H.; Walensky, Rochelle P.] Harvard Univ, Massachusetts Gen Hosp, Div Infect Dis, Sch Med, Boston, MA 02114 USA.
[Lorenzana, Sarah B.; Freedberg, Kenneth A.; Walensky, Rochelle P.] Harvard Univ, Massachusetts Gen Hosp, Div Gen Med, Sch Med, Boston, MA 02114 USA.
[Freedberg, Kenneth A.; Walensky, Rochelle P.] Harvard Univ, Massachusetts Gen Hosp, Dept Med, Sch Med, Boston, MA 02114 USA.
[Levison, Julie H.; Walensky, Rochelle P.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Lorenzana, Sarah B.; Freedberg, Kenneth A.; Weinstein, Milton C.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Grinsztejn, Beatriz; Luz, Paula Mendes] Fundacao Oswaldo Cruz, Inst Pesquisas Clin Evandro Chagas, Rio De Janeiro, Brazil.
[Collier, Ann C.] Univ Washington, Harborview Med Ctr, Sch Med, Seattle, WA 98104 USA.
[Wood, Robin] Univ Cape Town, Inst Infect Dis & Mol Med, Desmond Tutu HIV Ctr, ZA-7925 Cape Town, South Africa.
[Mugyenyi, Peter N.] Joint Clin Res Ctr, Kampala, Uganda.
[Salata, Robert] Case Western Reserve Univ, Sch Med, Div Infect Dis, Cleveland, OH 44106 USA.
[Schooley, Robert T.] Univ Calif San Diego, Div Infect Dis, San Diego, CA 92103 USA.
RP Walensky, RP (reprint author), Harvard Univ, Massachusetts Gen Hosp, Div Infect Dis, Sch Med, 50 Staniford St,9th Floor, Boston, MA 02114 USA.
EM rwalensky@partners.org
FU National Institute of Allergy and Infectious Diseases [R01 AI058736, K24
AI062476, P30 AI060354, AI069434]; AIDS Clinical Trials Group [U01
AI068636, U01 AI068634]; Merck Company; Schering-Plough
FX The work was supported by the National Institute of Allergy and
Infectious Diseases (R01 AI058736, K24 AI062476, P30 AI060354,
AI069434), and the AIDS Clinical Trials Group (U01 AI068636, U01
AI068634). The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.; A.C.C.
has current or recent past research support from Merck & Company and
Schering-Plough. She was a member of a Data, Safety, and Monitoring
Board for a Merck-sponsored study. She and an immediate family member
own stock in Abbott Laboratories, Bristol Myers Squibb, Johnson and
Johnson and Pfizer, Inc.; R.T.S. has served as a consultant to Merck &
Company. He serves as a consultant to Johnson and Johnson and to Gilead
Sciences. He serves as Chair of a Data, Safety, and Monitoring Board for
a Gilead-sponsored study.
NR 56
TC 8
Z9 8
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0269-9370
J9 AIDS
JI Aids
PD JUN 1
PY 2012
VL 26
IS 9
BP 1083
EP 1093
DI 10.1097/QAD.0b013e32835221eb
PG 11
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 946PK
UT WOS:000304364900004
PM 22343964
ER
PT J
AU Ho, JE
Scherzer, R
Hecht, FM
Maka, K
Selby, V
Martin, JN
Ganz, P
Deeks, SG
Hsue, PY
AF Ho, Jennifer E.
Scherzer, Rebecca
Hecht, Frederick M.
Maka, Kristinalisa
Selby, Van
Martin, Jeffrey N.
Ganz, Peter
Deeks, Steven G.
Hsue, Priscilla Y.
TI The association of CD4(+) T-cell counts and cardiovascular risk in
treated HIV disease
SO AIDS
LA English
DT Article
DE cardiovascular diseases; CD4 cell; HIV; risk factors; vasodilation
ID FLOW-MEDIATED DILATION; ANTIRETROVIRAL THERAPY; MYOCARDIAL-INFARCTION;
ENDOTHELIAL DYSFUNCTION; BRACHIAL-ARTERY; VIRAL LOAD; INFECTION;
ATHEROSCLEROSIS; VASODILATION; INDIVIDUALS
AB Objective: HIV-infected individuals are at high risk of developing cardiovascular disease. Whether earlier initiation of HIV therapy at higher CD4(+) cell counts has any effect on cardiovascular risk as assessed by endothelial function is unknown.
Design: Cross-sectional study of 74 antiretroviral-treated men with undetectable plasma HIV RNA levels.
Methods: Participants underwent noninvasive assessment of endothelial function using brachial artery flow-mediated dilation (FMD). The association of nadir and current CD4(+) T-cell count with FMD was assessed using multivariable linear regression.
Results: The median age was 47 years [interquartile range (IQR) 42-55], median current CD4(+) T-cell count was 659 cells/mu l (IQR 542-845), and nadir CD4 cell count was 314 cells/mu l (IQR 150-490). Twenty-eight percent had hypertension, and 32% hyperlipidemia. Nadir CD4(+) T-cell count less than 350 cells/mu l was associated with lower FMD in age-adjusted and race-adjusted analyses and remained an independent predictor of FMD after adjustment for cardiovascular risk factors (hypertension, diabetes, smoking, hyperlipidemia) and HIV-related characteristics (HIV duration, HAART duration). After multivariable adjustment, individuals with nadir CD4(+) T-cell count less than 350 cells/mu l had a 1.22% lower FMD compared with those with higher T-cell counts [95% confidence interval (CI) - 2.20 to 0.19-, P = 0.02]. Proximal CD4(+) T-cell count showed little association with FMD.
Conclusion: Among treated HIV-infected individuals, nadir CD4(+) T-cell count less than 350 cells/mu l is independently associated with lower FMD, suggesting that delayed therapy results in sustained harm to endothelial function. Our data support future prospective studies evaluating cardiovascular effects of HAART initiation at higher CD4(+) cell counts. (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins
C1 [Maka, Kristinalisa; Selby, Van; Ganz, Peter; Hsue, Priscilla Y.] Univ Calif San Francisco, San Francisco Gen Hosp, Dept Med, Div Cardiol, San Francisco, CA 94110 USA.
[Ho, Jennifer E.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Scherzer, Rebecca] Univ Calif San Francisco, Vet Adm Med Ctr, San Francisco, CA 94110 USA.
[Hecht, Frederick M.; Martin, Jeffrey N.; Deeks, Steven G.] Univ Calif San Francisco, Posit Hlth Program, San Francisco, CA 94110 USA.
[Martin, Jeffrey N.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94110 USA.
RP Hsue, PY (reprint author), Univ Calif San Francisco, San Francisco Gen Hosp, Dept Med, Div Cardiol, Room 5G1,1001 Potrero Ave, San Francisco, CA 94110 USA.
EM phsue@medsfgh.ucsf.edu
OI Ho, Jennifer/0000-0002-7987-4768
FU NIH/University of California, San Francisco-Gladstone Institute of
Virology and Immunology Center for AIDS Research [P30-AI027763]; NIH
[5R01-HL095130, 5K23-AI066885]; National Institute of Allergy and
Infectious Diseases [K24-AI069994]; CFAR Network of Integrated Clinical
Systems [R24 AI067039]; UCSF Clinical and Translational Science
Institute [UL1 RR024131-01]; Pfizer; Merck; Gilead
FX This research was supported by grants from the NIH/University of
California, San Francisco-Gladstone Institute of Virology and Immunology
Center for AIDS Research, P30-AI027763 (J.E.H); from the NIH,
5R01-HL095130, and 5K23-AI066885 (P.Y.H.); from the National Institute
of Allergy and Infectious Diseases, K24-AI069994 (S. G. D.), CFAR
Network of Integrated Clinical Systems, R24 AI067039; and the UCSF
Clinical and Translational Science Institute, UL1 RR024131-01.; P.Y.H.
has received honoraria from Gilead, and grant support from Pfizer. S. G.
D. has received grant support from Merck and Gilead and honoraria from
GlaxoSmithKline, ViiV, and Tobira.
NR 33
TC 35
Z9 36
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0269-9370
J9 AIDS
JI Aids
PD JUN 1
PY 2012
VL 26
IS 9
BP 1115
EP 1120
DI 10.1097/QAD.0b013e328352ce54
PG 6
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 946PK
UT WOS:000304364900007
PM 22382147
ER
PT J
AU Varraso, R
Camargo, CA
AF Varraso, Raphaelle
Camargo, Carlos A., Jr.
TI More evidence for the importance of nutritional factors in chronic
obstructive pulmonary disease
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Editorial Material
ID DIETARY PATTERNS; RISK-FACTORS; CURED MEATS; VITAMIN-D; US WOMEN; MEN;
METAANALYSIS; CONSUMPTION; BURDEN
C1 [Camargo, Carlos A., Jr.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Emergency Med, Boston, MA 02114 USA.
[Varraso, Raphaelle] INSERM, CESP Ctr Res Epidemiol & Populat Hlth, U1018, Resp & Environm Epidemiol Team, Villejuif, France.
[Varraso, Raphaelle] Univ Paris Sud 11, UMRS 1018, Villejuif, France.
RP Camargo, CA (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Emergency Med, 326 Cambridge St,Suite 410, Boston, MA 02114 USA.
EM ccamargo@partners.org
RI Varraso, Raphaelle/R-8740-2016
OI Varraso, Raphaelle/0000-0002-3338-7825
NR 20
TC 4
Z9 6
U1 1
U2 4
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD JUN
PY 2012
VL 95
IS 6
BP 1301
EP 1302
DI 10.3945/ajcn.112.039834
PG 2
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 946FT
UT WOS:000304337600002
PM 22552036
ER
PT J
AU McCaffery, JM
Papandonatos, GD
Peter, I
Huggins, GS
Raynor, HA
Delahanty, LM
Cheskin, LJ
Balasubramanyam, A
Wagenknecht, LE
Wing, RR
AF McCaffery, Jeanne M.
Papandonatos, George D.
Peter, Inga
Huggins, Gordon S.
Raynor, Hollie A.
Delahanty, Linda M.
Cheskin, Lawrence J.
Balasubramanyam, Ashok
Wagenknecht, Lynne E.
Wing, Rena R.
CA Genetic Subgrp Look AHEAD
Look AHEAD Res Grp
TI Obesity susceptibility loci and dietary intake in the Look AHEAD Trial
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; NEUROTROPHIC FACTOR BDNF; BODY-MASS INDEX;
DIABETES PREVENTION PROGRAM; ENERGY-INTAKE; FTO GENE; EATING FREQUENCY;
FOOD-FREQUENCY; ADULT OBESITY; LIFE-STYLE
AB Background: Genome-wide association studies (GWAS) have identified consistent associations with obesity. However, the mechanisms remain unclear.
Objective: The objective was to determine the association between obesity susceptibility loci and dietary intake.
Design: The association of GWAS-identified obesity risk alleles (FTO, MC4R, SH2B1, BDNF, INSIG2, TNNI3K, NISCH-STAB1, MTIF3, MAP2K5, QPCTL/GIPR, and PPARG) with dietary intake, measured through food-frequency questionnaires, was investigated in 2075 participants from the Look AHEAD (Action for Health in Diabetes) clinical trial. We adjusted for age, sex, population stratification, and study site.
Results: Obesity risk alleles at FTO rs1421085 significantly predicted more eating episodes per day (P = 0.001) an effect that persisted after adjustment for body weight (P = 0.004). Risk variants within BDNF were significantly associated with more servings from the dairy product and the meat, eggs, nuts, and beans food groups (P <= 0.004). The risk allele at SH2BI rs4788099 was significantly associated with more servings of dairy products (P = 0.001), whereas the risk allele at TNNI3K rs1514176 was significantly associated with a lower percentage of energy from protein (P = 0.002).
Conclusion: These findings suggest that obesity risk loci may affect the pattern and content of food consumption among overweight or obese individuals with type 2 diabetes. The Look AHEAD Genetic Ancillary Study was registered at clinicaltrials.gov as NCT01270763 and the Look AHEAD study as NCT00017953. Am J Clin Nutr 2012;95:1477-86.
C1 [McCaffery, Jeanne M.; Wing, Rena R.] Brown Univ, Weight Control & Diabet Res Ctr, Miriam Hosp, Providence, RI 02903 USA.
[McCaffery, Jeanne M.; Wing, Rena R.] Brown Univ, Warren Alpert Sch Med, Providence, RI 02903 USA.
[Papandonatos, George D.] Brown Univ, Ctr Stat Sci, Providence, RI 02903 USA.
[Peter, Inga] Mt Sinai Sch Med, Dept Genet & Genom Sci, New York, NY USA.
[Huggins, Gordon S.] Tufts Med Ctr, MCRI Ctr Translat Genom, Mol Cardiol Res Inst, Boston, MA USA.
[Raynor, Hollie A.] Univ Tennessee, Dept Nutr, Knoxville, TN 37996 USA.
[Delahanty, Linda M.] Massachusetts Gen Hosp, Ctr Diabet, Boston, MA 02114 USA.
[Delahanty, Linda M.] Harvard Univ, Sch Med, Boston, MA USA.
[Cheskin, Lawrence J.] Johns Hopkins Bloomberg Sch Publ Hlth, Johns Hopkins Weight Management Ctr, Dept Hlth Behav & Soc, Baltimore, MD USA.
[Balasubramanyam, Ashok] Baylor Coll Med, Diabet & Endocrinol Res Ctr, Translat Metab Unit, Houston, TX 77030 USA.
[Wagenknecht, Lynne E.] Wake Forest Univ, Div Publ Hlth Sci, Winston Salem, NC 27109 USA.
RP McCaffery, JM (reprint author), Brown Univ, Weight Control & Diabet Res Ctr, Miriam Hosp, 196 Richmond St, Providence, RI 02903 USA.
EM jeanne_mccaffery@brown.edu
RI Papandonatos, George/J-2328-2014;
OI Papandonatos, George/0000-0001-6770-932X
FU Look AHEAD [U01DK056992-11SI, DK072497]; Department of Health and Human
Services through NIH [DK57136, DK57149, DK56990, DK57177, DK57171,
DK57151, DK57182, DK57131, DK57002, DK57078, DK57154, DK57178, DK57219,
DK57008, DK57135, DK56992]; Johns Hopkins Medical Institutions Bayview
General Clinical Research Center [M01RR02719]; Massachusetts General
Hospital Mallinckrodt General Clinical Research Center [M01RR01066];
University of Colorado Health Sciences Center General Clinical Research
Center [M01RR00051]; Clinical Nutrition Research Unit [P30 DK48520];
University of Tennessee at Memphis General Clinical Research Center
[M01RR0021140]; University of Pittsburgh General Clinical Research
Center [M01RR000056 44]; NIH [DK072497, DK 046204]; University of
Washington/VA Puget Sound Health Care System Medical Research Service,
Department of Veterans Affairs; Frederic C Banter General Clinical
Research Center [M01RR01346]
FX Look AHEAD genetic ancillary study funding and support (U01DK056992-11SI
and DK072497). Look AHEAD is supported by the Department of Health and
Human Services through the following cooperative agreements from the
NIH: DK57136, DK57149, DK56990, DK57177, DK57171, DK57151, DK57182,
DK57131, DK57002, DK57078, DK57154, DK57178, DK57219, DK57008, DK57135,
and DK56992. The following federal agencies have contributed support:
National Institute of Diabetes and Digestive and Kidney Diseases
(Barbara Harrison, Van S Hubbard. and Susan Z Yanovski); National Heart,
Lung, and Blood Institute (Lawton S Cooper, Jeffrey Cutler, and Eva
Obarzanek); National Institute of Nursing Research; National Center on
Minority Health and Health Disparities; Office of Research on Women's
Health; and the CDC (Edward W Gregg, David F Williamson, and Ping
Zhang). Additional support was received from The Johns Hopkins Medical
Institutions Bayview General Clinical Research Center (M01RR02719); the
Massachusetts General Hospital Mallinckrodt General Clinical Research
Center (M01RR01066); the University of Colorado Health Sciences Center
General Clinical Research Center (M01RR00051) and Clinical Nutrition
Research Unit (P30 DK48520); the University of Tennessee at Memphis
General Clinical Research Center (M01RR0021140); the University of
Pittsburgh General Clinical Research Center (M01RR000056 44); NIH grants
(DK 046204 and DK072497); the University of Washington/VA Puget Sound
Health Care System Medical Research Service, Department of Veterans
Affairs; and Frederic C Banter General Clinical Research Center
(M01RR01346). The following organizations have committed to make major
contributions to Look AHEAD: Federal Express; Health Management
Resources; Johnson & Johnson, Life Scan Inc; Optifast-Novartis
Nutrition; Roche Pharmaceuticals; Ross Product Division of Abbott
Laboratories; Slim-Fast Foods Company; and Unilever.
NR 66
TC 46
Z9 48
U1 0
U2 11
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD JUN
PY 2012
VL 95
IS 6
BP 1477
EP 1486
DI 10.3945/ajcn.111.026955
PG 10
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 946FT
UT WOS:000304337600024
PM 22513296
ER
PT J
AU Weycker, D
Malin, J
Barron, R
Edelsberg, J
Kartashov, A
Oster, G
AF Weycker, Derek
Malin, Jennifer
Barron, Rich
Edelsberg, John
Kartashov, Alex
Oster, Gerry
TI Comparative Effectiveness of Filgrastim, Pegfilgrastim, and Sargramostim
as Prophylaxis Against Hospitalization for Neutropenic Complications in
Patients With Cancer Receiving Chemotherapy
SO AMERICAN JOURNAL OF CLINICAL ONCOLOGY-CANCER CLINICAL TRIALS
LA English
DT Article
DE filgrastim; pegfilgrastim; sargramostim; febrile neutropenia; outcomes
ID COLONY-STIMULATING FACTOR; SINGLE-ADMINISTRATION PEGFILGRASTIM;
BREAST-CANCER; MYELOSUPPRESSIVE CHEMOTHERAPY; FEBRILE NEUTROPENIA;
DOSE-INTENSITY; DOUBLE-BLIND; PHASE-III; RHUGM-CSF; MULTICENTER
AB Background: Comparative effectiveness of filgrastim, pegfilgrastim, and sargramostim in preventing hospitalization for febrile neutropenia (FN) during myelosuppressive chemotherapy has not been well characterized and is an important clinical question in oncology.
Methods: This study used a retrospective cohort design and US healthcare claims data. Source population included patients with solid tumors receiving filgrastim, pegfilgrastim, or sargramostim during their first observed course of chemotherapy between July 2001 and June 2007. For each patient, every unique chemotherapy cycle during the course was identified, along with each cycle in which filgrastim, pegfilgrastim, or sargramostim was administered by the fifth day of the cycle (ie, as prophylaxis). Risks of hospitalization for neutropenic complications (broad definition: admission with a diagnosis of neutropenia, fever, or infection; narrow definition: admission with a diagnosis of neutropenia) and for any reason were examined on a cycle-specific basis during all the cycles in which colony-stimulating factor prophylaxis was administered. Unadjusted and adjusted odds ratios (ORs) for hospitalization were estimated.
Results: Risk (unadjusted) of hospitalization for neutropenic complications (narrow definition) was 2.1% for filgrastim prophylaxis (n = 8286), 1.1% for pegfilgrastim prophylaxis (n = 67,247), and 2.5% for sargramostim prophylaxis (n = 1736). Corresponding risks of hospitalization based on the broad definition were 4.0%, 2.6%, and 5.1%. Risks of all-cause hospitalization were 7.9%, 5.3%, and 9.6%, respectively. Adjusted odds of hospitalization were significantly higher for filgrastim [OR (range across the 3 alternative measures of hospitalization): 1.58-1.79; P<0.001] and sargramostim (OR: 1.89-2.68; P<0.001) versus pegfilgrastim.
Conclusions: Risk of hospitalization for neutropenic complications during cancer chemotherapy is lower with pegfilgrastim prophylaxis than with filgrastim or sargramostim prophylaxis.
C1 [Weycker, Derek; Edelsberg, John; Kartashov, Alex; Oster, Gerry] PAI, Four Davis Court, Brookline, MA 02445 USA.
[Malin, Jennifer] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Barron, Rich] Amgen Inc, Global Hlth Econ, Thousand Oaks, CA 91320 USA.
RP Weycker, D (reprint author), PAI, Four Davis Court, Brookline, MA 02445 USA.
EM dweycker@pai2.com
FU Amgen Inc
FX Funding for this research was provided by Amgen Inc, to Policy Analysis
Inc (PAI).
NR 28
TC 18
Z9 18
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0277-3732
J9 AM J CLIN ONCOL-CANC
JI Am. J. Clin. Oncol.-Cancer Clin. Trials
PD JUN
PY 2012
VL 35
IS 3
BP 267
EP 274
DI 10.1097/COC.0b013e31820dc075
PG 8
WC Oncology
SC Oncology
GA 946QF
UT WOS:000304367400012
PM 21378538
ER
PT J
AU Alessi, CA
Vitiello, MV
AF Alessi, Cathy A.
Vitiello, Michael V.
TI Sleep Disturbance Among Older Adults in Long-Term Care: A Significant
Problem in an Important Clinical Setting
SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
LA English
DT Editorial Material
ID HOMES
C1 [Alessi, Cathy A.] Univ Calif Los Angeles, David Geffen Sch Med, Ctr Geriatr Res Educ & Clin, VA Greater Los Angeles Healthcare Syst, Los Angeles, CA 90095 USA.
[Vitiello, Michael V.] Univ Washington, Seattle, WA 98195 USA.
RP Alessi, CA (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Ctr Geriatr Res Educ & Clin, VA Greater Los Angeles Healthcare Syst, Los Angeles, CA 90095 USA.
EM cathy.alessi@va.gov
OI Vitiello, Michael/0000-0002-9776-0473
NR 12
TC 1
Z9 1
U1 2
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1064-7481
J9 AM J GERIAT PSYCHIAT
JI Am. J. Geriatr. Psychiatr.
PD JUN
PY 2012
VL 20
IS 6
BP 457
EP 459
DI 10.1097/JGP.0b013e31825688e4
PG 3
WC Geriatrics & Gerontology; Gerontology; Psychiatry
SC Geriatrics & Gerontology; Psychiatry
GA 945FC
UT WOS:000304257200001
PM 22517060
ER
PT J
AU Martin, JL
Jouldjian, S
Mitchell, MN
Josephson, KR
Alessi, CA
AF Martin, Jennifer L.
Jouldjian, Stella
Mitchell, Michael N.
Josephson, Karen R.
Alessi, Cathy A.
TI A Longitudinal Study of Poor Sleep After Inpatient Post-Acute
Rehabilitation: The Role of Depression and Pre-Illness Sleep Quality
SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
LA English
DT Article
DE Aging; depression; rehabilitation; sleep
ID HIP FRACTURE; RATING-SCALE; OLDER-ADULTS; RECOVERY; MORTALITY; SYMPTOMS
AB Objectives: To explore the unique impact of poor sleep and symptoms of depression on sleep quality for up to 1 year after inpatient post-acute rehabilitation among older adults. Design: Prospective longitudinal cohort study. Setting: Two inpatient post-acute rehabilitation facilities. Participants: A total of 245 individuals older than 65 years (mean age = 80 years, 38% women). Interventions: None. Measurements: Sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI) during the post-acute care stay twice to evaluate pre-illness sleep quality and sleep quality during the post-acute care stay, and again at 3-, 6-, 9-, and 12-month follow-up. Demographics, symptoms of depression, cognitive functioning, and comorbidities were also assessed. Results: Across time points, sleep was significantly disturbed for many individuals. Nested regression models predicting PSQI total score at 3, 6, 9, and 12 months showed that variables entered in Block 1 (age, gender, cognitive functioning, and comorbidities) were significant predictors of poor sleep at 6-month follow-up but not at 3-, 9-, or 12-month follow-up. Depression (Block 2) and pre-illness PSQI total score (Block 3) were significant predictors of PSQI total score at all follow-up time points. PSQI total score during post-acute care (Block 4) explained a significant proportion of variance only at the 3-month follow-up. Conclusions: This study confirms that chronic poor sleep is common among older adults during postacute rehabilitation and resolution of sleep disturbance after acute health events may be a lengthy process. Our findings expand understanding of the role of depressive symptoms and preexisting sleep complaints in predicting poor sleep over time among these vulnerable older adults. (Am J Geriatr Psychiatry 2012; 20:477-484)
C1 [Martin, Jennifer L.; Alessi, Cathy A.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Martin, Jennifer L.; Jouldjian, Stella; Mitchell, Michael N.; Josephson, Karen R.; Alessi, Cathy A.] VA Greater Los Angeles Healthcare Syst, Ctr Geriatr Res Educ & Clin, Los Angeles, CA USA.
RP Martin, JL (reprint author), VA GRECC 11E, 16111 Plummer St, North Hills, CA 91343 USA.
EM jennifer.martin@va.gov
FU NIA [K23 AG028452]; UCLA Claude Pepper Older Americans Independence
Center [AG-10415]; VA Greater Los Angeles Healthcare System Geriatric
Research, Education and Clinical Center; VA Health Services Research
Development [IIR-01-053-1, IIR 04-321-2, AIA-03-047]
FX This study was supported by NIA K23 AG028452; UCLA Claude Pepper Older
Americans Independence Center (AG-10415), VA Health Services Research &
Development IIR-01-053-1, IIR 04-321-2, and AIA-03-047; and VA Greater
Los Angeles Healthcare System Geriatric Research, Education and Clinical
Center.
NR 24
TC 2
Z9 3
U1 1
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1064-7481
J9 AM J GERIAT PSYCHIAT
JI Am. J. Geriatr. Psychiatr.
PD JUN
PY 2012
VL 20
IS 6
BP 477
EP 484
DI 10.1097/JGP.0b013e31824877c1
PG 8
WC Geriatrics & Gerontology; Gerontology; Psychiatry
SC Geriatrics & Gerontology; Psychiatry
GA 945FC
UT WOS:000304257200004
PM 22617164
ER
PT J
AU Fung, CH
Martin, JL
Chung, C
Fiorentino, L
Mitchell, M
Josephson, KR
Jouldjian, S
Alessi, C
AF Fung, Constance H.
Martin, Jennifer L.
Chung, Carol
Fiorentino, Lavinia
Mitchell, Michael
Josephson, Karen R.
Jouldjian, Stella
Alessi, Cathy
TI Sleep Disturbance Among Older Adults in Assisted Living Facilities
SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
LA English
DT Article
DE Assisted living facilities; long-term care; sleep
ID NURSING-HOME RESIDENTS; ALZHEIMERS-DISEASE; DEPRESSION; QUALITY;
SYMPTOMS; INSOMNIA; QUESTIONNAIRE; COMORBIDITY; COMPLAINTS; DIAGNOSIS
AB Objectives: To evaluate whether objectively and subjectively measured sleep disturbances persist among older adults in assisted living facilities (ALFs) and to identify predictors of sleep disturbance in this setting. Design: Prospective, observational cohort study. Setting and Participants: A total of 121 residents, age >= 65 years, in 18 ALFs in the Los Angeles area. Measurements: Objective (actigraphy) and subjective (Pittsburgh Sleep Quality Index) sleep measures were collected at baseline and 3- and 6-month follow-up. Predictors of baseline sleep disturbance tested in bivariate analyses and multiple regression models included demographics, Mini-Mental State Examination score, number of comorbidities, nighttime sedating medication use, functional status (activities of daily living; instrumental activities of daily living), restless legs syndrome, and sleep apnea risk. Results: Objective and subjective sleep measures were similar at baseline and 3- and 6-month follow-up (objective nighttime total sleep [hours] 6.3, 6.5, and 6.4; objective nighttime percent sleep 77.2, 77.7, and 78.3; and Pittsburgh Sleep Quality Index total score 8.0, 7.8, and 7.7, respectively). The mean baseline nighttime percent sleep decreased by 2% for each additional unit increase in baseline comorbid conditions (measured as the number of conditions), and increased by 4.5% for each additional unit increase in baseline activities of daily living (measured as the number of activities of daily living), in a multiple regression model. Conclusions: In this study, we found that objectively and subjectively measured sleep disturbances are persistent among ALF residents and are related to a greater number of comorbidities and poorer functional status at baseline. Interventions are needed to improve sleep in this setting. (Am J Geriatr Psychiatry 2012; 20:485-493)
C1 [Fung, Constance H.; Martin, Jennifer L.; Josephson, Karen R.; Jouldjian, Stella; Alessi, Cathy] Vet Adm Greater Los Angeles Healthcare Syst, GRECC, North Hills, CA 91343 USA.
[Martin, Jennifer L.; Chung, Carol; Mitchell, Michael; Alessi, Cathy] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Fiorentino, Lavinia] Univ Calif San Diego, Dept Psychiat, San Diego, CA 92103 USA.
RP Fung, CH (reprint author), VA Greater Los Angeles Healthcare Syst, GRECC 11E, 16111 Plummer St, North Hills, CA 91343 USA.
EM Connie.Fung@va.gov
FU VA Advanced Geriatrics Fellowship Program; NIH NIA [K23 AG028452]; NIMH
[T32 MH 019925-11]; UCLA Academic Senate Council on Research; VA Greater
Los Angeles Healthcare System, Geriatric Research, Education and
Clinical Center; VA Health Services Research and Development [IIR
04-321-2]; UCLA Cousins Center for Psychoneuroimmunology; Sepracor Inc.,
Marlborough, MA
FX This study was supported by the VA Advanced Geriatrics Fellowship
Program; NIH NIA K23 AG028452, NIMH T32 MH 019925-11; UCLA Academic
Senate Council on Research; VA Greater Los Angeles Healthcare System,
Geriatric Research, Education and Clinical Center; VA Health Services
Research and Development (IIR 04-321-2); and UCLA Cousins Center for
Psychoneuroimmunology. Additional financial support was provided by
Sepracor Inc., Marlborough, MA. The authors thank the study project
coordinators, Terry Vandenberg, MA, and Rebecca Saia, the research
staff, the staff at the participating facilities, and the ALF residents.
NR 39
TC 8
Z9 8
U1 1
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1064-7481
J9 AM J GERIAT PSYCHIAT
JI Am. J. Geriatr. Psychiatr.
PD JUN
PY 2012
VL 20
IS 6
BP 485
EP 493
DI 10.1097/JGP.0b013e318252e3e0
PG 9
WC Geriatrics & Gerontology; Gerontology; Psychiatry
SC Geriatrics & Gerontology; Psychiatry
GA 945FC
UT WOS:000304257200005
PM 22531104
ER
PT J
AU Armand, P
Sainvil, MM
Kim, HT
Rhodes, J
Cutler, C
Ho, VT
Koreth, J
Alyea, EP
Neufeld, EJ
Kwong, RY
Soiffer, RJ
Antin, JH
AF Armand, Philippe
Sainvil, Marie-Michele
Kim, Haesook T.
Rhodes, Joanna
Cutler, Corey
Ho, Vincent T.
Koreth, John
Alyea, Edwin P.
Neufeld, Ellis J.
Kwong, Raymond Y.
Soiffer, Robert J.
Antin, Joseph H.
TI Does iron overload really matter in stem cell transplantation?
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
ID PRETRANSPLANTATION SERUM FERRITIN; C-REACTIVE PROTEIN; PROGNOSTIC
IMPACT; RISK-FACTOR; MYELODYSPLASTIC SYNDROME; PREDICTOR; MALIGNANCIES;
RECIPIENTS; MORTALITY; SURVIVAL
AB A growing body of evidence suggests that iron overload is associated with inferior outcomes after myeloablative allogeneic hematopoietic stem cell transplantation (HSCT). However, all of those studies used surrogate markers of iron overload, especially serum ferritin, and most had a retrospective design. We conducted a prospective observational study in patients with myelodysplastic syndrome or acute leukemia undergoing myeloablative HSCT. Forty-five patients who were followed for over 1 year, with serial measurements of serum iron parameters, as well as liver and cardiac magnetic resonance imaging. There was no significant increase in ferritin, liver or cardiac iron content in the 12 months following HSCT. Although serum ferritin still appeared to have prognostic significance, as previously reported, pre-HSCT iron overload (as reflected in liver iron content) was not associated with increased mortality, relapse, or graft-versus-host disease. These results raise the possibility that the adverse prognostic impact of pre-HSCT hyperferritinemia may be related to factors independent of iron overload. Am. J. Hematol. 87:569572, 2012. (c) 2012 Wiley Periodicals, Inc.
C1 [Armand, Philippe; Sainvil, Marie-Michele; Cutler, Corey; Ho, Vincent T.; Koreth, John; Alyea, Edwin P.; Soiffer, Robert J.; Antin, Joseph H.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
[Kim, Haesook T.] Dana Farber Canc Inst, Dept Biostat, Boston, MA 02215 USA.
[Rhodes, Joanna] SUNY Stony Brook, Dept Med, Sch Med, Stony Brook, NY 11794 USA.
[Neufeld, Ellis J.] Childrens Hosp, Div Pediat Hematol Oncol, Boston, MA 02115 USA.
[Kwong, Raymond Y.] Brigham & Womens Hosp, Dept Cardiovasc Med, Boston, MA 02115 USA.
RP Armand, P (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 450 Brookline Ave, Boston, MA 02215 USA.
EM parmand@partners.org
FU Novartis; Novartis Oncology; National Institutes of Health
[CA142106-06]; Leukemia and Lymphoma Society; Conquer Cancer/ASCO
Foundation; American Society of Hematology
FX P.A. and E.N. have received research funding from Novartis.; Contract
grant sponsors: Novartis Oncology and the National Institutes of Health;
Contract grant number: CA142106-06.; Contract grant sponsors: Leukemia
and Lymphoma Society (Special Fellowship in Clinical Research). Contract
grant sponsors: Conquer Cancer/ASCO Foundation (Career Development
Award).; Contract grant sponsors: American Society of Hematology
(Scholar Award).
NR 26
TC 32
Z9 32
U1 2
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0361-8609
J9 AM J HEMATOL
JI Am. J. Hematol.
PD JUN
PY 2012
VL 87
IS 6
BP 569
EP 572
DI 10.1002/ajh.23188
PG 4
WC Hematology
SC Hematology
GA 945CC
UT WOS:000304249400001
PM 22473510
ER
PT J
AU Abel, GA
Friese, CR
Neville, BA
Wilson, KM
Hastings, BT
Earle, CC
Keating, NL
Richardson, LC
AF Abel, Gregory A.
Friese, Christopher R.
Neville, Bridget A.
Wilson, Katherine M.
Hastings, B. Taylor
Earle, Craig C.
Keating, Nancy L.
Richardson, Lisa C.
TI Referrals for suspected hematologic malignancy: A survey of primary care
physicians
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
ID MULTIPLE-MYELOMA; UNITED-STATES; CANCER; DIAGNOSIS; COMMUNICATION;
SYMPTOMS
C1 [Abel, Gregory A.; Neville, Bridget A.; Hastings, B. Taylor] Dana Farber Canc Inst, Dept Med Oncol, Div Populat Sci, Boston, MA 02215 USA.
[Abel, Gregory A.] Dana Farber Canc Inst, Dept Med Oncol, Ctr Leukaemia, Boston, MA 02215 USA.
[Friese, Christopher R.] Univ Michigan, Sch Nursing, Ann Arbor, MI 48109 USA.
[Wilson, Katherine M.; Richardson, Lisa C.] Ctr Dis Control & Prevent, Div Canc Prevent & Control, Atlanta, GA USA.
[Earle, Craig C.] Sunnybrook Hlth Sci Ctr, Inst Clin Evaluat Sci, Toronto, ON M4N 3M5, Canada.
[Keating, Nancy L.] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
[Keating, Nancy L.] Harvard Univ, Brigham & Womens Hosp, Div Gen Internal Med, Sch Med, Boston, MA 02115 USA.
RP Abel, GA (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Div Populat Sci, 450 Brookline Ave,Dana 1108, Boston, MA 02215 USA.
EM gregory_abel@dfci.harvard.edu
RI Friese, Christopher/D-2097-2013
OI Friese, Christopher/0000-0002-2281-2056
FU NINR NIH HHS [R00 NR010750]
NR 23
TC 3
Z9 3
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0361-8609
J9 AM J HEMATOL
JI Am. J. Hematol.
PD JUN
PY 2012
VL 87
IS 6
BP 634
EP 636
DI 10.1002/ajh.23172
PG 3
WC Hematology
SC Hematology
GA 945CC
UT WOS:000304249400014
PM 22473854
ER
PT J
AU Dolinay, T
Kim, YS
Howrylak, J
Hunninghake, GM
An, CH
Fredenburgh, L
Massaro, AF
Rogers, A
Gazourian, L
Nakahira, K
Haspel, JA
Landazury, R
Eppanapally, S
Christie, JD
Meyer, NJ
Ware, LB
Christiani, DC
Ryter, SW
Baron, RM
Choi, AMK
AF Dolinay, Tamas
Kim, Young Sam
Howrylak, Judie
Hunninghake, Gary M.
An, Chang Hyeok
Fredenburgh, Laura
Massaro, Anthony F.
Rogers, Angela
Gazourian, Lee
Nakahira, Kiichi
Haspel, Jeffrey A.
Landazury, Roberto
Eppanapally, Sabitha
Christie, Jason D.
Meyer, Nuala J.
Ware, Lorraine B.
Christiani, David C.
Ryter, Stefan W.
Baron, Rebecca M.
Choi, Augustine M. K.
TI Inflammasome-regulated Cytokines Are Critical Mediators of Acute Lung
Injury
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Article
DE acute respiratory distress syndrome; inflammasome; interleukin-18;
mechanical ventilation
ID RESPIRATORY-DISTRESS-SYNDROME; INTENSIVE-CARE-UNIT; NALP3 INFLAMMASOME;
IMMUNE-RESPONSES; IL-18 SECRETION; SEPSIS; ACTIVATION; CASPASE-1;
MORTALITY; MICE
AB Rationale: Despite advances in clinical management, there are currently no reliable diagnostic and therapeutic targets for acute respiratory distress syndrome (ARDS). The inflammasome/caspase-1 pathway regulates the maturation and secretion of proinflammatory cytokines (e.g., IL-18). IL-18 is associated with injury in animal models of systemic inflammation.
Objectives: We sought to determine the contribution of the inflammasome pathway in experimental acute lung injury and human ARDS.
Methods: We performed comprehensive gene expression profiling on peripheral blood from patients with critical illness. Gene expression changes were assessed using real-time polymerase chain reaction, and IL-18 levels were measured in the plasma of the critically ill patients. Wild-type mice or mice genetically deficient in IL-18 or caspase-1 were mechanically ventilated using moderate tidal volume (12 ml/kg). Lung injury parameters were assessed in lung tissue, serum, and bronchoalveolar lavage fluid.
Measurements and Main Results: In mice, mechanical ventilation enhanced IL-18 levels in the lung, serum, and bronchoalveolar lavage fluid. IL-18 neutralizing antibody treatment, or genetic deletion of IL-18 or caspase-1, reduced lung injury in response to mechanical ventilation. In human patients with ARDS, inflammasome-related mRNA transcripts (CASP1, IL1B, and IL18) were increased in peripheral blood. In samples from four clinical centers, IL-18 was elevated in the plasma of patients with ARDS (sepsis or trauma-induced ARDS) and served as a novel biomarker of intensive care unit morbidity and mortality.
Conclusions: The inflammasome pathway and its downstream cytokines play critical roles in ARDS development.
C1 [Choi, Augustine M. K.] Harvard Univ, Brigham & Womens Hosp, Div Pulm & Crit Care Med, Med Sch,Dept Med, Boston, MA 02115 USA.
[Eppanapally, Sabitha] Brigham & Womens Hosp, Dept Med, Div Renal Med, Boston, MA 02115 USA.
[Howrylak, Judie; Hunninghake, Gary M.; Rogers, Angela] Channing Labs, Boston, MA USA.
[Christie, Jason D.; Meyer, Nuala J.] Univ Penn, Dept Med, Div Pulm Allergy & Crit Care Med, Philadelphia, PA 19104 USA.
[Ware, Lorraine B.] Vanderbilt Univ, Dept Med, Div Allergy Pulm & Crit Care Med, Nashville, TN USA.
[Christiani, David C.] Massachusetts Gen Hosp, Pulm & Crit Care Unit, Boston, MA 02114 USA.
[Christiani, David C.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
RP Choi, AMK (reprint author), Harvard Univ, Brigham & Womens Hosp, Div Pulm & Crit Care Med, Med Sch,Dept Med, 75 Francis St, Boston, MA 02115 USA.
EM amchoi@rics.bwh.harvard.edu
FU National Institutes of Health [PO-HL108801, R01-HL079904]; FAMRI;
[R01-HL081619]; [P01-HL079063]
FX Supported by National Institutes of Health grants PO-HL108801,
R01-HL079904, and an FAMRI clinical innovator award (A.M.K.C.); and
R01-HL081619 and P01-HL079063 (J.D.C.).
NR 50
TC 126
Z9 136
U1 2
U2 20
PU AMER THORACIC SOC
PI NEW YORK
PA 25 BROADWAY, 18 FL, NEW YORK, NY 10004 USA
SN 1073-449X
EI 1535-4970
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD JUN 1
PY 2012
VL 185
IS 11
BP 1225
EP 1234
DI 10.1164/rccm.201201-0003OC
PG 10
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 946VC
UT WOS:000304384600016
PM 22461369
ER
PT J
AU Verma, S
Turkbey, B
Muradyan, N
Rajesh, A
Cornud, F
Haider, MA
Choyke, PL
Harisinghani, M
AF Verma, Sadhna
Turkbey, Baris
Muradyan, Naira
Rajesh, Arumugam
Cornud, Francois
Haider, Masoom A.
Choyke, Peter L.
Harisinghani, Mukesh
TI Overview of Dynamic Contrast-Enhanced MRI in Prostate Cancer Diagnosis
and Management
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Article
DE diffusion-weighted imaging; MR spectroscopy; prostate cancer; prostate
MRI; tumor angiogenesis
ID EXTERNAL-BEAM RADIOTHERAPY; RADICAL PROSTATECTOMY; PHARMACOKINETIC
PARAMETERS; LOCAL RECURRENCE; PERIPHERAL ZONE; DCE-MRI; LOCALIZATION;
DIFFUSION; TUMOR; GLAND
AB OBJECTIVE. This article is a primer on the technical aspects of performing a high-quality dynamic contrast-enhanced MRI (DCE-MRI) examination of the prostate gland.
CONCLUSION. DCE-MRI is emerging as a useful clinical technique as part of a multiparametric approach for evaluating the extent of primary and recurrent prostate cancer. Performing a high-quality DCE-MRI examination requires a good understanding of the technical aspects and limitations of image acquisition and postprocessing techniques.
C1 [Verma, Sadhna] Univ Cincinnati, Med Ctr, Dept Radiol, Cincinnati, OH 45267 USA.
[Turkbey, Baris; Choyke, Peter L.] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
[Muradyan, Naira] iCAD Inc, Nashua, NH USA.
[Rajesh, Arumugam] Univ Hosp Leicester NHS Trust, Leicester Gen Hosp, Leicester, Leics, England.
[Cornud, Francois] Hop Cochin, F-75674 Paris, France.
[Haider, Masoom A.] Univ Toronto, Dept Radiol, Toronto, ON M5S 1A1, Canada.
[Haider, Masoom A.] Univ Hlth Network, Toronto, ON, Canada.
[Harisinghani, Mukesh] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA USA.
RP Verma, S (reprint author), Univ Cincinnati, Med Ctr, Dept Radiol, 234 Goodman St,POB 670761, Cincinnati, OH 45267 USA.
EM drsadhnaverma@gmail.com
NR 67
TC 81
Z9 88
U1 1
U2 11
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD JUN
PY 2012
VL 198
IS 6
BP 1277
EP 1288
DI 10.2214/AJR.12.8510
PG 12
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 946ZX
UT WOS:000304397500030
PM 22623539
ER
PT J
AU Bai, XY
Wu, CL
AF Bai, Xiaoyan
Wu, Chin-Lee
TI Renal Cell Carcinoma and Mimics: Pathologic Primer for Radiologists
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Article
DE chromophobe renal cell carcinoma (RCC); clear cell RCC; papillary RCC;
primer; renal oncocytoma
ID TUBULOCYSTIC CARCINOMA; MOLECULAR CHARACTERIZATION; TRANSLOCATION
CARCINOMAS; KIDNEY; SPINDLE; NEUROBLASTOMA; EXPRESSION; NEOPLASIA;
DISTINCT; DISEASE
AB OBJECTIVE. The purpose of this article is to present a primer to review the gross and microscopic characteristics of the common types of renal cell carcinoma (RCC), such as clear cell RCC, papillary RCC, and chromophobe RCC. Renal oncocytoma and several new and emerging types of RCC are also described, such as tubulocystic carcinoma, acquired cystic kidney disease-associated RCC, clear cell papillary RCC, and oncocytic papillary RCC.
CONCLUSION. This primer provides a concise description of the pathologic characteristics fo RCC for radiologists
C1 [Bai, Xiaoyan] So Med Univ, Nanfang Hosp, Div Nephrol, Guangzhou, Guangdong, Peoples R China.
[Bai, Xiaoyan] Guangdong Prov Inst Nephrol, Guangzhou, Guangdong, Peoples R China.
[Wu, Chin-Lee] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol, Boston, MA 02114 USA.
[Wu, Chin-Lee] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Urol, Boston, MA 02114 USA.
RP Wu, CL (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol, 55 Fruit St, Boston, MA 02114 USA.
EM cwu2@partners.org
NR 24
TC 1
Z9 3
U1 0
U2 2
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD JUN
PY 2012
VL 198
IS 6
BP 1289
EP 1293
DI 10.2214/AJR.12.8586
PG 5
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 946ZX
UT WOS:000304397500031
PM 22623540
ER
PT J
AU Lichtenberger, JP
Sharma, A
Zachary, KC
Krishnam, MS
Greene, RE
Shepard, JAO
Wu, CC
AF Lichtenberger, John P., III
Sharma, Amita
Zachary, Kimon C.
Krishnam, Mayil S.
Greene, Reginald E.
Shepard, Jo-Anne O.
Wu, Carol C.
TI What a Differential a Virus Makes: A Practical Approach to Thoracic
Imaging Findings in the Context of HIV Infection-Part 1, Pulmonary
Findings
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Article
DE differential diagnosis; HIV; pulmonary; thoracic
ID LYMPHOCYTIC INTERSTITIAL PNEUMONIA; MULTICENTRIC CASTLEMAN-DISEASE;
PNEUMOCYSTIS-CARINII PNEUMONIA; HUMAN-IMMUNODEFICIENCY-VIRUS; CT
FINDINGS; KAPOSIS-SARCOMA; PATHOLOGICAL FINDINGS; UNITED-STATES;
LYMPHOPROLIFERATIVE DISORDERS; BACILLARY ANGIOMATOSIS
AB OBJECTIVE. The Centers for Disease Control and Prevention reported more than one million people with HIV infection in the United States in 2006, an increase of 11% over 3 years. Worldwide, nearly 34 million people are infected with HIV. Pulmonary disease accounts for 30-40% of acute hospitalizations of HIV-infected patients, underscoring the importance of understanding the pulmonary manifestations in this population. When presented with a chest radiograph or CT image of a patient with the clinical history of HIV infection, one approach is to start by identifying and categorizing key imaging findings. In some instances, the key findings may be further subcategorized to narrow the differential diagnosis, such as distinguishing between perilymphatic distribution and the random distribution of micronodules. The differential diagnosis of these key imaging findings can also be further refined by incorporating clinical data, such as patient demographics, CD4 count, and presenting symptoms. Finally, the change of thoracic disease and clinical status in response to treatment provides important diagnostic information. The purpose of this article is to discuss pulmonary findings in patients with HIV.
CONCLUSION. By developing a systematic and practical approach to key pulmonary imaging findings in HIV-infected patients, radiologists can generate clinically relevant and succinct differential diagnoses and thereby improve patient care.
C1 [Lichtenberger, John P., III; Sharma, Amita; Greene, Reginald E.; Shepard, Jo-Anne O.; Wu, Carol C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Thorac Imaging & Intervent,Dept Radiol, Boston, MA 02114 USA.
[Zachary, Kimon C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Internal Med,Div Infect Dis, Boston, MA 02114 USA.
[Krishnam, Mayil S.] Univ Calif Irvine, Med Ctr, Dept Radiol Sci, Div Diagnost Cardiovasc & Thorac Imaging, Orange, CA USA.
RP Lichtenberger, JP (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Thorac Imaging & Intervent,Dept Radiol, 55 Fruit St,Founders 202, Boston, MA 02114 USA.
EM john.lichtenberger@gmail.com
NR 52
TC 5
Z9 5
U1 0
U2 2
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD JUN
PY 2012
VL 198
IS 6
BP 1295
EP 1304
DI 10.2214/AJR.11.8003
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 946ZX
UT WOS:000304397500032
PM 22623541
ER
PT J
AU Lichtenberger, JP
Sharma, A
Zachary, KC
Krishnam, MS
Greene, RE
Shepard, JAO
Wu, CC
AF Lichtenberger, John P., III
Sharma, Amita
Zachary, Kimon C.
Krishnam, Mayil S.
Greene, Reginald E.
Shepard, Jo-Anne O.
Wu, Carol C.
TI What a Differential a Virus Makes: A Practical Approach to Thoracic
Imaging Findings in the Context of HIV Infection-Part 2, Extrapulmonary
Findings, Chronic Lung Disease, and Immune Reconstitution Syndrome
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Article
DE differential diagnosis; HIV; pulmonary; thoracic
ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; PULMONARY ARTERIAL-HYPERTENSION;
MULTICENTRIC CASTLEMAN-DISEASE; ANTIRETROVIRAL THERAPY; INFLAMMATORY
SYNDROME; CT FINDINGS; BACILLARY ANGIOMATOSIS; PERICARDIAL-EFFUSION;
KAPOSI-SARCOMA; AIDS
AB OBJECTIVE. The Centers for Disease Control and Prevention reported more than one million people with HIV infection in the United States in 2006, an increase of 11% over 3 years. Worldwide, nearly 34 million people are infected with HIV. Pulmonary disease accounts for 30-40% of acute hospitalizations of HIV-seropositive patients, underscoring the importance of understanding the range of cardiothoracic imaging findings associated with HIV infection. This article will cover extrapulmonary thoracic diseases, chronic lung diseases, and immune reconstitution inflammatory syndrome in HIV-infected patients. Our approach is focused on the radiologist's perspective by recognizing and categorizing key imaging findings to generate a differential diagnosis. The differential diagnosis can be further refined by incorporating clinical data, such as patient demographics, CD4 count, and presenting symptoms. In addition, with prolonged survival of HIV-infected patients in the era of highly active antiretroviral therapy, radiologists can also benefit from awareness of imaging features of a myriad of chronic cardiopulmonary diseases in this patient population. Finally, the change of imaging findings and clinical status in response to treatment provides important diagnostic information, such as in immune reconstitution syndrome.
CONCLUSION. Developing a practical approach to key cardiothoracic imaging findings in HIV-infected patients will aid the radiologist in generating a clinically relevant differential diagnosis and interpretation, thereby improving patient care.
C1 [Lichtenberger, John P., III; Sharma, Amita; Greene, Reginald E.; Shepard, Jo-Anne O.; Wu, Carol C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol,Div Thorac Imaging & Intervent, Boston, MA 02114 USA.
[Zachary, Kimon C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Internal Med,Div Infect Dis, Boston, MA 02114 USA.
[Krishnam, Mayil S.] Univ Calif Irvine, Med Ctr, Div Diagnost Cardiovasc & Thorac Imaging, Dept Radiol Sci, Orange, CA USA.
RP Lichtenberger, JP (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol,Div Thorac Imaging & Intervent, 55 Fruit St,Founders 202, Boston, MA 02114 USA.
EM john.lichtenberger@gmail.com
NR 48
TC 5
Z9 5
U1 0
U2 0
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD JUN
PY 2012
VL 198
IS 6
BP 1305
EP 1312
DI 10.2214/AJR.11.8004
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 946ZX
UT WOS:000304397500033
PM 22623542
ER
PT J
AU Guitchounts, G
Stewart, DS
Forman, SA
AF Guitchounts, Grigori
Stewart, Deirdre S.
Forman, Stuart A.
TI Two Etomidate Sites in alpha 1 beta 2 gamma 2 gamma-Aminobutyric Acid
Type A Receptors Contribute Equally and Noncooperatively to Modulation
of Channel Gating
SO ANESTHESIOLOGY
LA English
DT Article
ID ANESTHETIC BINDING-SITE; GABA(A) RECEPTOR; POTENTIATION; ARRANGEMENT;
ACTIVATION; MECHANISMS; MUTATIONS; SUBUNITS
AB Background: Etomidate is a potent hypnotic agent that acts via gamma-aminobutyric acid receptor type A (GABA(A)) receptors. Evidence supports the presence of two etomidate sites per GABA(A) receptor, and current models assume that each site contributes equally and noncooperatively to drug effects. These assumptions remain untested.
Methods: We used concatenated dimer (beta 2-alpha 1) and trimer (gamma 2-beta 2-alpha 1) GABA(A) subunit assemblies that form functional alpha 1 beta 2 gamma 2 channels, and inserted alpha 1M236W etomidate site mutations into both dimers (beta 2-alpha 1M236W) and trimers (gamma 2-beta 2-alpha 1M236W). Wild-type or mutant dimers (D-wt or D-alpha M236W) and trimers (T-wt or T-alpha M236W) were coexpressed in Xenopus oocytes to produce four types of channels: (DTwt)-T-wt, (DTwt)-T-alpha M236W, (DT alpha M236W)-T-wt, and (DT alpha M236W)-T-alpha M236W. For each channel type, two-electrode voltage clamp was performed to quantitatively assess GABA EC50, etomidate modulation (left shift), etomidate direct activation, and other functional parameters affected by alpha M236W mutations.
Results: Concatenated wild-type (DTwt)-T-wt channels displayed etomidate modulation and direct activation similar to alpha 1 beta 2 gamma 2 receptors formed with free subunits. (DT alpha M236W)-T-alpha M236W receptors also displayed altered GABA sensitivity and etomidate modulation similar to mutated channels formed with free subunits. Both single-site mutant receptors ((DTwt)-T-alpha M236W and (DT alpha M236W)-T-wt) displayed indistinguishable functional properties and equal gating energy changes for GABA activation (-4.9 +/- 0.48 vs. -4.7 +/- 0.48 kJ/mol, respectively) and etomidate modulation (-3.4 +/- 0.49 vs. -3.7 +/- 0.38 kJ/mol, respectively), which together accounted for the differences between (DTwt)-T-wt and (DT alpha M236W)-T-alpha M236W channels.
Conclusions: These results support the hypothesis that the two etomidate sites on alpha 1 beta 2 gamma 2 GABA(A) receptors contribute equally and noncooperatively to drug interactions and gating effects.
C1 [Stewart, Deirdre S.; Forman, Stuart A.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Guitchounts, Grigori] Boston Univ, Dept Neurobiol, Boston, MA 02215 USA.
RP Forman, SA (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Jackson 444,55 Fruit St, Boston, MA 02114 USA.
EM saforman@partners.org
FU National Institutes of Health, Bethesda, Maryland [R01GM089745,
P01GM58448]; Department of Anesthesia, Critical Care and Pain Medicine,
Massachusetts General Hospital
FX Received from the Department of Anesthesia, Critical Care and Pain
Medicine, Massachusetts General Hospital, Boston, Massachusetts.
Submitted for publication November 11, 2011. Accepted for publication
February 16, 2012. Supported by grant nos. R01GM089745 and P01GM58448
from National Institutes of Health, Bethesda, Maryland (to Dr. Forman),
and a research award from the Department of Anesthesia, Critical Care
and Pain Medicine, Massachusetts General Hospital (to Guitchounts).
Presented in part at the annual meeting of American Society of
Anesthesiologists, October 16, 2011, Chicago, Illinois, and the annual
meeting of Society for Neuroscience, November 14, 2011, Washington, D.C.
NR 25
TC 10
Z9 10
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-3022
J9 ANESTHESIOLOGY
JI Anesthesiology
PD JUN
PY 2012
VL 116
IS 6
BP 1235
EP 1244
DI 10.1097/ALN.0b013e3182567df3
PG 10
WC Anesthesiology
SC Anesthesiology
GA 946MR
UT WOS:000304356500014
PM 22531336
ER
PT J
AU Cusack, JC
Hughes, KS
AF Cusack, James C., Jr.
Hughes, Kevin S.
TI Managing Patients at High Risk for Hereditary Breast Cancer: A Guide for
the Practicing Physician
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Editorial Material
ID STATEMENT; SOCIETY
C1 [Cusack, James C., Jr.; Hughes, Kevin S.] Harvard Univ, Sch Med, Dept Surg, Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Cusack, JC (reprint author), Harvard Univ, Sch Med, Dept Surg, Massachusetts Gen Hosp, Boston, MA 02115 USA.
EM jcusack@partners.org
OI Hughes, Kevin/0000-0003-4084-6484
NR 7
TC 1
Z9 1
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9265
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD JUN
PY 2012
VL 19
IS 6
BP 1721
EP 1722
DI 10.1245/s10434-012-2255-0
PG 2
WC Oncology; Surgery
SC Oncology; Surgery
GA 944NF
UT WOS:000304209800001
PM 22411203
ER
PT J
AU Drohan, B
Roche, CA
Cusack, JC
Hughes, KS
AF Drohan, Brian
Roche, Constance A.
Cusack, James C., Jr.
Hughes, Kevin S.
TI Hereditary Breast and Ovarian Cancer and Other Hereditary Syndromes:
Using Technology to Identify Carriers
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Review
ID BRCA2; SUSCEPTIBILITY; BREAST/OVARIAN; PROBABILITIES; PENETRANCE;
PREDICTION; MUTATIONS; GENES; WOMEN; MODEL
AB Most patients who harbor a genetic mutation for hereditary breast cancer have not been identified, despite the availability of genetic testing. Developing an effective approach to the identification of high-risk individuals is the key to preventing and/or providing early diagnosis of cancer in this patient population. This educational review addresses these issues.
Using data available on the internet, and making assumptions regarding the types and results of genetic testing, we have estimated the number of mutation carriers in the country and the number who have been tested and identified as such. Overall, our ability to fund and more effectively manage carriers is weak. A technological solution is discussed.
C1 [Drohan, Brian; Roche, Constance A.; Cusack, James C., Jr.; Hughes, Kevin S.] Harvard Univ, Sch Med, Dept Surg,Massachusetts Gen Hosp, Avon Comprehens Breast Evaluat Ctr,Div Surg Oncol, Boston, MA 02115 USA.
[Hughes, Kevin S.] Harvard Univ, Bermuda Canc Genet & Risk Assessment Clin, Massachusetts Gen Hosp, Sch Med, Boston, MA 02115 USA.
RP Drohan, B (reprint author), Harvard Univ, Sch Med, Dept Surg,Massachusetts Gen Hosp, Avon Comprehens Breast Evaluat Ctr,Div Surg Oncol, Boston, MA 02115 USA.
EM jcusack@partners.org; kshughes@partners.org
OI Hughes, Kevin/0000-0003-4084-6484
FU Myriad Genetics
FX This educational review is part of a series, "Risk Assessment and
Genetic Testing for Hereditary Breast Cancer," which has been supported
by an educational grant from Myriad Genetics.
NR 21
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U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9265
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD JUN
PY 2012
VL 19
IS 6
BP 1732
EP 1737
DI 10.1245/s10434-012-2257-y
PG 6
WC Oncology; Surgery
SC Oncology; Surgery
GA 944NF
UT WOS:000304209800003
PM 22427173
ER
PT J
AU Pedroso, FE
Raut, CP
Xiao, H
Yeo, CJ
Koniaris, LG
AF Pedroso, Felipe E.
Raut, Chandrajit P.
Xiao, Hong
Yeo, Charles J.
Koniaris, Leonidas G.
TI Has the Survival Rate for Surgically Resected Gastric Gastrointestinal
Stromal Tumors Improved in the Tyrosine Kinase Inhibitor Era?
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Article
ID TERM-FOLLOW-UP; IMATINIB MESYLATE; PROGNOSTIC-FACTORS; DOSE IMATINIB;
MANAGEMENT; TRIAL; LEIOMYOSARCOMAS; STOMACH; RECURRENCE; DIAGNOSIS
AB Tyrosine kinase inhibitor (TKI) therapy for patients with gastrointestinal stromal tumors (GISTs) has been shown to improve overall outcomes. It remains unclear whether TKIs are delaying tumor recurrence or actually affecting cure rates. We sought to determine whether changes in overall and disease-specific survival (OS and DSS, respectively) for patients with surgically resected gastric GISTs have been observed after the introduction of TKI therapies by using population-based data.
The Surveillance, Epidemiology, and End Results (SEER) database was queried for patients with resected gastric mesenchymal tumors before the introduction of TKIs (pre-TKI: 1990-1994) and after their inception (post-TKI: 2002-2003).
Overall, 594 patients with gastric mesenchymal tumors were identified, and 189 and 405 underwent resection in the pre- and post-TKI eras, respectively. Between groups, there were no significant differences in patient demographics. The 1- and 6-year OS improved from 84 and 36 to 93 and 71%, respectively. The 1- and 6-year DSS improved from 92 and 62 to 96 and 90%, respectively. Through 6 years, OS and DSS significantly improved for all stages, tumor sizes, and extent of operation. By using multivariate analysis, undergoing treatment in the pre-TKI era was an independent negative predictor of OS, hazard ratio (HR, 2.98) and DSS (HR, 3.81).
The TKI era is associated with dramatic improvements in OS and DSS for patients with surgically resected gastric GISTs, irrespective of stage, tumor size, and extent of operation through 6 years of follow-up. It remains unclear, however, whether this survival advantage is a change in cure rate or simply a delay in disease progression.
C1 [Pedroso, Felipe E.; Yeo, Charles J.; Koniaris, Leonidas G.] Thomas Jefferson Univ, Jefferson Med Coll, Dept Surg, Philadelphia, PA 19107 USA.
[Raut, Chandrajit P.] Harvard Univ, Brigham & Womens Hosp, Dana Farber Canc Inst,Sch Med, Dept Surg,Ctr Sarcoma & Bone Oncol,Div Surg Oncol, Boston, MA 02115 USA.
[Xiao, Hong] Florida A&M Univ, Coll Pharm & Pharmaceut Sci, Div Econ Social & Adm Pharm, Tallahassee, FL 32307 USA.
RP Pedroso, FE (reprint author), Thomas Jefferson Univ, Jefferson Med Coll, Dept Surg, Philadelphia, PA 19107 USA.
EM leonidas.koniaris@jefferson.edu
FU NIH Supplement to Promote Diversity in Health-Related Research [R01
GM092758-01A1S1]
FX This work was partially supported by the following NIH Supplement to
Promote Diversity in Health-Related Research R01 GM092758-01A1S1
(F.E.P.).
NR 35
TC 5
Z9 5
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9265
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD JUN
PY 2012
VL 19
IS 6
BP 1748
EP 1758
DI 10.1245/s10434-012-2222-9
PG 11
WC Oncology; Surgery
SC Oncology; Surgery
GA 944NF
UT WOS:000304209800006
PM 22290567
ER
PT J
AU Seki, H
Hayashida, T
Jinno, H
Hirose, S
Sakata, M
Takahashi, M
Maheswaran, S
Mukai, M
Kitagawa, Y
AF Seki, Hirohito
Hayashida, Tetsu
Jinno, Hiromitsu
Hirose, Shigemichi
Sakata, Michio
Takahashi, Maiko
Maheswaran, Shyamala
Mukai, Makio
Kitagawa, Yuko
TI HOXB9 Expression Promoting Tumor Cell Proliferation and Angiogenesis Is
Associated with Clinical Outcomes in Breast Cancer Patients
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Article
ID EPITHELIAL-MESENCHYMAL TRANSITION; MICROVESSEL DENSITY; KI-67 ANTIGEN;
METASTASIS; CARCINOMA; SURVIVAL; GROWTH; BASAL; SECTIONS; THERAPY
AB Studies have suggested that HOXB9 expression in breast cancer cells promotes cellular invasiveness, metastatic ability, and tumor neovascularization in the surrounding tissue in and assays. These findings imply that HOXB9 overexpression may alter tumor-specific cell fates and the tumor stromal microenvironment, contributing to breast cancer progression. The objective of this study was to analyze whether these results could be applied to clinical practice.
A total of 141 consecutive, invasive ductal carcinoma patients who underwent surgical treatment were examined. Immunohistochemical staining was performed to evaluate the expression of HOXB9, Ki-67, CD31, and CD34, and the association of tumor proliferation and angiogenesis with HOXB9 expression was analyzed.
Of the 141 tumor specimens immunostained for HOXB9, 69 (48.9%) stained positive. Larger primary tumor size, hormone receptor negativity, HER2 positivity, higher nuclear grade, and number of pathologic nodal metastases were significant variables associated with HOXB9 expression. Notably, 12 (92.3%) of 13 triple-negative breast cancer cases showed HOXB9 expression. Disease-free survival and overall survival were significantly different between the HOXB9-positive and HOXB9-negative groups (hazard ratio 20.714, = 0.001; and hazard ratio 9.206, = 0.003, respectively). Multivariate analysis indicated that HOXB9 expression was the only independent prognostic factor for disease-free survival (hazard ratio 15.532, = 0.009). HOXB9-positive tumors showed a significant increase in the number of vasculature and the Ki-67 ratio compared with HOXB9-negative tumors.
HOXB9 expression, which promotes tumor proliferation and angiogenesis, is a significant prognostic factor in breast cancer.
C1 [Seki, Hirohito; Hayashida, Tetsu; Jinno, Hiromitsu; Sakata, Michio; Takahashi, Maiko; Kitagawa, Yuko] Keio Univ, Sch Med, Dept Surg, Tokyo 160, Japan.
[Hirose, Shigemichi; Mukai, Makio] Keio Univ, Sch Med, Div Diagnost Pathol, Tokyo 160, Japan.
[Maheswaran, Shyamala] Massachusetts Gen Hosp, Dept Surg, Charlestown, MA USA.
[Maheswaran, Shyamala] Harvard Univ, Sch Med, Charlestown, MA USA.
RP Seki, H (reprint author), Keio Univ, Sch Med, Dept Surg, Tokyo 160, Japan.
EM tetsu@z7.keio.jp
FU Ministry of Education, Culture, Sports, Science and Technology
[21791260, 23791499, 22591442, 21591677]; Keio University
FX The authors thank Chisato Saito, Hiroshi Okazaki, and Kazuhiro Miyao for
their technical support and helpful discussions. This research was
supported by the Ministry of Education, Culture, Sports, Science and
Technology Grants-in-Aid for Scientific Research [B] (21791260 and
23791499 to T.H.) and [C] (22591442 to H.J., 21591677 to M.T.), and a
Grant-in-Aid from the Global Center of Excellence Program entitled
"Education and Research Center for Stem Cell Medicine" (Keio
University).
NR 36
TC 18
Z9 19
U1 1
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9265
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD JUN
PY 2012
VL 19
IS 6
BP 1831
EP 1840
DI 10.1245/s10434-012-2295-5
PG 10
WC Oncology; Surgery
SC Oncology; Surgery
GA 944NF
UT WOS:000304209800016
PM 22396001
ER
PT J
AU Morikawa, T
Kuchiba, A
Qian, ZR
Mino-Kenudson, M
Hornick, JL
Yamauchi, M
Imamura, Y
Liao, XY
Nishihara, R
Meyerhardt, JA
Fuchs, CS
Ogino, S
AF Morikawa, Teppei
Kuchiba, Aya
Qian, Zhi Rong
Mino-Kenudson, Mari
Hornick, Jason L.
Yamauchi, Mai
Imamura, Yu
Liao, Xiaoyun
Nishihara, Reiko
Meyerhardt, Jeffrey A.
Fuchs, Charles S.
Ogino, Shuji
TI Prognostic Significance and Molecular Associations of Tumor Growth
Pattern in Colorectal Cancer
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Article
ID ISLAND METHYLATOR PHENOTYPE; POPULATION-BASED SAMPLE; BRAF V600E
MUTATION; MICROSATELLITE-INSTABILITY; COLON-CANCER; RECTAL-CANCER;
LINE-1 HYPOMETHYLATION; MULTIVARIATE-ANALYSIS; MISMATCH REPAIR; POOR
SURVIVAL
AB Infiltrative growth pattern at the tumor margin has been associated with shorter patient survival. However, little is known about the prognostic significance of tumor growth pattern, independent of tumoral molecular alterations and other histologic features.
Utilizing a database of 1139 colon and rectal cancer patients in two prospective cohort studies, histologic features including tumor growth pattern, tumor differentiation, lymphocytic reaction, mucinous component, and signet ring cell component were recorded by a single pathologist. Cox proportional hazard model was used to compute mortality hazard ratio, adjusting for clinical, pathologic, and tumor molecular features, including microsatellite instability, the CpG island methylator phenotype, long interspersed nucleotide element 1 (LINE-1) methylation, and and mutations.
Among 1139 colorectal cancers, we observed expansile growth pattern in 372 tumors (33%), intermediate growth pattern in 610 tumors (54%), and infiltrative growth pattern in 157 tumors (14%). Compared to patients with expansile growth pattern, those with infiltrative growth pattern experienced shorter cancer-specific survival (log rank < 0.0001; multivariate hazard ratio 1.74; 95% confidence interval 1.22-2.47) and overall survival (log rank < 0.0001; multivariate hazard ratio 1.78; 95% confidence interval 1.33-2.39). The prognostic association of infiltrative growth pattern was confined to patients with stage I-III disease ( (interaction) with stage = 0.0001).
Infiltrative growth pattern was associated with worse prognosis among stage I-III colorectal cancer patients, independent of other clinical, pathologic, and molecular characteristics.
C1 [Morikawa, Teppei; Kuchiba, Aya; Qian, Zhi Rong; Yamauchi, Mai; Imamura, Yu; Liao, Xiaoyun; Nishihara, Reiko; Meyerhardt, Jeffrey A.; Fuchs, Charles S.; Ogino, Shuji] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Morikawa, Teppei; Kuchiba, Aya; Qian, Zhi Rong; Mino-Kenudson, Mari; Hornick, Jason L.; Yamauchi, Mai; Imamura, Yu; Liao, Xiaoyun; Nishihara, Reiko; Meyerhardt, Jeffrey A.; Fuchs, Charles S.; Ogino, Shuji] Harvard Univ, Sch Med, Boston, MA USA.
[Mino-Kenudson, Mari] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Hornick, Jason L.; Ogino, Shuji] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Fuchs, Charles S.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
RP Morikawa, T (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
EM tmorikawa-tky@umin.ac.jp
OI Qian, Zhi rong/0000-0003-1633-4120
FU U.S. National Institute of Health (NIH) [P01 CA87969, P01 CA55075, P50
CA127003, R01 CA151993]; Bennett Family Fund; Entertainment Industry
Foundation through National Colorectal Cancer Research Alliance; Japan
Society for Promotion of Science
FX We thank the participants and staff of the Nurses' Health Study and the
Health Professionals Follow-up Study, for their valuable contributions
as well as the following state cancer registries for their help: AL, AZ,
AR, CA, CO, CT, DE, FL, GA, ID, IL, IN, IA, KY, LA, ME, MD, MA, MI, NE,
NH, NJ, NY, NC, ND, OH, OK, OR, PA, RI, SC, TN, TX, VA, WA, WY. This
work was supported by U.S. National Institute of Health (NIH) grants P01
CA87969 (to S. Hankinson), P01 CA55075 (to W. Willett), P50 CA127003 (to
C.S.F.), and R01 CA151993 (to S.O.) and by grants from the Bennett
Family Fund and the Entertainment Industry Foundation through National
Colorectal Cancer Research Alliance. T.M. was supported by a fellowship
grant from the Japan Society for Promotion of Science. The content is
solely the responsibility of the authors and does not necessarily
represent the official views of NCI or NIH. The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 50
TC 37
Z9 37
U1 0
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9265
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD JUN
PY 2012
VL 19
IS 6
BP 1944
EP 1953
DI 10.1245/s10434-011-2174-5
PG 10
WC Oncology; Surgery
SC Oncology; Surgery
GA 944NF
UT WOS:000304209800031
PM 22189472
ER
PT J
AU Lindquist, KA
Wager, TD
Kober, H
Bliss-Moreau, E
Barrett, LF
AF Lindquist, Kristen A.
Wager, Tor D.
Kober, Hedy
Bliss-Moreau, Eliza
Barrett, Lisa Feldman
TI The brain basis of emotion: A meta-analytic review
SO BEHAVIORAL AND BRAIN SCIENCES
LA English
DT Article
DE Discrete emotion; emotion experience; emotion perception; meta-analysis;
neuroimaging; psychological construction
ID MEDIAL PREFRONTAL CORTEX; MIDBRAIN PERIAQUEDUCTAL GRAY; BILATERAL
AMYGDALA DAMAGE; SKIN-CONDUCTANCE RESPONSE; ANTERIOR CINGULATE CORTEX;
VOXEL-BASED METAANALYSIS; TEMPORAL-LOBE EPILEPSY; MONKEYS
MACACA-MULATTA; ORBITOFRONTAL CORTEX; FACIAL EXPRESSIONS
AB Researchers have wondered how the brain creates emotions since the early days of psychological science. With a surge of studies in affective neuroscience in recent decades, scientists are poised to answer this question. In this target article, we present a meta-analytic summary of the neuroimaging literature on human emotion. We compare the locationist approach (i.e., the hypothesis that discrete emotion categories consistently and specifically correspond to distinct brain regions) with the psychological constructionist approach (i.e., the hypothesis that discrete emotion categories are constructed of more general brain networks not specific to those categories) to better understand the brain basis of emotion. We review both locationist and psychological constructionist hypotheses of brain-emotion correspondence and report meta-analytic findings bearing on these hypotheses. Overall, we found little evidence that discrete emotion categories can be consistently and specifically localized to distinct brain regions. Instead, we found evidence that is consistent with a psychological constructionist approach to the mind: A set of interacting brain regions commonly involved in basic psychological operations of both an emotional and non-emotional nature are active during emotion experience and perception across a range of discrete emotion categories.
C1 [Lindquist, Kristen A.] Harvard Univ, Sch Med, Dept Neurol, Massachusetts Gen Hosp,Martinos Ctr Biomed Imagin, Charlestown, MA 02129 USA.
[Lindquist, Kristen A.] Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA.
[Wager, Tor D.] Univ Colorado, Dept Psychol & Neurosci, Boulder, CO 80309 USA.
[Kober, Hedy] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT 06519 USA.
[Bliss-Moreau, Eliza] Univ Calif Davis, Calif Natl Primate Res Ctr, Davis, CA 95616 USA.
[Bliss-Moreau, Eliza] Univ Calif Davis, Dept Psychiat & Behav Sci, Davis, CA 95616 USA.
[Barrett, Lisa Feldman] Northeastern Univ, Dept Psychol, Boston, MA 02115 USA.
[Barrett, Lisa Feldman] Harvard Univ, Sch Med, Dept Radiol, Massachusetts Gen Hosp,Martinos Ctr Biomed Imagin, Charlestown, MA 02129 USA.
[Barrett, Lisa Feldman] Harvard Univ, Sch Med, Dept Psychiat, Massachusetts Gen Hosp,Martinos Ctr Biomed Imagin, Charlestown, MA 02129 USA.
RP Lindquist, KA (reprint author), Harvard Univ, Sch Med, Dept Neurol, Massachusetts Gen Hosp,Martinos Ctr Biomed Imagin, Charlestown, MA 02129 USA.
EM lindqukr@nmr.mgh.harvard.edu; tor.wager@colorado.edu;
hedy.kober@yale.edu; eblissmoreau@ucdavis.edu; l.barrett@neu.edu
FU National Science Foundation (NSF) [NSF 0631637]; Harvard University
Mind/Brain/Behavior Initiative; National Institute of Mental Health
(NIMH) [R01MH076136]; National Institutes of Health (NIH) [DP1OD003312];
National Institute on Aging (NIA) [R01 AG030311]; Army Reasearch
Institute (ARI) [W91WAW-08-C-0018]
FX We thank Amitai Shenhav for his insights into the amygdala's the role in
uncertainty, Natasha Sarkisian for her advice on logistic regression,
and Kurt Gray for his help with Figure 5. We also thank James Russell,
Elizabeth Kensinger, Hiram Brownell, Jerry Clore, and Stephan Hamann who
commented on an earlier draft of this manuscript. This project was
supported by a National Science Foundation (NSF) Graduate Research
Fellowship and a Harvard University Mind/Brain/Behavior Initiative
Postdoctoral Fellowship to Kristen Lindquist; a NSF Graduate Research
Fellowship to Hedy Kober; a NSF grant (NSF 0631637) and a National
Institute of Mental Health (NIMH) grant (R01MH076136) to Tor Wager; and
a National Institutes of Health (NIH) Director's Pioneer Award
(DP1OD003312), an National Institute on Aging (NIA) grant (R01
AG030311), and an Army Reasearch Institute (ARI) contract
(W91WAW-08-C-0018) to Lisa Feldman Barrett. The views, opinions, and/or
findings contained in this article are solely those of the authors and
should not be construed as an official Department of the Army or
Department of Defense position, policy, or decision.
NR 347
TC 406
Z9 414
U1 32
U2 217
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0140-525X
EI 1469-1825
J9 BEHAV BRAIN SCI
JI Behav. Brain Sci.
PD JUN
PY 2012
VL 35
IS 3
BP 121
EP 143
DI 10.1017/S0140525X11000446
PG 23
WC Psychology, Biological; Behavioral Sciences; Neurosciences
SC Psychology; Behavioral Sciences; Neurosciences & Neurology
GA 946ME
UT WOS:000304355000001
PM 22617651
ER
PT J
AU Lindquist, KA
Wager, TD
Bliss-Moreau, E
Kober, H
Barrett, LF
AF Lindquist, Kristen A.
Wager, Tor D.
Bliss-Moreau, Eliza
Kober, Hedy
Barrett, Lisa Feldman
TI What are emotions and how are they created in the brain? Response
SO BEHAVIORAL AND BRAIN SCIENCES
LA English
DT Article
ID SUBTHALAMIC NUCLEUS STIMULATION; FUNCTIONAL NEUROIMAGING DATA; FACIAL
EXPRESSIONS; BASIC EMOTIONS; PARKINSONS-DISEASE; PSYCHOLOGICAL
CONSTRUCTION; INDIVIDUAL-DIFFERENCES; CULTURAL-DIFFERENCES; CONGENITALLY
BLIND; ACCUMBENS DOPAMINE
AB In our response, we clarify important theoretical differences between basic emotion and psychological construction approaches. We evaluate the empirical status of the basic emotion approach, addressing whether it requires brain localization, whether localization can be observed with better analytic tools, and whether evidence for basic emotions exists in other types of measures. We then revisit the issue of whether the key hypotheses of psychological construction are supported by our meta-analytic findings. We close by elaborating on commentator suggestions for future research.
C1 [Lindquist, Kristen A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol,Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Lindquist, Kristen A.] Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA.
[Wager, Tor D.] Univ Colorado, Dept Psychol & Neurosci, Boulder, CO 80309 USA.
[Bliss-Moreau, Eliza] Univ Calif Davis, Calif Natl Primate Res Ctr, Davis, CA 95616 USA.
[Bliss-Moreau, Eliza] Univ Calif Davis, Dept Psychiat & Behav Sci, Davis, CA 95616 USA.
[Kober, Hedy] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT 06519 USA.
[Barrett, Lisa Feldman] Northeastern Univ, Dept Psychol, Boston, MA 02115 USA.
[Barrett, Lisa Feldman] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol,Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Barrett, Lisa Feldman] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat,Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
RP Lindquist, KA (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol,Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
EM lindqukr@nmr.mgh.harvard.edu; tor.wager@colorado.edu;
eblissmoreau@ucdavis.edu; hedy.kober@yale.edu; l.barrett@neu.edu
FU NIH HHS [DP1 OD003312]
NR 202
TC 11
Z9 15
U1 3
U2 56
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0140-525X
EI 1469-1825
J9 BEHAV BRAIN SCI
JI Behav. Brain Sci.
PD JUN
PY 2012
VL 35
IS 3
BP 172
EP 202
DI 10.1017/S0140525X1100183X
PG 31
WC Psychology, Biological; Behavioral Sciences; Neurosciences
SC Psychology; Behavioral Sciences; Neurosciences & Neurology
GA 946ME
UT WOS:000304355000030
PM 22783560
ER
PT J
AU Strakowski, SM
Adler, CM
Almeida, J
Altshuler, LL
Blumberg, HP
Chang, KKD
DelBello, MP
Frangou, S
McIntosh, A
Phillips, ML
Sussman, JE
Townsend, JD
AF Strakowski, Stephen M.
Adler, Caleb M.
Almeida, Jorge
Altshuler, Lori L.
Blumberg, Hilary P.
Chang, Kiki D.
DelBello, Melissa P.
Frangou, Sophia
McIntosh, Andrew
Phillips, Mary L.
Sussman, Jessika E.
Townsend, Jennifer D.
TI The functional neuroanatomy of bipolar disorder: a consensus model
SO BIPOLAR DISORDERS
LA English
DT Article
DE amygdala; bipolar disorder; connectivity; functional magnetic resonance
imaging (fMRI); neuroimaging; prefrontal cortex
ID VENTRAL PREFRONTAL CORTEX; ANTERIOR CINGULATE CORTEX; WHITE-MATTER
INTEGRITY; FACIAL EXPRESSIONS; AMYGDALA; ABNORMALITIES; FMRI;
ADOLESCENTS; ACTIVATION; DEPRESSION
AB Strakowski SM, Adler CM, Almeida J, Altshuler LL, Blumberg HP, Chang KD, DelBello MP, Frangou S, McIntosh A, Phillips ML, Sussman JE, Townsend JD. The functional neuroanatomy of bipolar disorder: a consensus model. ?Bipolar Disord 2012: 14: 313325. (c) 2012 The Authors. Journal compilation (c) 2012 John Wiley & Sons A/S. Objectives: Functional neuroimaging methods have proliferated in recent years, such that functional magnetic resonance imaging, in particular, is now widely used to study bipolar disorder. However, discrepant findings are common. A workgroup was organized by the Department of Psychiatry, University of Cincinnati (Cincinnati, OH, USA) to develop a consensus functional neuroanatomic model of bipolar I disorder based upon the participants work as well as that of others. Methods: Representatives from several leading bipolar disorder neuroimaging groups were organized to present an overview of their areas of expertise as well as focused reviews of existing data. The workgroup then developed a consensus model of the functional neuroanatomy of bipolar disorder based upon these data. Results: Among the participants, a general consensus emerged that bipolar I disorder arises from abnormalities in the structure and function of key emotional control networks in the human brain. Namely, disruption in early development (e.g., white matter connectivity and prefrontal pruning) within brain networks that modulate emotional behavior leads to decreased connectivity among ventral prefrontal networks and limbic brain regions, especially the amygdala. This developmental failure to establish healthy ventral prefrontallimbic modulation underlies the onset of mania and ultimately, with progressive changes throughout these networks over time and with affective episodes, a bipolar course of illness. Conclusions: This model provides a potential substrate to guide future investigations and areas needing additional focus are identified.
C1 [Strakowski, Stephen M.; Adler, Caleb M.; DelBello, Melissa P.] Univ Cincinnati, Coll Med, Dept Psychiat & Behav Neurosci, Cincinnati, OH 45267 USA.
[Almeida, Jorge; Phillips, Mary L.] Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA USA.
[Altshuler, Lori L.; Townsend, Jennifer D.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Semel Inst Neurosci & Human Behav, Los Angeles, CA 90095 USA.
[Altshuler, Lori L.] VA Greater Los Angeles Healthcare Syst, Dept Psychiat, Los Angeles, CA USA.
[Blumberg, Hilary P.] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA.
[Chang, Kiki D.] Stanford Univ, Pediat Bipolar Disorders Res Program, Div Child & Adolescent Psychiat, Dept Psychiat & Behav Sci,Sch Med, Stanford, CA 94305 USA.
[Frangou, Sophia] Kings Coll London, Sect Neurobiol Psychosis, Dept Psychosis Studies, Inst Psychiat, London WC2R 2LS, England.
[McIntosh, Andrew; Sussman, Jessika E.] Univ Edinburgh, Div Psychiat, Sch Mol & Clin Med, Edinburgh, Midlothian, Scotland.
[Phillips, Mary L.] Cardiff Univ Sch Med, Dept Psychol Med, Cardiff, S Glam, Wales.
RP Strakowski, SM (reprint author), Univ Cincinnati, Coll Med, Dept Psychiat, 260 Stetson Suite 3200, Cincinnati, OH 45267 USA.
EM stephen.strakowski@uc.edu
RI McIntosh, Andrew/B-9379-2008; Frangou, Sophia/A-2672-2013; Almeida,
Jorge/O-5185-2014
OI McIntosh, Andrew/0000-0002-0198-4588; Almeida, Jorge/0000-0002-1213-1986
FU NIH [P50 MH077138, R01 MH076971, R01 MH088371, 2R01MH070902,
1RC1MH088366, R01MH069747, 5R21MH075944, 1K24MH001848, 1R01MH084955, R01
MH077047, R01 MH080973, R01 MH078043]
FX This workgroup was supported in part by the Department of Psychiatry,
University of Cincinnati College of Medicine, Cincinnati, OH, USA. This
manuscript was supported in part by NIH grants P50 MH077138 (SMS); R01
MH076971 and R01 MH088371 (MLP); 2R01MH070902, 1RC1MH088366, and
R01MH069747 (HPB); 5R21MH075944, 1K24MH001848, and 1R01MH084955 (LLA);
R01 MH077047 (KDC); R01 MH080973 (MPD); and R01 MH078043 (CMA).
NR 72
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U1 7
U2 31
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1398-5647
J9 BIPOLAR DISORD
JI Bipolar Disord.
PD JUN
PY 2012
VL 14
IS 4
BP 313
EP 325
DI 10.1111/j.1399-5618.2012.01022.x
PG 13
WC Clinical Neurology; Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 947PE
UT WOS:000304441200001
PM 22631617
ER
PT J
AU Townsend, J
Altshuler, LL
AF Townsend, Jennifer
Altshuler, Lori L.
TI Emotion processing and regulation in bipolar disorder: a review
SO BIPOLAR DISORDERS
LA English
DT Review
DE amygdala; bipolar disorder; emotion processing; emotion regulation;
functional neuroimaging; vlPFC
ID INCREASED AMYGDALA ACTIVATION; FACIAL AFFECT RECOGNITION; MEDIAL
PREFRONTAL CORTEX; FUNCTIONAL CONNECTIVITY; NEGATIVE EMOTION; MOOD
DISORDERS; RHESUS-MONKEY; VOLUNTARY SUPPRESSION; ORBITOFRONTAL CORTEX;
COGNITIVE CONTROL
AB Townsend J, Altshuler LL. Emotion processing and regulation in bipolar disorder: a review. ?Bipolar Disord 2012: 14: 326339. (c) 2012 The Authors. Journal compilation (c) 2012 John Wiley & Sons A/S. Objectives: Bipolar disorder (BP) is characterized by a dysfunction of mood, alternating between states of mania/hypomania and depression. Thus, the primary abnormality appears to be an inability to regulate emotion, the result of which is emotional extremes. The purpose of this paper is to review the current functional magnetic resonance imaging (fMRI) literature on adult patients with BP using emotion processing or regulation paradigms. Methods: A search was conducted on PubMed using the keywords: bipolar disorder, fMRI, mania, bipolar depression, bipolar euthymia, emotion, and amygdala. Only those studies that were conducted in adult patients using an emotion activation task were included in the final review. Results: Using tasks that assess neural functioning during emotion processing and emotion regulation, many fMRI studies have examined BP subjects during mania and euthymia. Fewer fMRI studies have been conducted during depression, and fewer still have included the same subjects in multiple mood states. Despite these limitations, these studies have demonstrated specific abnormalities in frontallimbic regions. Using a variety of paradigms, investigators have specifically evaluated the amygdala (a structure within the limbic system known to be critical for emotion) and the prefrontal cortex (PFC) (a region known to have a regulatory function over the limbic system). Conclusions: These investigations reveal that amygdala activation varies as a function of mood state, while the PFC remains persistently hypoactivated across mood states. Emotional dysregulation and lability in mania and depression may reflect disruption of a frontallimbic functional neuroanatomical network.
C1 [Townsend, Jennifer; Altshuler, Lori L.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA.
[Townsend, Jennifer; Altshuler, Lori L.] Univ Calif Los Angeles, Semel Inst Neurosci & Human Behav, Los Angeles, CA 90095 USA.
[Altshuler, Lori L.] VA Greater Los Angeles Healthcare Syst, Dept Psychiat, Los Angeles, CA USA.
RP Altshuler, LL (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, 300 UCLA Med Plaza,Suite 1544,Box 957057, Los Angeles, CA 90095 USA.
EM laltshuler@mednet.ucla.edu
FU Forest Laboratories; Sepracor; Eli Lilly Co.
FX LLA has received past funding from Forest Laboratories (advisory board
honoraria, March 2008), Sepracor (advisory board honoraria, January
2010), and Eli Lilly & Co. (consultant, September 2010). JT does not
have any commercial associations that might pose a conflict of interest
in connection with this manuscript.
NR 117
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U1 12
U2 63
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1398-5647
J9 BIPOLAR DISORD
JI Bipolar Disord.
PD JUN
PY 2012
VL 14
IS 4
BP 326
EP 339
DI 10.1111/j.1399-5618.2012.01021.x
PG 14
WC Clinical Neurology; Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 947PE
UT WOS:000304441200002
PM 22631618
ER
PT J
AU Townsend, JD
Bookheimer, SY
Foland-Ross, LC
Moody, TD
Eisenberger, NI
Fischer, JS
Cohen, MS
Sugar, CA
Altshuler, LL
AF Townsend, Jennifer D.
Bookheimer, Susan Y.
Foland-Ross, Lara C.
Moody, Teena D.
Eisenberger, Naomi I.
Fischer, Jeffrey S.
Cohen, Mark S.
Sugar, Catherine A.
Altshuler, Lori L.
TI Deficits in inferior frontal cortex activation in euthymic bipolar
disorder patients during a response inhibition task
SO BIPOLAR DISORDERS
LA English
DT Article
DE bipolar disorder; fMRI; orbitofrontal cortex; response inhibition;
striatum
ID MEDIAL PREFRONTAL CORTEX; BRAIN ACTIVATION; I DISORDER; FMRI; MANIA;
ABNORMALITIES; MONKEYS; INTERFERENCE; IMPULSIVITY; DYSFUNCTION
AB Townsend JD, Bookheimer SY, Foland-Ross LC, Moody TD, Eisenberger NI, Fischer JS, Cohen MS, Sugar CA, Altshuler LL. Deficits in inferior frontal cortex activation in euthymic bipolar disorder patients during a response inhibition task. ?Bipolar Disord 2012: 14: 442450. (c) 2012 The Authors. Journal compilation (c) 2012 John Wiley & Sons A/S. Objectives: The inferior frontal corticalstriatal network plays an integral role in response inhibition in normal populations. While inferior frontal cortex (IFC) impairment has been reported in mania, this study explored whether this dysfunction persists in euthymia. Methods: Functional magnetic resonance imaging (fMRI) activation was evaluated in 32 euthymic patients with bipolar I disorder and 30 healthy subjects while performing the Go/NoGo response inhibition task. Behavioral data were collected to evaluate accuracy and response time. Within-group and between-group comparisons of activation were conducted using whole-brain analyses to probe significant group differences in neural function. Results: Both groups activated bilateral IFC. However, between-group comparisons showed a significantly reduced activation in this brain region in euthymic patients with bipolar disorder compared to healthy subjects. Other frontal and basal ganglia regions involved in response inhibition were additionally significantly reduced in bipolar disorder patients, in both the medicated and the unmedicated subgroups. No areas of greater activation were observed in bipolar disorder patients versus healthy subjects. Conclusions: Bipolar disorder patients, even during euthymia, have a persistent reduction in activation of brain regions involved in response inhibition, suggesting that reduced activation in the orbitofrontal cortex and striatum is not solely related to the state of mania. These findings may represent underlying trait abnormalities in bipolar disorder.
C1 [Townsend, Jennifer D.; Bookheimer, Susan Y.; Moody, Teena D.; Fischer, Jeffrey S.; Cohen, Mark S.; Altshuler, Lori L.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA.
[Foland-Ross, Lara C.] Univ Calif Los Angeles, David Geffen Sch Med, Lab NeuroImaging, Dept Neurol, Los Angeles, CA 90095 USA.
[Foland-Ross, Lara C.] Stanford Univ, Dept Psychol, Stanford, CA 94305 USA.
[Moody, Teena D.; Sugar, Catherine A.; Altshuler, Lori L.] Univ Calif Los Angeles, Sch Publ Hlth, Jane & Terry Semel Inst Neurosci & Human Behav, Los Angeles, CA 90095 USA.
[Eisenberger, Naomi I.] Univ Calif Los Angeles, Sch Publ Hlth, Dept Psychol, Los Angeles, CA 90095 USA.
[Sugar, Catherine A.] Univ Calif Los Angeles, Sch Publ Hlth, Dept Biostat, Los Angeles, CA 90095 USA.
[Altshuler, Lori L.] VA Greater Los Angeles Healthcare Syst, Dept Psychiat, W Los Angeles Healthcare Ctr, Los Angeles, CA USA.
RP Altshuler, LL (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, 300 UCLA Med Plaza,Suite 1544,Box 957057, Los Angeles, CA 90095 USA.
EM laltshuler@mednet.ucla.edu
RI Cohen, Mark/C-6610-2011
OI Cohen, Mark/0000-0001-6731-4053
FU Stanley Medical Research Institute; National Alliance for Research on
Schizophrenia and Depression; National Institute of Mental Health [K24
MH001848, R21 MH075944, 5F31MH078556]; National Center for Research
Resources [RR12169, RR13642, RR00865]; Forest Laboratories; Sepracor;
Eli Lilly Co.
FX This work was supported by The Stanley Medical Research Institute, the
National Alliance for Research on Schizophrenia and Depression, the
National Institute of Mental Health (K24 MH001848, R21 MH075944 and
5F31MH078556), and the National Center for Research Resources (RR12169,
RR13642 and RR00865). The authors also wish to thank the Brain Mapping
Medical Research Organization, the Brain Mapping Support Foundation, the
Pierson-Lovelace Foundation, The Ahmanson Foundation, the William M. and
Linda R. Dietel Philanthropic Fund at the Northern Piedmont Community
Foundation, the Tamkin Foundation, the Jennifer Jones-Simon Foundation,
the Capital Group Companies Charitable Foundation, the Robson Family,
and the Northstar Fund for generous support.; LLA has received past
funding from Forest Laboratories (advisory board honoraria, March 2008),
Sepracor (advisory board honoraria, January 2010), and Eli Lilly & Co.
(consultant, September 2010). JDT, SYB, LCF-R, TDM, NIE, JSF, MSC, and
CAS do not have any commercial associations that might pose a conflict
of interest in connection with this manuscript.
NR 38
TC 26
Z9 26
U1 3
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1398-5647
J9 BIPOLAR DISORD
JI Bipolar Disord.
PD JUN
PY 2012
VL 14
IS 4
BP 442
EP 450
DI 10.1111/j.1399-5618.2012.01020.x
PG 9
WC Clinical Neurology; Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 947PE
UT WOS:000304441200008
PM 22631623
ER
PT J
AU Gow, DW
AF Gow, David W., Jr.
TI The cortical organization of lexical knowledge: A dual lexicon model of
spoken language processing
SO BRAIN AND LANGUAGE
LA English
DT Review
DE Lexicon; Language; Spoken word recognition; Lexical access; Speech
perception; Speech production; Neuroimaging; Aphasia; Dual stream model;
Localization
ID EVENT-RELATED FMRI; ANTERIOR TEMPORAL CORTEX; WORD MEANING DEAFNESS;
TRANSCORTICAL SENSORY APHASIA; VOICE-ONSET TIME; SPEECH-PERCEPTION;
CONDUCTION APHASIA; SENTENCE COMPREHENSION; PAST-TENSE; WORKING-MEMORY
AB Current accounts of spoken language assume the existence of a lexicon where wordforms are stored and interact during spoken language perception, understanding and production. Despite the theoretical importance of the wordform lexicon, the exact localization and function of the lexicon in the broader context of language use is not well understood. This review draws on evidence from aphasia, functional imaging, neuroanatomy, laboratory phonology and behavioral results to argue for the existence of parallel lexica that facilitate different processes in the dorsal and ventral speech pathways. The dorsal lexicon, localized in the inferior parietal region including the supramarginal gyrus, serves as an interface between phonetic and articulatory representations. The ventral lexicon, localized in the posterior superior temporal sulcus and middle temporal gyrus, serves as an interface between phonetic and semantic representations. In addition to their interface roles, the two lexica contribute to the robustness of speech processing. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Gow, David W., Jr.] Massachusetts Gen Hosp, Neuropsychol Lab, Boston, MA 02114 USA.
[Gow, David W., Jr.] Salem State Univ, Dept Psychol, Salem, MA 01970 USA.
[Gow, David W., Jr.] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Gow, David W., Jr.] Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
RP Gow, DW (reprint author), Cognit Behav Neurol Grp, 175 Cambridge St,Suite S340, Boston, MA 02114 USA.
EM gow@helix.mgh.harvard.edu
FU National Institute of Deafness and Communicative Disorders [R01
DC003108]
FX I would like to thank David Caplan, Catherine Stoodley, and Joshua Levy
for their feedback during the preparation of this manuscript, and Matt
Davis and Greg Hickok for their thoughtful reviews of an earlier version
of this manuscript. This work was supported by the National Institute of
Deafness and Communicative Disorders (R01 DC003108). I have no conflicts
of interest to declare.
NR 199
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U1 3
U2 51
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0093-934X
J9 BRAIN LANG
JI Brain Lang.
PD JUN
PY 2012
VL 121
IS 3
BP 273
EP 288
DI 10.1016/j.bandl.2012.03.005
PG 16
WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences;
Psychology, Experimental
SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences &
Neurology; Psychology
GA 946GO
UT WOS:000304339700011
PM 22498237
ER
PT J
AU Togsverd-Bo, K
Haak, CS
Thaysen-Petersen, D
Wulf, HC
Anderson, RR
Haedesdal, M
AF Togsverd-Bo, K.
Haak, C. S.
Thaysen-Petersen, D.
Wulf, H. C.
Anderson, R. R.
Haedesdal, M.
TI Intensified photodynamic therapy of actinic keratoses with fractional
CO2 laser: a randomized clinical trial
SO BRITISH JOURNAL OF DERMATOLOGY
LA English
DT Article
ID TOPICAL METHYL AMINOLEVULINATE; PROTOPORPHYRIN-IX; 5-AMINOLEVULINIC
ACID; DOUBLE-BLIND; RED-LIGHT; FLUORESCENCE; MULTICENTER; LASER; FACE;
SKIN
AB Background Photodynamic therapy (PDT) with methyl aminolaevulinate (MAL) is effective for thin actinic keratoses (AKs) in field-cancerized skin. Ablative fractional laser resurfacing (AFXL) creates vertical channels that facilitate MAL uptake and may improve PDT efficacy.
Objectives To evaluate efficacy and safety of AFXL-assisted PDT (AFXL-PDT) compared with conventional PDT in field-directed treatment of AK.
Methods Fifteen patients with a total of 212 AKs (severity grade I-III) in field-cancerized skin of the face and scalp were randomized to one treatment with PDT and one treatment with AFXL-PDT in two symmetrical areas. Following curettage of both treatment areas, AFXL was applied to one area using 10 mJ per pulse, 0 12 mm spot, 5% density, single pulse (UltraPulse (R), DeepFx handpiece; Lumenis Inc., Santa Clara, CA, U. S. A.). MAL cream was then applied under occlusion for 3 h and illuminated with red light-emitting diode light at 37 J cm(-2). Fluorescence photography quantified protoporphyrin IX (PpIX) before and after illumination.
Results At 3-month follow-up, AFXL-PDT was significantly more effective than PDT for all AK grades. Complete lesion response of grade II-III AK was 88% after AFXL-PDT compared with 59% after PDT (P = 0.02). In grade I AK, 100% of lesions cleared after AFXL-PDT compared with 80% after PDT (P = 0.04). AFXL-PDT treated skin responded with significantly fewer new AK lesions (AFXL-PDT n = 3, PDT n = 11; P = 0.04) and more improved photoageing (moderate vs. minor improvement, P = 0.007) than PDT-treated skin. Pain scores during illumination (6.5 vs. 5.4; P = 0.02), erythema and crusting were more intense, and long-term pigmentary changes more frequent from AFXL-PDT than PDT (P = not significant). PpIX fluorescence was higher in AFXL-pretreated skin [7528 vs. 12 816 arbitrary units (AU); P = 0.003] and photobleached to equal intensities after illumination (AFXL-PDT 595 AU, PDT 454 AU; P = 0.59).
Conclusions AFXL-PDT is more effective than conventional PDT for treatment of AK in field-cancerized skin.
C1 [Togsverd-Bo, K.; Haak, C. S.; Thaysen-Petersen, D.; Wulf, H. C.; Haedesdal, M.] Univ Copenhagen, Dept Dermatol, Bispebjerg Hosp, DK-2400 Copenhagen, Denmark.
[Anderson, R. R.; Haedesdal, M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Wellman Ctr Photomed, Boston, MA 02114 USA.
RP Togsverd-Bo, K (reprint author), Univ Copenhagen, Dept Dermatol, Bispebjerg Hosp, DK-2400 Copenhagen, Denmark.
EM ktogsverdbo@dadlnet.dk
FU Department of Dermatology, Bispebjerg Hospital, University of
Copenhagen; A. P. Moller Foundation for the Advancement of Medical
Science. Lumenis Inc. (Santa Clara, CA, U.S.A.); Galderma
FX The study was funded by Department of Dermatology, Bispebjerg Hospital,
University of Copenhagen and A. P. Moller Foundation for the Advancement
of Medical Science. Lumenis Inc. (Santa Clara, CA, U.S.A.) lent the
ablative fractional CO2 laser but had no role in the design
or conduct of the trial and had no access to study data nor the
preparation of the manuscript.; K.T.-B. has received a travelling grant
from Galderma. C. S. H. and D. T.-P. have no disclosures. H. C. W. has
received fees for speaking and a travelling grant from Galderma. R. R.
A. is a consultant for Galderma (unrelated to this study). M. H. has
received fees from Galderma for speaking and is on the advisory board
for Galderma International regarding photodynamic therapy of organ
transplant recipients.
NR 31
TC 59
Z9 64
U1 0
U2 12
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-0963
J9 BRIT J DERMATOL
JI Br. J. Dermatol.
PD JUN
PY 2012
VL 166
IS 6
BP 1262
EP 1269
DI 10.1111/j.1365-2133.2012.10893.x
PG 8
WC Dermatology
SC Dermatology
GA 950QV
UT WOS:000304664700017
PM 22348388
ER
PT J
AU Bae, J
Song, WH
Smith, R
Daley, J
Tai, YT
Anderson, KC
Munshi, NC
AF Bae, Jooeun
Song, Weihua
Smith, Robert
Daley, John
Tai, Yu-Tzu
Anderson, Kenneth C.
Munshi, Nikhil C.
TI A novel immunogenic CS1-specific peptide inducing antigen-specific
cytotoxic T lymphocytes targeting multiple myeloma
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE Multiple myeloma; CS1; epitope; peptide vaccine
ID HUMANIZED MONOCLONAL-ANTIBODY; PLASMA-CELL DIFFERENTIATION; RECEPTOR;
EXPRESSION; LEUKEMIA; IMMUNOTHERAPY; THALIDOMIDE; APOPTOSIS; PARADIGM;
VACCINES
AB The CS1 antigen provides a unique target for the development of an immunotherapeutic strategy to treat patients with multiple myeloma (MM). This study aimed to identify HLA-A2+ immunogenic peptides from the CS1 antigen, which induce peptide-specific cytotoxic T lymphocytes (CTL) against HLA-A2+ MM cells. We identified a novel immunogenic HLA-A2-specific CS1239-247 (SLFVLGLFL) peptide, which induced CS1-specific CTL (CS1-CTL) to MM cells. The CS1-CTL showed a distinct phenotype, with an increased percentage of effector memory and activated CTL and a decreased percentage of naive CTL. CS1239-247 peptide-specific CD8+ T cells were detected by DimerX analyses and demonstrated functional activities specific to the peptide. The CTL displayed HLA-A2-restricted and antigen-specific cytotoxicity, proliferation, degranulation and ?-interferon (IFN-?) production against both primary MM cells and MM cell lines. In addition, the effector memory cells subset (CD45RO+CCR7-/CD3+CD8+) within CS1-CTL showed a higher level of CD107a degranulation and IFN-? production as compared to effector cells (CD45RO-CCR7-/CD3+CD8+) against HLA-A2+ primary MM cells or MM cell lines. In conclusion, this study introduced a novel immunogenic HLA-A2-specific CS1239-247 peptide capable of inducing antigen-specific CTL against MM cells that will provide a framework for its application as a novel MM immunotherapy.
C1 [Munshi, Nikhil C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol,Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA.
[Song, Weihua; Munshi, Nikhil C.] VA Boston Healthcare Syst, Boston, MA USA.
RP Munshi, NC (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol,Jerome Lipper Multiple Myeloma Ctr, 44 Binney St, Boston, MA 02115 USA.
EM nikhil_munshi@dfci.harvard.edu
FU National Institutes of Health [RO1-124929, P50-100007, PO1155258,
RO1-50947, PO1-155258, P50-100707, PO1-78378, RO1-129295]; American
Cancer Society; Department of Veteran's Affairs [RO1-50947]
FX This work was supported in part by grants from the National Institutes
of Health Grants RO1-124929 to Dr. Nikhil C. Munshi, P50-100007,
PO1-78378 and PO1155258 to Dr. Nikhil C. Munshi and Dr. Kenneth C.
Anderson and RO1-50947 to Dr. Kenneth C. Anderson. Dr. Anderson is an
American Cancer Society Clinical Research Professor. We also acknowledge
the generous support of the Stewart Nagler Research Fund. NIH grants
PO1-155258 (NCM); P50-100707 (KCA), and PO1-78378 (KCA), RO1-129295 and
Department of Veteran's Affairs merit review award (NCM) and RO1-50947
(KCA).
NR 45
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Z9 14
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1048
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD JUN
PY 2012
VL 157
IS 6
BP 687
EP 701
DI 10.1111/j.1365-2141.2012.09111.x
PG 15
WC Hematology
SC Hematology
GA 947PI
UT WOS:000304441600006
PM 22533610
ER
PT J
AU Leiba, M
Jakubikova, J
Klippel, S
Mitsiades, CS
Hideshima, T
Tai, YT
Leiba, A
Pines, M
Richardson, PG
Nagler, A
Anderson, KC
AF Leiba, Merav
Jakubikova, Jana
Klippel, Steffen
Mitsiades, Constantine S.
Hideshima, Teru
Tai, Yu-Tzu
Leiba, Adi
Pines, Mark
Richardson, Paul G.
Nagler, Arnon
Anderson, Kenneth C.
TI Halofuginone inhibits multiple myeloma growth in vitro and in vivo and
enhances cytotoxicity of conventional and novel agents
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE Halofuginone; TGF-ss; JNK; c-jun; p-53
ID CELL-GROWTH; HEPATOCELLULAR-CARCINOMA; MOLECULAR-MECHANISMS;
ANTITUMOR-ACTIVITY; BONE-MARROW; P38 MAPK; APOPTOSIS; PATHWAYS; JNK;
ANGIOGENESIS
AB Multiple Myeloma (MM), a malignancy of plasma cells, remains incurable despite the use of conventional and novel therapies. Halofuginone (HF), a synthetic derivative of quinazolinone alkaloid, has recently been shown to have anti-cancer activity in various preclinical settings. This study demonstrated the anti-tumour activity of HF against a panel of human MM cell lines and primary patient-derived MM cells, regardless of their sensitivity to conventional therapy or novel agents. HF showed anti-MM activity in vivo using a myeloma xenograft mouse model. HF suppressed proliferation of myeloma cells alone and when co-cultured with bone marrow stromal cells. Similarly, HF induced apoptosis in MM cells even in the presence of insulin-like growth factor 1 or interleukin 6. Importantly, HF, even at high doses, did not induce cytotoxicity against CD40 activated peripheral blood mononuclear cells from normal donors. HF treatment induced accumulation of cells in the G0/G1 cell cycle and induction of apoptotic cell death associated with depletion of mitochondrial membrane potential; cleavage of poly (ADP-ribose) polymerase and caspases-3, 8 and 9 as well as down-regulation of anti-apoptotic proteins including Mcl-1 and X-IAP. Multiplex analysis of phosphorylation of diverse components of signalling cascades revealed that HF induced changes in P38MAPK activation; increased phosphorylation of c-jun, c-jun NH(2)-terminal kinase (JNK), p53 and Hsp-27. Importantly, HF triggered synergistic cytotoxicity in combination with lenalidomide, melphalan, dexamethasone, and doxorubicin. Taken together, these preclinical studies provide the preclinical framework for future clinical studies of HF in MM.
C1 [Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol,Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02215 USA.
[Leiba, Merav; Jakubikova, Jana; Klippel, Steffen; Mitsiades, Constantine S.; Hideshima, Teru; Tai, Yu-Tzu; Richardson, Paul G.; Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol,LeBow Inst Myeloma, Boston, MA 02215 USA.
[Leiba, Merav; Nagler, Arnon] Chaim Sheba Med Ctr, Div Haematol & Bone Marrow Transplantat, IL-52621 Tel Hashomer, Israel.
[Jakubikova, Jana] Slovak Acad Sci, Canc Res Inst, Dept Tumour Immunol, Bratislava, Slovakia.
[Pines, Mark] Agr Res Org, Volcani Ctr, Inst Anim Sci, IL-50250 Bet Dagan, Israel.
RP Anderson, KC (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol,Jerome Lipper Multiple Myeloma Ctr, 430 Brookline Ave, Boston, MA 02215 USA.
EM Kenneth_Anderson@dfci.harvard.edu
FU NCI NIH HHS [P50 CA100707, R01 CA050947]
NR 52
TC 16
Z9 23
U1 2
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1048
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD JUN
PY 2012
VL 157
IS 6
BP 718
EP 731
DI 10.1111/j.1365-2141.2012.09120.x
PG 14
WC Hematology
SC Hematology
GA 947PI
UT WOS:000304441600009
PM 22533681
ER
PT J
AU Tomasetti, C
AF Tomasetti, Cristian
TI On the Probability of Random Genetic Mutations for Various Types of
Tumor Growth
SO BULLETIN OF MATHEMATICAL BIOLOGY
LA English
DT Article
DE Tumor growth; Genetic mutations; Drug resistance; Stem cells; Ordinary
differential equations; Branching processes
ID CHRONIC MYELOID-LEUKEMIA; DRUG-RESISTANCE; STEM-CELLS;
MATHEMATICAL-MODELS; CANCER-CHEMOTHERAPY; AMPLIFICATION; DIVISION;
SENSITIVITY; COMBINATION; DYNAMICS
AB In this work, we consider the problem of estimating the probability for a specific random genetic mutation to be present in a tumor of a given size. Previous mathematical models have been based on stochastic methods where the tumor was assumed to be homogeneous and, on average, growing exponentially. In contrast, we are able to obtain analytical results for cases where the exponential growth of cancer has been replaced by other, arguably more realistic types of growth of a heterogeneous tumor cell population. Our main result is that the probability that a given random mutation will be present by the time a tumor reaches a certain size, is independent of the type of curve assumed for the average growth of the tumor, at least for a general class of growth curves. The same is true for the related estimate of the expected number of mutants present in a tumor of a given size, if mutants are indeed present.
C1 [Tomasetti, Cristian] Harvard Univ, Dept Biostat, Boston, MA 02215 USA.
[Tomasetti, Cristian] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02215 USA.
RP Tomasetti, C (reprint author), Harvard Univ, Dept Biostat, CLS11007,450 Brookline Ave, Boston, MA 02215 USA.
EM cristian@jimmy.harvard.edu
OI Tomasetti, Cristian/0000-0003-3277-4804
FU National Institute of Health [T32 CA009337]; National Science
Foundation/National Institute of General Medical Sciences [DMS-0758374];
National Cancer Institute [R01CA130817]
FX The author wishes to thank Professor Dmitry Dolgopyat for his helpful
discussions and the reviewers for their valuable comments. The work of
CT was supported in part by the National Institute of Health under Grant
T32 CA009337, by the joint National Science Foundation/National
Institute of General Medical Sciences program under Grant DMS-0758374
and by the National Cancer Institute under Grant R01CA130817.
NR 36
TC 6
Z9 6
U1 1
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0092-8240
J9 B MATH BIOL
JI Bull. Math. Biol.
PD JUN
PY 2012
VL 74
IS 6
BP 1379
EP 1395
DI 10.1007/s11538-012-9717-1
PG 17
WC Biology; Mathematical & Computational Biology
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
Biology
GA 946ZD
UT WOS:000304395500005
PM 22311065
ER
PT J
AU Berkey, CS
Tamimi, RM
Rosner, B
Frazier, AL
Colditz, GA
AF Berkey, Catherine S.
Tamimi, Rulla M.
Rosner, Bernard
Frazier, A. Lindsay
Colditz, Graham A.
TI Young women with family history of breast cancer and their risk factors
for benign breast disease
SO CANCER
LA English
DT Article
DE adolescents; preteens; family history; alcohol; body mass index; height
growth spurt; peak height growth velocity; age at menarche; benign
breast disease; breast cancer
ID ALCOHOL-CONSUMPTION; NURSES HEALTH; GROWTH; AGE; ADOLESCENTS; COHORT;
GIRLS
AB BACKGROUND: Breast cancer (BC) patients wonder how their daughters might reduce their risk. The authors investigated childhood/adolescent risk factors for benign breast disease (BBD), a well-documented risk factor for BC, among girls with a family history. METHODS: GUTS (the Growing Up Today Study) includes females, aged 9 to 15 years in 1996, who completed annual questionnaires during 1996 to 2001, then in 2003, 2005, and 2007. Participants provided information regarding alcohol, menarche, height, and body mass index (BMI; kg/m2). Peak height growth velocity (PHV; in./y) was estimated from longitudinal heights. On 2005-2007 surveys, 6888 women (18-27 years old) reported whether they were diagnosed with biopsy-confirmed BBD (n = 67 cases); 6741 women (noncases) reported no BBD. Participants' mothers reported their own biopsy-confirmed BBD and BC, and BC in their sisters and mothers. Stratified by family history, logistic models investigated BBD risk factors. RESULTS: Young women whose mothers or aunts had BC were more likely to be diagnosed with BBD (odds ratio [OR], 2.34; P = .01), as were those with maternal BBD (OR, 1.59; P = .095). Adolescents with BC family history (mother, aunt, grandmother) who consumed alcohol (7 drinks/wk) doubled their BBD risk (OR, 2.28; P = .01), similar to those with maternal BBD (OR, 1.96; P = .02). Girls whose mother or aunt had BC saw their BBD risk elevated with higher PHV (OR, 1.82 [inch/yr]; P = .05). Among girls with no family history, BBD risk appeared to be related to other factors: childhood BMI, adolescent waist circumference, and adult height. CONCLUSIONS: Adolescents with family history may reduce their risk by avoiding alcohol. Separate risk factors were observed among girls with family history versus girls with no family history, possibly reflecting different causes of BC. Cancer 2011;. (c) 2011 American Cancer Society.
C1 [Berkey, Catherine S.; Tamimi, Rulla M.; Rosner, Bernard; Frazier, A. Lindsay] Brigham & Womens Hosp, Channing Lab, Dept Med, Boston, MA 02115 USA.
[Berkey, Catherine S.; Tamimi, Rulla M.; Rosner, Bernard; Frazier, A. Lindsay] Harvard Univ, Sch Med, Boston, MA USA.
[Frazier, A. Lindsay] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Colditz, Graham A.] Washington Univ, Alvin J Siteman Canc Ctr, Sch Med, St Louis, MO USA.
RP Berkey, CS (reprint author), Brigham & Womens Hosp, Channing Lab, Dept Med, 181 Longwood Ave, Boston, MA 02115 USA.
EM Catherine.Berkey@channing.harvard.edu
RI Colditz, Graham/A-3963-2009
OI Colditz, Graham/0000-0002-7307-0291
FU National Institutes of Health (Bethesda, Md) [DK46834]; Breast Cancer
Research foundation (New York, New York); American Institute for Cancer
Research; American Cancer Society
FX Grant DK46834 (principal investigator [PI], G. A. C.) from the National
Institutes of Health (Bethesda, Md) funded the initiation of the cohort
and the collection/management of the data during early years of
follow-up. The Breast Cancer Research foundation (New York, New York)
funded the design, conduct, and analysis of this specific article (PI,
G. A. C.). Neither sponsor was involved in the preparation, review, or
approval of the article. A. L. F. was supported by an award from the
American Institute for Cancer Research. G. A. C. was supported in part
by an American Cancer Society Clinical Research Professorship.
NR 33
TC 12
Z9 12
U1 0
U2 5
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 JUN 1
PY 2012
VL 118
IS 11
BP 2796
EP 2803
DI 10.1002/cncr.26519
PG 8
WC Oncology
SC Oncology
GA 944HA
UT WOS:000304188700004
PM 22083563
ER
PT J
AU Choy, E
Hornicek, F
MacConaill, L
Harmon, D
Tariq, Z
Garraway, L
Duan, ZF
AF Choy, Edwin
Hornicek, Francis
MacConaill, Laura
Harmon, David
Tariq, Zeeshan
Garraway, Levi
Duan, Zhenfeng
TI High-throughput genotyping in osteosarcoma identifies multiple mutations
in phosphoinositide-3-kinase and other oncogenes
SO CANCER
LA English
DT Article
DE genotyping; osteosarcoma; OncoMap; phosphoinositide-3-kinase; catalytic;
alpha polypeptide; mutation
ID GROWTH-FACTOR RECEPTOR; CELL LUNG-CANCER; IMATINIB MESYLATE; STAT3
PATHWAY; THERAPY; GENOME; RESISTANCE; INHIBITION; EXPRESSION; APOPTOSIS
AB BACKGROUND: The identification of new genes that are mutated in osteosarcomas is critical to developing a better understanding of the molecular pathogenesis of this disease and discovering new targets for therapeutic development. METHODS: The authors identified somatic nonsynonymous coding mutations in oncogenes associated with human cancers and hotspot mutations from tumor suppressor genes that were either well described in the literature or observed multiple times in human cancer sequencing efforts. Then, 961 mutations in 89 genes were systematically characterized across 98 osteosarcoma tumor samples and cell lines. All identified mutations were replicated on an independent platform using homogeneous mass extend matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. RESULTS: In total, 14 mutations were identified in at least 1 osteosarcoma tumor sample or cell line. Some of the genetic changes identified were in tumor suppressor genes previously identified as altered in osteosarcoma: p53 (arginine -> histidine at codon 273 [R273H], R -> cysteine at codon 723 [R273C], and tyrosine -> C at codon 163 [Y163C]) and retinoblastoma 1 (RB1) (glutamic acid ->* at codon 137 [E137*]). Notably, multiple mutations were identified in phosphoinositide-3-kinase (PI3K), catalytic, alpha polypeptide (PIK3CA) (H1047R, E -> lysine at codon 545 [E545K], and H -> proline at codon 701 [H701P]) that were not observed previously in osteosarcoma. In addition, mutations in v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) (glycine -> serine at codon 12 [G12S]); cubilin (CUBN) (isolucine -> valine at codon 3189 [I3189V]; observed in 2 separate tumor samples); cadherin 1, type 1, epithelial (CDH1) (alanine -> threonine at codon 617 [A617T]; observed in 2 separate tumor samples); catenin (cadherin-associated protein), beta 1, 88 kDa (CTNNB1) (asparagine -> S at codon 287 [N287S]); and fibrous sheath CABYR binding protein (FSCB) (S -> leucine at codon 775 [S775L]) were observed. CONCLUSIONS: In this largest mutational profiling of osteosarcoma to date, the authors identified for the first time several mutations involving the PI3K pathway, adding osteosarcoma to the growing list of malignancies with PI3K mutations. In addition, they initiated a mutational map detailing DNA sequence changes across a variety of osteosarcoma subtypes and offered new candidates for therapeutic targeting. Cancer 2011. (c) 2011 American Cancer Society.
C1 [Choy, Edwin; Harmon, David] Massachusetts Gen Hosp, Div Hematol & Oncol, Boston, MA 02114 USA.
[Choy, Edwin; Hornicek, Francis; Duan, Zhenfeng] Massachusetts Gen Hosp, Sarcoma Biol Lab, Ctr Sarcoma & Connect Tissue Oncol, Ctr Canc, Boston, MA 02114 USA.
[MacConaill, Laura; Garraway, Levi] Harvard Univ, Sch Med, Dana Farber Canc Inst, Ctr Canc Genome Discovery, Boston, MA 02115 USA.
[MacConaill, Laura; Garraway, Levi] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Tariq, Zeeshan] Univ Toledo, Dept Med, Med Ctr, Toledo, OH 43606 USA.
RP Choy, E (reprint author), Massachusetts Gen Hosp, Div Hematol & Oncol, 55 Fruit St, Boston, MA 02114 USA.
EM echoy@partners.org
OI Duan, Zhenfeng/0000-0002-8543-083X; Choy, Edwin/0000-0001-9896-8084
FU Jennifer Hunter Yates Foundation; Kenneth Stanton Osteosarcoma Research
Fund; Cassandra Moseley Berry Sarcoma Endowed Fund; Gategno Fund;
Wechsler Fund; Harvard Catalyst/The Harvard Clinical and Translational
Science Center (National Institutes of Health) [1KL2RR025757-01];
Harvard University; Amgen; Sanofi-Aventis; Novartis; Pharmacyclics
FX This project was supported in part by the Jennifer Hunter Yates
Foundation, the Kenneth Stanton Osteosarcoma Research Fund, the
Cassandra Moseley Berry Sarcoma Endowed Fund, the Gategno and Wechsler
Funds, and the KL2 Medical Research Investigator Training (MeRIT) grant
awarded to E.C. through Harvard Catalyst/The Harvard Clinical and
Translational Science Center (National Institutes of Health grant
1KL2RR025757-01), and by financial contributions from Harvard University
and its affiliated academic health care centers.; E.C. has received
financial and research support from Amgen, Sanofi-Aventis, Novartis, and
Pharmacyclics. L. G. is a consultant for Novartis and Foundation
Medicine and an equity holder in Foundation Medicine.
NR 51
TC 30
Z9 31
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
J9 CANCER-AM CANCER SOC
JI Cancer
PD JUN 1
PY 2012
VL 118
IS 11
BP 2905
EP 2914
DI 10.1002/cncr.26617
PG 10
WC Oncology
SC Oncology
GA 944HA
UT WOS:000304188700016
PM 22006429
ER
PT J
AU Kumar, A
Vanderplas, A
LaCasce, AS
Rodriguez, MA
Crosby, AL
Lepisto, E
Czuczman, MS
Nademanee, A
Niland, J
Gordon, LI
Millenson, M
Zelenetz, AD
Friedberg, JW
Abel, GA
AF Kumar, Anita
Vanderplas, Ann
LaCasce, Ann S.
Rodriguez, Maria A.
Crosby, Allison L.
Lepisto, Eva
Czuczman, Myron S.
Nademanee, Auayporn
Niland, Joyce
Gordon, Leo I.
Millenson, Michael
Zelenetz, Andrew D.
Friedberg, Jonathan W.
Abel, Gregory A.
TI Lack of benefit of central nervous system prophylaxis for diffuse large
B-cell lymphoma in the rituximab era
SO CANCER
LA English
DT Article
DE diffuse large B-cell lymphoma; central nervous system prophylaxis;
propensity score analysis; health services research
ID NON-HODGKINS-LYMPHOMA; STUDY-GROUP DSHNHL; RISK-FACTORS;
ELDERLY-PATIENTS; INTRATHECAL CHEMOTHERAPY; AGGRESSIVE LYMPHOMA;
INTERMEDIATE-GRADE; CHOP CHEMOTHERAPY; CNS PROPHYLAXIS; RELAPSE
AB BACKGROUND: Little is known about the utility of central nervous system (CNS) prophylaxis for diffuse large B-cell lymphoma (DLBCL) in the rituximab era. The objective of this study was to characterize patterns of CNS prophylaxis for patients who received combined rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) chemotherapy using the National Comprehensive Cancer Network Non-Hodgkin Lymphoma Outcomes Database, a prospective cohort study that collects clinical and outcomes data for patients at 7 participating centers. METHODS: Patients who were eligible for this analysis presented with newly diagnosed DLBCL between January 2001 and July 2008, had no evidence of baseline CNS disease, and had received R-CHOP within 180 days of diagnosis. The authors assessed incidence and covariates of prophylaxis, prophylaxis modality, and, using propensity score analysis, outcomes such as overall survival. RESULTS: Of 989 eligible patients, 117 received CNS prophylaxis (11.8%), most intrathecally (71.8%). Involvement of bone marrow, other high-risk site, >1 extranodal site, higher International Prognostic Index score, and higher stage were associated individually with the receipt of prophylaxis (all P < .0001). At a median follow-up of 2.5 years, there were 20 CNS recurrences (2% [95% confidence interval, 1.1%-2.9%]) among all patients, and overall survival was not affected by prophylaxis. CONCLUSIONS: Given the overall low rate of CNS recurrence and lack of prophylaxis-associated survival benefit, the current data called into question the practice of CNS prophylaxis in the rituximab era. Cancer 2011. (c) 2011 American Cancer Society.
C1 [Crosby, Allison L.; Abel, Gregory A.] Dana Farber Canc Inst, Div Populat Sci, Dept Med Oncol, Boston, MA 02215 USA.
[Vanderplas, Ann; Niland, Joyce] City Hope Natl Med Ctr, Div Informat Sci, Duarte, CA 91010 USA.
[Nademanee, Auayporn] City Hope Natl Med Ctr, Div Hematol & Bone Marrow Transplantat, Duarte, CA 91010 USA.
[LaCasce, Ann S.] Dana Farber Canc Inst, Div Hematol Malignancies, Dept Med Oncol, Boston, MA 02115 USA.
[Rodriguez, Maria A.] Univ Texas MD Anderson Canc Ctr, Dept Lymphoma Myeloma, Houston, TX 77030 USA.
[Czuczman, Myron S.] Roswell Pk Canc Inst, Div Med, Buffalo, NY 14263 USA.
[Gordon, Leo I.] Robert H Lurie Comprehens Canc Ctr, Div Hematol Oncol, Chicago, IL USA.
[Millenson, Michael] Fox Chase Canc Ctr, Dept Med Oncol, Philadelphia, PA 19111 USA.
[Zelenetz, Andrew D.] Mem Sloan Kettering Canc Ctr, Lymphoma Serv, New York, NY 10021 USA.
[Friedberg, Jonathan W.] James P Wilmot Canc Ctr, Div Hematol Oncol, Rochester, NY USA.
[Lepisto, Eva] Natl Comprehens Canc Network, NCCN VP Technol Res & Dev, Ft Washington, MD USA.
[Kumar, Anita; LaCasce, Ann S.; Abel, Gregory A.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
RP Abel, GA (reprint author), Dana Farber Canc Inst, Div Populat Sci, Dept Med Oncol, Boston, MA 02215 USA.
EM gregory_abel@dfci.harvard.edu
NR 27
TC 32
Z9 33
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
J9 CANCER-AM CANCER SOC
JI Cancer
PD JUN 1
PY 2012
VL 118
IS 11
BP 2944
EP 2951
DI 10.1002/cncr.26588
PG 8
WC Oncology
SC Oncology
GA 944HA
UT WOS:000304188700020
PM 22006274
ER
PT J
AU Corey, KE
Lai, M
Gelrud, LG
Misdraji, J
Barlow, LL
Zheng, H
Andersson, KL
Thiim, M
Pratt, DS
Chung, RT
AF Corey, Kathleen E.
Lai, Michelle
Gelrud, Louis G.
Misdraji, Joseph
Barlow, Lydia L.
Zheng, Hui
Andersson, Karin L.
Thiim, Michael
Pratt, Daniel S.
Chung, Raymond T.
TI Non-High-Density Lipoprotein Cholesterol as a Biomarker for Nonalcoholic
Steatohepatitis
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Diagnostic; Nonalcoholic Fatty Liver Disease; Blood Test; Clinical Trial
ID FATTY LIVER-DISEASE; NON-HDL CHOLESTEROL; TRIGLYCERIDE SYNTHESIS;
HEPATIC STEATOSIS; RISK; ATORVASTATIN
AB BACKGROUND & AIMS: There are no clinically available biomarkers for nonalcoholic steatohepatitis (NASH); differentiating between steatosis and NASH requires histologic evaluation. Noninvasive methods are needed to replace liver biopsy and its associated risks. Production of very low density lipoprotein (VLDL) contributes to the development of NASH and might be used to distinguish steatosis from NASH. However, it is not possible to measure levels of VLDL directly in the clinic. Non-high-density lipoprotein-cholesterol (non-HDL-C) encompasses all apolipoprotein-B-containing lipoproteins, including VLDL, and can be calculated from standard lipid panels without additional cost. METHODS: We evaluated the ability of non-HDL-C to differentiate steatosis from NASH in a prospective study of 218 patients with suspected NASH (steatosis, n = 100 and NASH, n = 118). RESULTS: Patients with NASH had a trend toward increased levels of non-HDL-C, compared with those with steatosis (P = .08). However, among subjects not on lipid-lowering medications, those with NASH had significantly higher levels of non-HDL-C (144.6 mg/dL) than those with steatosis (129.3 mg/dL; P = .025). This difference remained significant when adjusted for levels of cholesterol and triglycerides, indicating that the difference results from increased levels of apolipoprotein B including VLDL. These findings were validated in a cohort of 40 patients with steatosis or NASH who were not taking lipid-lowering agents. The NASH group had significantly higher levels of non-HDL-C than the steatosis group (162.8 vs 145.9 mg/dL; P = .04). CONCLUSIONS: NASH is associated with significantly higher levels of non-HDL-C than steatosis in patients who do not take lipid-lowering agents. This low-cost biomarker could be used in noninvasive differentiation between steatosis and NASH.
C1 [Corey, Kathleen E.; Barlow, Lydia L.; Andersson, Karin L.; Thiim, Michael; Pratt, Daniel S.; Chung, Raymond T.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[Misdraji, Joseph] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Zheng, Hui; Chung, Raymond T.] Massachusetts Gen Hosp, MGH Biostat Ctr, Boston, MA 02114 USA.
[Corey, Kathleen E.; Lai, Michelle; Misdraji, Joseph; Zheng, Hui; Andersson, Karin L.; Thiim, Michael; Pratt, Daniel S.; Chung, Raymond T.] Harvard Univ, Sch Med, Boston, MA USA.
[Lai, Michelle] Beth Israel Deaconess Med Ctr, Div Gastroenterol, Boston, MA 02215 USA.
[Gelrud, Louis G.] Bon Secours Richmond Hlth Syst, Dept Internal Med, Richmond, VA USA.
RP Chung, RT (reprint author), Massachusetts Gen Hosp, Gastrointestinal Unit, Warren 1007,55 Fruit St, Boston, MA 02114 USA.
EM rtchung@partners.org
FU American Association for the Study of Liver Disease; NIDDK
[5K23DK83439-2]; NIH [DK078772]
FX K.E.C. receives support from the American Association for the Study of
Liver Disease. M.L. received support from the NIDDK K23 grant number
5K23DK83439-2. R.T.C. receives support from NIH DK078772.
NR 28
TC 19
Z9 19
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1542-3565
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD JUN
PY 2012
VL 10
IS 6
BP 651
EP 656
DI 10.1016/j.cgh.2012.01.017
PG 6
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 948QJ
UT WOS:000304517400019
PM 22330232
ER
PT J
AU Saylor, PJ
Escudier, B
Michaelson, MD
AF Saylor, Philip J.
Escudier, Bernard
Michaelson, M. Dror
TI Importance of Fibroblast Growth Factor Receptor in Neovascularization
and Tumor Escape from Antiangiogenic Therapy
SO CLINICAL GENITOURINARY CANCER
LA English
DT Review
DE Angiogenesis; Cell signaling; Renal cell carcinoma; Vascular endothelial
growth factor receptor
ID RENAL-CELL CARCINOMA; PHASE-III TRIAL; TYROSINE KINASE INHIBITOR;
ENDOTHELIAL-CELLS; IN-VITRO; INTERFERON-ALPHA; SUPPRESSOR GENE; BINDING
PROTEIN; DOUBLE-BLIND; ANGIOGENESIS
AB Therapeutic inhibition of pathways involved in angiogenesis has become the standard of care in renal cell carcinoma (RCC). Most currently available antiangiogenic agents inhibit the vascular endothelial growth factor (VEGF) pathway. Although these drugs have produced exciting benefits, some tumors do not respond to these agents. In addition most if not all tumors that initially respond will eventually develop resistance. Tumor escape from antiangiogenic therapy may include various signaling pathways that are involved in angiogenesis, including the fibroblast growth factor (FGF) signaling pathway. Emerging preclinical data suggest that FGF and VEGF act distinctly and synergistically to promote tumor vascularization. The current review discusses the role of FGF signaling in resistance to anti-VEGF therapies and outlines potential therapeutic implications. Clinical Genitourinary Cancer, Vol. 10, No. 2, 77-83 (c) 2012 Elsevier Inc. All rights reserved.
C1 [Michaelson, M. Dror] Massachusetts Gen Hosp, Ctr Canc, Div Hematol Oncol, Boston, MA 02114 USA.
[Escudier, Bernard] Inst Gustave Roussy, Villejuif, France.
RP Michaelson, MD (reprint author), Massachusetts Gen Hosp, Ctr Canc, Div Hematol Oncol, Yawkey 7E, Boston, MA 02114 USA.
EM dmichaelson1@partners.org
OI Michaelson, Dror/0000-0001-9249-6338
FU Novartis Pharmaceuticals
FX Financial support for medical editorial assistance was provided by
Novartis Pharmaceuticals.
NR 80
TC 21
Z9 21
U1 0
U2 8
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1558-7673
J9 CLIN GENITOURIN CANC
JI Clin. Genitourin. Cancer
PD JUN
PY 2012
VL 10
IS 2
BP 77
EP 83
DI 10.1016/j.clgc.2012.01.010
PG 7
WC Oncology; Urology & Nephrology
SC Oncology; Urology & Nephrology
GA 944LG
UT WOS:000304202600003
PM 22382009
ER
PT J
AU Liu, G
Chen, YH
DiPaola, R
Carducci, M
Wilding, G
AF Liu, Glenn
Chen, Yu-Hui
DiPaola, Robert
Carducci, Michael
Wilding, George
TI Phase II Trial of Weekly Ixabepilone in Men With Metastatic
Castrate-Resistant Prostate Cancer (E3803): A Trial of the Eastern
Cooperative Oncology Group
SO CLINICAL GENITOURINARY CANCER
LA English
DT Article
DE BMS-247550; Chemotherapy; Epothilone; Microtubule-inhibitor;
NCT00087139; Version date; 2/20/2011
ID EPOTHILONE-B-ANALOG; ADVANCED SOLID TUMORS; ESTRAMUSTINE PHOSPHATE;
WEEKLY DOCETAXEL; 1-HOUR INFUSION; CLINICAL-TRIALS; DAILY SCHEDULE;
WORKING GROUP; BMS-247550; MITOXANTRONE
AB Ixabepilone is an epothilone B analogue with activity in a variety of solid malignancies, including prostate cancer. The main dose-limiting toxicity of ixabepilone is myelosuppression when administered by using an every 3-week schedule. Here we evaluate the activity of a weekly ixabepilone in men with metastatic castrate-resistant prostate cancer to minimize hematologic toxicity.
Purpose: BMS-247550 (ixabepilone) is an epothilone B analogue with activity in taxane-resistant cancer cell lines. Here we report the activity and toxicity of ixabepilone, administered by using a weekly schedule, in men with metastatic castrate-resistant prostate cancer (CRPC). Experimental Design: Patients with metastatic CRPC received ixabepilone at 20 mg/m(2) intravenous weekly x 3, in 4-week cycles. This noncomparative study stratified patients to either a chemotherapy naive (CN), prior taxane (Tax) only, or 2 prior cytotoxic (TCx) chemotherapy arm. The primary endpoint was prostate-specific antigen response by using PCWG (Prostate Cancer Working Group) 1 criteria. Secondary endpoints included radiographic response when using RECIST (Response Evaluation Criteria In Solid Tumors). Results: In total, 124 patients were enrolled, of whom, 109 were eligible (35 CN, 42 Tax, and 32 TCx) for the primary response determination in this study. Prostate-specific antigen responses were seen in 12 (34.3%) of 35, 12 (28.6%) of 42, and 7 (21.9%) of 32 patients with the partial objective response in 5 (22.7%) of 22, 2 (8.0%) of 25, and 0 (0.0%) of 24 patients for the CN, Tax, and TCx arms, respectively. Significant (grade 3/4) neutropenia was seen in 6 (15.4%), 7 (14.6%), and 9 (25.0%); and grade 3/4 sensory neuropathy was seen in 8 (20.5%), 12 ( 25.0%), and 12 (33.3%) for CN, Tax, and TCx, respectively. Grade 3/4 thrombocytopenia was infrequent and seen in only one patient on the CN and the TCx arm. Conclusion: Ixabepilone was found to have an acceptable toxicity profile when administered by using a weekly schedule with less myelosuppression compared with prior studies when using the every 3-week schedule. Single-agent activity was observed and met prespecified activity levels for the Tax treated arm. Clinical Genitourinary Cancer, Vol. 10, No. 2, 99-105 (c) 2012 Published by Elsevier Inc.
C1 [Liu, Glenn] Univ Wisconsin, Carbone Canc Ctr, Wisconsin Inst Med Res, Madison, WI 53705 USA.
[Chen, Yu-Hui] Dana Farber Canc Inst, Boston, MA 02115 USA.
[DiPaola, Robert] Canc Inst New Jersey, New Brunswick, NJ USA.
[Carducci, Michael] Johns Hopkins Kimmel Canc Ctr, Baltimore, MD USA.
RP Liu, G (reprint author), Univ Wisconsin, Carbone Canc Ctr, Wisconsin Inst Med Res, 1111 Highland Ave,Room 7051, Madison, WI 53705 USA.
EM gxl@medicine.wisc.edu
FU NCI NIH HHS [CA66636, U10 CA016116, CA107868, CA23318, U10 CA021076, U10
CA080775, CA21076, U10 CA066636, U10 CA023318, U10 CA021115, P30
CA016672, CA21115, U10 CA107868, CA16116, CA80775]
NR 26
TC 12
Z9 12
U1 1
U2 2
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1558-7673
EI 1938-0682
J9 CLIN GENITOURIN CANC
JI Clin. Genitourin. Cancer
PD JUN
PY 2012
VL 10
IS 2
BP 99
EP 105
DI 10.1016/j.clgc.2012.01.009
PG 7
WC Oncology; Urology & Nephrology
SC Oncology; Urology & Nephrology
GA 944LG
UT WOS:000304202600006
PM 22386239
ER
PT J
AU Calfee, CS
Gallagher, D
Abbott, J
Thompson, BT
Matthay, MA
AF Calfee, Carolyn S.
Gallagher, Diana
Abbott, Jason
Thompson, B. Taylor
Matthay, Michael A.
CA NHLBI ARDS Network
TI Plasma angiopoietin-2 in clinical acute lung injury: Prognostic and
pathogenetic significance
SO CRITICAL CARE MEDICINE
LA English
DT Article
DE acute respiratory distress syndrome; angiopoietin-2; biomarkers;
endothelial injury; pulmonary edema; von Willebrand factor
ID RESPIRATORY-DISTRESS-SYNDROME; VON-WILLEBRAND-FACTOR; CIRCULATING
ANGIOPOIETIN-2; CRITICALLY-ILL; FACTOR ANTIGEN; MORTALITY; RISK;
VENTILATION; PREDICTOR; SEPSIS
AB Background: Angiopoietin-2 is a proinflammatory mediator of endothelial injury in animal models, and increased plasma angiopoietin-2 levels are associated with poor outcomes in patients with sepsis-associated acute lung injury. Whether angiopoietin-2 levels are modified by treatment strategies in patients with acute lung injury is unknown.
Objectives: To determine whether plasma angiopoietin-2 levels are associated with clinical outcomes and affected by fluid management strategy in a broad cohort of patients with acute lung injury.
Design, Setting, and Participants:Plasma levels of angiopoietin-2 and von Willebrand factor (a traditional marker of endothelial injury) were measured in 931 subjects with acute lung injury enrolled in a randomized trial of fluid liberal vs. fluid conservative management.
Measurements and Main Results: The presence of infection (sepsis or pneumonia) as the primary acute lung injury risk factor significantly modified the relationship between baseline angiopoietin-2 levels and mortality (p = .01 for interaction). In noninfection-related acute lung injury, higher baseline angiopoietin-2 levels were strongly associated with increased mortality (odds ratio, 2.43 per 1-log increase in angiopoietin-2; 95% confidence interval, 1.57-3.75; p < .001). In infection-related acute lung injury, baseline angiopoietin-2 levels were similarly elevated in survivors and nonsurvivors; however, patients whose plasma angiopoietin-2 levels increased from day 0 to day 3 had more than double the odds of death compared with patients whose angiopoietin-2 levels declined over the same period of time (odds ratio, 2.29; 95% confidence interval, 1.54-3.43; p < .001). Fluid-conservative therapy led to a 15% greater decline in angiopoietin-2 levels from day 0 to day 3 (95% confidence interval, 4.6-24.8%; p = .006) compared with fluid-liberal therapy in patients with infection-related acute lung injury. In contrast, plasma levels of von Willebrand factor were significantly associated with mortality in both infection-related and noninfection-related acute lung injury and were not affected by fluid therapy.
Conclusions: Unlike von Willebrand factor, plasma angiopoietin-2 has differential prognostic value for mortality depending on the presence or absence of infection as an acute lung injury risk factor. Fluid conservative therapy preferentially lowers plasma angiopoietin-2 levels over time and thus may be beneficial in part by decreasing endothelial inflammation. (Crit Care Med 2012; 40:1731-1737)
C1 [Calfee, Carolyn S.; Matthay, Michael A.] Univ Calif San Francisco, Dept Med, Div Pulm & Crit Care Med, San Francisco, CA 94143 USA.
[Calfee, Carolyn S.; Abbott, Jason; Matthay, Michael A.] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA.
[Calfee, Carolyn S.; Matthay, Michael A.] Univ Calif San Francisco, Dept Anesthesia, San Francisco, CA 94143 USA.
[Gallagher, Diana] Beth Israel Deaconess Med Ctr, Dept Med, Div Pulm Crit Care & Sleep, Boston, MA 02215 USA.
[Thompson, B. Taylor] Massachusetts Gen Hosp, Dept Med, Pulm & Crit Care Med Unit, Boston, MA 02114 USA.
[Thompson, B. Taylor] Massachusetts Gen Hosp, Biostat Unit, Boston, MA 02114 USA.
RP Calfee, CS (reprint author), Univ Calif San Francisco, Dept Med, Div Pulm & Crit Care Med, San Francisco, CA 94143 USA.
EM carolyn.calfee@ucsf.edu
FU National Heart, Lung, and Blood Institute (NHLBI) [N01-HR 46046-64,
N01-HR-16146-54]; Flight Attendant Medical Research Institute; NCRR, a
component of the NIH [KL2RR024130]; [HL090833]; [HL 51856]
FX Supported, in part, by contracts (N01-HR 46046-64 and N01-HR-16146-54)
with the National Heart, Lung, and Blood Institute (NHLBI). Dr. Calfee
was supported by HL090833, by the Flight Attendant Medical Research
Institute, and by KL2RR024130 from the NCRR, a component of the NIH. Dr.
Matthay was supported by HL 51856.
NR 21
TC 58
Z9 64
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
J9 CRIT CARE MED
JI Crit. Care Med.
PD JUN
PY 2012
VL 40
IS 6
BP 1731
EP 1737
DI 10.1097/CCM.0b013e3182451c87
PG 7
WC Critical Care Medicine
SC General & Internal Medicine
GA 946EZ
UT WOS:000304335600006
PM 22610178
ER
PT J
AU Wilcox, SR
Bittner, EA
Elmer, J
Seigel, TA
Nguyen, NTP
Dhillon, A
Eikermann, M
Schmidt, U
AF Wilcox, Susan R.
Bittner, Edward A.
Elmer, Jonathan
Seigel, Todd A.
Nguyen, Nicole Thuy P.
Dhillon, Anahat
Eikermann, Matthias
Schmidt, Ulrich
TI Neuromuscular blocking agent administration for emergent tracheal
intubation is associated with decreased prevalence of procedure-related
complications
SO CRITICAL CARE MEDICINE
LA English
DT Article
DE airway management; anoxia; emergency treatment; hypoxia; intubation;
neuromuscular blockade
ID INTENSIVE-CARE-UNIT; DIFFICULT AIRWAY MANAGEMENT; RAPID-SEQUENCE
INTUBATION; ENDOTRACHEAL INTUBATION; MULTIPLE-CENTER; ROCURONIUM;
INDUCTION; ANESTHESIA; SUCCINYLCHOLINE; SEVOFLURANE
AB Background: Emergent intubation is associated with a high rate of complications. Neuromuscular blocking agents are routinely used in the operating room and emergency department to facilitate intubation. However, use of neuromuscular blocking agents during emergent airway management outside of the operating room and emergency department is controversial. We hypothesized that the use of neuromuscular blocking agents is associated with a decreased prevalence of hypoxemia and reduced rate of procedure-related complications.
Methods: Five hundred sixty-six patients undergoing emergent intubations in two tertiary care centers, Massachusetts General Hospital, Boston, MA, and the University of California Los Angeles, Ronald Reagan Medical Center, Los Angeles, CA, were enrolled in a prospective, observational study. The 112 patients intubated during cardiopulmonary resuscitation were excluded, leaving 454 patients for analysis. All intubations were supervised by attendings trained in Critical Care Medicine. We measured intubating conditions, oxygen saturation during and 5 mins following intubation. We assessed the prevalence of procedure-related complications defined as esophageal intubation, traumatic intubation, aspiration, dental injury, and endobronchial intubation.
Results: The use of neuromuscular blocking agents was associated with a lower prevalence of hypoxemia (10.1% vs. 17.4%, p = .022) and a lower prevalence of procedure-related complications (3.1% vs. 8.3%, p = .012). This association persisted in a multivariate analysis, which controlled for airway grade, sedation, and institution. Use of neuromuscular blocking agents was associated with significantly improved intubating conditions (laryngeal view, p = .014; number of intubation attempts, p = .049). After controlling for the number of intubation attempts and laryngoscopic view, muscle relaxant use is an independent predictor of complications associated with emergency intubation (p = .037), and there is a trend towards improvement of oxygenation (p = .07).
Conclusion: The use of neuromuscular blocking agents, when used by intensivists with a high level of training and experience, is associated with a decrease in procedure-related complications. (Crit Care Med 2012; 40:1808-1813)
C1 [Wilcox, Susan R.; Bittner, Edward A.; Elmer, Jonathan; Eikermann, Matthias] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Wilcox, Susan R.] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
[Elmer, Jonathan] Brigham & Womens Hosp, Dept Emergency Med, Boston, MA 02115 USA.
[Seigel, Todd A.] Brown Univ, Rhode Isl Hosp, Warren Alpert Sch Med, Dept Emergency Med, Providence, RI 02903 USA.
[Nguyen, Nicole Thuy P.] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Dhillon, Anahat] Univ Calif Los Angeles, Dept Anesthesia, Ronald Reagan Med Ctr, Los Angeles, CA USA.
RP Wilcox, SR (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
EM swilcox1@partners.org
OI Wilcox, Susan/0000-0001-7477-7531
FU Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts
General Hospital, Boston, MA
FX This work was funded by the Department of Anesthesia, Critical Care and
Pain Medicine, Massachusetts General Hospital, Boston, MA.
NR 33
TC 33
Z9 37
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
J9 CRIT CARE MED
JI Crit. Care Med.
PD JUN
PY 2012
VL 40
IS 6
BP 1808
EP 1813
DI 10.1097/CCM.0b013e31824e0e67
PG 6
WC Critical Care Medicine
SC General & Internal Medicine
GA 946EZ
UT WOS:000304335600016
PM 22610185
ER
PT J
AU Glynn, SM
AF Glynn, Shirley M.
TI Family Interventions in Schizophrenia: Promise and Pitfalls over 30
Years
SO CURRENT PSYCHIATRY REPORTS
LA English
DT Article
DE Schizophrenia; Family treatment; Psychosocial interventions; Family
therapy; Family interventions; Psychosis; Evidence-based practice;
Relatives
ID RANDOMIZED CONTROLLED-TRIAL; COGNITIVE-BEHAVIOR THERAPY; SUBSTANCE USE
DISORDERS; SERIOUS MENTAL-ILLNESS; TREATMENT RECOMMENDATIONS; RELATIVES;
PROGRAM; EDUCATION; RECOVERY; OUTCOMES
AB The stress of living with unpredictable, disturbing schizophrenic symptoms can erode interpersonal relationships. Stressful family interactions are associated with poorer prognosis. Several investigators have developed educational or more intensive skills-based family programs to increase illness knowledge and improve prognosis in schizophrenia. An extensive body of research supports the benefits of participating in family-based treatments for schizophrenia, especially those of longer duration and emphasizing skill development, in reducing relapse rates. In spite of the data, these programs are underimplemented and underutilized. Barriers to their use likely arise from patients, relatives, and mental health professionals. Newer programs, which include novel engagement strategies, target subpopulations with poor prognoses, or use innovative technologies, may make these programs more accessible to a wider range of families. Engaging individuals with schizophrenia and their loved ones in a collaborative effort to design new, more consumer-driven family interventions is warranted.
C1 Univ Calif Los Angeles, VA Greater Los Angeles Healthcare Syst W Los Ange, Semel Inst, Los Angeles, CA 90073 USA.
RP Glynn, SM (reprint author), Univ Calif Los Angeles, VA Greater Los Angeles Healthcare Syst W Los Ange, Semel Inst, B151j,11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM sglynn@ucla.edu
NR 49
TC 7
Z9 7
U1 5
U2 30
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1523-3812
J9 CURR PSYCHIAT REP
JI Curr. Psychiatry Rep.
PD JUN
PY 2012
VL 14
IS 3
BP 237
EP 243
DI 10.1007/s11920-012-0265-z
PG 7
WC Psychiatry
SC Psychiatry
GA 940AL
UT WOS:000303862300011
PM 22437626
ER
PT J
AU Zuleger, CL
Albertini, MR
AF Zuleger, Cindy L.
Albertini, Mark R.
TI OMIP-008: Measurement of Th1 and Th2 cytokine polyfunctionality of human
T cells
SO CYTOMETRY PART A
LA English
DT Article
DE immunophenotype; T cells; intracellular cytokine staining; melanoma
C1 [Albertini, Mark R.] William S Middleton Mem Vet Adm Med Ctr, Med Serv, Madison, WI 53705 USA.
[Zuleger, Cindy L.; Albertini, Mark R.] Univ Wisconsin, Carbone Canc Ctr, Madison, WI USA.
[Zuleger, Cindy L.] Univ Wisconsin, Sch Med & Publ Hlth, Dept Dermatol, Madison, WI USA.
[Albertini, Mark R.] Univ Wisconsin, Dept Med, Sch Med & Publ Hlth, Madison, WI USA.
RP Albertini, MR (reprint author), William S Middleton Mem Vet Adm Med Ctr, Med Serv, Room B-5057,2500 Overlook Terrace, Madison, WI 53705 USA.
EM mralbert@wisc.edu
FU National Cancer Institute [P30 CA014520]; Office of Research and
Development, Biomedical Laboratory Research and Development Service,
Department of Veterans Affairs; Gretchen and Andrew Dawes Melanoma
Research Fund; Ann's Hope Foundation; Steve Leuthold Family; U.S. PHS
[T32AR055893]; Tim Eagle Memorial
FX Grant sponsor: National Cancer Institute; Grant number: P30 CA014520;
Grant sponsors: Office of Research and Development, Biomedical
Laboratory Research and Development Service, Department of Veterans
Affairs; Gretchen and Andrew Dawes Melanoma Research Fund; Ann's Hope
Foundation; Jay Van Sloan Memorial from the Steve Leuthold Family; Tim
Eagle Memorial. Grant sponsor: CLZ was supported by a postdoctoral
fellowship by U.S. PHS; Grant number: T32AR055893.
NR 5
TC 5
Z9 5
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4922
J9 CYTOM PART A
JI Cytom. Part A
PD JUN
PY 2012
VL 81A
IS 6
BP 450
EP 452
DI 10.1002/cyto.a.22035
PG 3
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 945FO
UT WOS:000304258400005
PM 22431369
ER
PT J
AU Lopes-Virella, MF
Baker, NL
Hunt, KJ
Lyons, TJ
Jenkins, AJ
Virella, G
AF Lopes-Virella, Maria F.
Baker, Nathaniel L.
Hunt, Kelly J.
Lyons, Timothy J.
Jenkins, Alicia J.
Virella, Gabriel
CA DCCT EDIC Study Grp
TI High Concentrations of AGE-LDL and Oxidized LDL in Circulating Immune
Complexes Are Associated With Progression of Retinopathy in Type 1
Diabetes
SO DIABETES CARE
LA English
DT Article
ID INTIMA-MEDIA THICKNESS; COMPLICATIONS TRIAL; ADVANCED GLYCATION; HUMAN
MACROPHAGES; MELLITUS; EPIDEMIOLOGY; LIPOPROTEIN; PRODUCTS; CELLS;
INFLAMMATION
AB OBJECTIVE-To determine whether immunocomplexes (ICs) containing advanced glycation end product (AGE)-LDL (AGE-LDL) and oxidized LDL (oxLDL) contribute to the development of retinopathy over a 16-year period in subjects with type 1 diabetes.
RESEARCH DESIGN AND METHODS-Levels of AGE-LDL and oxLDL in ICs were measured in 517 patients of the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) cohort. Retinopathy was assessed by stereoscopic fundus photography. Cox proportional hazards models were used to assess the effect of AGE-LDL-ICs and oxLDL-ICs on retinopathy progression.
RESULTS-In unadjusted models, higher baseline levels of AGE-LDL-ICs and oxLDL-ICs significantly predicted progression of diabetic retinopathy outcomes. After adjustment by study-design variables (treatment group, retinopathy cohort, duration of type 1 diabetes, and baseline albumin excretion rate [AER], hemoglobin A(1c) (HbA(1c)), and Early Treatment Diabetic Retinopathy Study [ETDRS] score), one SD increase in IC levels was associated with 47% (hazard ratio [HR] 1.47 [95% CI 1.19-1.81]; AGE-LDL-IC) and 45% (1.45 [1.17-1.80]; oxLDL-IC) increased risk of developing proliferative diabetic retinopathy (PDR) and 37% (1.37 [1.12-1.66]; to both ICs) increased risk of progressing to severe nonproliferative retinopathy. Analyses were stratified by retinopathy cohort because results differed between primary and secondary cohorts. For AGE-LDL-ICs, FIR for progression to PDR was 2.38 (95% CI 1.30-4.34) in the primary cohort and attenuated in the secondary cohort (1.29 [1.03-1.62]). Similar results were observed for oxLDL-ICs.
CONCLUSIONS-Increased levels of AGE-LDL and oxLDL in ICs are associated with increased risk for progression to advanced retinopathy in patients with type 1 diabetes, indicating that the antibody response to modified LDL plays a significant role in retinopathy progression.
C1 [Lopes-Virella, Maria F.; Baker, Nathaniel L.; Hunt, Kelly J.] Med Univ S Carolina, Dept Med, Charleston, SC 29425 USA.
[Lopes-Virella, Maria F.; Hunt, Kelly J.] Ralph H Johnson VA Med Ctr, Charleston, SC USA.
[Lyons, Timothy J.; Jenkins, Alicia J.] Univ Oklahoma, Hlth Sci Ctr, Harold Hamm Oklahoma Diabet Ctr, Oklahoma City, OK USA.
[Lyons, Timothy J.; Jenkins, Alicia J.] Univ Oklahoma, Hlth Sci Ctr, Sect Endocrinol & Diabet, Oklahoma City, OK USA.
[Virella, Gabriel] Med Univ S Carolina, Dept Microbiol & Immunol, Charleston, SC 29425 USA.
RP Lopes-Virella, MF (reprint author), Med Univ S Carolina, Dept Med, Charleston, SC 29425 USA.
EM virellam@musc.edu
FU National Institutes of Health(NIH)/National Heart, Lung, and Blood
Institute [P01-HL-55782]; NIH/National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK) [R01-DK-081352, R01-DK-088778];
Juvenile Diabetes Research Foundation [2006-49]; Research Service of the
Ralph H. Johnson VA Medical Center; Division of Diabetes, Endocrinology,
and Metabolic Diseases (NIDDK) of the NIH; National Center for Research
Resources; Genentech Inc.; NIDDK
FX This work was supported by a Program Project funded by the National
Institutes of Health(NIH)/National Heart, Lung, and Blood Institute
(P01-HL-55782), R01 grants funded by NIH/National Institute of Diabetes
and Digestive and Kidney Diseases (NIDDK) (R01-DK-081352 and
R01-DK-088778), and by a Juvenile Diabetes Research Foundation grant
(2006-49). This work was also supported by the Research Service of the
Ralph H. Johnson VA Medical Center. The DCCT/EDIC was sponsored through
research contracts from the Division of Diabetes, Endocrinology, and
Metabolic Diseases (NIDDK) of the NIH. Additional support was provided
by the National Center for Research Resources through the General
Clinical Research Centers program and by Genentech Inc., through a
Cooperative Research and Development Agreement with the NIDDK. No other
potential conflicts of interest relevant to this article were reported.
NR 41
TC 20
Z9 21
U1 0
U2 6
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
EI 1935-5548
J9 DIABETES CARE
JI Diabetes Care
PD JUN
PY 2012
VL 35
IS 6
BP 1333
EP 1340
DI 10.2337/dc11-2040
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 950DY
UT WOS:000304631000023
PM 22511260
ER
PT J
AU de Boer, IH
Katz, R
Chonchol, MB
Fried, LF
Ix, JH
Kestenbaum, B
Mukamal, KJ
Peralta, CA
Siscovick, DS
AF de Boer, Ian H.
Katz, Ronit
Chonchol, Michel B.
Fried, Linda F.
Ix, Joachim H.
Kestenbaum, Bryan
Mukamal, Kenneth J.
Peralta, Carmen A.
Siscovick, David S.
TI Insulin Resistance, Cystatin C, and Mortality Among Older Adults
SO DIABETES CARE
LA English
DT Article
ID HOMEOSTASIS MODEL ASSESSMENT; INCIDENT CARDIOVASCULAR-DISEASE; CHRONIC
KIDNEY-DISEASE; METABOLIC SYNDROME; SERUM CREATININE; HEART-DISEASE;
RISK; POPULATION; HYPERINSULINEMIA; INDIVIDUALS
AB OBJECTIVE-Insulin resistance is a risk factor for cardiovascular and noncardiovascular diseases. Impaired kidney function is linked with insulin resistance and may affect relationships of insulin resistance with health outcomes.
RESEARCH DESIGN AND METHODS-We performed a cohort study of 3,138 Cardiovascular Health Study participants (age >= 65years) without diabetes. Insulin sensitivity index (ISI) was calculated from fasting and 2-h postload insulin and glucose concentrations. Associations of ISI and fasting insulin concentration with all-cause mortality were tested using Cox proportional hazards models, adjusting for demographic variables, prevalent cardiovascular disease, lifestyle variables, waist circumference, and LDL cholesterol. Subsequent models were additionally adjusted for or stratified by glomerular filtration rate estimated using serum cystatin C (eGFR).
RESULTS-A total of 1,810 participants died during the 14.7-year median follow-up. Compared with the highest quartile of ISI, the lowest quartile (most insulin resistant) was associated with 21% (95% CI 6-41) and 11% (-3 to 29) higher risks of death without and with adjustment for eGFR, respectively. Compared with the lowest quartile of fasting insulin concentration, the highest quartile was associated with 22% (4-43) and 4% (-12 to 22) higher risks of death without and with adjustment for eGFR, respectively. Similar attenuation by eGFR was observed when blood pressure, triglycerides, HDL cholesterol, and C-reactive protein were included in models.
CONCLUSIONS-Insulin resistance measured as ISI or fasting insulin concentration is associated with increased risk of death among older adults, adjusting for conventional confounding characteristics. Impaired kidney function may mediate or confound this relationship. Diabetes Care 35:1355-1360,2012
C1 [de Boer, Ian H.; Katz, Ronit; Kestenbaum, Bryan; Siscovick, David S.] Univ Washington, Seattle, WA 98195 USA.
[Chonchol, Michel B.] Univ Colorado, Denver, CO 80202 USA.
[Fried, Linda F.] Vet Affairs Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Ix, Joachim H.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Mukamal, Kenneth J.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Peralta, Carmen A.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RP de Boer, IH (reprint author), Univ Washington, Seattle, WA 98195 USA.
EM deboer@u.washington.edu
FU National Heart, Lung, and Blood Institute [N01-HC-85079, N01-HC-85086,
N01-HC-35129, N01-HC-15103, N01-HC-55222, N01-HC-75150, N01-HC-45133,
U01-HL-080295]; National Institutes of Health [R01-AG-027002,
R01-DK-087726]; National Institute of Neurologic Disorders and Stroke
FX The research reported in this article was supported by Contracts
N0I-HC-85079 through N01-HC-85086, N01-HC-35129, N01-HC-15103,
N01-HC-55222, N01-HC-75150, and N01-HC-45133 and Grant U01-HL-080295
from the National Heart, Lung, and Blood Institute, with additional
contribution from the National Institute of Neurologic Disorders and
Stroke. Additional support came from National Institutes of Health
Grants R01-AG-027002 and R01-DK-087726. A full list of principal CHS
investigators and 10. institutions can be found at hup://www.chs-nhIbi.
org/pi.htm.
NR 36
TC 13
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U1 0
U2 2
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD JUN
PY 2012
VL 35
IS 6
BP 1355
EP 1360
DI 10.2337/dcl1-1657
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 950DY
UT WOS:000304631000026
PM 22432118
ER
PT J
AU Khalili, H
Chan, AT
AF Khalili, Hamed
Chan, Andrew T.
TI Is Diabetes a Risk Factor for Colorectal Cancer?
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Editorial Material
ID GROWTH-FACTOR-I; BINDING PROTEIN-3; COLON-CARCINOMA; PLASMA-INSULIN;
MELLITUS; RECEPTORS; COHORT; P21RAS; TYPE-2; MEN
C1 [Khalili, Hamed; Chan, Andrew T.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[Khalili, Hamed; Chan, Andrew T.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Chan, Andrew T.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
RP Chan, AT (reprint author), Massachusetts Gen Hosp, Gastrointestinal Unit, 55 Fruit St,GRJ-728A, Boston, MA 02114 USA.
EM achan@partners.org
FU NCI NIH HHS [CA137178]
NR 30
TC 3
Z9 3
U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD JUN
PY 2012
VL 57
IS 6
BP 1427
EP 1429
DI 10.1007/s10620-012-2175-7
PG 3
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 946ZP
UT WOS:000304396700001
PM 22531890
ER
PT J
AU Houser, CR
Zhang, NH
Peng, ZC
Huang, CS
Cetina, Y
AF Houser, Carolyn R.
Zhang, Nianhui
Peng, Zechun
Huang, Christine S.
Cetina, Yliana
TI Neuroanatomical clues to altered neuronal activity in epilepsy: From
ultrastructure to signaling pathways of dentate granule cells
SO EPILEPSIA
LA English
DT Article
DE Electron microscopy; Extracellular signal-regulated kinase; Fos; Mossy
fiber sprouting; Seizure; Temporal lobe epilepsy
ID TEMPORAL-LOBE EPILEPSY; REGULATED KINASE ACTIVATION; MOSSY FIBER
SYNAPSES; PILOCARPINE-INDUCED SEIZURES; KAPPA-OPIOID RECEPTORS;
LONG-TERM POTENTIATION; ACID-TREATED RATS; SYNAPTIC REORGANIZATION;
HIPPOCAMPAL-FORMATION; FASCIA-DENTATA
AB The dynamic aspects of epilepsy, in which seizures occur sporadically and are interspersed with periods of relatively normal brain function, present special challenges for neuroanatomical studies. Although numerous morphologic changes can be identified during the chronic period, the relationship of many of these changes to seizure generation and propagation remains unclear. Mossy fiber sprouting is an example of a frequently observed morphologic change for which a functional role in epilepsy continues to be debated. This review focuses on neuroanatomically identified changes that would support high levels of activity in reorganized mossy fibers and potentially associated granule cell activation. Early ultrastructural studies of reorganized mossy fiber terminals in human temporal lobe epilepsy tissue have identified morphologic substrates for highly efficacious excitatory connections among granule cells. If similar connections in animal models contribute to seizure activity, activation of granule cells would be expected. Increased labeling with two activity-related markers, Fos and phosphorylated extracellular signalregulated kinase, has suggested increased activity of dentate granule cells at the time of spontaneous seizures in a mouse model of epilepsy. However, neuroanatomical support for a direct link between activation of reorganized mossy fiber terminals and increased granule cell activity remains elusive. As novel activity-related markers are developed, it may yet be possible to demonstrate such functional links and allow mapping of seizure activity throughout the brain. Relating patterns of neuronal activity during seizures to the underlying morphologic changes could provide important new insights into the basic mechanisms of epilepsy and seizure generation.
C1 [Houser, Carolyn R.; Zhang, Nianhui; Peng, Zechun; Huang, Christine S.; Cetina, Yliana] Univ Calif Los Angeles, Dept Neurobiol, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Houser, Carolyn R.] Univ Calif Los Angeles, Brain Res Inst, Los Angeles, CA 90095 USA.
[Houser, Carolyn R.] Vet Adm Greater Angeles Healthcare Syst, Res Serv, Los Angeles, CA USA.
RP Houser, CR (reprint author), Univ Calif Los Angeles, Dept Neurobiol, David Geffen Sch Med, CHS 73-235,10833 Le Conte Ave, Los Angeles, CA 90095 USA.
EM houser@mednet.ucla.edu
FU Veterans Affairs Medical Research Funds; National Institutes of Health
[NS046524, NS051311]
FX This work was supported by Veterans Affairs Medical Research Funds
(C.R.H.) and the National Institutes of Health grants NS046524 and
NS051311 (C.R.H.). We are grateful to Drs. J.R. Rich, P.S. Dwan, B.E.
Swartz, G.O. Walsh, and A.V. Delgado-Escueta, and to their patients, for
invaluable contributions to our early studies of human temporal lobe
epilepsy tissue. This review is contributed as a tribute to H. Jurgen
Wenzel in recognition of his careful, detailed morphologic studies,
which have been linked consistently to function, and his great interest
in mossy fibers of the dentate gyrus, from their early development
(Wenzel et al., 1981) to their functionally associated transporters
(Wenzel et al., 1997), and to their reorganization in epilepsy (Wenzel
et al., 2000).
NR 73
TC 15
Z9 15
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD JUN
PY 2012
VL 53
SU 1
SI SI
BP 67
EP 77
DI 10.1111/j.1528-1167.2012.03477.x
PG 11
WC Clinical Neurology
SC Neurosciences & Neurology
GA 945FH
UT WOS:000304257700010
PM 22612811
ER
PT J
AU D'Ascenzo, F
Presutti, DG
Picardi, E
Moretti, C
Omede, P
Sciuto, F
Novara, M
Yan, AT
Goodman, S
Mahajan, N
Kosuge, M
Palazzuoli, A
Jong, GP
Isma'eel, H
Budoff, MJ
Rubinshtein, R
Gewirtz, H
Reed, MJ
Theroux, P
Biondi-Zoccai, G
Modena, MG
Sheiban, I
Gaita, F
AF D'Ascenzo, Fabrizio
Presutti, Davide Giacomo
Picardi, Elisa
Moretti, Claudio
Omede, Pierluigi
Sciuto, Filippo
Novara, Marco
Yan, Andrew T.
Goodman, Shaun
Mahajan, Nitin
Kosuge, Masami
Palazzuoli, Alberto
Jong, Gwo-Ping
Isma'eel, Hussain
Budoff, Matthew J.
Rubinshtein, Ronen
Gewirtz, Henry
Reed, Matthew J.
Theroux, Pierre
Biondi-Zoccai, Giuseppe
Modena, Maria Grazia
Sheiban, Imad
Gaita, Fiorenzo
TI Prevalence and non-invasive predictors of left main or three-vessel
coronary disease: evidence from a collaborative international
meta-analysis including 22 740 patients
SO HEART
LA English
DT Article
ID ST-SEGMENT ELEVATION; ACUTE MYOCARDIAL-INFARCTION; TIMI RISK SCORE;
ARTERY-DISEASE; LEAD AVR; HEART-FAILURE; 12-LEAD ELECTROCARDIOGRAPHY;
ANGIOGRAPHIC FINDINGS; SYSTEMATIC REVIEWS; PROGNOSTIC VALUE
AB Background Left main disease (LMD) and three-vessel disease (3VD) have important prognostic value in patients with coronary artery disease. However, uncertainties still exist about their prevalence and predictors in patients with acute coronary syndrome (ACS) and also in patients with stable coronary disease. Thus the aim of this study was to perform an international collaborative systematic review and meta-analysis to appraise the prevalence and predictors of LMD and 3VD.
Methods Medline/PubMed were systematically searched for eligible studies published up to 2010, reporting multivariate predictors of LMD or 3VD. Study features, patient characteristics, and prevalence and predictors of LMD and 3VD were abstracted and pooled with random-effect methods (95% CIs).
Results 17 studies (22 740 patients) were included, 11 focusing on ACS (17 896 patients) and six on stable coronary disease (4844 patients). In the ACS subgroup, LMD or 3VD occurred in 20% (95% CI 7.2% to 33.4%), LMD in 12% (95% CI 10.5% to 13.5%), and 3VD in 25% (95% CI 23.1% to 27.0%). Heart failure at admission and extent of ST-segment elevation in lead aVR on 12-lead ECG were the most powerful predictors of LMD or 3VD. In the stable disease subgroup, LMD or 3VD was found in 36% (95% CI 18.5% to 48.8%), with the most powerful predictors being transient ischaemic dilation during the imaging stress test, extent of ST-segment elevation in aVR and V1 during the stress test, and hyperlipidaemia.
Conclusions This meta-analysis demonstrated that severe coronary disease-that is, LMD or 3VD-is more common in patients with ACS or stable coronary disease than generally perceived, and that simple and low-cost tools may help in the selection of the most appropriate therapeutic approach.
C1 [D'Ascenzo, Fabrizio; Presutti, Davide Giacomo; Picardi, Elisa; Moretti, Claudio; Omede, Pierluigi; Sciuto, Filippo; Novara, Marco; Sheiban, Imad; Gaita, Fiorenzo] Univ Turin, Div Cardiol, I-10126 Turin, Italy.
[Yan, Andrew T.; Goodman, Shaun] Maimonides Hosp, Dept Med, Brooklyn, NY 11219 USA.
[Mahajan, Nitin] Yokohama City Univ, Med Ctr, Div Cardiol, Yokohama, Kanagawa 232, Japan.
[Kosuge, Masami] Univ Siena, Cardiol Sect, Dept Internal Med & Metab Dis, I-53100 Siena, Italy.
[Palazzuoli, Alberto] Natl Yang Ming Univ, Inst Publ Hlth, Community Med Res Ctr, Yang Ming, Peoples R China.
[Jong, Gwo-Ping] Amer Univ Beirut, Med Ctr, Beirut, Lebanon.
[Isma'eel, Hussain; Budoff, Matthew J.] Technion IIT, Ruth & Bruce Rappaport Sch Med, Haifa, Israel.
[Isma'eel, Hussain; Budoff, Matthew J.] Technion IIT, Lady Davis Carmel Med Ctr, Dept Cardiovasc Med, Haifa, Israel.
[Rubinshtein, Ronen] Harvard Univ, Sch Med, Dept Med, Cardiol Div,Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Gewirtz, Henry] Univ Toronto, St Michaels Hosp, Toronto, ON M5B 1W8, Canada.
[Gewirtz, Henry] Canadian Heart Res Ctr, Toronto, ON, Canada.
[Reed, Matthew J.; Biondi-Zoccai, Giuseppe; Modena, Maria Grazia] Univ Modena & Reggio Emilia, Div Cardiol, Modena, Italy.
[D'Ascenzo, Fabrizio; Moretti, Claudio; Theroux, Pierre; Biondi-Zoccai, Giuseppe] Meta Anal & Evidence Based Med Training Cardiol M, Ospedaletti, Italy.
RP D'Ascenzo, F (reprint author), Univ Turin, Div Cardiol, S Giovanni Battista Molinette Hosp, Corso Bramante 88-90, I-10126 Turin, Italy.
EM fabrizio.dascenzo@gmail.com
RI MORETTI, CLAUDIO/G-4396-2012; modena, maria grazia/N-2442-2015;
OI modena, maria grazia/0000-0002-4704-4663; MORETTI,
CLAUDIO/0000-0002-4475-7289; Reed, Matthew/0000-0003-1308-4824
NR 57
TC 26
Z9 28
U1 0
U2 5
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1355-6037
J9 HEART
JI Heart
PD JUN
PY 2012
VL 98
IS 12
BP 914
EP 919
DI 10.1136/heartjnl-2011-301596
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 947FM
UT WOS:000304414000005
PM 22626899
ER
PT J
AU Kim, H
Miller, LM
Byl, N
Abrams, GM
Rosen, J
AF Kim, Hyunchul
Miller, Levi Makaio
Byl, Nancy
Abrams, Gary M.
Rosen, Jacob
TI Redundancy Resolution of the Human Arm and an Upper Limb Exoskeleton
SO IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING
LA English
DT Article
DE Exoskeleton; inverse kinematic; redundancy; swivel angle
ID POWERED EXOSKELETON; INVERSE KINEMATICS; COMPLEX MOVEMENTS;
MICROSTIMULATION; CONFIGURATION; CORTEX
AB The human arm has 7 degrees of freedom (DOF) while only 6 DOF are required to position the wrist and orient the palm. Thus, the inverse kinematics of an human arm has a nonunique solution. Resolving this redundancy becomes critical as the human interacts with a wearable robot and the inverse kinematics solution of these two coupled systems must be identical to guarantee an seamless integration. The redundancy of the arm can be formulated by defining the swivel angle, the rotation angle of the plane defined by the upper and lower arm around a virtual axis that connects the shoulder and wrist joints. Analyzing reaching tasks recorded with a motion capture system indicates that the swivel angle is selected such that when the elbow joint is flexed, the palm points to the head. Based on these experimental results, a new criterion is formed to resolve the human arm redundancy. This criterion was implemented into the control algorithm of an upper limb 7-DOF wearable robot. Experimental results indicate that by using the proposed redundancy resolution criterion, the error between the predicted and the actual swivel angle adopted by the motor control system is less then 5 degrees.
C1 [Kim, Hyunchul] Univ Calif Santa Cruz, Dept Elect Engn, Santa Cruz, CA 95064 USA.
[Kim, Hyunchul] Optodynamics Inc, Songnam 463870, South Korea.
[Miller, Levi Makaio] Univ Washington, Dept Mech Engn, Seattle, WA 98195 USA.
[Miller, Levi Makaio] Carbon Design Grp, Seattle, WA 98105 USA.
[Byl, Nancy] Univ Calif San Francisco, Dept Phys Therapy & Rehabil Sci, Sch Med, San Francisco, CA 94158 USA.
[Abrams, Gary M.] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA.
[Abrams, Gary M.] San Francisco VA Med Ctr, San Francisco, CA 94121 USA.
[Rosen, Jacob] Univ Calif Santa Cruz, Dept Comp Engn, Santa Cruz, CA 95064 USA.
[Rosen, Jacob] Univ Calif Santa Cruz, Bion Lab, Santa Cruz, CA 95064 USA.
RP Kim, H (reprint author), Atromax Inc, Santa Clara, CA USA.
EM hyunchul78@gmail.com; makaio@uw.edu; BylN@ptrehab.ucsf.edu;
Gary.Abrams@ucsf.edu; rosen@ucsc.edu
NR 26
TC 26
Z9 26
U1 2
U2 33
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 0018-9294
J9 IEEE T BIO-MED ENG
JI IEEE Trans. Biomed. Eng.
PD JUN
PY 2012
VL 59
IS 6
BP 1770
EP 1779
DI 10.1109/TBME.2012.2194489
PG 10
WC Engineering, Biomedical
SC Engineering
GA 944ZQ
UT WOS:000304242700029
PM 22510944
ER
PT J
AU Luo, G
Peli, E
AF Luo, Gang
Peli, Eli
TI Methods for Automated Identification of Informative Behaviors in Natural
Bioptic Driving
SO IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING
LA English
DT Article
DE Bioptic driving; driving behavior; instrumented vehicle; natural driving
study
ID TELESCOPIC SPECTACLE; OLDER DRIVERS; MOTOR-VEHICLE; ACCIDENTS; HAZARD
AB Visually impaired people may legally drive if wearing bioptic telescopes in some developed countries. To address the controversial safety issue of the practice, we have developed a low-cost in-car recording system that can be installed in study participants' own vehicles to record their daily driving activities. We also developed a set of automated identification techniques of informative behaviors to facilitate efficient manual review of important segments submerged in the vast amount of uncontrolled data. Here, we present the methods and quantitative results of the detection performance for six types of driving maneuvers and behaviors that are important for bioptic driving: bioptic telescope use, turns, curves, intersections, weaving, and rapid stops. The testing data were collected from one normally sighted and two visually impaired subjects across multiple days. The detection rates ranged from 82% up to 100%, and the false discovery rates ranged from 0% to 13%. In addition, two human observers were able to interpret about 80% of targets viewed through the telescope. These results indicate that with appropriate data processing the low-cost system is able to provide reliable data for natural bioptic driving studies.
C1 [Luo, Gang; Peli, Eli] Massachusetts Eye & Ear Infirm, Schepens Eye Res Inst, Boston, MA 02114 USA.
[Luo, Gang; Peli, Eli] Harvard Univ, Dept Ophthalmol, Sch Med, Cambridge, MA 02138 USA.
RP Luo, G (reprint author), Massachusetts Eye & Ear Infirm, Schepens Eye Res Inst, Boston, MA 02114 USA.
EM gang.luo@schepens.harvard.edu; eli.peli@schepens.harvard.edu
FU National Institute of Health [AG034553, EY12890]
FX This work was supported in part by the National Institute of Health
under Grant AG034553 (GL) and Grant EY12890 (EP).
NR 27
TC 0
Z9 0
U1 0
U2 3
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 0018-9294
J9 IEEE T BIO-MED ENG
JI IEEE Trans. Biomed. Eng.
PD JUN
PY 2012
VL 59
IS 6
BP 1780
EP 1786
DI 10.1109/TBME.2012.2191406
PG 7
WC Engineering, Biomedical
SC Engineering
GA 944ZQ
UT WOS:000304242700030
PM 22514200
ER
PT J
AU Lambert, A
Picardeau, M
Haake, DA
Sermswan, RW
Srikram, A
Adler, B
Murray, GA
AF Lambert, Ambroise
Picardeau, Mathieu
Haake, David A.
Sermswan, Rasana W.
Srikram, Amporn
Adler, Ben
Murray, Gerald A.
TI FlaA Proteins in Leptospira interrogans Are Essential for Motility and
Virulence but Are Not Required for Formation of the Flagellum Sheath
SO INFECTION AND IMMUNITY
LA English
DT Article
ID BORRELIA-BURGDORFERI; PERIPLASMIC FLAGELLA; INACTIVATION; MUTAGENESIS;
GENE; INVOLVEMENT; CHEMOTAXIS; TRANSPOSON; MUTANT
AB Spirochetes have periplasmic flagella composed of a core surrounded by a sheath. The pathogen Leptospira interrogans has four flaB (proposed core subunit) and two flaA (proposed sheath subunit) genes. The flaA genes are organized in a locus with flaA2 immediately upstream of flaA1. In this study, flaA1 and flaA2 mutants were constructed by transposon mutagenesis. Both mutants still produced periplasmic flagella. The flaA 1 mutant did not produce FlaA1 but continued to produce FlaA2 and retained normal morphology and virulence in a hamster model of infection but had reduced motility. The flaA2 mutant did not produce either the FlaA1 or the FlaA2 protein. Cells of the flaA2 mutant lacked the distinctive hook-shaped ends associated with L. interrogans and lacked translational motility in liquid and semisolid media. These observations were confirmed with a second, independent flaA2 mutant. The flaA2 mutant failed to cause disease in animal models of acute infection. Despite lacking FlaA proteins, the flagella of the flaA2 mutant were of the same thickness as wild-type flagella, as measured by electron microscopy, and exhibited a normal flagellum sheath, indicating that FlaA proteins are not essential for the synthesis of the flagellum sheath, as observed for other spirochetes. This study shows that FlaA subunits contribute to leptospiral translational motility, cellular shape, and virulence.
C1 [Adler, Ben; Murray, Gerald A.] Monash Univ, Dept Microbiol, Australian Res Council Ctr Excellence Struct & Fu, Clayton, Vic 3168, Australia.
[Sermswan, Rasana W.; Srikram, Amporn] Khon Kaen Univ, Melioidosis Res Ctr, Khon Kaen, Thailand.
[Sermswan, Rasana W.] Khon Kaen Univ, Dept Biochem, Khon Kaen, Thailand.
[Haake, David A.] Univ Calif Los Angeles, Sch Med, Dept Med, Los Angeles, CA 90024 USA.
[Haake, David A.] Vet Affairs Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Lambert, Ambroise] Univ Paris Diderot, Paris, France.
[Lambert, Ambroise; Picardeau, Mathieu] Inst Pasteur, Unite Biol Spirochetes, Paris, France.
RP Adler, B (reprint author), Monash Univ, Dept Microbiol, Australian Res Council Ctr Excellence Struct & Fu, Clayton, Vic 3168, Australia.
EM ben.adler@monash.edu
FU Australian Research Council; National Health and Medical Research
Council; Institut Pasteur; French Ministry of Research [ANR-08-MIE-018];
University Paris Diderot; VA Medical Research funds; Public Health
Service from the National Institute of Allergy and Infectious Diseases
[AI-034431]
FX This work was supported by the Australian Research Council, the National
Health and Medical Research Council, the Institut Pasteur, the French
Ministry of Research (ANR-08-MIE-018), the doctoral program of the
University Paris Diderot, VA Medical Research funds, and Public Health
Service grant AI-034431 from the National Institute of Allergy and
Infectious Diseases.
NR 33
TC 44
Z9 44
U1 1
U2 6
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0019-9567
J9 INFECT IMMUN
JI Infect. Immun.
PD JUN
PY 2012
VL 80
IS 6
BP 2019
EP 2025
DI 10.1128/IAI.00131-12
PG 7
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 946WH
UT WOS:000304387700008
PM 22451522
ER
PT J
AU Hoeppner, BB
Redding, CA
Rossi, JS
Pallonen, UE
Prochaska, JO
Velicer, WF
AF Hoeppner, Bettina B.
Redding, Colleen A.
Rossi, Joseph S.
Pallonen, Unto E.
Prochaska, James O.
Velicer, Wayne F.
TI Factor Structure of Decisional Balance and Temptations Scales for
Smoking: Cross-Validation in Urban Female African-American Adolescents
SO INTERNATIONAL JOURNAL OF BEHAVIORAL MEDICINE
LA English
DT Article
DE Transtheoretical model; Decisional Balance; Temptations; Smoking;
African-Americans; Adolescents
ID 12 PROBLEM BEHAVIORS; HEALTH BEHAVIORS; SELF-EFFICACY; TRANSTHEORETICAL
MODEL; WEAK PRINCIPLES; FIT INDEXES; CESSATION; PRECONTEMPLATION;
ASSOCIATION; DISPARITIES
AB Background The transtheoretical model is an influential theoretical model in health psychology, particularly in its application to smoking cessation research. Decisional Balance (DB) and Temptations are key constructs within this framework.
Purpose This study examines the psychometric properties of the DB and Temptations scales for smoking in a predominantly African-American sample of urban adolescent girls.
Methods We used confirmatory factor analysis to compare the fit of previously published factor structures in smokers (n=233) and nonsmokers (n=598). External validity was tested by examining stages of change differences in the retained subscales.
Results Results supported the internal and external validity of the DB scale for smokers and nonsmokers. Notably, previously published three-factor (Social Pros, Coping Pros, Cons) and four-factor (Cons split into "Aesthetic Cons" and "Health Cons") models fit equally well, with Cons subscales correlating highly. For Temptations, a previously published three-factor (Negative Affect, Social, Weight Control) hierarchical model fit well in nonsmokers. In smokers, previously published subscales were reliably measured, but their structural relationship remained unclear. Stage difference tests showed medium to large effect sizes of DB and Temptation subscales in smokers and nonsmokers.
Conclusions The use of DB was validated for both smokers and nonsmokers in this sample of primarily African-American adolescent females, where Cons can be combined or separated into "Aesthetic Cons" and "Health Cons" based on practical utility and preference. For Temptations, more research is needed but large stage differences in Temptations subscales underscore the importance of this concept in smoking acquisition and cessation.
C1 [Hoeppner, Bettina B.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Addict Med, Boston, MA 02114 USA.
[Hoeppner, Bettina B.] Brown Univ, Ctr Alcohol & Addict Studies, Providence, RI 02912 USA.
[Redding, Colleen A.; Rossi, Joseph S.; Prochaska, James O.; Velicer, Wayne F.] Univ Rhode Isl, Canc Prevent Res Ctr, Kingston, RI 02881 USA.
[Pallonen, Unto E.] Univ Texas Hlth Sci Ctr Houston, Sch Publ Hlth, Houston, TX USA.
RP Hoeppner, BB (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Addict Med, 60 Staniford St, Boston, MA 02114 USA.
EM bhoeppner@partners.org; credding@uri.edu
RI Redding, Colleen /J-8261-2012
OI Redding, Colleen /0000-0002-5044-3155
FU NCI NIH HHS [CA50087, CA63045, P01 CA050087]; NIAAA NIH HHS [T32
AA007459, T32 AA007459-21]; NIDA NIH HHS [L30 DA025511, L30 DA025511-02,
R01 DA023191]
NR 45
TC 4
Z9 4
U1 2
U2 11
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1070-5503
J9 INT J BEHAV MED
JI Int. J. Behav. Med.
PD JUN
PY 2012
VL 19
IS 2
BP 217
EP 227
DI 10.1007/s12529-011-9145-x
PG 11
WC Psychology, Clinical
SC Psychology
GA 947AR
UT WOS:000304399500010
PM 21279493
ER
PT J
AU Mukherjee, A
Larson, EA
Carlos, AS
Belknap, JK
Rotwein, P
Klein, RF
AF Mukherjee, Aditi
Larson, Emily A.
Carlos, Amy S.
Belknap, John K.
Rotwein, Peter
Klein, Robert F.
TI Congenic mice provide in vivo evidence for a genetic locus that
modulates intrinsic transforming growth factor beta 1-mediated signaling
and bone acquisition
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Article
DE HEREDITY; GENETICS; TRANSFORMING GROWTH FACTOR; BONE STRENGTH;
OSTEOPOROSIS
ID QUANTITATIVE TRAIT LOCI; INHIBITS OSTEOBLAST DIFFERENTIATION; TGF-BETA
ACTIVATION; MINERAL DENSITY; MECHANICAL-PROPERTIES; PARATHYROID-HORMONE;
COMPLEX TRAITS; OSTEOPOROSIS; MOUSE; IDENTIFICATION
AB Osteoporosis, the most common skeletal disorder, is characterized by low bone mineral density (BMD) and an increased risk of fragility fractures. BMD is the best clinical predictor of future osteoporotic fracture risk, but is a complex trait controlled by multiple environmental and genetic determinants with individually modest effects. Quantitative trait locus (QTL) mapping is a powerful method for identifying chromosomal regions encompassing genes involved in shaping complex phenotypes, such as BMD. Here we have applied QTL analysis to male and female genetically-heterogeneous F2 mice derived from a cross between C57BL/6 and DBA/2 strains, and have identified 11 loci contributing to femoral BMD. Further analysis of a QTL on mouse chromosome 7 following the generation of reciprocal congenic strains has allowed us to determine that the high BMD trait, which tracks with the DBA/2 chromosome and exerts equivalent effects on male and female mice, is manifested by enhanced osteogenic differentiation of mesenchymal stem cells (MSCs) in vitro and by increased growth of metatarsal bones in short-term primary culture. An insertion/deletion DNA polymorphism in Ltbp4 exon 12 that causes the in-frame removal of 12 codons in the DBA/2-derived gene maps within 0.6?Mb of the marker most tightly linked to the QTL. LTBP4, one of four paralogous mouse proteins that modify the bioavailability of the transforming growth factor beta (TGF-beta) family of growth factors, is expressed in differentiating MSC-derived osteoblasts and in long bones, and reduced responsiveness to TGF-beta 1 is observed in MSCs of mice homozygous for the DBA/2 chromosome 7. Taken together, our results identify a potential genetic and biochemical relationship between decreased TGF-beta 1mediated signaling and enhanced femoral BMD that may be regulated by a variant LTBP4 molecule. (C) 2012 American Society for Bone and Mineral Research.
C1 [Larson, Emily A.; Carlos, Amy S.; Klein, Robert F.] Oregon Hlth & Sci Univ, Bone & Mineral Res Unit, Dept Med, Portland, OR 97201 USA.
[Mukherjee, Aditi; Rotwein, Peter] Oregon Hlth & Sci Univ, Dept Biochem & Mol Biol, Portland, OR 97201 USA.
[Belknap, John K.] Oregon Hlth & Sci Univ, Dept Behav Neurosci, Portland, OR 97201 USA.
[Belknap, John K.; Klein, Robert F.] Portland VA Med Ctr, Portland, OR USA.
RP Klein, RF (reprint author), Oregon Hlth & Sci Univ, Bone & Mineral Res Unit CR113, 3181 SW Sam Jackson Pk Rd, Portland, OR 97201 USA.
EM kleinro@ohsu.edu
FU National Institutes of Health [R01 DK42748, P50 AA10760, R01 AR44659];
VA Medical Research Service
FX These studies were supported in part by National Institutes of Health
grants R01 DK42748 (to PR), P50 AA10760 (to JKB), R01 AR44659 (to RFK),
and the VA Medical Research Service (to RFK). We thank Dr. Lynn Sakai
for polyclonal antibodies to LTBP4.
NR 59
TC 8
Z9 8
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD JUN
PY 2012
VL 27
IS 6
BP 1345
EP 1356
DI 10.1002/jbmr.1590
PG 12
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 943QY
UT WOS:000304141500012
PM 22407846
ER
PT J
AU Heckman, CJ
Cohen-Filipic, J
AF Heckman, Carolyn J.
Cohen-Filipic, Jessye
TI Brief Report: Ultraviolet Radiation Exposure, Considering Acculturation
Among Hispanics (Project URECAH)
SO JOURNAL OF CANCER EDUCATION
LA English
DT Article
DE Hispanics; Skin cancer; Prevention; Acculturation
ID SUN PROTECTION PRACTICES; BEHAVIORS
AB Very few studies have examined acculturation of Hispanics as it relates to skin cancer prevention attitudes and behaviors. This pilot study used the Abbreviated Acculturation Rating Scale for Mexican Americans-II to classify 14-25-year-old Hispanics as traditional, bicultural, or acculturated. More acculturated individuals reported significantly higher perceived benefits of ultraviolet radiation exposure and lower worry about skin damage than traditional individuals. Bicultural individuals reported using sunscreen significantly more often than acculturated individuals. These preliminary data suggest that more acculturated Hispanic young adults may demonstrate riskier skin cancer-related attitudes and behaviors than others.
C1 [Heckman, Carolyn J.] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[Cohen-Filipic, Jessye] Portland VA Med Ctr, Portland, OR 97239 USA.
RP Heckman, CJ (reprint author), Fox Chase Canc Ctr, 333 Cottman Ave, Philadelphia, PA 19111 USA.
EM Carolyn.Heckman@fccc.edu; JessyeCohen@gmail.com
FU NCI NIH HHS [K07 CA108685, K07 CA108685-05]
NR 15
TC 7
Z9 7
U1 1
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0885-8195
J9 J CANCER EDUC
JI J. Cancer Educ.
PD JUN
PY 2012
VL 27
IS 2
BP 342
EP 346
DI 10.1007/s13187-011-0308-x
PG 5
WC Oncology; Education, Scientific Disciplines; Public, Environmental &
Occupational Health
SC Oncology; Education & Educational Research; Public, Environmental &
Occupational Health
GA 943SC
UT WOS:000304144500021
PM 22228464
ER
PT J
AU Safren, SA
O'Cleirigh, CM
Bullis, JR
Otto, MW
Stein, MD
Pollack, MH
AF Safren, Steven A.
O'Cleirigh, Conall M.
Bullis, Jacqueline R.
Otto, Michael W.
Stein, Michael D.
Pollack, Mark H.
TI Cognitive Behavioral Therapy for Adherence and Depression (CBT-AD) in
HIV-Infected Injection Drug Users: A Randomized Controlled Trial
SO JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY
LA English
DT Article
DE HIV/AIDS; antiretroviral therapy (ART); depression; adherence; substance
abuse
ID ACTIVE ANTIRETROVIRAL THERAPY; HUMAN-IMMUNODEFICIENCY-VIRUS; VIRAL LOAD;
MEDICATION ADHERENCE; VIROLOGICAL RESPONSE; PSYCHOSOCIAL FACTORS;
DISEASE PROGRESSION; INCREASE ADHERENCE; INHIBITOR THERAPY; METAANALYSIS
AB Objective: Depression and substance use, the most common comorbidities with HIV, are both associated with poor treatment adherence. Injection drug users comprise a substantial portion of individuals with HIV in the United States and globally. The present study tested cognitive behavioral therapy for adherence and depression (CBT-AD) in patients with HIV and depression in active substance abuse treatment for injection drug use. Method: This is a 2-arm, randomized controlled trial (N = 89) comparing CBT-AD with enhanced treatment as usual (ETAU). Analyses were conducted for two time-frames: (a) baseline to post-treatment and (b) post-treatment to follow-up at 3 and 6 months after intervention discontinuation. Results: At post-treatment, the CBT-AD condition showed significantly greater improvement than ETAU in MEMS (electronic pill cap) based adherence, gamma(slope) = 0.8873, t(86) = 2.38, p = .02; d(GMA-raw), = 0.64, and depression, assessed by blinded assessor: Mongomery-Asberg Depression Rating Scale, F(1, 79) = 6.52, p < .01, d = 0.55; clinical global impression, F(1, 79) = 14.77, p < .001, d = 0.85. After treatment discontinuation, depression gains were maintained, but adherence gains were not. Viral load did not differ across condition; however, the CBT-AD condition had significant improvements in CD4 cell counts over time compared with ETAU, gamma(slope) = 2.09, t(76) = 2.20,p = .03, d(GMA-raw) = 0.60. Conclusions: In patients managing multiple challenges including HIV, depression, substance dependence, and adherence, CBT-AD is a useful way to integrate treatment of depression with an adherence intervention. Continued adherence counseling is likely needed, however, to maintain or augment adherence gains in this population.
C1 [Safren, Steven A.; O'Cleirigh, Conall M.; Pollack, Mark H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Safren, Steven A.; O'Cleirigh, Conall M.; Bullis, Jacqueline R.; Pollack, Mark H.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Bullis, Jacqueline R.; Otto, Michael W.] Boston Univ, Dept Psychol, Boston, MA 02215 USA.
[Stein, Michael D.] Butler Hosp, Providence, RI 02906 USA.
[Stein, Michael D.] Brown Univ, Providence, RI 02912 USA.
RP Safren, SA (reprint author), MGH Behav Med, 1 Bowdoin Sq,7th Floor, Boston, MA 02114 USA.
EM ssafren@partners.org
FU NIDA NIH HHS [R01 DA018603, R01 DA018603-01, R01DA018603]
NR 55
TC 60
Z9 61
U1 6
U2 28
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0022-006X
J9 J CONSULT CLIN PSYCH
JI J. Consult. Clin. Psychol.
PD JUN
PY 2012
VL 80
IS 3
BP 404
EP 415
DI 10.1037/a0028208
PG 12
WC Psychology, Clinical
SC Psychology
GA 948MT
UT WOS:000304508000009
PM 22545737
ER
PT J
AU Ghosh, PM
Shu, ZJ
Zhu, B
Lu, ZD
Ikeno, YJ
Barnes, JL
Yeh, CK
Zhang, BX
Katz, MS
Kamat, A
AF Ghosh, Paramita M.
Shu, Zhen-Ju
Zhu, Bing
Lu, Zhongding
Ikeno, Yuji
Barnes, Jeffrey L.
Yeh, Chih-Ko
Zhang, Bin-Xian
Katz, Michael S.
Kamat, Amrita
TI Role of beta-adrenergic receptors in regulation of hepatic fat
accumulation during aging
SO JOURNAL OF ENDOCRINOLOGY
LA English
DT Article
ID ISOLATED RAT HEPATOCYTES; LIVER-DISEASE; MYOCARDIAL-INFARCTION;
METABOLIC SYNDROME; ADENYLATE-CYCLASE; FISCHER-344 RATS; ADIPOSE-TISSUE;
AGE; EXPRESSION; ADRENOCEPTOR
AB Excessive fat accumulation in liver (hepatic steatosis) predisposes to hepatic functional and structural impairment and overall metabolic risk. Previous studies noted an association between hepatic steatosis and age in humans and rodents. However, the mechanisms leading to age-associated hepatic fat accumulation remain unknown. Earlier work from our group showed that beta-adrenergic receptor (beta-AR) levels and beta-AR-stimulated adenylyl cyclase activity increase in rat liver during aging. Herewe investigated whether age-associated increases in beta-AR signaling play a role in augmenting hepatic lipid accumulation. We demonstrate an increase in hepatic lipid content during senescence and a significant correlation between hepatic fat content and stimulation of adenylyl cyclase activity by the beta-AR agonist isoproterenol in rat liver. Isoproterenol administration to young and old rodents in vivo increased hepatic lipid accumulation. Furthermore, in vitro overexpression of b1-and b2-AR subtypes in hepatocytes from young rodents increased cellular lipid content, whereas inhibition of beta-ARs by receptor subtype-specific inhibitors reduced lipid levels in hepatocytes from senescent animals. Isoproterenol-induced hepatic lipid accumulation in vivo was prevented by the beta-AR nonselective blocker propranolol, suggesting a novel therapeutic effect of this class of drugs in hepatic steatosis. Acipimox, which inhibits adipose tissue lipolysis, did not alter isoproterenolmediated hepatic fat accumulation; thus beta-AR responsive hepatic lipid accumulation does not appear to be related primarily to altered lipolysis. These findings suggest that augmented hepatic beta-AR signaling during aging may increase lipid accumulation in liver and advocate a possible role for beta-adrenergic blockers in preventing or retarding the development of hepatic steatosis. Journal of Endocrinology (2012) 213, 251-261
C1 [Ghosh, Paramita M.; Yeh, Chih-Ko; Zhang, Bin-Xian; Katz, Michael S.; Kamat, Amrita] S Texas Vet Hlth Care Syst, Audie L Murphy Div, Geriatr Res Educ & Clin Ctr 182, San Antonio, TX 78229 USA.
[Shu, Zhen-Ju; Barnes, Jeffrey L.; Zhang, Bin-Xian; Katz, Michael S.; Kamat, Amrita] Univ Texas Hlth Sci Ctr San Antonio, Dept Med, San Antonio, TX 78229 USA.
[Zhu, Bing; Lu, Zhongding; Yeh, Chih-Ko; Katz, Michael S.] Univ Texas Hlth Sci Ctr San Antonio, Dept Comprehens Dent, San Antonio, TX 78229 USA.
[Ikeno, Yuji] Univ Texas Hlth Sci Ctr San Antonio, Dept Pathol, San Antonio, TX 78229 USA.
[Ikeno, Yuji; Yeh, Chih-Ko; Kamat, Amrita] Univ Texas Hlth Sci Ctr San Antonio, Barshop Inst Longev & Aging Studies, San Antonio, TX 78229 USA.
RP Kamat, A (reprint author), S Texas Vet Hlth Care Syst, Audie L Murphy Div, Geriatr Res Educ & Clin Ctr 182, 7400 Merton Minter Blvd, San Antonio, TX 78229 USA.
EM kamat@uthscsa.edu
FU Department of Veterans Affairs VISN 17; American Heart Association;
Kronos Longevity Research Institute
FX Grant sponsor: Department of Veterans Affairs VISN 17 award to A K;
grant sponsor: American Heart Association grant in aid to A K; and grant
sponsor: Kronos Longevity Research Institute award to M S K.
NR 53
TC 14
Z9 14
U1 1
U2 5
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA EURO HOUSE, 22 APEX COURT WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT,
ENGLAND
SN 0022-0795
J9 J ENDOCRINOL
JI J. Endocrinol.
PD JUN
PY 2012
VL 213
IS 3
BP 251
EP 261
DI 10.1530/JOE-11-0406
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 946PZ
UT WOS:000304366600006
PM 22457517
ER
PT J
AU Shiner, B
D'Avolio, LW
Nguyen, TM
Zayed, MH
Watts, BV
Fiore, L
AF Shiner, Brian
D'Avolio, Leonard W.
Nguyen, Thien M.
Zayed, Maha H.
Watts, Bradley V.
Fiore, Louis
TI Automated classification of psychotherapy note text: implications for
quality assessment in PTSD care
SO JOURNAL OF EVALUATION IN CLINICAL PRACTICE
LA English
DT Article
DE health care quality; access; and evaluation; natural language
processing; psychotherapy; quality assurance; health care; quality of
health care; stress disorders; post-traumatic
ID POSTTRAUMATIC-STRESS-DISORDER; MENTAL-HEALTH; VETERANS; CLINICS
C1 [Shiner, Brian; Zayed, Maha H.; Watts, Bradley V.] VA Med Ctr, White River Jct, VT 05009 USA.
[Shiner, Brian; Watts, Bradley V.] VA New England Healthcare Engn Partnership, White River Jct, VT USA.
[Shiner, Brian; Watts, Bradley V.] Dartmouth Med Sch, Hanover, NH USA.
[D'Avolio, Leonard W.; Nguyen, Thien M.; Fiore, Louis] VA Boston Healthcare Syst, Boston, MA USA.
[D'Avolio, Leonard W.; Nguyen, Thien M.; Fiore, Louis] Massachusetts Vet Epidemiol Res & Informat Ctr, Boston, MA USA.
[D'Avolio, Leonard W.] Ctr Surg & Publ Hlth, Boston, MA USA.
[D'Avolio, Leonard W.] Harvard Univ, Sch Med, Boston, MA USA.
[Fiore, Louis] Boston Univ, Sch Publ Hlth, Boston, MA USA.
RP Shiner, B (reprint author), VA Med Ctr, 215 N Main St 11Q, White River Jct, VT 05009 USA.
EM brian.shiner@va.gov
FU Veterans Administration; Health Services Research & Development through
the Consortium for Healthcare Informatics Research (CHIR)
FX Dr Shiner's time is supported by the VA-New England Early Career
Development Award Program. This work is made possible by funding from
the Veterans Administration Cooperative Studies Program (CSP) and Health
Services Research & Development through the Consortium for Healthcare
Informatics Research (CHIR).
NR 13
TC 10
Z9 10
U1 2
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1356-1294
J9 J EVAL CLIN PRACT
JI J. Eval. Clin. Pract.
PD JUN
PY 2012
VL 18
IS 3
BP 698
EP 701
DI 10.1111/j.1365-2753.2011.01634.x
PG 4
WC Health Care Sciences & Services; Medical Informatics; Medicine, General
& Internal
SC Health Care Sciences & Services; Medical Informatics; General & Internal
Medicine
GA 939KA
UT WOS:000303807600031
PM 21668796
ER
PT J
AU Suh, JY
Cho, G
Song, Y
Lee, CK
Kang, JS
Kang, MR
Park, SB
Kim, YR
Kim, JK
AF Suh, Ji-Yeon
Cho, Gyunggoo
Song, Youngkyu
Lee, Chang Kyung
Kang, Jong Soon
Kang, Moo Rim
Park, Sung Bin
Kim, Young Ro
Kim, Jeong Kon
TI Is apparent diffusion coefficient reliable and accurate for monitoring
effects of antiangiogenic treatment in a longitudinal study?
SO JOURNAL OF MAGNETIC RESONANCE IMAGING
LA English
DT Article
DE outcome; treatment; diffusion magnetic resonance imaging; inhibitors;
angiogenesis
ID TUMOR XENOGRAFTS; EARLY THERAPY; LYMPH-NODES; FEASIBILITY; CANCER;
EXPERIENCE; PERFUSION; ANTIBODY; SU11248; MRI
AB Purpose: To evaluate the reliability and accuracy of the apparent diffusion coefficient (ADC) for monitoring antiangiogenic treatment in a longitudinal study. Materials and Methods: Tumor volume and ADC were monitored by T2-weighted magnetic resonance imaging (MRI) and diffusion-weighted MRI, respectively, in 18 mice with angiogenesis-dependent tumors (U118MG) before (day 0) and after 2, 7, 14, and 21 days of administration of the antiangiogenic agent sunitinib maleate (n = 12) or vehicle (n = 6). Percent changes in tumor volume and ADC were calculated and correlations between tumor volume and ADC were evaluated. Results: Tumor volume and ADC showed a negative correlation at 69 of the 72 (96%) follow-up measurements. In the 13 mice with tumor regrowth, ADC started to decrease before (27%) or at the same time (73%) as tumor regrowth. Pretreatment ADC and percent change in ADC change on days 02 were similar in mice with positive and negative responses to treatment (0.851 vs. 0.999, 24% vs. 16%). Percent change of ADC showed significant negative correlation with percent change in tumor volume in both the control (r = -0.69) and treated (r = -0.65) groups. Conclusion: Percent change in ADC is a reliable and accurate marker for monitoring the effects of antiangiogenic treatment, whereas pretreatment ADC and early changes in ADC (ie, days 02) are limited in predicting treatment outcome. J. Magn. Reson. Imaging 2012;. (c) 2012 Wiley Periodicals, Inc.
C1 [Suh, Ji-Yeon; Lee, Chang Kyung; Kim, Jeong Kon] Univ Ulsan, Coll Med, Dept Radiol, Res Inst Radiol,Asan Med Ctr, Seoul 138736, South Korea.
[Suh, Ji-Yeon; Cho, Gyunggoo; Song, Youngkyu] Korea Basic Sci Inst, Div Magnet Resonance, Cheongwon, Chungbuk, South Korea.
[Kang, Jong Soon; Kang, Moo Rim] Korea Res Inst Biosci & Biotechnol, Cheongwon, Chungbuk, South Korea.
[Park, Sung Bin] Cheil Gen Hosp, Dept Radiol, Seoul, South Korea.
[Park, Sung Bin] Kwandong Univ, Coll Med, Womens Healthcare Ctr, Seoul, South Korea.
[Kim, Young Ro] Massachusetts Gen Hosp, Dept Radiol, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA USA.
RP Kim, JK (reprint author), Univ Ulsan, Coll Med, Dept Radiol, Res Inst Radiol,Asan Med Ctr, 388-1 Poongnap Dong, Seoul 138736, South Korea.
EM kim.jeongkon@gmail.com
FU National Research Foundation of Korea (NRF); Ministry of Education,
Science of Technology [2011-0005480, 2010-0025731]; Ministry for Health,
Welfare Family Affairs [A090754]
FX Contract grant sponsor: Basic Science Research Program through the
National Research Foundation of Korea (NRF) funded by the Ministry of
Education, Science of Technology; Contract grant number: 2011-0005480,
2010-0025731; Contract grant sponsor: Korea Healthcare Technology R&D
Project, Ministry for Health, Welfare & Family Affairs; Contract grant
number: A090754.
NR 26
TC 4
Z9 4
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1053-1807
J9 J MAGN RESON IMAGING
JI J. Magn. Reson. Imaging
PD JUN
PY 2012
VL 35
IS 6
BP 1430
EP 1436
DI 10.1002/jmri.23574
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 942HP
UT WOS:000304035100021
PM 22314928
ER
PT J
AU Adams, JM
Potempa, K
AF Adams, Jeffrey M.
Potempa, Kathleen
TI Influencing Nursing Education, Policy, Practice, and Research An
Interview With Kathleen Potempa
SO JOURNAL OF NURSING ADMINISTRATION
LA English
DT Editorial Material
C1 [Adams, Jeffrey M.] Yvonne L Munn Ctr Nursing Res, Boston, MA USA.
[Adams, Jeffrey M.] Ctr Innovat Patient Care, Boston, MA USA.
[Potempa, Kathleen] AACN, Aliso Viejo, CA USA.
[Potempa, Kathleen] Univ Michigan, Sch Nursing, Ann Arbor, MI 48109 USA.
RP Adams, JM (reprint author), Massachusetts Gen Hosp, 275 Cambridge St,POB 4, Boston, MA 02114 USA.
EM jadams9@partners.org
NR 1
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0002-0443
J9 J NURS ADMIN
JI J. Nurs. Adm.
PD JUN
PY 2012
VL 42
IS 6
BP 318
EP 320
PG 3
WC Nursing
SC Nursing
GA 947MV
UT WOS:000304435000006
ER
PT J
AU Foreyt, J
Kleinman, R
Brown, RJ
Lindstrom, R
AF Foreyt, John
Kleinman, Ronald
Brown, Rebecca J.
Lindstrom, Rachel
TI The Use of Low-Calorie Sweeteners by Children: Implications for Weight
Management
SO JOURNAL OF NUTRITION
LA English
DT Article
ID FOOD-INTAKE; BEVERAGE CONSUMPTION; ENERGY-INTAKE; TASTE RECEPTORS;
CHILDHOOD OBESITY; SELF-REGULATION; UNITED-STATES; BODY-WEIGHT;
ARTIFICIAL SWEETENERS; INTENSE SWEETENERS
AB The rise in pediatric obesity since the 1970s has been well established in the United States and is becoming a major concern worldwide. As a potential means to help slow the obesity epidemic, low-calorie sweeteners (LCS) have gained attention as dietary tools to assist in adherence to weight loss plans or prevention of excess weight gain. Observational studies tend to show positive correlations between LCS consumption and weight gain in children and adolescents. Although the data are intriguing, these epidemiologic studies do not establish that LCS cause weight gain, because there are likely many lifestyle and genetic differences between children and families who choose to consume LCS and those who do not. Short-term randomized controlled trials have shown LCS use to be BMI neutral or to have modest weight-reducing effects in overweight and obese adolescents. The long-term effects of LCS in children and adolescents are unknown. Some compelling research is currently underway and may provide needed insight into the potential role of LCS in weight management. The paucity of data regarding the effects of LCS use in children and adolescents creates challenges in decision-making for health care providers and parents. J. Nutr. 142: 1155S-1162S, 2012.
C1 [Foreyt, John] Baylor Coll Med, Houston, TX 77030 USA.
[Kleinman, Ronald] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Massachusetts Gen Hosp Children, Boston, MA USA.
[Brown, Rebecca J.] NIH, Bethesda, MD 20892 USA.
[Lindstrom, Rachel] Amer Move Fdn, Aurora, CO USA.
RP Foreyt, J (reprint author), Baylor Coll Med, Houston, TX 77030 USA.
EM jforeyt@bcm.edu
FU Kellogg Company; Committee on Low-Calorie Sweeteners of the North
American Branch of the International Life Sciences Institute; National
Institute of Diabetes, Digestive, and Kidney Diseases
FX Published in a supplement to The Journal of Nutrition. Presented at the
conference Low-Calorie Sweeteners, Appetite and Weight Control: What the
Science Tells Us, held in Washington, DC, April 7-8, 2011. The
conference was sponsored by the Committee on Low-calorie Sweeteners of
the International Life Sciences Institute North America. The views
expressed in these papers are not necessarily those of the supplement
coordinator or guest editors. The supplement coordinator for this
supplement was Adam Drewnowski, University of Washington. Supplement
Coordinator disclosures: Adam Drewnowski received travel reimbursement
for participation in the Low-Calorie Sweeteners Conference. The
supplement is the responsibility of the Guest Editor to whom the Editor
of The Journal of Nutrition has delegated supervision of both technical
conformity to the published regulations of The Journal of Nutrition and
general oversight of the scientific merit of each article. The Guest
Editor for this supplement was Sibylle Kranz. Guest Editor disclosure:
Sibylle Kranz has received funding from The Kellogg Company to conduct
research projects unrelated to this supplement material. She has also
been an invited speaker at a roundtable discussion funded by The Kellogg
Company. Publication costs for this supplement were defrayed in part by
the payment of page charges. This publication must therefore be hereby
marked "advertisement" in accordance with 18 USC section 1734 solely to
indicate this fact. The opinions expressed in this publication are those
of the authors and are not attributable to the sponsors or the
publisher, Editor, or Editorial Board of The Journal of Nutrition.;
Supported by the Committee on Low-Calorie Sweeteners of the North
American Branch of the International Life Sciences Institute. J. Foreyt,
R. Kleinman, and R. Lindstrom received a modest honorarium for their
participation in the workshop and development of the manuscript, as well
as travel funding to attend the workshop.; Author disclosures: R.
Kleinman has served on an advisory committee for Ajinomoto. J. Foreyt
has received consulting fees, honoraria, and unrestricted grants from
food, beverage, and pharmaceutical companies and from government and
nonprofit sources. R. J. Brown's research was supported in part by the
Intramural Research Program of the National Institute of Diabetes,
Digestive, and Kidney Diseases. R. Lindstrom, no conflicts of interest.
NR 64
TC 10
Z9 10
U1 10
U2 56
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-3166
J9 J NUTR
JI J. Nutr.
PD JUN
PY 2012
VL 142
IS 6
BP 1155S
EP 1162S
DI 10.3945/jn.111.149609
PG 8
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 946EY
UT WOS:000304335500028
PM 22573780
ER
PT J
AU Rhodes, ET
Goran, MI
Lieu, TA
Lustig, RH
Prosser, LA
Songer, TJ
Weigensberg, MJ
Weinstock, RS
Gonzalez, T
Rawluk, K
Zoghbi, RM
Ludwig, DS
Laffel, LM
AF Rhodes, Erinn T.
Goran, Michael I.
Lieu, Tracy A.
Lustig, Robert H.
Prosser, Lisa A.
Songer, Thomas J.
Weigensberg, Marc J.
Weinstock, Ruth S.
Gonzalez, Tessa
Rawluk, Kaitlin
Zoghbi, Roula M.
Ludwig, David S.
Laffel, Lori M.
TI Health-Related Quality of Life in Adolescents with or at Risk for Type 2
Diabetes Mellitus
SO JOURNAL OF PEDIATRICS
LA English
DT Article
ID GLYCEMIC CONTROL; CARDIOVASCULAR-DISEASE; FAMILY CONFLICT; OBESE
CHILDREN; YOUTH; OVERWEIGHT; PREFERENCES; PREVALENCE; IMPACT; CHALLENGES
AB Objective To evaluate how adolescents with or at risk for type 2 diabetes mellitus (T2DM) and their parent/guardians (parents) perceive adolescents' health-related quality of life.
Study design We interviewed overweight/obese, 12- to 18-year-old youth with T2DM, prediabetes, or insulin resistance and one parent from 5 US sites. Assessments included Pediatric Quality of Life Inventory (PedsQL), Health Utilities Index, family conflict, and diabetes burden.
Results In 108 adolescents, diagnoses included 40.7% with T2DM, 25.0% with prediabetes, and 34.3% with insulin resistance. PedsQL summary score (SS) was higher in adolescents than parents (P = .02). Parents rated physical functioning lower than adolescents (P < .0001), but there were no differences in psychosocial health. Adolescent PedsQL SS did not differ with diagnosis, but was inversely associated with adolescent body mass index z-score (P = .0004) and family conflict (P < .0001) and associated with race/ethnicity (P < .0001). Number of adolescent co-morbidities (P = .007) and burden of diabetes care (P < .05) were inversely associated with parent PedsQL SS. There were no differences in the Health Utilities Index-Mark 3 multi-attribute utility score.
Conclusions Parents perceive their adolescents' physical functioning as more impaired than adolescents themselves. Contextual factors including severity of obesity, race/ethnicity, family conflict, and burden of diabetes care influence health-related quality of life. Family-based approaches to treatment and prevention of T2DM may benefit from increased attention to the biopsychosocial context. (J Pediatr 2011;square:square-square).
C1 [Rhodes, Erinn T.; Ludwig, David S.] Childrens Hosp, Div Endocrinol, Boston, MA 02115 USA.
[Lieu, Tracy A.] Childrens Hosp, Div Gen Pediat, Boston, MA 02115 USA.
[Rhodes, Erinn T.; Lieu, Tracy A.; Ludwig, David S.; Laffel, Lori M.] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
[Goran, Michael I.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Goran, Michael I.; Weigensberg, Marc J.] Univ So Calif, Keck Sch Med, Dept Pediat, Los Angeles, CA 90033 USA.
[Lieu, Tracy A.; Prosser, Lisa A.] Harvard Pilgrim Hlth Care Inst, Dept Populat Med, Ctr Child Hlth Care Studies, Boston, MA USA.
[Lustig, Robert H.] Univ Calif San Francisco, Dept Pediat, San Francisco, CA USA.
[Prosser, Lisa A.] Univ Michigan, Div Gen Pediat, Child Hlth Evaluat & Res Unit, Ann Arbor, MI 48109 USA.
[Songer, Thomas J.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
[Weinstock, Ruth S.] SUNY Upstate Med Univ, Dept Med, Syracuse, NY USA.
[Gonzalez, Tessa] Palmetto Hlth Childrens Hosp, Dept Pediat, Columbia, SC USA.
[Rawluk, Kaitlin] Duke Univ, Sch Med, Durham, NC USA.
[Zoghbi, Roula M.] Texas Childrens Hosp, Houston, TX 77030 USA.
[Laffel, Lori M.] Joslin Diabet Ctr, Pediat Adolescent & Young Adult Sect, Boston, MA 02215 USA.
RP Rhodes, ET (reprint author), Childrens Hosp, Div Endocrinol, 300 Longwood Ave,6th Floor, Boston, MA 02115 USA.
EM Erinn.Rhodes@childrens.harvard.edu
OI Songer, Thomas/0000-0002-5253-2514
FU Centers for Disease Control and Prevention [K01DP000089]; Katherine
Adler Astrove Youth Education Fund; Maria Griffin Drury Fund; National
Institute of Diabetes and Digestive and Kidney Diseases [K24DK082730];
New Balance Foundation; Bayer
FX Supported by the Centers for Disease Control and Prevention (grant
K01DP000089 to E. R.). Investigators were also supported by the
Katherine Adler Astrove Youth Education Fund (to L. L.), Maria Griffin
Drury Fund (to L. L.), National Institute of Diabetes and Digestive and
Kidney Diseases (grant K24DK082730 to D. L.), and the New Balance
Foundation (E. R. and D. L.). The contents of this paper are solely the
responsibility of the authors and do not necessarily represent the
official views of the funding agencies. E. R. was formerly Chief Medical
Officer for Pediatric Weight Management Centers' Great Moves! Program, a
company that was privately owned and operated in collaboration with the
physicians of Children's Hospital Boston. E. R. provided contracted
clinical and administrative services for the company, but neither had
nor has equity or other economic interest in the business. E. R. also
received salary support from an unrestricted, philanthropic grant from
the New Balance Foundation. E.R.'s spouse owns stock in Bristol Meyers
Squibb and Pfizer. L. L. is a consultant for Sanofi-Aventis, Johnson &
Johnson, Lilly, Bristol Myers Squibb, Astra Zeneca, and Menarini and
receives grant support from Bayer. The remaining authors declare no
conflicts of interest.
NR 40
TC 10
Z9 11
U1 3
U2 14
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-3476
J9 J PEDIATR-US
JI J. Pediatr.
PD JUN
PY 2012
VL 160
IS 6
DI 10.1016/j.jpeds.2011.11.026
PG 7
WC Pediatrics
SC Pediatrics
GA 946TC
UT WOS:000304377300008
PM 22217471
ER
PT J
AU Shames, S
Koczo, A
Hahn, R
Jin, ZZ
Picard, MH
Gillam, LD
AF Shames, Sofia
Koczo, Agnes
Hahn, Rebecca
Jin, Zhezhen
Picard, Michael H.
Gillam, Linda D.
TI Flow Characteristics of the SAPIEN Aortic Valve: The Importance of
Recognizing In-Stent Flow Acceleration for the Echocardiographic
Assessment of Valve Function
SO JOURNAL OF THE AMERICAN SOCIETY OF ECHOCARDIOGRAPHY
LA English
DT Editorial Material
DE Echocardiography; Transcatheter aortic valve
ID DOPPLER-ECHOCARDIOGRAPHY; TRANSCATHETER; IMPLANTATION; STENOSIS;
OUTCOMES; COREVALVE; RECOMMENDATIONS; VALIDATION; EXPERIENCE
AB Background: The percutaneously implanted Edwards SAPIEN valve (Edwards Lifesciences, Irvine, CA) consists of cusps mounted within a stent. The individual impact of the stent and cusps on transvalvular flow and its implications for the echocardiographic assessment of valve function have not been previously reported.
Methods: The study group consisted of 40 patients who underwent successful implantation with the SAPIEN valve. Pulsed Doppler was recorded with sample volumes immediately proximal to the stent (prestent), within the stent but proximal to the cusps (in-stent precusp), and distal to the cusps (in-stent postcusp). The Doppler velocity index and effective orifice area were calculated using both prestent and in-stent precusp velocities to represent "subvalvular" flow and continuous-wave recordings of the left ventricular outflow tract and aortic valve to represent postvalvular flow.
Results: In all patients, there was flow acceleration at two levels: in-stent precusp and in-stent postcusp. The mean in-stent precusp peak velocities were significantly higher than the prestent values (1.5 +/- 0.2 vs 1.0 +/- 0.2 m/sec, P < .0001). Effective orifice area and Doppler velocity index calculated using the prestent versus in-stent precusp velocities were also significantly different (1.79 +/- 0.34 vs 2.54 +/- 0.46 cm(2), P < .0001, and 0.48 +/- 0.12 vs 0.73 +/- 0.13, P < .0001, respectively).
Conclusions: The SAPIEN valve demonstrates flow acceleration at two levels, representing contributions of both the stent and valve cusps to the total valve gradient. Failure to recognize this phenomenon may result in inappropriate selection of the in-stent precusp pulsed Doppler spectrum to represent "subvalvular" flow, thereby overestimating the effective orifice area and Doppler velocity index. (J Am Soc Echocardiogr 2012;square:square-square-.)
C1 [Shames, Sofia; Koczo, Agnes; Hahn, Rebecca] Columbia Univ Coll Phys & Surg, New York Presbyterian Hosp, Div Cardiol, New York, NY 10032 USA.
[Jin, Zhezhen] Columbia Univ, Mailman Sch Publ Hlth, Dept Biostat, New York, NY USA.
[Picard, Michael H.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Gillam, Linda D.] Morristown Med Ctr, Dept Cardiovasc Med, Morristown, NJ USA.
RP Gillam, LD (reprint author), Morristown Mem Hosp, Gagnon Cardiovasc Inst, Cardiac Adm 5, 100 Madison Ave, Morristown, NJ 07962 USA.
EM linda.gillam@atlantichealth.org
OI Picard, Michael/0000-0002-9264-3243
NR 18
TC 20
Z9 20
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0894-7317
J9 J AM SOC ECHOCARDIOG
JI J. Am. Soc. Echocardiogr.
PD JUN
PY 2012
VL 25
IS 6
BP 603
EP 609
DI 10.1016/j.echo.2012.02.013
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 946OK
UT WOS:000304361700004
PM 22425590
ER
PT J
AU Perrault, LP
Moskowitz, AJ
Kron, IL
Acker, MA
Miller, MA
Horvath, KA
Thourani, VH
Argenziano, M
D'Alessandro, DA
Blackstone, EH
Moy, CS
Mathew, JP
Hung, J
Gardner, TJ
Parides, MK
AF Perrault, Louis P.
Moskowitz, Alan J.
Kron, Irving L.
Acker, Michael A.
Miller, Marissa A.
Horvath, Keith A.
Thourani, Vinod H.
Argenziano, Michael
D'Alessandro, David A.
Blackstone, Eugene H.
Moy, Claudia S.
Mathew, Joseph P.
Hung, Judy
Gardner, Timothy J.
Parides, Michael K.
TI Optimal surgical management of severe ischemic mitral regurgitation: To
repair or to replace?
SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY
LA English
DT Article
ID VALVULAR HEART-DISEASE; PAPILLARY-MUSCLE; NORMATIVE DATA; VALVE REPAIR;
ANNULOPLASTY; RELIABILITY; DYSFUNCTION
AB Background: Ischemic mitral regurgitation, a complication of myocardial infarction and coronary artery disease more generally, is associated with a high mortality rate and is estimated to affect 2.8 million Americans. With 1-year mortality rates as high as 40%, recent practice guidelines of professional societies recommend repair or replacement, but there remains a lack of conclusive evidence supporting either intervention. The choice between therapeutic options is characterized by the trade-off between reduced operative morbidity and mortality with repair versus a better long-term correction of mitral insufficiency with replacement. The long-term benefits of repair versus replacement remain unknown, which has led to significant variation in surgical practice.
Methods and Results: This article describes the design of a prospective randomized clinical trial to evaluate the safety and effectiveness of mitral valve repair and replacement in patients with severe ischemic mitral regurgitation. This trial is being conducted as part of the Cardiothoracic Surgical Trials Network. This article addresses challenges in selecting a feasible primary end point, characterizing the target population (including the degree of mitral regurgitation) and analytical challenges in this high mortality disease.
Conclusions: The article concludes by discussing the importance of information on functional status, survival, neurocognition, quality of life, and cardiac physiology in therapeutic decision making. (J Thorac Cardiovasc Surg 2012;143:1396-403)
C1 [Moskowitz, Alan J.; Parides, Michael K.] Mt Sinai Sch Med, Dept Hlth Evidence & Policy, InCHOIR, New York, NY USA.
[Perrault, Louis P.] Univ Montreal, Montreal Heart Inst, Dept Surg, Montreal, PQ, Canada.
[Kron, Irving L.] Univ Virginia, Sch Med, Div Thorac & Cardiovasc Surg, Charlottesville, VA 22908 USA.
[Acker, Michael A.] Univ Penn, Div Cardiovasc Surg, Philadelphia, PA 19104 USA.
[Miller, Marissa A.] NHLBI, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
[Horvath, Keith A.] Suburban Hosp, NIH Heart Ctr, Bethesda, MD USA.
[Thourani, Vinod H.] Emory Univ Hosp Midtown, Div Cardiothorac Surg, Atlanta, GA USA.
[Argenziano, Michael] Columbia Univ, Med Ctr, Div Cardiothorac Surg, New York, NY USA.
[D'Alessandro, David A.] Montefiore Einstein Heart Ctr, Dept Cardiovasc & Thorac Surg, New York, NY USA.
[Blackstone, Eugene H.] Cleveland Clin, Dept Thorac & Cardiovasc Surg, Cleveland, OH 44106 USA.
[Moy, Claudia S.] Natl Inst Neurol Disorders & Stroke, Bethesda, MD USA.
[Mathew, Joseph P.] Duke Univ, Med Ctr, Dept Anesthesiol, Durham, NC 27710 USA.
[Hung, Judy] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Gardner, Timothy J.] Christiana Care Hlth Syst, Ctr Heart & Vasc Hlth, Newark, DE USA.
RP Parides, MK (reprint author), Mt Sinai Sch Med, Dept Hlth Evidence & Policy, InCHOIR, New York, NY USA.
EM michael.parides@mssm.edu
OI Moskowitz, Alan/0000-0002-4412-9450
FU NHLBI NIH HHS [U01 HL088942, R01 HL092101]
NR 31
TC 18
Z9 22
U1 1
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5223
J9 J THORAC CARDIOV SUR
JI J. Thorac. Cardiovasc. Surg.
PD JUN
PY 2012
VL 143
IS 6
BP 1396
EP 1403
DI 10.1016/j.jtcvs.2011.05.030
PG 8
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 943HE
UT WOS:000304110700025
PM 22054660
ER
PT J
AU Cuffe, S
Bourredjem, A
Graziano, S
Pignon, JP
Domerg, C
Ezzalfani, M
Seymour, L
Strevel, E
Burkes, R
Capelletti, M
Janne, PA
Tsao, MS
Shepherd, FA
AF Cuffe, Sinead
Bourredjem, Abderrahmane
Graziano, Stephen
Pignon, Jean-Pierre
Domerg, Caroline
Ezzalfani, Monia
Seymour, Lesley
Strevel, Elizabeth
Burkes, Ronald
Capelletti, Marzia
Jaenne, Pasi A.
Tsao, Ming-Sound
Shepherd, Frances A.
TI A Pooled Exploratory Analysis of the Effect of Tumor Size and KRAS
Mutations on Survival Benefit From Adjuvant Platinum-Based Chemotherapy
in Node-Negative Non-Small Cell Lung Cancer
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Article
DE Non-small-cell lung cancer; KRAS mutations; Adjuvant chemotherapy; TNM
staging; Tumor size
ID FORTHCOMING 7TH EDITION; VINORELBINE PLUS CISPLATIN; TNM CLASSIFICATION;
STAGING PROJECT; PROGNOSTIC-SIGNIFICANCE; MALIGNANT-TUMORS; PROPOSALS;
REVISION; RAS; GROUPINGS
AB Introduction: The staging of node-negative non-small-cell lung cancer is modified in the 7th edition TNM classification. Here, we pool data from the National Cancer Institute of Canada Clinical Trials Group JBR. 10 trial and the Cancer and Leukemia Group B-9633 trial to explore the prognostic and predictive effects of the new T-size descriptors and KRAS mutation status.
Methods: Node-negative patients were reclassified as T2a (>3-<= 5 cm), T2b (>5-<= 7 cm), T3 (>7 cm) or T <= 3 cm (<= 3 cm, but other T2 characteristics).
Results: Of 538 eligible patients, 288 (53.5%) were T2a, 111 (21%) T2b, 62 (11.5%) T3, whereas 77 (14%) T <= 3 cm were excluded to avoid confounding. KRAS mutations were detected in 104 of 390 patients (27%). T-size was prognostic for disease-free survival (p = 0.03), but borderline for overall survival (OS; p = 0.10), on multivariable analysis. Significant interaction between the prognostic value of KRAS and tumor size was observed for OS (p = 0.01), but not disease-free survival (p = 0.10). There was a nonsignificant trend (p = 0.24) for increased chemotherapy effect on OS with advancing T-size (hazard ratio [HR] T2a 0.90, [0.63-1.30]; T2b 0.69, [0.38-1.24]; and T3 0.57, [0.28-1.17]). The HR for chemotherapy effect on OS in T2a patients with KRAS wild-type tumors was 0.81 (p = 0.36), whereas a trend for detrimental effect was observed in those with mutant tumors (HR 2.11; p = 0.09; interaction p = 0.05). Similar trends were observed in T2b to T3 patients with wild-type (HR 0.86; p = 0.62), and KRAS mutant tumors (HR 1.16; p = 0.74; interaction p = 0.58).
Conclusion: Chemotherapy effect seems to increase with tumor size. However, this small study could not identify subgroups of patients who did or did not derive significant benefit from adjuvant chemotherapy based on T-size or KRAS status.
C1 [Cuffe, Sinead; Tsao, Ming-Sound; Shepherd, Frances A.] Univ Hlth Network, Princess Margaret Hosp, Dept Med Oncol & Hematol, Toronto, ON M5G 2M9, Canada.
[Cuffe, Sinead; Tsao, Ming-Sound; Shepherd, Frances A.] Univ Toronto, Toronto, ON, Canada.
[Bourredjem, Abderrahmane; Pignon, Jean-Pierre; Domerg, Caroline; Ezzalfani, Monia] Inst Gustave Roussy, Dept Biostat & Epidemiol, Villejuif, France.
[Graziano, Stephen] SUNY Upstate Med Univ, Dept Med, Syracuse, NY USA.
[Seymour, Lesley] Queens Univ, NCIC Clin Trials Grp, Kingston, ON, Canada.
[Strevel, Elizabeth] Credit Valley Hosp, Dept Med Oncol, Mississauga, ON, Canada.
[Burkes, Ronald] Mt Sinai Hosp, Dept Med Oncol, Toronto, ON M5G 1X5, Canada.
[Capelletti, Marzia; Jaenne, Pasi A.] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Shepherd, FA (reprint author), Univ Hlth Network, Princess Margaret Hosp, Dept Med Oncol & Hematol, Suite 5-104,610 Univ Ave, Toronto, ON M5G 2M9, Canada.
EM frances.shepherd@uhn.on.ca
FU French Ligue Nationale Contre le Cancer; Sanofi; Canadian Cancer
Society; National Cancer Institute of the United States; National Cancer
Institute [CA31946, CA33601]
FX Supported by the French Ligue Nationale Contre le Cancer and an
unrestricted grant from Sanofi. The JBR. 10 trial was supported by the
Canadian Cancer Society and the National Cancer Institute of the United
States. The research for CALGB 9633 was supported, in part, by grants
from the National Cancer Institute (CA31946) to the Cancer and Leukemia
Group B (M.M.B.) and to the CALGB Statistical Center (D.J.S., CA33601).
The content of this manuscript is solely the responsibility of the
authors and does not necessarily reflect the official views of the
National Cancer Institute.
NR 29
TC 11
Z9 11
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD JUN
PY 2012
VL 7
IS 6
BP 963
EP 972
DI 10.1097/JTO.0b013e31824fe9e6
PG 10
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA 943IK
UT WOS:000304114000003
PM 22588152
ER
PT J
AU Westover, KD
Seco, J
Adams, JA
Lanuti, M
Choi, NC
Engelsman, M
Willers, H
AF Westover, Kenneth D.
Seco, Joao
Adams, Judith A.
Lanuti, Michael
Choi, Noah C.
Engelsman, Martijn
Willers, Henning
TI Proton SBRT for Medically Inoperable Stage I NSCLC
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Article
DE Stereotactic body radiation therapy; Proton therapy; Non-small-cell lung
cancer
ID STEREOTACTIC BODY RADIOTHERAPY; CELL LUNG-CARCINOMA; RADIATION-THERAPY;
QUALITY-ASSURANCE; BEAM RADIOTHERAPY; CANCER; TUMORS; TOXICITY
AB Introduction: The physical properties of proton beam radiation may offer advantages for treating patients with non-small-cell lung cancer (NSCLC). However, its utility for the treatment of medically inoperable stage I NSCLC patients with stereotactic body radiation therapy (SBRT) is unknown.
Methods: Outcomes for patients with medically inoperable stage I NSCLC treated with proton SBRT were retrospectively analyzed. Proton SBRT was selected as the treatment modality based on pulmonary comorbidities (n = 5), prior chest radiation or/and multiple primary tumors (n = 7), or other reasons (n = 3). Treatments were administered using 2 to 3 proton beams. Treatment toxicity was scored according to common toxicity criteria for adverse events version 4 criteria.
Results: Fifteen consecutive patients and 20 tumors were treated with proton SBRT to 42 to 50 Gy(relative biological effectiveness) in 3 to 5 fractions between July 2008 and September 2010. Treatments were well tolerated with only one case of grade 2 fatigue, one case of grade 2 dermatitis, three cases of rib fracture (maximum grade 2), and one case of grade 3 pneumonitis in a patient with severe chronic obstructive pulmonary disease. With a median follow-up of 24.1 months, 2-year overall survival and local control rates were 64% (95% confidence limits, 34%-83%) and 100% (83%-100%), respectively.
Conclusions: We conclude that proton SBRT is effective and well tolerated in this unfavorable group of patients. Prospective clinical trials testing the utility of proton SBRT in stage I NSCLC are warranted.
C1 [Seco, Joao; Adams, Judith A.; Engelsman, Martijn; Willers, Henning] Massachusetts Gen Hosp, Dept Radiat Oncol, Div Radiat Phys, Boston, MA 02114 USA.
[Westover, Kenneth D.] Harvard Radiat Oncol Program, Boston, MA USA.
[Lanuti, Michael] Harvard Univ, Sch Med, Dept Surg, Div Thorac Surg,Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Willers, H (reprint author), Massachusetts Gen Hosp, Dept Radiat Oncol, Div Radiat Phys, Cox 3,55 Fruit St, Boston, MA 02114 USA.
EM hwillers@partners.org
RI Seco, Joao/J-4451-2012
FU Federal Share of program; Proton Therapy Research and Treatment Center
[C06 CA059267]
FX The project was supported by the Federal Share of program income earned
by Massachusetts General Hospital on C06 CA059267, Proton Therapy
Research and Treatment Center.
NR 23
TC 22
Z9 23
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD JUN
PY 2012
VL 7
IS 6
BP 1021
EP 1025
DI 10.1097/JTO.0b013e31824de0bf
PG 5
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA 943IK
UT WOS:000304114000010
PM 22551902
ER
PT J
AU Oxnard, GR
Miller, VA
Robson, ME
Azzoli, CG
Pao, W
Ladanyi, M
Arcila, ME
AF Oxnard, Geoffrey R.
Miller, Vincent A.
Robson, Mark E.
Azzoli, Christopher G.
Pao, William
Ladanyi, Marc
Arcila, Maria E.
TI Screening for Germline EGFR T790M Mutations Through Lung Cancer
Genotyping
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Article
ID TYROSINE KINASE INHIBITORS; SUSCEPTIBILITY LOCUS; NEVER-SMOKERS;
ADENOCARCINOMAS; RESISTANCE
AB Introduction: The study of patients carrying germline endothelial growth factor receptor (EGFR) mutations, which have been found in cases of familial lung adenocarcinoma, could provide unique insight into lung cancer risk and carcinogenesis in never-smokers. However, investigations into the biology of germline EGFR mutations have been hampered by the lack of an effective strategy for screening for carriers. We hypothesized that patients with lung cancers found to harbor the EGFR T790M resistance mutation before treatment, an uncommon occurrence, would be likely to carry underlying germline T790M mutations.
Methods: Eleven unrelated patients with lung cancer, harboring an EGFR T790M mutation, were identified from a 7-year institutional experience with tumor genotyping. Ten patients had benign tissue available, which was anonymously tested for the presence of germline EGFR mutations.
Results: Five of 10 cases carried a germline T790M mutation (50%, confidence interval 27%-73%). One patient's cancer exhibited a distinctive indolent growth, which has also been described in preclinical studies of T790M-mutant cancers. A second patient underwent resection of six separate primary lung adenocarcinomas, each carrying different sensitizing EGFR mutations and T790M.
Conclusions: Genotyping of lung cancers, now commonly performed to predict benefit from treatment with EGFR tyrosine kinase inhibitors, can also be used as a screening tool to identify patients at risk of carrying germline EGFR mutations. Once identified, these patients and their families can be studied prospectively to explore appropriate lung cancer screening strategies. Further studies using existing oncogenomic data to provide insight into underlying germline genetics are warranted.
C1 [Oxnard, Geoffrey R.; Miller, Vincent A.; Azzoli, Christopher G.] Mem Sloan Kettering Canc Ctr, Thorac Oncol Serv, Dept Med, New York, NY 10021 USA.
[Robson, Mark E.] Mem Sloan Kettering Canc Ctr, Dept Med, Clin Genet Serv, New York, NY 10021 USA.
[Pao, William] Vanderbilt Ingram Canc Ctr, Dept Med, Nashville, TN USA.
[Ladanyi, Marc; Arcila, Maria E.] Mem Sloan Kettering Canc Ctr, Dept Pathol, Mol Diagnost Serv, New York, NY 10021 USA.
RP Oxnard, GR (reprint author), Dana Farber Canc Inst, 450 Brookline Ave,D1234, Boston, MA 02215 USA.
EM goxnard@partners.org
RI Mendez, Pedro /J-8955-2016;
OI Mendez, Pedro /0000-0001-6713-7907; Robson, Mark/0000-0002-3109-1692
FU National Cancer Institute; Astra-Zeneca; Enzon; Xcovery; Symphogen;
American Society of Clinical Oncology; National Cancer Institute at the
National Institutes of Health [P01-CA129243]
FX Vincent A. Miller's institution has received a P01 grant from the
National Cancer Institute and he hold patents relating to this work.
Christopher G. Azzoli's institution has received a P01 grant from the
National Cancer Institute. Geoffrey R. Oxnard's institution has received
a P01 grant from the National Cancer Institute, and he has served on the
advisory board of Genentech. Mark Robson has served as a consultant to
Sanofi-Aventis, Abbott, Pfizer, and General Electric, and has received
grants from Astra-Zeneca. Marc Ladanyi has served as a consultant to
Astra Zeneca (Canada), Daiichi-Sankyo, and Genzyme. William Pao serves
as a consultant to MolecularMD, AstraZeneca, Bristol-Myers Squibb,
Symphony Evolution, and Clovis Oncology. William Pao has received grants
from Enzon, Xcovery, AstraZeneca, and Symphogen. Rights to EGFR T790M
testing were licensed on behalf of William Pao and others by MSKCC to
MolecularMD.; Supported in part by a Young Investigator Award from the
American Society of Clinical Oncology; and from the National Cancer
Institute at the National Institutes of Health (P01-CA129243).
NR 18
TC 38
Z9 38
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD JUN
PY 2012
VL 7
IS 6
BP 1049
EP 1052
DI 10.1097/JTO.0b013e318250ed9d
PG 4
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA 943IK
UT WOS:000304114000014
PM 22588155
ER
PT J
AU Lo, RC
Bensley, RP
Hamdan, AD
Wyers, M
Chaikof, E
Adams, JE
Schermerhorn, ML
AF Lo, Ruby C.
Bensley, Rodney P.
Hamdan, Allen D.
Wyers, Mark
Chaikof, Elliot
Adams, Julie E.
Schermerhorn, Marc L.
TI Gender Differences in Aortic Aneurysm Presentation, Repair, and
Mortality in the VSGNE
SO JOURNAL OF VASCULAR SURGERY
LA English
DT Meeting Abstract
CT Vascular Annual Meeting of the Society-for-Vascular-Surgery (SVS)
CY JUN 07-09, 2012
CL Natl Harbor, MD
SP Soc Vasc Surg (SVS)
C1 [Lo, Ruby C.; Bensley, Rodney P.; Hamdan, Allen D.; Wyers, Mark; Chaikof, Elliot; Schermerhorn, Marc L.] BIDMC, Boston, MA USA.
[Adams, Julie E.] Univ Vermont, Coll Med, Burlington, VT USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0741-5214
J9 J VASC SURG
JI J. Vasc. Surg.
PD JUN
PY 2012
VL 55
IS 6
SU S
BP 10
EP 11
PG 2
WC Surgery; Peripheral Vascular Disease
SC Surgery; Cardiovascular System & Cardiology
GA 947AL
UT WOS:000304398900016
ER
PT J
AU Kang, JW
Patel, VI
Mukhopadhyay, S
Garg, A
Cambria, MR
Conrad, MF
LaMuraglia, GM
Cambria, RP
AF Kang, Jeanwan
Patel, Virendra I.
Mukhopadhyay, Shankha
Garg, Ashu
Cambria, Matthew R.
Conrad, Mark F.
LaMuraglia, Glenn M.
Cambria, Richard P.
TI Long-term Clinical and Anatomic Outcomes Following Carotid
Endarterectomy
SO JOURNAL OF VASCULAR SURGERY
LA English
DT Meeting Abstract
CT Vascular Annual Meeting of the Society-for-Vascular-Surgery (SVS)
CY JUN 07-09, 2012
CL Natl Harbor, MD
SP Soc Vasc Surg (SVS)
C1 [Kang, Jeanwan; Patel, Virendra I.; Mukhopadhyay, Shankha; Garg, Ashu; Cambria, Matthew R.; Conrad, Mark F.; LaMuraglia, Glenn M.; Cambria, Richard P.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 1
Z9 1
U1 1
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0741-5214
J9 J VASC SURG
JI J. Vasc. Surg.
PD JUN
PY 2012
VL 55
IS 6
SU S
BP 12
EP 13
PG 2
WC Surgery; Peripheral Vascular Disease
SC Surgery; Cardiovascular System & Cardiology
GA 947AL
UT WOS:000304398900020
ER
PT J
AU Wang, JY
Gupta, N
Raffetto, JD
Haider, SA
Silva, R
Ebaugh, JL
Sulkin, M
Fox, R
AF Wang, Jeffrey Y.
Gupta, Naren
Raffetto, Joseph D.
Haider, Shan-Ali
Silva, Richard
Ebaugh, James L.
Sulkin, Michael
Fox, Robert
TI Ambulatory Venous Thrombectomy for Acute Deep Venous Thrombosis
SO JOURNAL OF VASCULAR SURGERY
LA English
DT Meeting Abstract
CT Vascular Annual Meeting of the Society-for-Vascular-Surgery (SVS)
CY JUN 07-09, 2012
CL Natl Harbor, MD
SP Soc Vasc Surg (SVS)
C1 [Wang, Jeffrey Y.; Haider, Shan-Ali; Silva, Richard; Sulkin, Michael; Fox, Robert] Shady Grove Adventist Hosp, Rockville, MD USA.
[Gupta, Naren; Raffetto, Joseph D.; Ebaugh, James L.] VA Boston Healthcare Syst, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0741-5214
J9 J VASC SURG
JI J. Vasc. Surg.
PD JUN
PY 2012
VL 55
IS 6
SU S
BP 102
EP 102
PG 1
WC Surgery; Peripheral Vascular Disease
SC Surgery; Cardiovascular System & Cardiology
GA 947AL
UT WOS:000304398900195
ER
PT J
AU Danczyk, RC
Mitchell, EL
Burk, C
Singh, S
Liem, TK
Landry, GJ
Petersen, BD
Moneta, GL
AF Danczyk, Rachel C.
Mitchell, Erica L.
Burk, Chad
Singh, Sarguni
Liem, Timothy K.
Landry, Gregory J.
Petersen, Bryan D.
Moneta, Gregory L.
TI Comparing patient outcomes between multiple ipsilateral iliac artery
stents and isolated iliac artery stents
SO JOURNAL OF VASCULAR SURGERY
LA English
DT Article; Proceedings Paper
CT 26th Annual Meeting of the Western-Vascular-Society
CY SEP 17-20, 2011
CL Kauai, HI
SP Western Vasc Soc
ID PERCUTANEOUS TRANSLUMINAL ANGIOPLASTY; AORTOILIAC OCCLUSIVE DISEASE;
CONSENSUS-CLASS-C; ENDOVASCULAR TREATMENT; PREDICTORS; LESIONS;
MULTICENTER; EXPERIENCE; ISCHEMIA; THERAPY
AB Objective: Endovascular stents are accepted therapy for iliac artery stenoses and occlusions. Surgery is the recommended therapy for patients with severe iliac artery disease, including those with the combination of ipsilateral common iliac artery (CIA) and external iliac artery (EIA) stenoses/occlusions. This study compared patient outcomes, including late open conversion rates, for combined ipsilateral CIA and EIA stenting vs CIA or EIA stents alone.
Methods: Between 1998 and 2010, 588 patients underwent iliac artery stenting at two institutions. Patient comorbidities and outcomes were retrospectively reviewed, and analyses were performed using multivariate regression and Kaplan-Meier methods.
Results: There were 436 extremities with CIA stents, 195 with EIA stents, and 157 with CIA and EIA stents. The groups did not differ significantly in demographics, comorbidities, or treatment indications. During follow-up, 183 patients died, 95 underwent an endovascular reintervention, and 48 required late open conversion. For patients in the CIA or EIA stent group, the mean +/- standard error survival was 5.3 +/- 0.3 years, secondary endovascular intervention-free survival was 7.4 +/- 0.6 years, late open conversion-free survival was 9.8 +/- 0.4 years, and amputation-free survival was 7.6 +/- 0.4 years. In the CIA and EIA stent group, survival was 6.1 +/- 0.6 years, secondary endovascular intervention-free survival was 7.2 +/- 0.6 years, late open conversion-free survival was 9.0 +/- 1.1 years, and amputation-free survival was 8.4 +/- 0.5 years. Survival, reintervention-free survival, late open conversion-free survival, and amputation-free survival were all similar between patient groups (all P > .05). CIA and EIA stenting in combination was not a predictor of death, reintervention, late open conversion, or amputation.
Conclusions: Outcomes are similar for patients with CIA or EIA stents and for those with combined ipsilateral CIA and EIA stents. Late open conversions for iliac artery stent failure are uncommon and not influenced by the location or extent of prior iliac artery stent placement. Endovascular therapy for aortoiliac disease should be extended to consider selected patients with ipsilateral CIA and EIA stenoses/occlusions. (J Vasc Surg 2012; 55: 1637-46.)
C1 [Danczyk, Rachel C.; Mitchell, Erica L.; Burk, Chad; Singh, Sarguni; Liem, Timothy K.; Landry, Gregory J.; Moneta, Gregory L.] Oregon Hlth & Sci Univ, Div Vasc Surg, Portland, OR 97239 USA.
[Petersen, Bryan D.] Oregon Hlth & Sci Univ, Dotter Inst, Portland, OR 97239 USA.
[Petersen, Bryan D.] Oregon Hlth & Sci Univ, Portland Vet Affairs Med Ctr, Portland, OR 97239 USA.
RP Mitchell, EL (reprint author), Oregon Hlth & Sci Univ, Div Vasc Surg, OP11, Portland, OR 97239 USA.
EM mitcheer@ohsu.edu
NR 21
TC 3
Z9 4
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0741-5214
J9 J VASC SURG
JI J. Vasc. Surg.
PD JUN
PY 2012
VL 55
IS 6
BP 1637
EP U411
DI 10.1016/j.jvs.2011.12.048
PG 16
WC Surgery; Peripheral Vascular Disease
SC Surgery; Cardiovascular System & Cardiology
GA 944MF
UT WOS:000304206000014
PM 22360919
ER
PT J
AU Raffetto, JD
Yu, P
Reslan, OM
Xia, Y
Khalil, RA
AF Raffetto, Joseph D.
Yu, Peng
Reslan, Ossama M.
Xia, Yin
Khalil, Raouf A.
TI Endothelium-dependent nitric oxide and hyperpolarization-mediated venous
relaxation pathways in rat inferior vena cava
SO JOURNAL OF VASCULAR SURGERY
LA English
DT Article; Proceedings Paper
CT 23rd Annual Meeting of the American-Venous-Forum
CY FEB 23-26, 2011
CL San Diego, CA
SP Amer Venous Forum
ID POTASSIUM CHANNEL OPENERS; VARICOSE-VEIN FORMATION; K+-CHANNELS;
HYDROGEN-PEROXIDE; SAPHENOUS-VEIN; SMALL ARTERIES; FEMORAL VEINS;
PREGNANT RATS; FACTOR EDHF; CYCLIC-GMP
AB Introduction: The vascular endothelium plays a major role in the control of arterial tone; however, its role in venous tissues is less clear. The purpose of this study was to determine the role of endothelium in the control of venous function and the relaxation pathways involved.
Methods: Circular segments of inferior vena cava (IVC) from male Sprague-Dawley rats were suspended between two wires and isometric contraction to phenylephrine (Phe; 10(-5)M) and 96 mM KCl was measured. Acetylcholine (Ach; 10(-10) to 10(-5)M) was added and the percentage of venous relaxation was measured. To determine the role of nitric oxide (NO) and prostacyclin (PGI(2)), vein relaxation was measured in the presence of the nitric oxide synthase inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME; 3 x 10(-4) M) and the cyclooxygenase inhibitor indomethacin (10(-5) M). To measure the role of hyperpolarization, vein relaxation was measured in the presence of K+ channel activator cromakalim (10(-11) to 10(-6) M), and the nonselective K+ channel blocker tetraethylammonium (TEA; 10(-3) M). To test for the contribution of a specific K+ channel, the effects of K+ channel blockers: glibenclamide (adenosine triphosphate [ATP]-sensitive K-ATP, 10(-5) M), 4-aminopyridine (4-AP; voltage-dependent K-v, 10(-3) M), apamin (small conductance Ca2+-dependent SKCa, 10(-7) M), and iberiotoxin (large conductance Ca2+-dependent BKCa, 10(-8) M) on Ach-induced relaxation were tested.
Results: Ach caused concentration-dependent relaxation of Phe contraction (maximum 49.9 +/- 4.9%). Removal of endothelium abolished Ach-induced relaxation. IVC treatment with L-NAME partially reduced Ach relaxation (32.8 +/- 4.9%). In IVC treated with L-NAME plus indomethacin, significant Ach-induced relaxation (33.6 +/- 3.2%) could still be observed, suggesting a role of endothelium-derived hyperpolarizing factor (EDHF). In IVC treated with L-NAME, indomethacin and TEA, Ach relaxation was abolished, supporting a role of EDHF. In veins stimulated with high KCl, Ach caused relaxation (maximum 59.5 +/- 3.5%) that was abolished in the presence of L-NAME and indomethacin suggesting that any Ach-induced EDHF is blocked in the presence of high KCl depolarizing solution, which does not favor outward movement of K+ ion and membrane hyperpolarization. Cromakalim, an activator of K-ATP, caused significant IVC relaxation when applied alone or on top of maximal Ach-induced relaxation, suggesting that the Ach response may not involve K-ATP. Ach-induced relaxation was not inhibited by glibenclamide, 4-AP, or apamin, suggesting little role of K-ATP, K-v or SKCa, respectively. In contrast, iberiotoxin significantly inhibited Ach-induced relaxation, suggesting a role of BKCa.
Conclusions: Thus, endothelium-dependent venous relaxation plays a major role in the control of venous function. In addition to NO, an EDHF pathway involving BKCa may play a role in endothelium-dependent venous relaxation. (J Vasc Surg 2012;55:1716-25.)
C1 [Raffetto, Joseph D.; Khalil, Raouf A.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Raffetto, Joseph D.; Yu, Peng; Reslan, Ossama M.; Xia, Yin; Khalil, Raouf A.] Brigham & Womens Hosp, Div Vasc & Endovasc Surg, Boston, MA 02115 USA.
[Raffetto, Joseph D.] VA Boston Healthcare Syst, W Roxbury, MA USA.
RP Khalil, RA (reprint author), Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Vasc Surg, 75 Francis St, Boston, MA 02115 USA.
EM raouf_khalil@hms.harvard.edu
FU NHLBI NIH HHS [R21 HL098724, R21 HL098724-01A1, R01 HL065998-10,
HL-98724, R01 HL065998, R01 HL065998-09, R01 HL070659-05, R01 HL070659,
HL-65998, R21 HL098724-02]; NICHD NIH HHS [HD-60702, R03 HD060702-01,
R03 HD060702-02, R03 HD060702]
NR 57
TC 5
Z9 5
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0741-5214
J9 J VASC SURG
JI J. Vasc. Surg.
PD JUN
PY 2012
VL 55
IS 6
BP 1716
EP 1725
DI 10.1016/j.jvs.2011.10.124
PG 10
WC Surgery; Peripheral Vascular Disease
SC Surgery; Cardiovascular System & Cardiology
GA 944MF
UT WOS:000304206000025
PM 22209615
ER
PT J
AU Moldt, B
Shibata-Koyama, M
Rakasz, EG
Schultz, N
Kanda, Y
Dunlop, DC
Finstad, SL
Jin, CG
Landucci, G
Alpert, MD
Dugast, AS
Parren, PWHI
Nimmerjahn, F
Evans, DT
Alter, G
Forthal, DN
Schmitz, JE
Iida, S
Poignard, P
Watkins, DI
Hessell, AJ
Burton, DR
AF Moldt, Brian
Shibata-Koyama, Mami
Rakasz, Eva G.
Schultz, Niccole
Kanda, Yutaka
Dunlop, D. Cameron
Finstad, Samantha L.
Jin, Chenggang
Landucci, Gary
Alpert, Michael D.
Dugast, Anne-Sophie
Parren, Paul W. H. I.
Nimmerjahn, Falk
Evans, David T.
Alter, Galit
Forthal, Donald N.
Schmitz, Jorn E.
Iida, Shigeru
Poignard, Pascal
Watkins, David I.
Hessell, Ann J.
Burton, Dennis R.
TI A Nonfucosylated Variant of the anti-HIV-1 Monoclonal Antibody b12 Has
Enhanced Fc gamma RIIIa-Mediated Antiviral Activity In Vitro but Does
Not Improve Protection against Mucosal SHIV Challenge in Macaques
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID DEPENDENT CELLULAR CYTOTOXICITY; SIMIAN IMMUNODEFICIENCY VIRUS; HIV
PRECLINICAL INTERVENTIONS; EFFECTOR-CELLS; NEUTRALIZING ANTIBODIES;
NONHUMAN-PRIMATES; BINDING; RESPONSES; RECEPTOR; INFECTION
AB Eliciting neutralizing antibodies is thought to be a key activity of a vaccine against human immunodeficiency virus (HIV). However, a number of studies have suggested that in addition to neutralization, interaction of IgG with Fc gamma receptors (Fc gamma R) may play an important role in antibody-mediated protection. We have previously obtained evidence that the protective activity of the broadly neutralizing human IgG1 anti-HIV monoclonal antibody (MAb) b12 in macaques is diminished in the absence of Fc gamma R binding capacity. To investigate antibody-dependent cellular cytotoxicity (ADCC) as a contributor to Fc gamma R-associated protection, we developed a nonfucosylated variant of b12 (NFb12). We showed that, compared to fully fucosylated (referred to as wild-type in the text) b12, NFb12 had higher affinity for human and rhesus macaque Fc gamma RIIIa and was more efficient in inhibiting viral replication and more effective in killing HIV-infected cells in an ADCC assay. Despite these more potent in vitro antiviral activities, NFb12 did not enhance protection in vivo against repeated low-dose vaginal challenge in the simian-human immunodeficiency virus (SHIV)/macaque model compared to wild-type b12. No difference in protection, viral load, or infection susceptibility was observed between animals given NFb12 and those given fully fucosylated b12, indicating that Fc gamma R-mediated activities distinct from Fc gamma RIIIa-mediated ADCC may be important in the observed protection against SHIV challenge.
C1 [Moldt, Brian; Schultz, Niccole; Dunlop, D. Cameron; Poignard, Pascal; Hessell, Ann J.; Burton, Dennis R.] Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
[Moldt, Brian; Schultz, Niccole; Dunlop, D. Cameron; Poignard, Pascal; Hessell, Ann J.; Burton, Dennis R.] Scripps Res Inst, IAVI Neutralizing Antibody Ctr, La Jolla, CA USA.
[Shibata-Koyama, Mami; Kanda, Yutaka] Kyowa Hakko Kirin Calif Inc, La Jolla, CA USA.
[Rakasz, Eva G.; Watkins, David I.] Univ Wisconsin Madison, Dept Pathol, Madison, WI USA.
[Rakasz, Eva G.; Watkins, David I.] Univ Wisconsin Madison, Lab Med, Madison, WI USA.
[Finstad, Samantha L.; Jin, Chenggang; Schmitz, Jorn E.] Harvard Univ, Sch Med, Beth Israel Med Ctr, Div Vial Pathogenesis, Boston, MA USA.
[Landucci, Gary; Forthal, Donald N.] Univ Calif Irvine, Dept Med, Div Infect Dis, Irvine, CA 92717 USA.
[Alpert, Michael D.; Evans, David T.] Harvard Univ, Sch Med, New England Primate Res Ctr, Dept Microbiol & Mol Genet, Southborough, MA USA.
[Dugast, Anne-Sophie; Alter, Galit; Burton, Dennis R.] Massachusetts Gen Hosp, Ragon Inst, Massachusetts Inst Technol & Harvard, Boston, MA USA.
[Parren, Paul W. H. I.] Genmab, Utrecht, Netherlands.
[Nimmerjahn, Falk] Univ Erlangen Nurnberg, Inst Genet, Dept Biol, D-91054 Erlangen, Germany.
[Iida, Shigeru] Kyowa Hakko Kirin, Tokyo, Japan.
[Poignard, Pascal] Int AIDS Vaccine Initiat, New York, NY USA.
[Hessell, Ann J.] Oregon Hlth & Sci Univ, Oregon Natl Primate Res Ctr, Beaverton, OR USA.
[Hessell, Ann J.] Oregon Hlth & Sci Univ, Vaccine & Gene Therapy Inst, Beaverton, OR USA.
RP Burton, DR (reprint author), Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
EM hessell@ohsu.edu; burton@scripps.edu
RI Nimmerjahn, Falk/J-4986-2013; poignard, pascal/N-6678-2013; Dugast,
AnneSophie/L-9541-2015;
OI Finstad, Samantha/0000-0002-3460-6428; Nimmerjahn,
Falk/0000-0002-5418-316X
FU NIH/NIAID [R01 AI055332]; Center for HIV/AIDS Vaccine Immunology NIAID
[U19 AI067854]; International AIDS Vaccine Initiative through the
Neutralizing Antibody Consortium; The Ragon Institute of MGH; The Ragon
Institute of MIT; The Ragon Institute of Harvard; Alfred Benzon
Fellowship
FX This work was funded by NIH/NIAID grant R01 AI055332 (D.R.B.), by the
Center for HIV/AIDS Vaccine Immunology NIAID grant U19 AI067854 (S.L.F.,
C.J., and J.E.S.), by the International AIDS Vaccine Initiative through
the Neutralizing Antibody Consortium (D.R.B.), by The Ragon Institute of
MGH, MIT, and Harvard, and by an Alfred Benzon Fellowship (B.M.).
NR 50
TC 58
Z9 58
U1 0
U2 5
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD JUN
PY 2012
VL 86
IS 11
BP 6189
EP 6196
DI 10.1128/JVI.00491-12
PG 8
WC Virology
SC Virology
GA 944UM
UT WOS:000304229300020
PM 22457527
ER
PT J
AU Abel, GA
Vanderplas, A
Rodriguez, MA
Crosby, AL
Czuczman, MS
Niland, JC
Gordon, LI
Millenson, M
Zelenetz, AD
Friedberg, JW
LaCasce, AS
AF Abel, Gregory A.
Vanderplas, Ann
Rodriguez, Maria A.
Crosby, Allison L.
Czuczman, Myron S.
Niland, Joyce C.
Gordon, Leo I.
Millenson, Michael
Zelenetz, Andrew D.
Friedberg, Jonathan W.
LaCasce, Ann S.
TI High rates of surveillance imaging for treated diffuse large B-cell
lymphoma: findings from a large national database
SO LEUKEMIA & LYMPHOMA
LA English
DT Article
DE Diff use large B-cell lymphoma; diagnostic imaging; health services
research
ID NON-HODGKINS-LYMPHOMA; POSITRON-EMISSION-TOMOGRAPHY; FOLLOW-UP; COMPLETE
REMISSION; CANCER; RELAPSE; SCANS; PET
AB We aimed to characterize surveillance imaging and circumstances of relapse for patients with diffuse large B-cell lymphoma (DLBCL) in the National Comprehensive Cancer Network Non-Hodgkin's Lymphoma Outcomes Database, a prospective cohort study collecting clinical and outcome data at seven comprehensive cancer centers. Patients presenting with newly diagnosed DLBCL in remission >= 3 months after initial therapy and who had accrued 2 years of follow-up were eligible for analysis (n = 625). The median number of imaging studies was 2.5/year (institutional range 0.5-3.5, p < 0.0001); 48.4% received only dedicated computed tomography (CT) scans, 14.6% received only positron emission tomography (PET)-inclusive modalities, 32.8% received a combination and 4.2% received no imaging. Among all eligible patients, 50 (8.0%) experienced relapse, and approximately one-quarter of subclinical relapses were detected through routine imaging. Our results suggest that despite limited data regarding its effect on outcomes, surveillance imaging is prevalent in DLBCL, and a majority of patients receive PET scans at some point during follow-up.
C1 [Abel, Gregory A.; Crosby, Allison L.; Niland, Joyce C.; LaCasce, Ann S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Abel, Gregory A.; LaCasce, Ann S.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Vanderplas, Ann] City Hope Natl Med Ctr, Duarte, CA 91010 USA.
[Rodriguez, Maria A.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Czuczman, Myron S.] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[Gordon, Leo I.] Robert H Lurie Comprehens Canc Ctr, Chicago, IL USA.
[Millenson, Michael] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[Zelenetz, Andrew D.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Friedberg, Jonathan W.] James P Wilmot Canc Ctr, Rochester, NY USA.
RP Abel, GA (reprint author), Dana Farber Canc Inst, Boston, MA 02115 USA.
EM Gregory_Abel@dfci.harvard.edu
OI Zelenetz, Andrew/0000-0003-1403-6883; Gordon, Leo/0000-0003-1666-7064
NR 18
TC 20
Z9 20
U1 0
U2 1
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1042-8194
J9 LEUKEMIA LYMPHOMA
JI Leuk. Lymphoma
PD JUN
PY 2012
VL 53
IS 6
BP 1113
EP 1116
DI 10.3109/10428194.2011.639882
PG 4
WC Oncology; Hematology
SC Oncology; Hematology
GA 945XZ
UT WOS:000304311500017
PM 22098406
ER
PT J
AU Lane, AA
Armand, P
Feng, Y
Neuberg, DS
Abramson, JS
Brown, JR
Fisher, DC
LaCasce, AS
Jacobsen, ED
McAfee, SL
Spitzer, TR
Freedman, AS
Chen, YB
AF Lane, Andrew A.
Armand, Philippe
Feng, Yang
Neuberg, Donna S.
Abramson, Jeremy S.
Brown, Jennifer R.
Fisher, David C.
LaCasce, Ann S.
Jacobsen, Eric D.
McAfee, Steven L.
Spitzer, Thomas R.
Freedman, Arnold S.
Chen, Yi-Bin
TI Risk factors for development of pneumonitis after high-dose chemotherapy
with cyclophosphamide, BCNU and etoposide followed by autologous stem
cell transplant
SO LEUKEMIA & LYMPHOMA
LA English
DT Article
DE Transplant toxicity; clinical results; lymphoma and Hodgkin disease
ID BONE-MARROW-TRANSPLANTATION; REFRACTORY HODGKINS-DISEASE; BREAST-CANCER;
LYMPHOID MALIGNANCIES; PREPARATIVE REGIMENS; CARMUSTINE; TOXICITY;
THERAPY; EFFICACY
AB Pneumonitis is a complication of high-dose chemotherapy and autologous stem cell transplant (HDC-ASCT) regimens containing BCNU. Our goal was to define the incidence and risk factors for pneumonitis in patients with lymphoma receiving a uniform conditioning regimen in the modern era. We studied 222 patients who received HDC-ASCT using cyclophosphamide, BCNU and VP-16 (CBV). Pneumonitis incidence was 22%, with 19% receiving systemic corticosteroid treatment and 8% requiring inpatient hospitalization for pneumonitis. Three patients died secondary to pneumonitis-related complications. The following variables were independently associated with pneumonitis: prior mediastinal radiation (odds ratio [OR] 6.5, 95% confi dence interval [CI] 2.3 -18.9, p = 0.0005), total BCNU dose above 1000 mg (OR 3.4, 95% CI 1.3-8.7, p = 0.012) and age less than 54 (OR 3.0, 95% CI 1.4-6.5, p = 0.0037). Increased vigilance for symptoms of pneumonitis is warranted for patients with prior mediastinal radiation and for younger patients, and dose reduction may be considered for patients who would receive greater than 1000 mg of BCNU.
C1 [Chen, Yi-Bin] Massachusetts Gen Hosp, Dept Hematol Oncol, Div Bone Marrow Transplantat, Ctr Canc, Boston, MA 02114 USA.
[Lane, Andrew A.; Armand, Philippe; Brown, Jennifer R.; Fisher, David C.; LaCasce, Ann S.; Jacobsen, Eric D.; Freedman, Arnold S.; Chen, Yi-Bin] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Feng, Yang; Neuberg, Donna S.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
RP Chen, YB (reprint author), Massachusetts Gen Hosp, Dept Hematol Oncol, Div Bone Marrow Transplantat, Ctr Canc, 55 Fruit St, Boston, MA 02114 USA.
EM ychen6@partners.org
FU Leukemia & Lymphoma Society; NIH [T32 CA071345]
FX Y.-B.C. is a recipient of a career development award from the Leukemia &
Lymphoma Society. Additional support provided was by NIH T32 CA071345
(A.A.L.).
NR 28
TC 9
Z9 9
U1 0
U2 0
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1042-8194
J9 LEUKEMIA LYMPHOMA
JI Leuk. Lymphoma
PD JUN
PY 2012
VL 53
IS 6
BP 1130
EP 1136
DI 10.3109/10428194.2011.645208
PG 7
WC Oncology; Hematology
SC Oncology; Hematology
GA 945XZ
UT WOS:000304311500020
PM 22132836
ER
PT J
AU Wiernik, PH
Li, HL
Weller, E
Hochster, HS
Horning, SJ
Nazeer, T
Gordon, LI
Habermann, TM
Minniti, CJ
Shapiro, GR
Cassileth, PA
AF Wiernik, Peter H.
Li, Hailun
Weller, Edie
Hochster, Howard S.
Horning, Sandra J.
Nazeer, Tipu
Gordon, Leo I.
Habermann, Thomas M.
Minniti, Carl J., Jr.
Shapiro, Gary R.
Cassileth, Peter A.
TI Activity of topotecan 21-day infusion in patients with previously
treated large cell lymphoma: long-term follow-up of an Eastern
Cooperative Oncology Group study (E5493)
SO LEUKEMIA & LYMPHOMA
LA English
DT Article
DE Lymphoma and Hodgkin disease; chemotherapeutic approaches; topotecan
ID NON-HODGKINS-LYMPHOMA; CHRONIC MYELOMONOCYTIC LEUKEMIA; EPITHELIAL
OVARIAN-CANCER; PHASE-II; TOPOISOMERASE-I; CAMPTOTHECIN; LENALIDOMIDE;
MALIGNANCIES; PACLITAXEL; INHIBITOR
AB The purpose of this study was to determine the activity of topotecan given by 21-day continuous infusion in patients previously treated with one prior therapy for a diffuse large-cell lymphoma or immunoblastic lymphoma. Patients with appropriate histology and measurable disease who had been treated with one prior chemotherapy regimen were eligible for study. Slides of tumor biopsies were submitted for central review of pathology. Patients were required to have an Eastern Cooperative Oncology Group (ECOG) performance status of 0, 1 or 2 and adequate bone marrow function. Patients were treated with continuous infusion topotecan, 0.4 mg/m(2)/day x 21 days. Therapy could be escalated to 0.5 and then 0.6 mg/m(2)/day in subsequent cycles if there was no dose-limiting toxicity at the initial dose level. Patients were treated with two cycles after achieving a complete response or until disease progression or unacceptable toxicity occurred. Thirty-seven patients were enrolled. However, only 26 cases were eligible due to a performance status of > 2 (n = 2), more than one prior chemotherapy (n = 1) and wrong histology on review (n = 8). Due to the unexpectedly high ineligibility rate, two sets of analysis were done for all 37 patients enrolled and for the 26 eligible patients, respectively. Of the 37 patients (15 males and 22 females), the International Prognostic Index included 11% low risk, 30% low intermediate risk, 46% high intermediate risk and 8% high risk. The median follow-up was 77 months. A total of 136 cycles of therapy were given with a median of 3 cycles per patient. Grade 4 toxicities included: 14% grade 4 thrombocytopenia; 14% grade 4 granulocytopenia, 8% leukopenia, 3% each anemia, hemorrhage, infection, vomiting, thrombosis, liver toxicity and neuromotor toxicity. The response analysis including all 37 patients showed five complete responses (CRs) and four partial responses (PRs) for a total response rate of 24% (90% two-stage confidence interval 13-39%). Median progression-free survival (PFS) was 3.7 months, with 1- and 2-year PFS of 21% and 6%, respectively (90% confidence interval 11-34% and 2-15%). Median overall survival (OS) was 10.5 months, with 1- and 2-year OS of 41% and 27%, respectively (90% confidence interval 27-53% and 16-39%). Analysis including only eligible patients showed similar response rates and survival outcomes. Single agent topotecan has moderate activity for previously treated high-grade lymphoma equivalent to that of several newer agents, and should be considered for incorporation into multi-drug salvage chemotherapy programs.
C1 [Wiernik, Peter H.] Beth Israel Deaconess Med Ctr, New York, NY 10003 USA.
[Wiernik, Peter H.] St Lukes Roosevelt Hosp, New York, NY USA.
[Li, Hailun; Weller, Edie] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Hochster, Howard S.] NYU, Sch Med, New York, NY USA.
[Horning, Sandra J.] Stanford Univ, Stanford, CA 94305 USA.
[Nazeer, Tipu] Albany Med Coll, Albany, NY 12208 USA.
[Gordon, Leo I.] Northwestern Univ, Chicago, IL 60611 USA.
[Habermann, Thomas M.] Mayo Clin, Rochester, MN USA.
[Minniti, Carl J., Jr.] Minniti Ctr Oncol Hematol, Mickleton, NJ USA.
[Shapiro, Gary R.] Aurora Sinai Med Ctr, Milwaukee, WI USA.
[Cassileth, Peter A.] Univ Miami, Miami, FL USA.
RP Wiernik, PH (reprint author), Montefiore N Div, Ctr Canc, 600 E 233rd St, Bronx, NY 10466 USA.
EM pwiernik@aol.com
OI Gordon, Leo/0000-0003-1666-7064
FU Public Health Service [CA23318, CA66636, CA21115, CA14958, CA17145,
CA13650, CA27525, CA 16116, CA21076]; National Cancer Institute,
National Institutes of Health; Department of Health and Human Services
FX This study was conducted by the Eastern Cooperative Oncology Group
(Robert L. Comis, MD, Chair) and supported in part by Public Health
Service Grants CA23318, CA66636, CA21115, CA14958, CA17145, CA13650,
CA27525, CA 16116, CA21076 and from the National Cancer Institute,
National Institutes of Health and the Department of Health and Human
Services. Its contents are solely the responsibility of the authors and
do not necessarily represent the official views of the National Cancer
Institute.
NR 21
TC 4
Z9 4
U1 0
U2 0
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1042-8194
J9 LEUKEMIA LYMPHOMA
JI Leuk. Lymphoma
PD JUN
PY 2012
VL 53
IS 6
BP 1137
EP 1142
DI 10.3109/10428194.2011.643406
PG 6
WC Oncology; Hematology
SC Oncology; Hematology
GA 945XZ
UT WOS:000304311500021
PM 22111940
ER
PT J
AU Cook, DB
Stegner, AJ
Nagelkirk, PR
Meyer, JD
Togo, F
Natelson, BH
AF Cook, Dane B.
Stegner, Aaron J.
Nagelkirk, Paul R.
Meyer, Jacob D.
Togo, Fumiharu
Natelson, Benjamin H.
TI Responses to Exercise Differ for Chronic Fatigue Syndrome Patients with
Fibromyalgia
SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
LA English
DT Article
DE PAIN; FATIGUE; IMPEDANCE CARDIOGRAPHY; STROKE VOLUME; RPE
ID PHYSIOLOGICAL-RESPONSES; CARDIOVASCULAR-RESPONSE; RESISTANCE EXERCISE;
WOMEN; ILLNESS; MUSCLE; PAIN; SYMPTOMS; CAPACITY
AB COOK, D. B., A. J. STEGNER, P. R. NAGELKIRK, J. D. MEYER, F. TOGO, and B. H. NATELSON. Responses to Exercise Differ for Chronic Fatigue Syndrome Patients with Fibromyalgia. Med. Sci. Sports Exerc., Vol. 44, No. 6, pp. 1186-1193, 2012. Chronic fatigue syndrome (CFS) and fibromyalgia (FM) are chronic multisymptom illnesses with substantial clinical and diagnostic overlap. We have previously shown that, when controlling for aerobic fitness and accounting for comorbid FM, CFS patients do not exhibit abnormal cardiorespiratory responses during maximal aerobic exercise compared with healthy controls, despite differences in pain and exertion. Purpose: The purpose of the present study was to examine cardiac and perceptual responses to steady-state submaximal exercise in CFS patients and healthy controls. Methods: Twenty-one CFS patients (13 CFS with comorbid FM (CFS + FM)) and 14 controls completed 20 min of submaximal cycling exercise. Impedance cardiography was used to determine cardiac responses during exercise. Systolic blood pressure (SBP), RPE, and leg muscle pain were also measured. Data were analyzed using a doubly multivariate, repeated-measures MANOVA to model the exercise response. Results: There was a significant multivariate time-by-group interaction (P < 0.05). The CFS + FM group exhibited an exercise response characterized by higher stroke index, ventilatory equivalents for oxygen and carbon dioxide and RPE, lower SBP, and similar HR responses compared to controls. Conclusions: The present results extend on our previous work with maximal exercise and show that CFS and CFS + FM differ in their responses to steady-state exercise. These results highlight the importance of accounting for comorbid conditions when conducting CFS research, particularly when examining psychophysiological responses to exercise.
C1 [Cook, Dane B.; Stegner, Aaron J.; Meyer, Jacob D.] Univ Wisconsin Madison, Dept Kinesiol, Madison, WI 53706 USA.
[Cook, Dane B.; Stegner, Aaron J.] William S Middleton Mem Vet Adm Med Ctr, Res Serv, Madison, WI USA.
[Nagelkirk, Paul R.] Ball State Univ, Sch Phys Educ Sport & Exercise Sci, Muncie, IN 47306 USA.
[Togo, Fumiharu] Univ Tokyo, Grad Sch Educ, Tokyo, Japan.
[Natelson, Benjamin H.] Beth Israel Deaconess Med Ctr, Pain & Fatigue Study Ctr, New York, NY 10003 USA.
RP Cook, DB (reprint author), Univ Wisconsin Madison, Dept Kinesiol, 2000 Observ Dr, Madison, WI 53706 USA.
EM dcook@education.wisc.edu
FU National Institutes of Health [AI-32247]
FX This research was supported by the National Institutes of Health grant
AI-32247.
NR 40
TC 10
Z9 10
U1 1
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0195-9131
J9 MED SCI SPORT EXER
JI Med. Sci. Sports Exerc.
PD JUN
PY 2012
VL 44
IS 6
BP 1186
EP 1193
DI 10.1249/MSS.0b013e3182417b9a
PG 8
WC Sport Sciences
SC Sport Sciences
GA 944TQ
UT WOS:000304227100027
PM 22157881
ER
PT J
AU Morioka, T
Dishinger, JF
Reid, KR
Liew, CW
Zhang, T
Inaba, M
Kennedy, RT
Kulkarni, RN
AF Morioka, Tomoaki
Dishinger, John. F.
Reid, Kendra. R.
Liew, Chong Wee
Zhang, Ting
Inaba, Masaaki
Kennedy, Robert. T.
Kulkarni, Rohit. N.
TI Enhanced GLP-1-and Sulfonylurea-Induced Insulin Secretion in Islets
Lacking Leptin Signaling
SO MOLECULAR ENDOCRINOLOGY
LA English
DT Article
ID PANCREATIC BETA-CELLS; ACTIVATION; GLUCOSE; RAT; RECEPTOR; CHANNELS;
CRI-G1; GROWTH; LINE; CAMP
AB We have previously reported that the absence of leptin signaling in beta-cells enhances glucose-stimulated insulin secretion and improves glucose tolerance in vivo. To investigate the relevance of beta-cell leptin signaling in the context of postprandial or therapeutic insulin secretion, we examined the cross talk between leptin and glucagon-like peptide (GLP)-1 and sulfonylurea actions. Single and size-matched islets isolated from control or pancreas-specific leptin receptor knockout (pancreas-ObR-KO) mice were treated either with GLP-1 or with glibenclamide. Leptin suppressed GLP-1-stimulated intracellular Ca2+ concentrations ([Ca2+](i)) increase that paralleled the decrease in insulin secretion in controls. In contrast, and as expected, the ObR-KO islets were nonresponsive to leptin, and instead, showed a 2.8-fold greater GLP-1-stimulated [Ca2+](i) increase and a 1.7-fold greater insulin secretion. Phosphorylation of cAMP-responsive element binding protein was enhanced, and phosphodiesterase enzymatic activity was suppressed in MIN6 beta-cells with ObR knockdown compared with controls. The ObR-KO islets also showed significantly higher glibenclamide-induced insulin secretion compared with control islets, whereas [Ca2+](i) was similar to the controls. These data support enhanced insulinotropic effects of glucose, GLP-1, and sulfonyl-ureas in the islets lacking leptin signaling with potential therapeutic implications. (Molecular Endocrinology 26: 967-976, 2012)
C1 [Morioka, Tomoaki; Liew, Chong Wee; Kulkarni, Rohit. N.] Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02115 USA.
[Morioka, Tomoaki; Liew, Chong Wee; Kulkarni, Rohit. N.] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[Dishinger, John. F.; Reid, Kendra. R.; Zhang, Ting; Kennedy, Robert. T.] Univ Michigan, Dept Chem, Ann Arbor, MI 48109 USA.
[Dishinger, John. F.; Reid, Kendra. R.; Zhang, Ting; Kennedy, Robert. T.] Univ Michigan, Dept Pharmacol, Ann Arbor, MI 48109 USA.
[Morioka, Tomoaki; Inaba, Masaaki] Osaka City Univ, Grad Sch Med, Osaka 5458585, Japan.
RP Kulkarni, RN (reprint author), 602 1 Joslin Pl, Boston, MA 02215 USA.
EM Rohit.Kulkarni@joslin.harvard.edu
RI Kennedy, Robert/G-9095-2016
OI Kennedy, Robert/0000-0003-2447-7471
FU American Diabetes Association [7-07-RA-84]; National Institutes of
Health [RO1 DK67536, 1-K99 DK090210-01]; Japanese Ministry of Education,
Culture, Sports, Science and Technology [B 21790878]; The Osaka Medical
Research Foundation for Incurable Diseases
FX This work was supported by an American Diabetes Association Research
Award (7-07-RA-84) (to R.N.K.) and in part by National Institutes of
Health Grant RO1 DK67536. T.M. was supported by the Japanese Ministry of
Education, Culture, Sports, Science and Technology (Grant-in-Aid for
Young Scientists B 21790878) and The Osaka Medical Research Foundation
for Incurable Diseases. C.W.L. is supported by National Institutes of
Health Grant 1-K99 DK090210-01.
NR 31
TC 5
Z9 5
U1 0
U2 8
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0888-8809
J9 MOL ENDOCRINOL
JI Mol. Endocrinol.
PD JUN
PY 2012
VL 26
IS 6
BP 967
EP 976
DI 10.1210/me.2011-1306
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 946PM
UT WOS:000304365100008
PM 22474124
ER
PT J
AU Hoh, BL
Neal, DW
Kleinhenz, DT
Hoh, DJ
Mocco, J
Barker, FG
AF Hoh, Brian L.
Neal, Daniel W.
Kleinhenz, Dominic T.
Hoh, Daniel J.
Mocco, J.
Barker, Fred G., II
TI Higher Complications and No Improvement in Mortality in the ACGME
Resident Duty-Hour Restriction Era: An Analysis of More Than 107000
Neurosurgical Trauma Patients in the Nationwide Inpatient Sample
Database
SO NEUROSURGERY
LA English
DT Article
DE Complications; Medical errors; Mortality; Neurosurgery; Residency;
Training; Trauma
ID STAFF WORKING HOURS; ACCREDITATION-COUNCIL; SLEEP-DEPRIVATION;
INTERNAL-MEDICINE; SURGICAL RESIDENTS; HOURS REGULATIONS; IMPACT; CARE;
EDUCATION; REFORM
AB BACKGROUND: The Accreditation Council for Graduate Medical Education resident duty-hour restrictions were implemented in July 2003 based on the supposition that resident fatigue contributes to medical errors.
OBJECTIVE: To examine the effect of duty-hour restrictions on outcome in neurotrauma patients.
METHODS: The Nationwide Inpatient Sample database was analyzed for a time period with no restrictions (years 1999-2002) compared with a period with restrictions (years 2005-2008) for (1) mortality and (2) complications. We analyzed both teaching and nonteaching hospitals to account for potential differences attributed to nonresident-related factors.
RESULTS: There were 107 006 teaching hospital and 115 604 nonteaching hospital admissions for neurotrauma. Multivariate logistic regression demonstrated significantly more complications in the time period with restrictions in teaching hospitals. In nonteaching hospitals, there was no difference in complications. In both teaching and nonteaching hospitals, there was no difference in mortality between the 2 time periods. For teaching and nonteaching hospitals, there was no difference in hospital length of stay, but hospital charges were significantly higher in the period with restrictions. The occurrence of a complication was significantly associated with longer hospital length of stay and higher hospital charges in both time periods in both teaching and nonteaching hospitals.
CONCLUSION: The implementation of the Accreditation Council for Graduate Medical Education resident duty-hour restrictions was associated with increased complications and no change in mortality for neurotrauma patients in teaching hospitals. In nonteaching hospitals, there was no change in complications and mortality. The occurrence of a complication was associated with longer length of stay and higher hospital charges in both time periods in both teaching and nonteaching hospitals.
C1 [Hoh, Brian L.; Kleinhenz, Dominic T.; Hoh, Daniel J.; Mocco, J.] Univ Florida, Dept Neurosurg, Gainesville, FL 32610 USA.
[Neal, Daniel W.] Univ Florida, Dept Biostat, Gainesville, FL 32610 USA.
[Barker, Fred G., II] Massachusetts Gen Hosp, Neurosurg Serv, Boston, MA 02114 USA.
RP Hoh, BL (reprint author), Univ Florida, Dept Neurosurg, POB 100265, Gainesville, FL 32610 USA.
EM brian.hoh@neurosurgery.ufl.edu
FU Codman Neurovascular
FX Dr Mocco received an unrestricted educational grant from Codman
Neurovascular and is a consultant to Actelion Pharmaceuticals, Nfocus,
and Lazarus Effect. The other authors have no personal financial or
institutional interest in any of the drugs, materials, or devices
described in this article.
NR 45
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U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0148-396X
J9 NEUROSURGERY
JI Neurosurgery
PD JUN
PY 2012
VL 70
IS 6
BP 1369
EP 1381
DI 10.1227/NEU.0b013e3182486a75
PG 13
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 946RV
UT WOS:000304372600020
PM 22227483
ER
PT J
AU Taylor, JJ
Borckardt, JJ
George, MS
AF Taylor, Joseph J.
Borckardt, Jeffrey J.
George, Mark S.
TI Endogenous opioids mediate left dorsolateral prefrontal cortex
rTMS-induced analgesia
SO PAIN
LA English
DT Article
DE Pain modulation; Endogenous opioids; rTMS; Analgesia; Prefrontal cortex
ID TRANSCRANIAL MAGNETIC STIMULATION; ROSTRAL VENTROMEDIAL MEDULLA;
ANTERIOR CINGULATE CORTEX; PERIAQUEDUCTAL GRAY; HEALTHY-VOLUNTEERS;
PLACEBO ANALGESIA; BRAIN-STEM; CORTICAL PROJECTIONS; PAIN THRESHOLDS;
MOOD DISORDERS
AB The concurrent rise of undertreated pain and opiate abuse poses a unique challenge to physicians and researchers alike. A focal, noninvasive form of brain stimulation called repetitive transcranial magnetic stimulation (rTMS) has been shown to produce acute and chronic analgesic effects when applied to dorsolateral prefrontal cortex (DLPFC), but the anatomical and pharmacological mechanisms by which prefrontal rTMS induces analgesia remain unclear. Data suggest that DLPFC mediates top-down analgesia via gain modulation of the supraspinal opioidergic circuit. This potential pathway might explain how prefrontal rTMS reduces pain. The purpose of this sham-controlled, double-blind, crossover study was to determine whether left DLPFC rTMS-induced analgesia was sensitive to l-opioid blockade. Twenty-four healthy volunteers were randomized to receive real or sham TMS after either intravenous saline or naloxone pretreatment. Acute hot and cold pain via quantitative sensory testing and hot allodynia via block testing on capsaicin-treated skin were assessed at baseline and at 0, 20, and 40 minutes after TMS treatment. When compared to sham, real rTMS reduced hot pain and hot allodynia. Naloxone pretreatment significantly reduced the analgesic effects of real rTMS. These results demonstrate that left DLPFC rTMS-induced analgesia requires opioid activity and suggest that rTMS drives endogenous opioidergic pain relief in the human brain. Further studies with chronic dosing regimens of drugs that block or augment the actions of opiates are needed to determine whether TMS can augment opiates in chronic or postoperative pain management. (C) 2012 International Association for the Study of Pain. Published by Elsevier B. V. All rights reserved.
C1 [Taylor, Joseph J.] Med Univ S Carolina, Inst Psychiat, Brain Stimulat Lab, Dept Psychiat, Charleston, SC 29414 USA.
[George, Mark S.] Ralph H Johnson VA Med Ctr, Charleston, SC USA.
RP Taylor, JJ (reprint author), Med Univ S Carolina, Inst Psychiat, Brain Stimulat Lab, Dept Psychiat, 67 President St,Room 504 N, Charleston, SC 29414 USA.
EM taylorjj@musc.edu
FU NIDA NIH HHS [F30 DA033748]
NR 72
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U1 0
U2 12
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-3959
J9 PAIN
JI Pain
PD JUN
PY 2012
VL 153
IS 6
BP 1219
EP 1225
DI 10.1016/j.pain.2012.02.030
PG 7
WC Anesthesiology; Clinical Neurology; Neurosciences
SC Anesthesiology; Neurosciences & Neurology
GA 945BZ
UT WOS:000304249100017
PM 22444187
ER
PT J
AU Briere, LC
Roberts, AE
Joshi, V
AF Briere, Lauren C.
Roberts, Amy E.
Joshi, Victoria
TI Correspondence regarding genetic assessment following increased nuchal
translucency and normal karyotype
SO PRENATAL DIAGNOSIS
LA English
DT Article
ID NOONAN-SYNDROME; SOS1; MUTATIONS
C1 [Briere, Lauren C.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Roberts, Amy E.] Childrens Hosp, Boston, MA 02115 USA.
[Joshi, Victoria] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Briere, LC (reprint author), Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
EM lcbriere@bidmc.harvard.edu
FU European Union [037244]; Canada-Israel industrial RD Fund (CIIRDF) [39]
FX This study was funded part by the European Union FP6 grant Pregenesys #
037244 (HM) and the Canada-Israel industrial R&D Fund (CIIRDF) # 39
(HM).
NR 4
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0197-3851
J9 PRENATAL DIAG
JI Prenat. Diagn.
PD JUN
PY 2012
VL 32
IS 6
BP 607
EP 608
DI 10.1002/pd.2920
PG 2
WC Genetics & Heredity; Obstetrics & Gynecology
SC Genetics & Heredity; Obstetrics & Gynecology
GA 946XJ
UT WOS:000304390500017
PM 22622833
ER
PT J
AU Yagi, M
Murray, J
Strand, K
Blystone, S
Interlandi, G
Suda, Y
Sobel, M
AF Yagi, Mayumi
Murray, Jacqueline
Strand, Kurt
Blystone, Scott
Interlandi, Gianluca
Suda, Yasuo
Sobel, Michael
TI Heparin modulates the conformation and signaling of platelet integrin
alpha IIb beta 3
SO THROMBOSIS RESEARCH
LA English
DT Article
DE Heparin; Integrin alpha IIb beta 3 (platelet glycoprotein IIbIIIa);
Platelet activation; Src kinase; Surface plasmon resonance; Tyrosine
phosphorylation
ID PERCUTANEOUS CORONARY INTERVENTION; MOLECULAR-WEIGHT HEPARIN;
UNFRACTIONATED-HEPARIN; TYROSINE PHOSPHORYLATION; BINDING DOMAIN;
LIGAND-BINDING; ACTIVATION; AGGREGATION; ADHESION; IIIA
AB Introduction: The glycosaminoglycan heparin has been shown to bind to platelet integrin alpha IIb beta 3 and induce platelet activation and aggregation, although the relationship between binding and activation is unclear. We analyzed the interaction of heparin and alpha IIb beta 3 in detail, to obtain a better understanding of the mechanism by which heparin acts on platelets.
Methods: We assessed conformational changes in alpha IIb beta 3 by flow cytometry of platelets exposed to unfractionated heparin. In human platelets and K562 cells engineered to express alpha IIb beta 3, we assayed the effect of heparin on key steps in integrin signaling: phosphorylation of the beta 3 chain cytoplasmic tail, and activation of src kinase. We measured the heparin binding affinity of purified alpha IIb beta 3, and of recombinant fragments of alpha IIb and beta 3, by surface plasmon resonance.
Results and conclusions: Heparin binding results in conformational changes in alpha IIb beta 3, similar to those observed upon ligand binding. Heparin binding alone is not sufficient to induce tyrosine phosphorylation of the integrin beta 3 cytoplasmic domain, but the presence of heparin increased both beta 3 phosphorylation and src kinase activation in response to ligand binding. Specific recombinant fragments derived from alpha IIb bound heparin, while recombinant beta 3 did not bind. This pattern of heparin binding, compared to the crystal structure of alpha IIb beta 3, suggests that heparin-binding sites are located in clusters of basic amino acids in the headpiece and/or leg domains of alpha IIb. Binding of heparin to these clusters may stabilize the transition of alpha IIb beta 3 to an open conformation with enhanced affinity for ligand, facilitating outside-in signaling and platelet activation. Published by Elsevier Ltd.
C1 [Yagi, Mayumi; Murray, Jacqueline; Strand, Kurt; Sobel, Michael] VA Puget Sound Hlth Care Syst, Res & Dev, Seattle, WA 98108 USA.
[Murray, Jacqueline; Sobel, Michael] Univ Washington, Dept Surg, Div Vasc Surg, Seattle, WA 98195 USA.
[Blystone, Scott] SUNY Upstate Med Univ, Dept Cell & Dev Biol, Syracuse, NY USA.
[Interlandi, Gianluca] Univ Washington, Dept Bioengn, Seattle, WA 98195 USA.
[Suda, Yasuo] Kagoshima Univ, Dept Nanostruct & Adv Mat, Grad Sch Sci & Engn, Kagoshima 890, Japan.
RP Yagi, M (reprint author), VA Puget Sound Hlth Care Syst, Res & Dev 151, Seattle Div, 1660 S Columbian Way, Seattle, WA 98108 USA.
EM myagi@uw.edu
FU National Institutes of Health [HL39903]; Department of Veterans Affairs
FX This work was supported by grants from the National Institutes of Health
(HL39903) and the Department of Veterans Affairs to MS.
NR 38
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U1 1
U2 6
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0049-3848
J9 THROMB RES
JI Thromb. Res.
PD JUN
PY 2012
VL 129
IS 6
BP 743
EP 749
DI 10.1016/j.thromres.2011.11.054
PG 7
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA 945HG
UT WOS:000304263100013
PM 22197178
ER
PT J
AU Sumorok, NT
Asplin, JR
Eisner, BH
Stoller, ML
Goldfarb, DS
AF Sumorok, Nicola T.
Asplin, John R.
Eisner, Brian H.
Stoller, Marshall L.
Goldfarb, David S.
TI Effect of diet orange soda on urinary lithogenicity
SO UROLOGICAL RESEARCH
LA English
DT Article
DE Alkalies; Carbonated beverages; Citrates; Nephrolithiasis; Urolithiasis
ID STONE RISK; HYPOCITRATURIC NEPHROLITHIASIS; CALCIUM NEPHROLITHIASIS;
LEMONADE; MANIPULATION; PARAMETERS; VOLUME; JUICE
AB Studies have shown that certain beverages decrease urinary lithogenicity by increasing urine citrate excretion. Diet Sunkist Orange soda had the highest concentration of citrate and total alkali content among 12 diet sodas previously assayed. We studied the effect of Diet Sunkist Orange soda consumption on urinary chemistry. Nine healthy men and women ages 26-54 years completed the study. During the control period, subjects drank 36 oz of water for 3 days in addition to their own, self-selected diet and recorded a food diary. During the study period, the subjects drank three 12-oz cans of Diet Sunkist Orange soda a day instead of water, and replicated their diets from the control period. In each period, the subjects performed 24-h urine collections on days 2 and 3. Urine chemical analysis was performed, including urinary citrate levels and pH. Diet Sunkist Orange soda increased urinary citrate excretion by 60 mg/day, which was not statistically significant (95% CI -75 to 195, value 0.34). There was no significant change in pH from the control period to the study period (pH: 6.29-6.21; 95% CI: -0.09 to 0.25, = 0.30). Urine volumes and creatinine excretions were not significantly different between the control and study periods. Despite the relatively high citrate and total alkali content of Diet Sunkist Orange soda, the volume consumed in this study (36 oz per day) did not provide sufficient potential base to significantly alter urine composition in healthy subjects with normocitraturia. The effect of Diet Sunkist Orange soda on urinary chemistry in patients with hypocitraturia and nephrolithiasis is not likely to have a clinically significant effect to prevent calcium or uric acid stones.
C1 [Goldfarb, David S.] New York Harbor VA Hlth Care Syst, Nephrol Sect 111G, New York, NY 10010 USA.
[Sumorok, Nicola T.; Goldfarb, David S.] NYU, Dept Med, Langone Med Ctr, New York, NY 10016 USA.
[Sumorok, Nicola T.; Goldfarb, David S.] NYU, Div Nephrol, Langone Med Ctr, New York, NY USA.
[Asplin, John R.] Univ Chicago, Sch Med, Litholink Corp & Renal Sect, Chicago, IL 60637 USA.
[Eisner, Brian H.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Urol, Boston, MA USA.
[Stoller, Marshall L.] Univ Calif San Francisco, Dept Urol, San Francisco, CA USA.
RP Goldfarb, DS (reprint author), New York Harbor VA Hlth Care Syst, Nephrol Sect 111G, E 23 St, New York, NY 10010 USA.
EM david.goldfarb@va.gov
OI Goldfarb, David/0000-0002-9215-1273
NR 18
TC 6
Z9 6
U1 0
U2 11
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0300-5623
J9 UROL RES
JI Urol. Res.
PD JUN
PY 2012
VL 40
IS 3
BP 237
EP 241
DI 10.1007/s00240-011-0418-2
PG 5
WC Urology & Nephrology
SC Urology & Nephrology
GA 944MT
UT WOS:000304208200008
PM 21858427
ER
PT J
AU Aspinall, SL
Smith, KJ
Good, CB
Zhao, X
Stone, RA
Tonnu-Mihara, IQ
Cunningham, FE
AF Aspinall, S. L.
Smith, K. J.
Good, C. B.
Zhao, X.
Stone, R. A.
Tonnu-Mihara, I. Q.
Cunningham, F. E.
TI INCREMENTAL COST-EFFECTIVENESS OF PHARMACIST-MANAGED
ERYTHROPOIESIS-STIMULATING AGENTS CLINICS FOR NON-DIALYSIS CHRONIC
KIDNEY DISEASE PATIENTS
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Aspinall, S. L.; Good, C. B.; Cunningham, F. E.] VA Ctr Medicat Safety, Hines, IL USA.
[Smith, K. J.; Stone, R. A.] Univ Pittsburgh, Pittsburgh, PA USA.
[Zhao, X.] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Tonnu-Mihara, I. Q.] VA Long Beach Healthcare Syst, Long Beach, CA USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1098-3015
J9 VALUE HEALTH
JI Value Health
PD JUN
PY 2012
VL 15
IS 4
BP A155
EP A156
PG 2
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 947XP
UT WOS:000304468200806
ER
PT J
AU Choi, S
Neuwirth, R
Cakana, A
San Miguel, JF
Richardson, PG
AF Choi, S.
Neuwirth, R.
Cakana, A.
San Miguel, J. F.
Richardson, P. G.
TI PATIENT-REPORTED OUTCOME (PRO) INSTRUMENT FOR DETECTION OF PERIPHERAL
NEUROPATHY (PN) IN PATIENTS WITH MULTIPLE MYELOMA (MM): THE FACT/GOG-NTX
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Choi, S.; Neuwirth, R.] Millennium Pharmaceut Inc, Cambridge, MA USA.
[Cakana, A.] Janssen Cilag Pty Ltd, High Wycombe, Bucks, England.
[San Miguel, J. F.] Hosp Univ Salamanca, CIC, IBMCC USAL CSIC, Salamanca, Spain.
[Richardson, P. G.] 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 1098-3015
J9 VALUE HEALTH
JI Value Health
PD JUN
PY 2012
VL 15
IS 4
BP A106
EP A106
PG 1
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 947XP
UT WOS:000304468200548
ER
PT J
AU Forrest, G
Larson, K
Crompton, M
Patel, H
Boening, AJ
AF Forrest, G.
Larson, K.
Crompton, M.
Patel, H.
Boening, A. J.
TI HEALTH OUTCOMES WITH DAPTOMYCIN (DAP) IN THE TREATMENT OF METHICILLIN
RESISTANT STAPHYLOCOCCUS AUREUS BACTEREMIA (MRSA-B) WITH VANCOMYCIN
(VAN) MINIMUM INHIBITORY CONCENTRATION (MIC)=2 mu G/Ml
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Forrest, G.] OHSU, Portland, OR USA.
[Forrest, G.] Portland VA Med Ctr, Portland, OR USA.
[Larson, K.; Crompton, M.; Patel, H.; Boening, A. J.] Cubist Pharmaceut Inc, Lexington, MA 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 1098-3015
J9 VALUE HEALTH
JI Value Health
PD JUN
PY 2012
VL 15
IS 4
BP A237
EP A237
PG 1
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 947XP
UT WOS:000304468201425
ER
PT J
AU Ganapathy, V
Hay, JW
Smoot, KJ
Lawler, E
Weber, HC
Grotzinger, KM
AF Ganapathy, V
Hay, J. W.
Smoot, K. J.
Lawler, E.
Weber, H. C.
Grotzinger, K. M.
TI RESOURCE UTILIZATION IN THROMBOCYTOPENIA OF CHRONIC LIVER DISEASES IN
THE VETERANS AFFAIRS POPULATION
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Ganapathy, V; Hay, J. W.] Univ So Calif, Los Angeles, CA USA.
[Smoot, K. J.; Lawler, E.] Massachusetts Vet Epidemiol Res & Informat Ctr MA, Boston, MA USA.
[Weber, H. C.] VA Boston Healthcare Syst, Boston, MA USA.
[Grotzinger, K. M.] SmithKline Beecham Pharmaceut, Collegeville, PA USA.
NR 0
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 1098-3015
J9 VALUE HEALTH
JI Value Health
PD JUN
PY 2012
VL 15
IS 4
BP A137
EP A137
PG 1
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 947XP
UT WOS:000304468200710
ER
PT J
AU Hatoum, IJ
Hunter, TD
Francis, DM
Steinbuch, M
Kaplan, LM
AF Hatoum, I. J.
Hunter, T. D.
Francis, D. M.
Steinbuch, M.
Kaplan, L. M.
TI IDENTIFICATION OF BARIATRIC SURGICAL PROCEDURES, COMORBIDITIES AND
ADVERSE EVENTS IN PAYOR DATA
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Hatoum, I. J.; Kaplan, L. M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Hunter, T. D.] S2 Stat Solut Inc, Cincinnati, OH USA.
[Francis, D. M.] Ethicon Endosurg Inc, Cincinnati, OH USA.
[Steinbuch, M.] Johnson & Johnson, Cincinnati, OH 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 1098-3015
J9 VALUE HEALTH
JI Value Health
PD JUN
PY 2012
VL 15
IS 4
BP A80
EP A80
PG 1
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 947XP
UT WOS:000304468200417
ER
PT J
AU Landsman-Blumberg, P
Wei, W
Douglas, D
Smith, DM
Camargo, CA
AF Landsman-Blumberg, P.
Wei, W.
Douglas, D.
Smith, D. M.
Camargo, C. A.
TI A LARGE-SCALE RETROSPECTIVE STUDY OF EMERGENCY DEPARTMENT VISITS OR
HOSPITALIZATIONS FOR ANAPHYLAXIS AMONG PATIENTS WITH EMPLOYER-SPONSORED
HEALTH INSURANCE
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Landsman-Blumberg, P.; Smith, D. M.] Thomson Reuters, Washington, DC USA.
[Wei, W.] Sanofi Aventis, Bridgewater, NJ USA.
[Douglas, D.] Rutgers State Univ, Ernest Mario Sch Pharm, Piscataway, NJ USA.
[Camargo, C. A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1098-3015
J9 VALUE HEALTH
JI Value Health
PD JUN
PY 2012
VL 15
IS 4
BP A60
EP A60
PG 1
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 947XP
UT WOS:000304468200307
ER
PT J
AU Romley, J
Jena, A
Goldman, D
AF Romley, J.
Jena, A.
Goldman, D.
TI HOSPITAL SPENDING AND INPATIENT MORTALITY
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Romley, J.; Goldman, D.] Univ So Calif, Los Angeles, CA USA.
[Jena, A.] 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 1098-3015
J9 VALUE HEALTH
JI Value Health
PD JUN
PY 2012
VL 15
IS 4
BP A20
EP A20
PG 1
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 947XP
UT WOS:000304468200100
ER
PT J
AU Sansgiry, S
Naik, AD
Brown, AC
Latini, DM
AF Sansgiry, S.
Naik, A. D.
Brown, A. C.
Latini, D. M.
TI VARIATION IN ATTACHMENT STYLE AND HEALTH OUTCOMES OF DIABETES PATIENTS
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Sansgiry, S.; Naik, A. D.] Baylor Coll Med, VA HSR&D Ctr Excellence, Michael E DeBakey VA Med Ctr, Houston, TX 77030 USA.
[Latini, D. M.] San Francisco VA Med Ctr, Baylor Coll Med, Scott Dept Urol, Houston, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1098-3015
J9 VALUE HEALTH
JI Value Health
PD JUN
PY 2012
VL 15
IS 4
BP A184
EP A185
PG 2
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 947XP
UT WOS:000304468201151
ER
PT J
AU Spiegel, B
Poysophon, P
Snyder, B
Agarwal, N
Yen, L
Hodgkins, P
Cohen, E
Vu, M
Kurzbard, N
Atia, M
Sheen, V
Kaneshiro, M
Fuller, G
Bolus, R
AF Spiegel, B.
Poysophon, P.
Snyder, B.
Agarwal, N.
Yen, L.
Hodgkins, P.
Cohen, E.
Vu, M.
Kurzbard, N.
Atia, M.
Sheen, V
Kaneshiro, M.
Fuller, G.
Bolus, R.
TI RESOURCE UTILIZATION AND COSTS ASSOCIATED WITH DIVERTICULITIS INPATIENT
ADMISSIONS: AN ANALYSIS OF THE ECONOMIC BURDEN OF DIVERTICULITIS
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Spiegel, B.; Poysophon, P.; Snyder, B.; Agarwal, N.; Cohen, E.; Vu, M.; Kurzbard, N.; Atia, M.; Sheen, V; Kaneshiro, M.; Fuller, G.; Bolus, R.] Univ Calif Los Angeles, Cedars Sinai Med Ctr, David Geffen Sch Med, VA Greater Los Angeles Healthcare Syst, Los Angeles, CA 90048 USA.
[Yen, L.; Hodgkins, P.] Shire Dev LLC, Wayne, PA USA.
NR 0
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 1098-3015
J9 VALUE HEALTH
JI Value Health
PD JUN
PY 2012
VL 15
IS 4
BP A139
EP A139
PG 1
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 947XP
UT WOS:000304468200722
ER
PT J
AU Zhang, B
Cella, DF
Durie, BG
Kuter, D
Moreau, P
Bartlett, JB
Kroog, GS
Wagner, S
AF Zhang, B.
Cella, D. F.
Durie, B. G.
Kuter, D.
Moreau, P.
Bartlett, J. B.
Kroog, G. S.
Wagner, S.
TI DESIGN AND RATIONALE OF THE MULTIPLE MYELOMA PREAMBLE STUDY: A
PROSPECTIVE, NON-INTERVENTIONAL, MULTI-CENTER COHORT STUDY
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Zhang, B.] Bristol Myers Squibb Co, Plainsboro, NJ USA.
[Cella, D. F.] Northwestern Univ, Chicago, IL 60611 USA.
[Durie, B. G.] IMF, Los Angeles, CA USA.
[Durie, B. G.] Cedars Sinai Comprehens Canc Ctr, Los Angeles, CA USA.
[Kuter, D.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Moreau, P.] Univ Hosp Hotel Dieu, Nantes, France.
[Bartlett, J. B.; Kroog, G. S.; Wagner, S.] Bristol Myers Squibb Co, Princeton, NJ USA.
RI richard, chrystelle/K-8595-2015
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 1098-3015
J9 VALUE HEALTH
JI Value Health
PD JUN
PY 2012
VL 15
IS 4
BP A210
EP A210
PG 1
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 947XP
UT WOS:000304468201284
ER
PT J
AU Hong, SC
Holbrook, EH
Leopold, DA
Hummel, T
AF Hong, Seok-Chan
Holbrook, Eric H.
Leopold, Donald A.
Hummel, Thomas
TI Distorted olfactory perception: A systematic review
SO ACTA OTO-LARYNGOLOGICA
LA English
DT Review
DE Olfactory nerve diseases; olfaction disorders; smell
ID UPPER RESPIRATORY-TRACT; TERM FOLLOW-UP; BULB VOLUME; DYSFUNCTION;
PAROSMIA; SMELL; TRANSECTION; PHANTOSMIA; INFECTION; DISORDERS
AB The sense of smell provides people with valuable input from the chemical environment around them. The human sense of smell generally fails in three ways; one is an intensity reduction and the other two are the quality of changes. Smell disorders can be classified into central or peripheral depending on their origin. Central causes can be related to an area of hyper-functioning brain cells generating this odor perception, thus olfactory distortions have also been observed with epilepsy and migraine. In this paper, we present a review of the current clinical understanding of olfactory distortions and discuss how they can be evaluated and therapies to treat this debilitating condition.
C1 [Hong, Seok-Chan] Konkuk Univ Hosp, Dept Otorhinolaryngol, Seoul 412, South Korea.
[Holbrook, Eric H.] Harvard Univ, Sch Med, Dept Otolaryngol, Massachusetts Eye & Ear Infirm, Boston, MA 02115 USA.
[Leopold, Donald A.] Univ Nebraska Med Ctr, Dept Otolaryngol Head & Neck Surg, Omaha, NE USA.
[Hummel, Thomas] Univ Dresden, Dept Otorhinolaryngol, Sch Med, Dresden, Germany.
RP Hong, SC (reprint author), Konkuk Univ Hosp, Dept Otorhinolaryngol, Seoul 412, South Korea.
EM 20050692@kuh.ac.kr
FU Konkuk University
FX This work was supported by the Konkuk University.
NR 27
TC 12
Z9 12
U1 2
U2 19
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0001-6489
J9 ACTA OTO-LARYNGOL
JI Acta Oto-Laryngol.
PD JUN
PY 2012
VL 132
SU 1
BP S27
EP S31
DI 10.3109/00016489.2012.659759
PG 5
WC Otorhinolaryngology
SC Otorhinolaryngology
GA 943FT
UT WOS:000304106600005
PM 22582778
ER
PT J
AU Ingelfinger, JR
AF Ingelfinger, Julie R.
TI Selective, Isolated Proximal Tubular Angiotensinogen Overexpression and
Salt-Sensitive Hypertension
SO AMERICAN JOURNAL OF HYPERTENSION
LA English
DT Editorial Material
ID NEPHRON; SYSTEM
C1 [Ingelfinger, Julie R.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Ingelfinger, Julie R.] Massachusetts Gen Hosp, MassGen Hosp Children, Boston, MA 02114 USA.
RP Ingelfinger, JR (reprint author), Harvard Univ, Sch Med, Boston, MA 02115 USA.
EM jingelfinger@partners.org
NR 5
TC 1
Z9 1
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0895-7061
J9 AM J HYPERTENS
JI Am. J. Hypertens.
PD JUN
PY 2012
VL 25
IS 6
BP 628
EP 628
DI 10.1038/ajh.2012.23
PG 1
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 944GZ
UT WOS:000304188600001
PM 22592314
ER
PT J
AU Dong, F
Wang, CF
Farris, AB
Wu, SL
Lee, H
Olumi, AF
McDougal, WS
Young, RH
Wu, CL
AF Dong, Fei
Wang, Chaofu
Farris, A. Brad
Wu, Shulin
Lee, Hang
Olumi, Aria F.
McDougal, W. Scott
Young, Robert H.
Wu, Chin-Lee
TI Impact on the Clinical Outcome of Prostate Cancer by the 2005
International Society of Urological Pathology Modified Gleason Grading
System
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE Gleason score; grading; prostate cancer; prognosis; classification
ID RADICAL PROSTATECTOMY; CONSENSUS CONFERENCE; CARCINOMA; STAGE;
SPECIMENS; BIOPSY; SCORE; TIME
AB The 2005 International Society of Urological Pathology (ISUP) Consensus Conference modified the Gleason grading system for prostate cancer. In the modified criteria, ill-defined glands with poorly formed lumina and large cribriform glands with smooth borders, classically described as Gleason pattern 3 adenocarcinoma, were redefined as Gleason pattern 4. To evaluate the clinical outcome of patients upgraded by the ISUP criteria, the histologic slides of 1240 consecutive radical prostatectomy specimens at a single institution were reviewed, and each case of adenocarcinoma was graded on the basis of the original and modified Gleason criteria. A total of 806 patients with prostate cancer of classical Gleason score 3 + 3 = 6 or 3 + 4 = 7 and modified Gleason score 6 to 8 were analyzed with a median overall follow-up of 12.6 years. In the study population, 34% of patients with classical Gleason score 3 + 3 = 6 prostate cancer were upgraded to modified Gleason score 7 or 8 by the ISUP criteria. Compared to patients with modified Gleason score 3 + 3 = 6 and patients with classical Gleason score 3 + 4 = 7, the upgraded patients were at intermediate risk for biochemical progression (paired log-rank P <= 0.003) and metastasis (paired log-rank P <= 0.04) after radical prostatectomy. The hazard ratio for upgrading was 1.60 (95% confidence interval, 1.09-2.35, P = 0.02) for biochemical recurrence and 5.02 (95% confidence interval, 1.77-14.2, P = 0.003) for metastasis. These results validate the prognostic value of the modified Gleason grading system and suggest that the recognition of an intermediate-risk histological pattern may be useful in the prognosis of patients with prostate cancer.
C1 [Dong, Fei; Wang, Chaofu; Farris, A. Brad; Wu, Shulin; Young, Robert H.; Wu, Chin-Lee] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Olumi, Aria F.; McDougal, W. Scott; Wu, Chin-Lee] Massachusetts Gen Hosp, Dept Urol, Boston, MA 02114 USA.
[Lee, Hang] Massachusetts Gen Hosp, Ctr Biostat, Boston, MA 02114 USA.
RP Wu, CL (reprint author), Massachusetts Gen Hosp, Dept Pathol, Warren Bldg 225,55 Fruit St, Boston, MA 02114 USA.
EM cwu2@partners.org
NR 21
TC 42
Z9 47
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0147-5185
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD JUN
PY 2012
VL 36
IS 6
BP 838
EP 843
DI 10.1097/PAS.0b013e3182486faf
PG 6
WC Pathology; Surgery
SC Pathology; Surgery
GA 944KP
UT WOS:000304200700006
PM 22592143
ER
PT J
AU Yamato, M
Ketten, DR
Arruda, J
Cramer, S
Moore, K
AF Yamato, Maya
Ketten, Darlene R.
Arruda, Julie
Cramer, Scott
Moore, Kathleen
TI The Auditory Anatomy of the Minke Whale (Balaenoptera acutorostrata): A
Potential Fatty Sound Reception Pathway in a Baleen Whale
SO ANATOMICAL RECORD-ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY
BIOLOGY
LA English
DT Article
DE cetacea; mysticete; hearing; ear; acoustic fat; imaging
ID TURSIOPS-TRUNCATUS; HEARING; DOLPHIN; TRANSMISSION; SENSITIVITY;
TISSUES; LIPIDS; JAW
AB Cetaceans possess highly derived auditory systems adapted for underwater hearing. Odontoceti (toothed whales) are thought to receive sound through specialized fat bodies that contact the tympanoperiotic complex, the bones housing the middle and inner ears. However, sound reception pathways remain unknown in Mysticeti (baleen whales), which have very different cranial anatomies compared to odontocetes. Here, we report a potential fatty sound reception pathway in the minke whale (Balaenoptera acutorostrata), a mysticete of the balaenopterid family. The cephalic anatomy of seven minke whales was investigated using computerized tomography and magnetic resonance imaging, verified through dissections. Findings include a large, well-formed fat body lateral, dorsal, and posterior to the mandibular ramus and lateral to the tympanoperiotic complex. This fat body inserts into the tympanoperiotic complex at the lateral aperture between the tympanic and periotic bones and is in contact with the ossicles. There is also a second, smaller body of fat found within the tympanic bone, which contacts the ossicles as well. This is the first analysis of these fatty tissues' association with the auditory structures in a mysticete, providing anatomical evidence that fatty sound reception pathways may not be a unique feature of odontocete cetaceans. Anat Rec, 2012. (c) 2012 Wiley Periodicals, Inc.
C1 [Yamato, Maya; Ketten, Darlene R.; Arruda, Julie; Cramer, Scott] Woods Hole Oceanog Inst, Dept Biol, Woods Hole, MA 02543 USA.
[Ketten, Darlene R.] Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA.
[Arruda, Julie] Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
[Moore, Kathleen] Int Fund Anim Welf Marine Mammal Rescue & Res, Yarmouth Port, MA USA.
RP Yamato, M (reprint author), Woods Hole Oceanog Inst, Dept Biol, 266 Woods Hole Rd,MS 50, Woods Hole, MA 02543 USA.
EM myamato@whoi.edu
FU National Science Foundation; Ocean Life Institute; WHOI; Princeton
University Ecology and Evolutionary Biology Department; Joint Industry
Program; Office of Naval Research; Naval Operations Energy and
Environmental Readiness Division
FX Grant sponsors: National Science Foundation Graduate Research
Fellowship, Ocean Life Institute Graduate Fellowship, WHOI Summer
Student Fellowship, WHOI Minority Fellowship, Princeton University
Ecology and Evolutionary Biology Department Senior Thesis Fund, Joint
Industry Program, Office of Naval Research Marine Mammal Program, Chief
of Naval Operations Energy and Environmental Readiness Division.
NR 43
TC 20
Z9 20
U1 0
U2 48
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1932-8486
J9 ANAT REC
JI Anat. Rec.
PD JUN
PY 2012
VL 295
IS 6
BP 991
EP 998
DI 10.1002/ar.22459
PG 8
WC Anatomy & Morphology
SC Anatomy & Morphology
GA 940SY
UT WOS:000303914600012
PM 22488847
ER
PT J
AU Conrad, C
Konuk, Y
Werner, PD
Cao, CG
Warshaw, AL
Rattner, DW
Stangenberg, L
Ott, HC
Jones, DB
Miller, DL
Gee, DW
AF Conrad, Claudius
Konuk, Yusuf
Werner, Paul D.
Cao, Caroline G.
Warshaw, Andrew L.
Rattner, David W.
Stangenberg, Lars
Ott, Harald C.
Jones, Daniel B.
Miller, Diane L.
Gee, Denise W.
TI A Quality Improvement Study on Avoidable Stressors and Countermeasures
Affecting Surgical Motor Performance and Learning
SO ANNALS OF SURGERY
LA English
DT Article
ID LAPAROSCOPIC TASK; MUSIC EXPERIENCE; NOISE; SURGEONS
AB Objective: To explore how the 2 most important components of surgical performance-speed and accuracy-are influenced by different forms of stress and what the impact of music is on these factors.
Background: On the basis of a recently published pilot study on surgical experts, we designed an experiment examining the effects of auditory stress, mental stress, and music on surgical performance and learning and then correlated the data psychometric measures to the role of music in a novice surgeon's life.
Methods: Thirty-one surgeons were recruited for a crossover study. Surgeons were randomized to 4 simple standardized tasks to be performed on the SurgicalSIM VR laparoscopic simulator (Medical Education Technologies, Inc, Sarasota, FL), allowing exact tracking of speed and accuracy. Tasks were performed under a variety of conditions, including silence, dichotic music (auditory stress), defined classical music (auditory relaxation), and mental loading (mental arithmetic tasks). Tasks were performed twice to test for memory consolidation and to accommodate for baseline variability. Performance was correlated to the brief Musical Experience Questionnaire (MEQ).
Results: Mental loading influences performance with respect to accuracy, speed, and recall more negatively than does auditory stress. Defined classical music might lead to minimally worse performance initially but leads to significantly improved memory consolidation. Furthermore, psychologic testing of the volunteers suggests that surgeons with greater musical commitment, measured by the MEQ, perform worse under the mental loading condition.
Conclusions: Mental distraction and auditory stress negatively affect specific components of surgical learning and performance. If used appropriately, classical music may positively affect surgical memory consolidation. It also may be possible to predict surgeons' performance and learning under stress through psychological tests on the role of music in a surgeon's life. Further investigation is necessary to determine the cognitive processes behind these correlations.
C1 [Conrad, Claudius; Jones, Daniel B.] Harvard Univ, Sch Med, Dept Surg, Beth Israel Deaconess Med Ctr, Boston, MA 02114 USA.
[Conrad, Claudius; Konuk, Yusuf; Warshaw, Andrew L.; Rattner, David W.; Stangenberg, Lars; Ott, Harald C.; Gee, Denise W.] Harvard Univ, Sch Med, Dept Surg, Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Werner, Paul D.] Alliant Int Univ, Calif Sch Profess Psychol, San Francisco, CA USA.
[Cao, Caroline G.] Tufts Univ, Dept Mech Engn, Medford, MA 02155 USA.
[Miller, Diane L.] Tufts Univ, Sch Med, Boston, MA 02111 USA.
RP Conrad, C (reprint author), Harvard Univ, Sch Med, Dept Surg, Beth Israel Deaconess Med Ctr, 55 Fruit St, Boston, MA 02114 USA.
EM Cconrad1@partners.org
FU NIBIB NIH HHS [R01 EB005807, R01 EB009362, R01 EB010037, R01
EB010037-01, R01 EB010037-02, R01 EB010037-03, R01 EB014305]
NR 24
TC 10
Z9 10
U1 1
U2 15
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-4932
J9 ANN SURG
JI Ann. Surg.
PD JUN
PY 2012
VL 255
IS 6
BP 1190
EP 1194
DI 10.1097/SLA.0b013e318250b332
PG 5
WC Surgery
SC Surgery
GA 943DQ
UT WOS:000304101100037
PM 22584632
ER
PT J
AU Fung, TT
Hu, FB
Schulze, M
Pollak, M
Wu, TY
Fuchs, CS
Giovannucci, E
AF Fung, Teresa T.
Hu, Frank B.
Schulze, Matthias
Pollak, Michael
Wu, Tianying
Fuchs, Charles S.
Giovannucci, Edward
TI A dietary pattern that is associated with C-peptide and risk of
colorectal cancer in women
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Colorectal cancer; Diet; C-peptide
ID FOOD-FREQUENCY QUESTIONNAIRE; GROWTH-FACTOR-I; CARDIOVASCULAR-DISEASE;
DECAFFEINATED COFFEE; BINDING-PROTEINS; INSULIN INDEX; LOAD;
REPRODUCIBILITY; BIOMARKERS; VALIDITY
AB Higher serum C-peptide concentrations have shown to be associated with an increased risk of colorectal cancer (CRC). Therefore, we used diet information to identify food groups that correlated with fasting serum concentrations of C-peptide and assess the association of this dietary pattern and CRC risk.
Major food contributors to fasting C-peptide concentrations were identified with stepwise linear regression in a subsample ( = 833) of women from a large cohort. We then summed the consumption frequency of the major food contributors to form a C-peptide dietary pattern for the entire cohort ( = 66,714). Risk for CRC was computed using Cox proportional hazard model with the C-peptide dietary pattern score as the predictor.
In up to 20 years of follow-up, we ascertained 985 cases of CRC and 758 colon cancer. After adjusting for confounders, the C-peptide dietary pattern, characterized by higher meat, fish, and sweetened beverage intake, but lower coffee, high fat dairy, and whole grains intake, showed direct association with CRC risk (RR comparing extreme quintiles = 1.29, 95 % CI = 1.05-1.58, trend = 0.048). The same comparison was slightly stronger for colon cancer (RR = 1.35, 95 % CI = 1.07-1.70, trend = 0.009). In stratified analysis, there was no association between the C-peptide dietary pattern and colon cancer among lean and active women. However, for overweight or sedentary women, RR for the same comparison was 1.58 (95 % CI = 1.20-2.07, trend = 0.002) ( for interaction = 0.007).
We derived a dietary pattern that correlated with C-peptide concentrations. This pattern was associated with an increase in colon cancer, especially among women who were overweight or sedentary.
C1 [Fung, Teresa T.] Simmons Coll, Dept Nutr, Boston, MA 02115 USA.
[Fung, Teresa T.; Hu, Frank B.; Giovannucci, Edward] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Hu, Frank B.; Giovannucci, Edward] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Hu, Frank B.; Giovannucci, Edward] Harvard Univ, Sch Med, Boston, MA USA.
[Schulze, Matthias] Tech Univ Munich, Munich, Germany.
[Schulze, Matthias] German Inst Human Nutr, Munich, Germany.
[Pollak, Michael] McGill Univ, Lady Davis Inst Med Res, Montreal, PQ, Canada.
[Wu, Tianying] Univ Cincinnati, Dept Environm Hlth, Cincinnati, OH USA.
[Fuchs, Charles S.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Fung, TT (reprint author), Simmons Coll, Dept Nutr, 300 Fenway, Boston, MA 02115 USA.
EM fung@simmons.edu
RI Pollak, Michael/G-9094-2011;
OI Pollak, Michael/0000-0003-3047-0604; Yang, Shuman/0000-0002-9638-0890;
Schulze, Matthias B./0000-0002-0830-5277
FU National Institute of Health [CA87969, HL60712, CA95589]
FX We would like to thank the participants and staff of the Nurses' Health
Study for their valuable contributions as well as the following state
cancer registries for their help: AL, AZ, AR, CA, CO, CT, DE, FL, GA,
ID, IL, IN, IA, KY, LA, ME, MD, MA, MI, NE, NH, NJ, NY, NC, ND, OH, OK,
OR, PA, RI, SC, TN, TX, VA, WA, WY. This work is funded by the National
Institute of Health research grants CA87969, HL60712, and CA95589.
NR 26
TC 9
Z9 9
U1 0
U2 6
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD JUN
PY 2012
VL 23
IS 6
BP 959
EP 965
DI 10.1007/s10552-012-9969-y
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 943FK
UT WOS:000304105700017
PM 22535146
ER
PT J
AU Lanternier, F
Sun, HY
Ribaud, P
Singh, N
Kontoyiannis, DP
Lortholary, O
AF Lanternier, Fanny
Sun, Hsin-Yun
Ribaud, Patricia
Singh, Nina
Kontoyiannis, Dimitrios P.
Lortholary, Olivier
TI Mucormycosis in Organ and Stem Cell Transplant Recipients
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID INVASIVE FUNGAL-INFECTIONS; LIPOSOMAL AMPHOTERICIN-B; SURVEILLANCE
NETWORK TRANSNET; MOLD INFECTIONS; HEMATOLOGIC MALIGNANCY; ANTIFUNGAL
THERAPY; MURINE ZYGOMYCOSIS; RHIZOPUS-ORYZAE; IRON OVERLOAD;
RISK-FACTORS
AB Mucormycosis is a devastating invasive fungal disease whose incidence has increased during the past decade. Mucormycosis now represents a major threat in transplant recipients, accounting for 2% and 8% of invasive fungal infections in recent cohorts of solid-organ and allogeneic stem-cell transplant recipients, respectively. Mucormycosis most often occurs late, >3 months after transplantation, although cases occurring early have been observed, especially among liver transplant recipients and in cases of graft-transmitted infection. Recent guidelines have emphasized the direct examination of the involved fluid or tissue and culture from a sterile site as the most appropriate diagnostic strategy and the use of lipid formulations of amphotericin B and major surgery when feasible as the most appropriate first-line therapeutic strategy for mucormycosis in organ and stem cell transplant recipients.
C1 [Lanternier, Fanny; Lortholary, Olivier] Univ Paris 05, Hop Necker Enfants Malad, Ctr Infect Necker Pasteur, F-75105 Paris, France.
[Lanternier, Fanny; Lortholary, Olivier] IHU Imagine, Paris, France.
[Lanternier, Fanny; Lortholary, Olivier] Ctr Natl Reference Mycol & Antifong, Inst Pasteur, Paris, France.
[Lortholary, Olivier] CNRS, URA 3012, Paris, France.
[Sun, Hsin-Yun; Singh, Nina] Univ Pittsburgh, Pittsburgh, PA 15260 USA.
[Sun, Hsin-Yun; Singh, Nina] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Sun, Hsin-Yun] Natl Taiwan Univ Hosp, Dept Internal Med, Taipei 100, Taiwan.
[Sun, Hsin-Yun] Natl Taiwan Univ, Coll Med, Taipei 10764, Taiwan.
[Ribaud, Patricia] Univ Paris 07, UFR Denis Diderot, F-75221 Paris 05, France.
[Ribaud, Patricia] Hop St Louis, Assistance Publ Hop Paris, Serv Hematol Greffe Moelle, Paris, France.
[Kontoyiannis, Dimitrios P.] Univ Texas MD Anderson Canc Ctr, Dept Infect Dis, Houston, TX 77030 USA.
RP Lortholary, O (reprint author), Univ Paris 05, Hop Necker Enfants Malad, Ctr Infect Necker Pasteur, 149 Rue Sevres, F-75105 Paris, France.
EM olivier.lortholary@nck.aphp.fr
OI SUN, HSIN-YUN/0000-0003-0074-7721
NR 62
TC 37
Z9 39
U1 0
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD JUN 1
PY 2012
VL 54
IS 11
BP 1629
EP 1636
DI 10.1093/cid/cis195
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 942MO
UT WOS:000304048400020
PM 22431807
ER
PT J
AU Stanley, TL
Falutz, J
Marsolais, C
Morin, J
Soulban, G
Mamputu, JC
Assaad, H
Turner, R
Grinspoon, SK
AF Stanley, Takara L.
Falutz, Julian
Marsolais, Christian
Morin, Josee
Soulban, Graziella
Mamputu, Jean-Claude
Assaad, Hani
Turner, Ralph
Grinspoon, Steven K.
TI Reduction in Visceral Adiposity Is Associated With an Improved Metabolic
Profile in HIV-Infected Patients Receiving Tesamorelin
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID GROWTH-HORMONE TREATMENT; ABDOMINAL FAT ACCUMULATION; PLACEBO-CONTROLLED
TRIAL; BODY-COMPOSITION; REDISTRIBUTION-SYNDROME; INSULIN-RESISTANCE;
SAFETY EXTENSION; FACTOR ANALOG; TISSUE; LIPODYSTROPHY
AB Background. Tesamorelin, a growth hormone-releasing hormone analogue, decreases visceral adipose tissue (VAT) by 15%-20% over 6-12 months in individuals with human immunodeficiency virus (HIV)-associated abdominal adiposity, but it is unknown whether VAT reduction is directly associated with endocrine and metabolic changes.
Methods. In 2 phase III, randomized, double-blind studies, men and women with HIV-associated abdominal fat accumulation were randomly assigned (ratio, 2:1) to receive tesamorelin or placebo for 26 weeks. At week 26, patients initially receiving tesamorelin were randomly assigned to continue receiving tesamorelin or to receive placebo for an additional 26 weeks. In per-protocol analysis of 402 subjects initially randomly assigned to receive tesamorelin, those with >= 8% reduction in VAT were defined a priori as responders per the statistical analysis plan. Post hoc analyses were performed to assess differences between responders and nonresponders.
Results. Compared with tesamorelin nonresponders, responders experienced greater mean (+/- SD) reduction in triglyceride levels (26 weeks: -0.6 +/- 1.7 mmol/L vs -0.1 +/- 1.2 mmol/L [P = .005]; 52 weeks: -0.8 +/- 1.8 mmol/L vs 0.0 +/- 1.1 mmol/L [P = .003]) and attenuated changes in fasting glucose levels (26 weeks: 1 +/- 16 mg/dL vs 5 +/- 14 mg/dL [P = .01]; 52 weeks: -1 +/- 14 mg/dL vs 8 +/- 17 mg/dL [P < .001]), hemoglobin A1c levels (26 weeks: 0.1 +/- 0.3% vs 0.3 +/- 0.4% [P < .001]; 52 weeks: 0.0 +/- 0.3% vs 0.2 +/- 0.5% [P = .003]), and other parameters of glucose homeostasis. Similar patterns were seen for adiponectin levels, with significant improvement in responders vs nonresponders. Changes in lipid levels and glucose homeostasis were significantly associated with percentage change in VAT.
Conclusions. In contrast to nonresponders, HIV-infected patients receiving tesamorelin with >= 8% reduction in VAT have significantly improved triglyceride levels, adiponectin levels, and preservation of glucose homeostasis over 52 weeks of treatment.
Clinicaltrials.gov Registration. NCT00123253, NCT00435136, NCT00608023.
C1 [Stanley, Takara L.; Grinspoon, Steven K.] Massachusetts Gen Hosp, Program Nutr Metab, Boston, MA 02114 USA.
[Stanley, Takara L.; Grinspoon, Steven K.] Harvard Univ, Sch Med, Boston, MA USA.
[Falutz, Julian] McGill Univ, Ctr Hlth, Montreal, PQ, Canada.
[Marsolais, Christian; Morin, Josee; Soulban, Graziella; Mamputu, Jean-Claude; Assaad, Hani] Theratechnol, Montreal, PQ, Canada.
[Turner, Ralph] Phase Technol 5, Wellesley, MA USA.
RP Grinspoon, SK (reprint author), Massachusetts Gen Hosp, Program Nutr Metab, 5 Longfellow Pl,Ste 207, Boston, MA 02114 USA.
EM sgrinspoon@partners.org
OI Mamputu, Jean-Claude/0000-0001-8493-959X
FU Theratechnologies; National Institute of Diabetes and Digestive and
Kidney Diseases at the National Institutes of Health [K23 DK089910, K24
DK064545]
FX This work was supported by Theratechnologies and by the National
Institute of Diabetes and Digestive and Kidney Diseases at the National
Institutes of Health (grant K23 DK089910 to T. L. S. and grant K24
DK064545 to S. K. G.).
NR 34
TC 8
Z9 8
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD JUN 1
PY 2012
VL 54
IS 11
BP 1642
EP 1651
DI 10.1093/cid/cis251
PG 10
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 942MO
UT WOS:000304048400022
PM 22495074
ER
PT J
AU Musher, DM
Stager, C
AF Musher, Daniel M.
Stager, Charles
TI Diagnosis of Clostridium difficile Infection
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Letter
C1 [Musher, Daniel M.] Baylor Coll Med, Houston, TX 77030 USA.
[Stager, Charles] Baylor Coll Med, Michael E DeBakey Vet Affairs Med Ctr, Lab Serv Care Line, Infect Dis Sect, Houston, TX 77030 USA.
[Musher, Daniel M.] Baylor Coll Med, Dept Med, Houston, TX 77030 USA.
[Stager, Charles] Baylor Coll Med, Dept Pathol, Houston, TX 77030 USA.
RP Musher, DM (reprint author), Baylor Coll Med, Houston, TX 77030 USA.
EM dmusher@bcm.edu
NR 4
TC 6
Z9 6
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD JUN 1
PY 2012
VL 54
IS 11
BP 1675
EP 1675
DI 10.1093/cid/cis259
PG 1
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 942MO
UT WOS:000304048400027
PM 22503848
ER
PT J
AU Bedair, H
Ting, N
Bozic, KJ
Della Valle, CJ
Sporer, SM
AF Bedair, Hany
Ting, Nicholas
Bozic, Kevin J.
Della Valle, Craig J.
Sporer, Scott M.
TI Reply to Letter to the Editor: Treatment of Early Postoperative
Infections After THA: A Decision Analysis
SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH
LA English
DT Letter
C1 [Bedair, Hany] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Orthopaed Surg, Boston, MA 02114 USA.
[Ting, Nicholas; Della Valle, Craig J.; Sporer, Scott M.] Rush Univ, Med Ctr, Dept Orthopaed Surg, Chicago, IL 60612 USA.
[Bozic, Kevin J.] Univ Calif San Francisco, Dept Orthopaed Surg, Philip R Lee Inst Hlth Policy, San Francisco, CA USA.
RP Bedair, H (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Orthopaed Surg, 55 Fruit St,YAW 3B, Boston, MA 02114 USA.
EM hbedair@gmail.com
NR 3
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0009-921X
J9 CLIN ORTHOP RELAT R
JI Clin. Orthop. Rel. Res.
PD JUN
PY 2012
VL 470
IS 6
BP 1793
EP 1794
DI 10.1007/s11999-012-2360-1
PG 2
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 943BG
UT WOS:000304094800039
ER
PT J
AU Borrero, S
Mor, MK
Zhao, XH
McNeil, M
Ibrahim, S
Hayes, P
AF Borrero, Sonya
Mor, Maria K.
Zhao, Xinhua
McNeil, Melissa
Ibrahim, Said
Hayes, Patricia
TI Contraceptive care in the VA health care system
SO CONTRACEPTION
LA English
DT Article
DE VA; Women's health; Contraception; Race/ethnicity
ID OF-VETERANS-AFFAIRS; INTRAUTERINE-DEVICE; WOMEN VETERANS; DELIVERY;
AVAILABILITY; ORGANIZATION; PHYSICIANS; INNOVATION; KNOWLEDGE; ATTITUDES
AB Background: Little is known about contraceptive care within the Veterans Affairs (VA) health care system. This study was conducted to assess the prevalence of documented contraception by race/ethnicity within the VA and to examine the association between receiving primary care in women's health clinics (WHCs) and having a documented contraceptive method.
Study Design: We examined national VA administrative and pharmacy data for 103,950 female veterans aged 18-45 years who made at least one primary care clinic visit in 2008. Multivariable regression models were used to examine the associations between race/ethnicity and receipt of care in a WHC with having a method of contraception while controlling for confounders.
Results: Only 22% of women veterans had a documented method of contraception during 2008. After adjusting for potential confounders, Hispanic and African-American women were significantly less likely to have a method compared to whites [odds ratio (OR): 0.82; 95% confidence interval (CI): 0.76-0.88 and OR: 0.85; 95% CI: 0.81-0.89, respectively]. Women who went to WHCs were significantly more likely to have a method of contraception compared to women who went to traditional primary care clinics (OR: 2.05; 95% CI: 1.97-2.14).
Conclusions: Overall contraceptive prevalence in the VA is low, but receiving care in a WHC is associated with a significantly higher likelihood of having a contraceptive method. Published by Elsevier Inc.
C1 [Borrero, Sonya; Mor, Maria K.; Zhao, Xinhua] VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA 15206 USA.
[Borrero, Sonya; McNeil, Melissa] Univ Pittsburgh, Dept Med, Pittsburgh, PA 15261 USA.
[Mor, Maria K.] Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA 15213 USA.
[Ibrahim, Said] Philadelphia Vet Adm, Med Ctr, Philadelphia, PA 19104 USA.
[Ibrahim, Said] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Hayes, Patricia] US Dept Vet Affairs, Women Vet Hlth Strateg Hlth Care Grp, Off Publ Hlth & Environm Hazards, Washington, DC 20420 USA.
RP Borrero, S (reprint author), VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, 7180 Highland Dr,151C-H, Pittsburgh, PA 15206 USA.
EM borrerosp@upmc.edu
FU Department of Veterans Affairs, Veteran Health Administration, Office of
Research and Development, VISN 4 CHERP
FX This study was supported by the Department of Veterans Affairs, Veteran
Health Administration, Office of Research and Development, VISN 4 CHERP
Pilot Project Award (PI: Sonya Borrero). Dr. Borrero had full access to
all the data in the study and takes responsibility for the integrity of
the data and the accuracy of the data analysis. The contents of this
manuscript do not represent the views of the Department of Veterans
Affairs or the United States Government. The abstract of this manuscript
was presented at The Society of General Internal Medicine annual meeting
in Phoenix, AZ, in May 2011.
NR 20
TC 11
Z9 11
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0010-7824
J9 CONTRACEPTION
JI Contraception
PD JUN
PY 2012
VL 85
IS 6
BP 580
EP 588
DI 10.1016/j.contraception.2011.10.010
PG 9
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 944FP
UT WOS:000304185000009
PM 22176794
ER
PT J
AU Cecere, LM
Slatore, CG
Uman, JE
Evans, LE
Udris, EM
Bryson, CL
Au, DH
AF Cecere, Laura M.
Slatore, Christopher G.
Uman, Jane E.
Evans, Laura E.
Udris, Edmunds M.
Bryson, Chris L.
Au, David H.
TI Adherence to Long-Acting Inhaled Therapies among Patients with Chronic
Obstructive Pulmonary Disease (COPD)
SO COPD-JOURNAL OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE
LA English
DT Article
DE Medication adherence; Pulmonary diseases; Chronic disease;
Pharmacoepidemiology
ID CLINICAL-TRIAL; MEDICATION NONADHERENCE; ASTHMATIC-PATIENTS;
CORTICOSTEROIDS; MANAGEMENT; BELIEFS; PERSISTENCE; VALIDATION; CHILDREN;
UNDERUSE
AB Background: Long-acting inhaled medications are an important component of the treatment of patients with chronic obstructive pulmonary disease (COPD), yet few studies have examined the determinants of medication adherence among this patient population. Objective: We sought to identify factors associated with adherence to long-acting beta-agonists (LABA) and inhaled corticosteroids (ICS) among patients with COPD. Methods: We performed secondary analysis of baseline data collected in a randomized trial of 376 Veterans with spirometrically confirmed COPD. We used electronic pharmacy records to assess adherence, defined as a medication possession ratio of >= 0.80. We investigated the following exposures: patient characteristics, disease severity, medication regimen complexity, health behaviors, confidence in self-management, and perceptions of provider skill. We performed multivariable logistic regression, clustered by provider, to estimate associations. Results: Of the 167 patients prescribed LABA, 54% (n = 90) were adherent to therapy while only 40% (n = 74) of 184 the patients prescribed ICS were adherent. Higher adherence to LABA and ICS was associated with patient perception of their provider as being an "expert" in diagnosing and managing lung disease [For LABA: OR = 21.70 (95% CI 6.79, 69.37); For ICS OR = 7.93 (95% CI 1.71, 36.67)]. Factors associated with adherence to LABA, but not ICS, included: age, education, race, COPD severity, smoking status, and confidence in self-management. Conclusions: Adherence to long-acting inhaled medications among patients with COPD is poor, and determinants of adherence likely differ by medication class. Patient perception of clinician expertise in lung disease was the factor most highly associated with adherence to long-acting therapies.
C1 [Cecere, Laura M.; Uman, Jane E.; Udris, Edmunds M.; Bryson, Chris L.; Au, David H.] Dept Vet Affairs Puget Sound Hlth Care Syst, Hlth Serv Res & Dev, Seattle, WA USA.
[Cecere, Laura M.; Au, David H.] Univ Washington, Dept Med, Div Pulm & Crit Care Med, Seattle, WA USA.
[Slatore, Christopher G.] Dept Vet Affairs Med Ctr, Portland, OR USA.
[Slatore, Christopher G.] Oregon Hlth & Sci Univ, Dept Med, Div Pulm & Crit Care Med, Portland, OR 97201 USA.
[Evans, Laura E.] NYU, Med Ctr, Div Pulm & Crit Care Med, Dept Med, New York, NY 10016 USA.
RP Cecere, LM (reprint author), VA Puget Sound Hlth Care Syst, Hlth Serv Res & Dev, 1100 Olive Way,Suite 1400, Seattle, WA 98101 USA.
EM lcecere@u.washington.edu
OI Slatore, Christopher/0000-0003-0958-8122
FU VA Advanced Fellowship Program in Health Services Research and
Development [TPM 61-037]; Department of Veterans Affairs, Veterans
Health Administration, Office of Research and Development [IIR 02-292];
Portland VA Medical Center, Portland, OR; Firland Foundation
FX This material is based upon work supported by a VA Advanced Fellowship
Program in Health Services Research and Development [TPM 61-037] and a
Department of Veterans Affairs, Veterans Health Administration, Office
of Research and Development grant [IIR 02-292]. Dr. Slatore is supported
by a Veterans Affairs HSR&D Career Development Award and resources from
the Portland VA Medical Center, Portland, OR. Additional support also
comes from the Firland Foundation. The views expressed in this article
are those of the authors and do not necessarily reflect the position or
policy of the Department of Veterans Affairs. Some of the results of
this work were presented in abstract form at the American Thoracic
Society International Conference, in Denver, Colorado on May 15, 2011.
NR 35
TC 23
Z9 23
U1 1
U2 6
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1541-2555
J9 COPD
JI COPD-J. Chronic Obstr. Pulm. Dis.
PD JUN
PY 2012
VL 9
IS 3
BP 251
EP 258
DI 10.3109/15412555.2011.650241
PG 8
WC Respiratory System
SC Respiratory System
GA 942ZM
UT WOS:000304090200008
PM 22497533
ER
PT J
AU Tamura, RE
de Vasconcellos, JF
Sarkar, D
Libermann, TA
Fisher, PB
Zerbini, LF
AF Tamura, R. E.
de Vasconcellos, J. F.
Sarkar, D.
Libermann, T. A.
Fisher, P. B.
Zerbini, L. F.
TI GADD45 Proteins: Central Players in Tumorigenesis
SO CURRENT MOLECULAR MEDICINE
LA English
DT Review
DE Apoptosis; cancer; GADD45 family; survival
ID NF-KAPPA-B; ENDOTHELIAL GROWTH-FACTOR; CELL-CYCLE ARREST; HISTONE
DEACETYLASE INHIBITOR; DNA-DAMAGING AGENTS; HUMAN BREAST-CANCER;
EXPRESSING MDA-7/IL-24-MEDIATED APOPTOSIS; NONSTEROIDAL ANTIINFLAMMATORY
AGENTS; DIFFERENTIATION-ASSOCIATED GENE; VASCULAR-PERMEABILITY FACTOR
AB The Growth Arrest and DNA Damage-inducible 45 (GADD45) proteins have been implicated in regulation of many cellular functions including DNA repair, cell cycle control, senescence and genotoxic stress. However, the pro-apoptotic activities have also positioned GADD45 as an essential player in oncogenesis. Emerging functional evidence implies that GADD45 proteins serve as tumor suppressors in response to diverse stimuli, connecting multiple cell signaling modules. Defects in the GADD45 pathway can be related to the initiation and progression of malignancies. Moreover, induction of GADD45 expression is an essential step for mediating anti-cancer activity of multiple chemotherapeutic drugs and the absence of GADD45 might abrogate their effects in cancer cells. In this review, we present a comprehensive discussion of the functions of GADD45 proteins, linking their regulation to effectors of cell cycle arrest, DNA repair and apoptosis. The ramifications regarding their roles as essential and central players in tumor growth suppression are also examined. We also extensively review recent literature to clarify how different chemotherapeutic drugs induce GADD45 gene expression and how its up-regulation and interaction with different molecular partners may benefit cancer chemotherapy and facilitate novel drug discovery.
C1 [Tamura, R. E.; Zerbini, L. F.] Int Ctr Genet Engn & Biotechnol, ZA-7925 Cape Town, South Africa.
[Tamura, R. E.; Zerbini, L. F.] Univ Cape Town, Med Biochem Div, ZA-7925 Cape Town, South Africa.
[de Vasconcellos, J. F.] Ctr Infantil Boldrini, Mol Biol Lab, Campinas, SP, Brazil.
[de Vasconcellos, J. F.] Univ Estadual Campinas, Fac Med Sci, Dept Med Genet, Campinas, SP, Brazil.
[Sarkar, D.; Fisher, P. B.] Virginia Commonwealth Univ, Dept Human & Mol Genet, VCU Inst Mol Med, VCU Massey Canc Ctr,Sch Med, Richmond, VA USA.
[Libermann, T. A.; Zerbini, L. F.] Beth Israel Deaconess Med Ctr, BIDMC Genom & Prote Ctr, Boston, MA 02215 USA.
[Libermann, T. A.; Zerbini, L. F.] Harvard Univ, Sch Med, Boston, MA USA.
RP Zerbini, LF (reprint author), Int Ctr Genet Engn & Biotechnol, Wernher & Beit Bldg S,UCT Campus,Anzio Rd, ZA-7925 Cape Town, South Africa.
EM luiz.zerbini@uct.ac.za
RI tamura, rodrigo/O-9846-2014; Zerbini, Luiz /B-7720-2015
OI tamura, rodrigo/0000-0001-7767-0887;
FU International Centre for Genetic Engineering and Biotechnology; CAPES
[1102-08-7]; FAPESP [06/01158-3]; NIH [1R01 CA85467, P50 CA090381, P50
CA105009, 1R01 CA097318, 1R01 CA127641, P01 CA104177, R01 CA138540];
Hershey Foundation; Samuel Waxman Cancer Research Foundation; National
Foundation for Cancer Research; Department of Defense [PC051217,
OC0060439]
FX R.E.T. was supported by an International Centre for Genetic Engineering
and Biotechnology fellowship. J.F.V. was recipient of a CAPES
international fellowship (1102-08-7) and FAPESP 06/01158-3. This work
was supported by NIH grants 1R01 CA85467, P50 CA090381, P50 CA105009 and
the Hershey Foundation (T.A.L.); NIH grants 1R01 CA097318, 1R01
CA127641, P01 CA104177 and grants from the Samuel Waxman Cancer Research
Foundation and the National Foundation for Cancer Research (P.B.F.); NIH
grant R01 CA138540 (D.S.); and Department of Defense grants PC051217 and
OC0060439 (L.F.Z.). D.S. is a Harrison Endowed Scholar in Cancer
Research and a Blick Scholar. P.B.F. holds the Thelma Newmeyer Corman
Chair in Cancer Research in the VCU Massey Cancer Center and is a SWCRF
and a NFCR Investigator.
NR 195
TC 60
Z9 64
U1 2
U2 13
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1566-5240
J9 CURR MOL MED
JI Curr. Mol. Med.
PD JUN
PY 2012
VL 12
IS 5
BP 634
EP 651
PG 18
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 942MD
UT WOS:000304047300012
PM 22515981
ER
PT J
AU Sosenko, JM
Skyler, JS
Herold, KC
Palmer, JP
AF Sosenko, Jay M.
Skyler, Jay S.
Herold, Kevan C.
Palmer, Jerry P.
CA Type 1 Diabet TrialNet Study Grp
Diabet Prevention Trial-Type 1
TI The Metabolic Progression to Type 1 Diabetes as Indicated by Serial Oral
Glucose Tolerance Testing in the Diabetes Prevention Trial-Type 1
SO DIABETES
LA English
DT Article
ID BETA-CELL FUNCTION; INSULIN-RESISTANCE; C-PEPTIDE;
CLINICAL-MANIFESTATIONS; NATURAL-HISTORY; RISK SCORE; MELLITUS; ONSET;
SECRETION; RELATIVES
C1 [Sosenko, Jay M.; Skyler, Jay S.] Univ Miami, Miller Sch Med, Div Endocrinol, Miami, FL 33136 USA.
[Herold, Kevan C.] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT USA.
[Palmer, Jerry P.] Univ Washington, VA Puget Sound Hlth Care Syst, Div Endocrinol Metab & Nutr, Seattle, WA 98195 USA.
RP Sosenko, JM (reprint author), Univ Miami, Miller Sch Med, Div Endocrinol, Miami, FL 33136 USA.
EM jsosenko@med.miami.edu
RI Skyler, Jay/F-4211-2016;
OI Gallagher, Mary/0000-0002-5844-2309
FU Type 1 Diabetes TrialNet Study Group; National Institutes of Health
(NTH) through the National Institute of Diabetes and Digestive and
Kidney Diseases; National Institute of Allergy and Infectious Diseases;
Eunice Kennedy Shriver National Institute of Child Health and Human
Development [U01 DK-061010, U01 DK-061016, U01 DK-061034, U01 DK-061036,
U01 DK-061040, U01 DK-061041, U01 DK-061042, U01 DK-061055, U01
DK-061058, U01 DK-084565, U01 DK-085453, U01 DK-085461, U01 DK-085463,
U01 DK-085466, U01 DK-085499, U01 DK-085505, U01 DK-085509,
HHSN267200800019C]; National Center for Research Resources [UL1
RR-024131, UL1 RR-024139, UL1 RR-024153, UL1 RR-024975, UL1 RR-024982,
UL1 RR-025744, UL1 RR-025761, UL1 RR-025780, UL1 RR-029890, UL1
RR-031986]; General Clinical Research Center [M01 RR-00400]; Juvenile
Diabetes Research Foundation International (JDRF); ADA
FX The sponsor of the study was the Type 1 Diabetes TrialNet Study Group.
Type 1 Diabetes TrialNet Study Group is a clinical trials network funded
by the National Institutes of Health (NTH) through the National
Institute of Diabetes and Digestive and Kidney Diseases, the National
Institute of Allergy and Infectious Diseases, and the Eunice Kennedy
Shriver National Institute of Child Health and Human Development,
through the cooperative agreements U01 DK-061010, U01 DK-061016, U01
DK-061034, U01 DK-061036, U01 DK-061040, U01 DK-061041, U01 DK-061042,
U01 DK-061055, U01 DK-061058, U01 DK-084565, U01 DK-085453, U01
DK-085461, U01 DK-085463, U01 DK-085466, U01 DK-085499, U01 DK-085505,
and U01 DK-085509, and a contract HHSN267200800019C; the National Center
for Research Resources, through Clinical Translational Science Awards
UL1 RR-024131, UL1 RR-024139, UL1 RR-024153, UL1 RR-024975, UL1
RR-024982, UL1 RR-025744, UL1 RR-025761, UL1 RR-025780, UL1 RR-029890,
and UL1 RR-031986, and General Clinical Research Center Award M01
RR-00400; the Juvenile Diabetes Research Foundation International
(JDRF); and the ADA. The contents of this article are solely the
responsibility of the authors and do not necessarily represent the
official views of the NIH, JDRF, or ADA.
NR 50
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PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD JUN
PY 2012
VL 61
IS 6
BP 1331
EP 1337
DI 10.2337/db11-1660
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 948FX
UT WOS:000304490100004
PM 22618768
ER
PT J
AU Haiman, CA
Fesinmeyer, MD
Spencer, KL
Buzkova, P
Voruganti, VS
Wan, P
Haessler, J
Franceschini, N
Monroe, KR
Howard, BV
Jackson, RD
Florez, JC
Kolonel, LN
Buyske, S
Goodloe, RJ
Liu, SM
Manson, JE
Meigs, JB
Waters, K
Mukamal, KJ
Pendergrass, SA
Shrader, P
Wilkens, LR
Hindorff, LA
Ambite, JL
North, KE
Peters, U
Crawford, DC
Le Marchand, L
Pankow, JS
AF Haiman, Christopher A.
Fesinmeyer, Megan D.
Spencer, Kylee L.
Buzkova, Petra
Voruganti, V. Saroja
Wan, Peggy
Haessler, Jeff
Franceschini, Nora
Monroe, Kristine R.
Howard, Barbara V.
Jackson, Rebecca D.
Florez, Jose C.
Kolonel, Laurence N.
Buyske, Steven
Goodloe, Robert J.
Liu, Simin
Manson, JoAnn E.
Meigs, James B.
Waters, Kevin
Mukamal, Kenneth J.
Pendergrass, Sarah A.
Shrader, Peter
Wilkens, Lynne R.
Hindorff, Lucia A.
Ambite, Jose Luis
North, Kari E.
Peters, Ulrike
Crawford, Dana C.
Le Marchand, Loic
Pankow, James S.
TI Consistent Directions of Effect for Established Type 2 Diabetes Risk
Variants Across Populations
SO DIABETES
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; LARGE-SCALE ASSOCIATION; TCF7L2 GENE;
CARDIOVASCULAR-DISEASE; ATHEROSCLEROSIS RISK; SUSCEPTIBILITY LOCI;
AFRICAN-AMERICANS; DESIGN; INDIANS; CDKAL1
AB Common genetic risk variants for type 2 diabetes (T2D) have primarily been identified in populations of European and Asian ancestry. We tested whether the direction of association with 20 T2D risk variants generalizes across six major racial/ethnic groups in the U.S. as part of the Population Architecture using Genomics and Epidemiology Consortium (16,235 diabetes case and 46,122 control subjects of European American, African American, Hispanic, East Asian, American Indian, and Native Hawaiian ancestry). The percentage of positive (odds ratio [OR] >1 for putative risk allele) associations ranged from 69% in American Indians to 100% in European Americans. Of the nine variants where we observed significant heterogeneity of effect by racial/ethnic group (P-heterogeneity < 0.05), eight were positively associated with risk (OR >1) in at least five groups. The marked directional consistency of association observed for most genetic variants across populations implies a shared functional common variant in each region. Fine-mapping of all loci will be required to reveal markers of risk that are important within and across populations. Diabetes 61:1642-1647, 2012
C1 [Haiman, Christopher A.; Wan, Peggy; Monroe, Kristine R.; Waters, Kevin] Univ So Calif, Keck Sch Med, Norris Comprehens Canc Ctr, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Fesinmeyer, Megan D.; Haessler, Jeff; Peters, Ulrike] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA.
[Spencer, Kylee L.; Goodloe, Robert J.; Pendergrass, Sarah A.; Crawford, Dana C.] Vanderbilt Univ, Dept Mol Physiol & Biophys, Ctr Human Genet Res, Nashville, TN 37232 USA.
[Buzkova, Petra] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Voruganti, V. Saroja] Texas Biomed Res Inst, Dept Genet, San Antonio, TX USA.
[Franceschini, Nora; North, Kari E.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Howard, Barbara V.] Georgetown Univ, Washington, DC USA.
[Howard, Barbara V.] Medstar Hlth Res Inst, Washington, DC USA.
[Jackson, Rebecca D.] Ohio State Univ, Dept Internal Med, Columbus, OH 43210 USA.
[Florez, Jose C.; Manson, JoAnn E.; Meigs, James B.] Harvard Univ, Sch Med, Boston, MA USA.
[Florez, Jose C.] Massachusetts Gen Hosp, Diabet Unit, Boston, MA 02114 USA.
[Florez, Jose C.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Florez, Jose C.] Broad Inst, Program Med & Populat Genet, Cambridge, MA USA.
[Kolonel, Laurence N.; Wilkens, Lynne R.] Univ Hawaii, Ctr Canc, Program Epidemiol, Honolulu, HI 96822 USA.
[Buyske, Steven] Rutgers State Univ, Dept Genet & Stat, Piscataway, NJ USA.
[Liu, Simin] Univ Calif Los Angeles, Sch Publ Hlth, Dept Epidemiol, Los Angeles, CA 90024 USA.
[Manson, JoAnn E.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Meigs, James B.; Shrader, Peter] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[Mukamal, Kenneth J.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
NHGRI, NIH, Off Populat Gen, Bethesda, MD 20892 USA.
[Ambite, Jose Luis] Univ So Calif, Inst Informat Sci, Los Angeles, CA USA.
[Pankow, James S.] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
RP Haiman, CA (reprint author), Univ So Calif, Keck Sch Med, Norris Comprehens Canc Ctr, Dept Prevent Med, Los Angeles, CA 90033 USA.
EM haiman@usc.edu
RI Crawford, Dana/C-1054-2012; Liu, Simin/I-3689-2014;
OI Liu, Simin/0000-0003-2098-3844; Pankow, James/0000-0001-7076-483X
FU National Human Genome Research Institute; [U01HG004803];
[U01HG004798]; [U01HG004802]; [U01HG004790]; [U01HG004801]
FX The PAGE program is funded by the National Human Genome Research
Institute, supported by U01HG004803 (CALiCo [Causal Variants Across the
Life Course]), U01HG004798 (EAGLE [Epidemiologic Architecture of Genes
Linked to Environment]), U01HG004802 (MEG [Multiethnic Cohort]),
U01HG004790 ('WHI [Women's Health Initiative]), and UO1HG004801
(Coordinating Center).
NR 44
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U1 0
U2 8
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD JUN
PY 2012
VL 61
IS 6
BP 1642
EP 1647
DI 10.2337/db11-1296
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 948FX
UT WOS:000304490100043
PM 22474029
ER
PT J
AU Rapuano, BE
Lee, JJE
MacDonald, DE
AF Rapuano, Bruce E.
Lee, Jani J. E.
MacDonald, Daniel E.
TI Titanium alloy surface oxide modulates the conformation of adsorbed
fibronectin to enhance its binding to alpha(5)beta(1) integrins in
osteoblasts
SO EUROPEAN JOURNAL OF ORAL SCIENCES
LA English
DT Article
DE conformation; fibronectin; integrins; osteoblast; titanium alloy
ID HUMAN PLASMA FIBRONECTIN; ATOMIC-FORCE MICROSCOPY; AMINO-ACID-SEQUENCE;
CELL-ADHESION; CHEMICAL-MODIFICATION; BONE SIALOPROTEIN; SYNERGY SITE;
NET CHARGE; IN-VITRO; ATTACHMENT
AB Rapuano BE, Lee JJE, MacDonald DE. Titanium alloy surface oxide modulates the conformation of adsorbed fibronectin to enhance its binding to a5 beta 1 integrins in osteoblasts. ?Eur J Oral Sci 2012; 120: 185194. (C) 2012 Eur J Oral Sci Our laboratory has previously demonstrated that heat (600 degrees C) or radiofrequency plasma glow discharge (RFGD) pretreatment of a titanium alloy (Ti6Al4V) increased the net negative charge of the alloy's surface oxide and the attachment of osteoblastic cells to adsorbed fibronectin. The purpose of the current study was to investigate the biological mechanism by which these surface pretreatments enhance the capacity of fibronectin to stimulate osteoblastic cell attachment. Each pretreatment was found to increase the binding (measured by ELISA) of a monoclonal anti-fibronectin Ig to the central integrin-binding domain of adsorbed fibronectin, and to increase the antibody's inhibition of osteogenic cell attachment (measured by hexosaminidase assay). Pretreatments also increased the binding (measured by ELISA) of anti-integrin IgGs to the a5 and beta 1 integrin subunits that became attached to fibronectin during cell incubation. These findings suggest that negatively charged surface oxides of Ti6Al4V cause conformational changes in fibronectin that increase the availability of its integrin-binding domain to a5 beta 1 integrins.
C1 [Rapuano, Bruce E.; Lee, Jani J. E.; MacDonald, Daniel E.] Cornell Univ, Weill Med Coll, Hosp Special Surg, New York, NY 10021 USA.
[MacDonald, Daniel E.] James J Peters VA Med Ctr, Bronx, NY USA.
[MacDonald, Daniel E.] Columbia Univ, Langmuir Ctr Colloids & Interfaces, New York, NY USA.
RP MacDonald, DE (reprint author), Cornell Univ, Weill Med Coll, Hosp Special Surg, 535 E 70th St, New York, NY 10021 USA.
EM dem14@columbia.edu
FU NIH [RO1 DE017695]; National Center for Research Resources, NIH [C06-
RR12538-01]
FX The project described was supported by Grant Number NIH RO1 DE017695
(awarded to D.E.M.). This material is also the result of work supported
with resources and the use of facilities at the James J. Peters VA
Medical Center, Bronx, New York. This investigation was also conducted
at the HSS research facility constructed with support of Grant C06-
RR12538-01 from the National Center for Research Resources, NIH. We
would like to acknowledge Dr Stephen Doty and Tony Labisserie for their
help with scanning electron microscopy. Special thanks go to Tiffany
Leung, Ryan Jeong, and Kyle Hackshaw for their technical assistance.
NR 51
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U1 1
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0909-8836
J9 EUR J ORAL SCI
JI Eur. J. Oral Sci.
PD JUN
PY 2012
VL 120
IS 3
BP 185
EP 194
DI 10.1111/j.1600-0722.2012.954_e.x
PG 10
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 944HC
UT WOS:000304188900002
PM 22607334
ER
PT J
AU Yamauchi, M
Lochhead, P
Morikawa, T
Huttenhower, C
Chan, AT
Giovannucci, E
Fuchs, C
Ogino, S
AF Yamauchi, Mai
Lochhead, Paul
Morikawa, Teppei
Huttenhower, Curtis
Chan, Andrew T.
Giovannucci, Edward
Fuchs, Charles
Ogino, Shuji
TI Colorectal cancer: a tale of two sides or a continuum?
SO GUT
LA English
DT Article
ID ISLAND METHYLATOR PHENOTYPE; MOLECULAR PATHOLOGICAL EPIDEMIOLOGY;
POPULATION-BASED SAMPLE; COLON-CANCER; MICROSATELLITE INSTABILITY;
BIRTH-COHORT; TRENDS; DISTAL; EXPRESSION; MORTALITY
C1 [Ogino, Shuji] Harvard Univ, Sch Med, Brigham & Womens Hosp, Ctr Mol Oncol Pathol,Dana Farber Canc Inst,Dept M, Boston, MA 02215 USA.
[Yamauchi, Mai; Lochhead, Paul; Morikawa, Teppei; Chan, Andrew T.; Giovannucci, Edward; Fuchs, Charles; Ogino, Shuji] Harvard Univ, Sch Med, Boston, MA 02215 USA.
[Huttenhower, Curtis] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02215 USA.
[Chan, Andrew T.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[Chan, Andrew T.; Giovannucci, Edward; Fuchs, Charles] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Giovannucci, Edward] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02215 USA.
[Giovannucci, Edward] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02215 USA.
[Ogino, Shuji] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
RP Ogino, S (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Ctr Mol Oncol Pathol,Dana Farber Canc Inst,Dept M, 450 Brookline Ave,Room JF 215C, Boston, MA 02215 USA.
EM shuji_ogino@dfci.harvard.edu
OI Huttenhower, Curtis/0000-0002-1110-0096
FU US National Institute of Health [P01 CA87969, P01 CA55075, P50 CA127003,
R01 CA118553, R01 CA151993, R01 CA137178]; US National Science
Foundation [DBI-1053486]; Harvard University; Japan Society for
Promotion of Science
FX This work was supported by US National Institute of Health grants (P01
CA87969 to S E Hankinson, P01 CA55075 to W C Willett, P50 CA127003 to
CSF, R01 CA118553 to CSF, R01 CA151993 to SO and R01 CA137178 to ATC)
and a US National Science Foundation grant (DBI-1053486 to CH). PL is a
Scottish Government Clinical Academic Fellow and is supported by a
Harvard University Knox Memorial Fellowship. TM was supported by a
fellowship grant from the Japan Society for Promotion of Science. The
content is solely the responsibility of the authors and does not
necessarily represent the official views of US NIH. Funding agencies did
not have any role in the design of the study; the collection, analysis,
or interpretation of the data; the decision to submit the manuscript for
publication; or the writing of the manuscript.
NR 53
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U1 0
U2 11
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0017-5749
J9 GUT
JI Gut
PD JUN
PY 2012
VL 61
IS 6
BP 794
EP 797
DI 10.1136/gutjnl-2012-302014
PG 4
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 941WG
UT WOS:000303997800005
PM 22490520
ER
PT J
AU Yamauchi, M
Morikawa, T
Kuchiba, A
Imamura, Y
Qian, ZR
Nishihara, R
Liao, XY
Waldron, L
Hoshida, Y
Huttenhower, C
Chan, AT
Giovannucci, E
Fuchs, C
Ogino, S
AF Yamauchi, Mai
Morikawa, Teppei
Kuchiba, Aya
Imamura, Yu
Qian, Zhi Rong
Nishihara, Reiko
Liao, Xiaoyun
Waldron, Levi
Hoshida, Yujin
Huttenhower, Curtis
Chan, Andrew T.
Giovannucci, Edward
Fuchs, Charles
Ogino, Shuji
TI Assessment of colorectal cancer molecular features along bowel subsites
challenges the conception of distinct dichotomy of proximal versus
distal colorectum
SO GUT
LA English
DT Article
ID ISLAND METHYLATOR PHENOTYPE; POPULATION-BASED SAMPLE; BODY-MASS INDEX;
DNA METHYLATION; COLON-CANCER; MICROSATELLITE INSTABILITY; LINE-1
HYPOMETHYLATION; P-GLYCOPROTEIN; BRAF MUTATION; EXPRESSION
AB Objective Colorectal cancer is typically classified into proximal colon, distal colon and rectal cancer. Tumour genetic and epigenetic features differ by tumour location. Considering a possible role of bowel contents (including microbiome) in carcinogenesis, this study hypothesised that tumour molecular features might gradually change along bowel subsites, rather than change abruptly at splenic flexure.
Design Utilising 1443 colorectal cancers in two US nationwide prospective cohort studies, the frequencies of molecular features (CpG island methylator phenotype (CIMP), microsatellite instability (MSI), LINE-1 methylation and BRAF, KRAS and PIK3CA mutations) were examined along bowel subsites (rectum, rectosigmoid junction, sigmoid, descending colon, splenic flexure, transverse colon, hepatic flexure, ascending colon and caecum). The linearity and non-linearity of molecular relations along subsites were statistically tested by multivariate logistic or linear regression analysis.
Results The frequencies of CIMP-high, MSI-high and BRAF mutations gradually increased from the rectum (<2.3%) to ascending colon (36-40%), followed by falls in the caecum (12-22%). By linearity tests, these molecular relations were significantly linear from rectum to ascending colon (p<0.0001), and there was little evidence of non-linearity (p>0.09). Caecal cancers exhibited the highest frequency of KRAS mutations (52% vs 27-35% in other sites; p<0.0001).
Conclusions The frequencies of CIMP-high, MSI-high and BRAF mutations in cancer increased gradually along colorectum subsites from the rectum to ascending colon. These novel data challenge the common conception of discrete molecular features of proximal versus distal colorectal cancers, and have a substantial impact on clinical, translational and epidemiology research, which has typically been performed with the dichotomous classification of proximal versus distal tumours.
C1 [Ogino, Shuji] Harvard Univ, Sch Med, Brigham & Womens Hosp, Ctr Mol Oncol Pathol,Dana Farber Canc Inst,Dept M, Boston, MA 02215 USA.
[Yamauchi, Mai; Morikawa, Teppei; Kuchiba, Aya; Imamura, Yu; Qian, Zhi Rong; Nishihara, Reiko; Liao, Xiaoyun; Waldron, Levi; Chan, Andrew T.; Giovannucci, Edward; Fuchs, Charles; Ogino, Shuji] Harvard Univ, Sch Med, Boston, MA 02215 USA.
[Waldron, Levi; Huttenhower, Curtis] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02215 USA.
[Waldron, Levi] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Hoshida, Yujin] Broad Inst Massachusetts Inst Technol & Harvard U, Canc Program, Cambridge, MA USA.
[Chan, Andrew T.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[Chan, Andrew T.; Giovannucci, Edward; Fuchs, Charles] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Giovannucci, Edward] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02215 USA.
[Giovannucci, Edward] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02215 USA.
[Ogino, Shuji] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
RP Ogino, S (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Ctr Mol Oncol Pathol,Dana Farber Canc Inst,Dept M, 450 Brookline Ave,Room JF 215C, Boston, MA 02215 USA.
EM shuji_ogino@dfci.harvard.edu
OI Qian, Zhi rong/0000-0003-1633-4120; Waldron, Levi/0000-0003-2725-0694;
Huttenhower, Curtis/0000-0002-1110-0096
FU US National Institutes of Health [P01CA87969, P01CA55075, P50CA127003,
R01CA151993, R01CA137178]; Bennett Family Fund for Targeted Therapies
Research; Entertainment Industry Foundation through National Colorectal
Cancer Research Alliance; Japan Society for the Promotion of Science
FX This work was supported by US National Institutes of Health grants
(P01CA87969 (to SE Hankinson), P01CA55075 (to WC Willett), P50CA127003
(to CSF), R01CA151993 (to SO) and R01CA137178 (to ATC)); the Bennett
Family Fund for Targeted Therapies Research; and the Entertainment
Industry Foundation through National Colorectal Cancer Research
Alliance. TM was supported by a fellowship grant from the Japan Society
for the Promotion of Science. The content is solely the responsibility
of the authors and does not necessarily represent the official views of
NCI or NIH. Funding agencies did not have any role in the design of the
study, the collection, analysis, or interpretation of the data, the
decision to submit the manuscript for publication or the writing of the
manuscript.
NR 57
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Z9 190
U1 4
U2 26
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0017-5749
J9 GUT
JI Gut
PD JUN
PY 2012
VL 61
IS 6
BP 847
EP 854
DI 10.1136/gutjnl-2011-300865
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 941WG
UT WOS:000303997800013
PM 22427238
ER
PT J
AU Williams, DR
Kontos, EZ
Viswanath, K
Haas, JS
Lathan, CS
MacConaill, LE
Chen, JV
Ayanian, JZ
AF Williams, David R.
Kontos, Emily Z.
Viswanath, K.
Haas, Jennifer S.
Lathan, Christopher S.
MacConaill, Laura E.
Chen, Jarvis
Ayanian, John Z.
TI Integrating Multiple Social Statuses in Health Disparities Research: The
Case of Lung Cancer
SO HEALTH SERVICES RESEARCH
LA English
DT Article
DE Health care disparities; smoking; lung cancer; race; ethnicity;
socioeconomic status; gender
ID SOCIOECONOMIC-STATUS; UNITED-STATES; RACIAL-DIFFERENCES;
CIGARETTE-SMOKING; RESIDENTIAL SEGREGATION; ETHNIC DISPARITIES;
AFRICAN-AMERICANS; RACE; US; MORTALITY
AB Objective To illustrate the complex patterns that emerge when race/ethnicity, socioeconomic status (SES), and gender are considered simultaneously in health care disparities research and to outline the needed research to understand them by using disparities in lung cancer risks, treatment, and outcomes as an example. Principal Findings SES, gender, and race/ethnicity are social categories that are robust predictors of variations in health and health services utilization. These are usually considered separately, but intersectionality theory indicates that the impact of each depends on the others. Each reflects historically and culturally contingent variations in social, economic, and political status. Distinct patterns of risk and resilience emerge at the intersections of multiple social categories and shape the experience of health, health care access, utilization, quality, and outcomes where these categories intersect. Intersectional approaches call for greater attention to understand social processes at multiple levels of society and require the collection of relevant data and utilization of appropriate analytic approaches to understand how multiple risk factors and resources combine to affect the distribution of disease and its management. Conclusions Understanding how race/ethnicity, gender, and SES are interactive, interdependent, and social identities can provide new knowledge to enhance our efforts to effectively address health disparities.
C1 [Williams, David R.; Kontos, Emily Z.; Chen, Jarvis] Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Boston, MA 02215 USA.
[Viswanath, K.] Harvard Univ, Sch Publ Hlth, Dept Med Oncol, Dana Farber Canc Inst, Boston, MA 02215 USA.
[Haas, Jennifer S.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Gen Med & Primary Care, Boston, MA 02215 USA.
[Lathan, Christopher S.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Adult Oncol,Dept Med, Boston, MA 02215 USA.
[MacConaill, Laura E.] Dana Farber Canc Inst, Ctr Canc Genome Discovery, Boston, MA 02115 USA.
[Ayanian, John Z.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Hlth Care Policy,Div Gen Med, Boston, MA 02215 USA.
RP Kontos, EZ (reprint author), Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, 401 Pk Dr,4th Floor W, Boston, MA 02215 USA.
EM ekontos@hsph.harvard.edu
FU National Cancer Institute's Lung Cancer Disparities Center
[1P50CA148596]; Harvard Catalyst \ The Harvard Clinical and
Translational Science Center (NIH) [UL1 RR 025758]; Harvard University
FX This work was conducted with support from the National Cancer
Institute's Lung Cancer Disparities Center grant 1P50CA148596 and in
part (for Drs. Ayanian and Haas) with support from Harvard Catalyst
vertical bar The Harvard Clinical and Translational Science Center (NIH
Award UL1 RR 025758 and financial contributions from Harvard University
and its affiliated academic health care centers). The content is solely
the responsibility of the authors and does not necessarily represent the
official views of Harvard Catalyst, Harvard University and its
affiliated academic health care centers, the National Center for
Research Resources, or the National Institutes of Health. The authors
would also like to thank the Center's Program Coordinator, Maria
Simoneau, for her dedication to the formatting of this manuscript and
the administrative oversight of the submission process. The co-authors
report no conflict of interest.
NR 84
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U1 2
U2 36
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0017-9124
J9 HEALTH SERV RES
JI Health Serv. Res.
PD JUN
PY 2012
VL 47
IS 3
BP 1255
EP 1277
DI 10.1111/j.1475-6773.2012.01404.x
PN 2
PG 23
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 939HO
UT WOS:000303800300003
PM 22568674
ER
PT J
AU Lapatin, S
Goncalves, M
Nillni, A
Chavez, L
Quinn, RL
Green, A
Alegria, M
AF Lapatin, Sheri
Goncalves, Marta
Nillni, Anna
Chavez, Ligia
Quinn, Roxana Llerena
Green, Alexander
Alegria, Margarita
TI Lessons from the Use of Vignettes in the Study of Mental Health Service
Disparities
SO HEALTH SERVICES RESEARCH
LA English
DT Article
DE Vignettes; disparities; mental health services
ID RHEUMATOID-ARTHRITIS; CLINICAL JUDGMENT
AB Objective To examine the development, feasibility, and use of a vignette approach as an important tool in health services disparities research. Data Source Interviews with vignette developers and qualitative data from a novel mental health services disparities study that used vignettes in two samples: (1) predominantly low-income parents of children attending mental health specialty care who were Latino or non-Latino White and (2) Latino and non-Latino mental health clinicians who treat children in their practice. Study Design We conduct a content analysis of qualitative data from patients and providers in the Ethnic Differences Study to explore the feasibility of vignette methodology in health services disparities research, and we identify lessons learned that may guide future vignette development. Principal Findings Vignettes provide a valuable approach that is acceptable to participants, elicits important insight on participant experience and services, and sheds light on factors that can help optimize study design for exploring health disparities questions. Conclusions Researchers, clinicians, and others should consider a set of factors that help determine when a vignette approach is warranted in research, training, or for other uses, including how best to address identified weaknesses.
C1 [Lapatin, Sheri; Alegria, Margarita] Harvard Univ, Sch Med, Ctr Multicultural Mental Hlth Res, Cambridge Hlth Alliance, Somerville, MA 02143 USA.
[Goncalves, Marta] Harvard Univ, Sch Med, Cambridge Hlth Alliance,Mental Hlth Res, Lisbon Univ Inst ISCTE IUL,Ctr Multicultural, Lisbon, Portugal.
[Nillni, Anna] NYU, Steinhardt Sch Media Culture & Commun, New York, NY USA.
[Chavez, Ligia] Univ Puerto Rico, San Juan, PR 00936 USA.
[Quinn, Roxana Llerena] Childrens Hosp Boston, Dept Psychiat, Boston, MA USA.
[Green, Alexander] Massachusetts Gen Hosp, Disparities Solut Ctr, Boston, MA 02114 USA.
RP Lapatin, S (reprint author), Harvard Univ, Sch Med, Ctr Multicultural Mental Hlth Res, Cambridge Hlth Alliance, 120 Beacon St,4th Floor, Somerville, MA 02143 USA.
EM slapatin@charesearch.com
OI Goncalves, Marta/0000-0002-0232-2631; Markle, Sheri/0000-0002-6768-3569
FU NIH [1P50MH 073469]; National Institute of Mental Health; National
Institute on Minority Health and Health Disparities [P60 MD 002261]
FX This study was supported by NIH Research Grant 1P50MH 073469 funded by
the National Institute of Mental Health and P60 MD 002261 (NIMHD) funded
by the National Institute on Minority Health and Health Disparities. The
authors thank Norah Mulvaney-Day, Marcela Horvitz-Lennon, Benjamin Cook,
John Ayanian, LeRoi Hicks, and Emily Zobel Kontos for their valuable
feedback on previous drafts; Yaminette Diaz, for her contributions to
study setup and implementation in Boston site; Sabrina Gonzalez for
conducting parent interviews; and Rachel Shapiro for her input on
recruitment.
NR 27
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U1 1
U2 10
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0017-9124
J9 HEALTH SERV RES
JI Health Serv. Res.
PD JUN
PY 2012
VL 47
IS 3
BP 1345
EP 1362
DI 10.1111/j.1475-6773.2011.01360.x
PN 2
PG 18
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 939HO
UT WOS:000303800300007
PM 22150766
ER
PT J
AU Shields, AE
Crown, WH
AF Shields, Alexandra E.
Crown, William H.
TI Looking to the Future: Incorporating Genomic Information into
Disparities Research to Reduce Measurement Error and Selection Bias
SO HEALTH SERVICES RESEARCH
LA English
DT Article
DE Health economics; social determinants of health; racial; ethnic
differences in health and health care; personalized medicine; genomics
ID HER2-POSITIVE BREAST-CANCER; ELECTRONIC HEALTH RECORDS; GENE-ENVIRONMENT
INTERACTION; AFRICAN-AMERICANS; ADJUVANT CHEMOTHERAPY; SUSCEPTIBILITY
LOCI; WIDE ASSOCIATION; MEDICAL-RECORDS; NATIONAL-SURVEY; LUNG-CANCER
AB Objective To extend recent conceptual and methodological advances in disparities research to include the incorporation of genomic information in analyses of racial/ethnic disparities in health care and health outcomes. Data Sources Published literature on human genetic variation, the role of genetics in disease and response to treatment, and methodological developments in disparities research. Study Design We present a conceptual framework for incorporating genomic information into the Institute of Medicine definition of racial/ethnic disparities in health care, identify key concepts used in disparities research that can be informed by genomics research, and illustrate the incorporation of genomic information into current methods using the example of HER-2 mutations guiding care for breast cancer. Principal Findings Genomic information has not yet been incorporated into disparities research, though it has direct relevance to concepts of race/ethnicity, health status, appropriate care, and socioeconomic status. The HER-2 example demonstrates how available genetic information can be incorporated into current disparities methods to reduce selection bias and measurement error. Advances in health information infrastructure may soon make standardized genetic information more available to health services researchers. Conclusion Genomic information can refine measurement of racial/ethnic disparities in health care and health outcomes and should be included wherever possible in disparities research.
C1 [Shields, Alexandra E.] Massachusetts Gen Hosp, Harvard MGH Ctr Genom Vulnerable Populat & Hlth D, Boston, MA 02114 USA.
[Shields, Alexandra E.] Massachusetts Gen Hosp, Mongan Inst Hlth Policy, Boston, MA 02114 USA.
[Crown, William H.] OptumInsight Life Sci, Waltham, MA USA.
RP Shields, AE (reprint author), 50 Staniford St,Suite 901, Boston, MA 02114 USA.
EM ashields@partners.org
FU Harvard Catalyst \ The Harvard Clinical and Translational Science Center
(NIH) [UL1 RR 025758]; Harvard University; National Human Genome
Research Institute [R01 HG003475-03]; OptumInsight Fellowship Program
FX The authors thank Tom McGuire, Wylie Burke, Mehdi Najafzadeh, and John
Ayanian for comments on earlier drafts of this manuscript. Carly
Hudelson, Marcelo Cerullo, and Anna Boonin Schachter also deserve
special thanks for their superb research assistance. This work was
conducted with support from Harvard Catalyst vertical bar The Harvard
Clinical and Translational Science Center (NIH Award UL1 RR 025758 and
financial contributions from Harvard University and its affiliated
academic health care centers). The content is solely the responsibility
of the authors and does not necessarily represent the official views of
Harvard Catalyst, Harvard University and its affiliated academic health
care centers, the National Center for Research Resources, or the
National Institutes of Health. This work was also supported by a grant
from the National Human Genome Research Institute R01 HG003475-03 (A.
Shields) and the OptumInsight Fellowship Program (W. Crown).
NR 79
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U1 3
U2 10
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0017-9124
J9 HEALTH SERV RES
JI Health Serv. Res.
PD JUN
PY 2012
VL 47
IS 3
BP 1387
EP 1410
DI 10.1111/j.1475-6773.2012.01413.x
PN 2
PG 24
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 939HO
UT WOS:000303800300009
PM 22515190
ER
PT J
AU Qi, H
Liu, JP
Deng, CY
Zhou, HX
Deng, SP
Li, FR
AF Qi, Hui
Liu, Jin-Peng
Deng, Chun-Yan
Zhou, Han-Xin
Deng, Shao-Ping
Li, Fu-Rong
TI A role for anti-CD45RB monoclonal antibody treatment upon dendritic
cells
SO IMMUNOLOGIC RESEARCH
LA English
DT Article
DE Anti-CD45RB monoclonal antibody; Dendritic cells; Exosome; Immune
tolerance
ID REGULATORY T-CELLS; ISLET ALLOGRAFT SURVIVAL; TRANSPLANT TOLERANCE;
EXOSOMES; ACTIVATION; MATURATION; RECEPTOR; CD45; IMMUNOSUPPRESSION;
PHOSPHATASE
AB Selective interference with CD45RB isoform by monoclonal antibody (anti-CD45RBmAb) reliably induces donor-specific tolerance. Dendritic cells (DCs) are the most potent antigen-presenting cells that are capable of activating na < ve T cells. The purposes of the present study were to investigate the roles of anti-CD45RBmAb on the phenotypes and functioning of DCs and to further illustrate the mechanism of anti-CD45RBmAb-inducing immunologic tolerance. DCs from C57BL/6 mice were cultured and treated with various doses of anti-CD45RB monoclonal antibody. Cell phenotype, cycle and phagocytic ability were detected by flow cytometry. The production of IL-10 and IL-12 in the supernatants of mature DCs was measured with ELISA. Exosomes (Dex) were recovered from the supernatant of DCs cultured for 6 days in depleted medium, and effects of DCs and Dex on the ability of T-cell proliferation were detected by mixed lymphocyte culture. Anti-CD45RBmAb could inhibit DCs maturation in a dose-dependent manner, and the effects of exosomes (Dex) on DCs enhance or inhibition proliferation of T cells were also in a dose-dependent manner. Anti-CD45RBmAb could profoundly inhibit the maturation and functioning of DCs and generate tolerogenic dendritic cells (tDCs) as well as Dex, suggesting mechanistic contributions to tolerance development from the DCs through interactions with T cells.
C1 [Qi, Hui; Liu, Jin-Peng; Deng, Chun-Yan; Zhou, Han-Xin; Deng, Shao-Ping; Li, Fu-Rong] Jinan Univ, Shenzhen Peoples Hosp, Clin Med Res Ctr, Clin Med Coll 2, Shenzhen 518020, Peoples R China.
[Deng, Shao-Ping] Harvard Univ, Sch Med, Dept Surg, Massachusetts Gen Hosp, Boston, MA USA.
[Li, Fu-Rong] Shenzhen Inst Gerontol, Shenzhen 518020, Peoples R China.
RP Li, FR (reprint author), Jinan Univ, Shenzhen Peoples Hosp, Clin Med Res Ctr, Clin Med Coll 2, 1017 Dongmen N Rd, Shenzhen 518020, Peoples R China.
EM dengs60@yahoo.com.cn; frli62@yahoo.com
FU National Natural Science Foundation of China [30772042]; The Natural
Science Foundation of Guangdong [6027540]; The Science and Technology
Project of Shenzhen [200601017]; Medical Science and Technology
Foundation of Guangdong [B2008158]
FX This work was supported by the National Natural Science Foundation of
China (No. 30772042), The Natural Science Foundation of Guangdong (No.
6027540) and The Science and Technology Project of Shenzhen (No.
200601017) and the Medical Science and Technology Foundation of
Guangdong (No. B2008158).
NR 31
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U1 1
U2 8
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0257-277X
J9 IMMUNOL RES
JI Immunol. Res.
PD JUN
PY 2012
VL 52
IS 3
BP 250
EP 257
DI 10.1007/s12026-012-8336-0
PG 8
WC Immunology
SC Immunology
GA 943HD
UT WOS:000304110600009
PM 22539131
ER
PT J
AU Labbe, C
Boucher, G
Foisy, S
Alikashani, A
Nkwimi, H
David, G
Beaudoin, M
Goyette, P
Charron, G
Xavier, RJ
Rioux, JD
AF Labbe, Catherine
Boucher, Gabrielle
Foisy, Sylvain
Alikashani, Azadeh
Nkwimi, Herbert
David, Genevieve
Beaudoin, Melissa
Goyette, Philippe
Charron, Guy
Xavier, Ramnik J.
Rioux, John D.
TI Genome-wide expression profiling implicates a MAST3-regulated gene set
in colonic mucosal inflammation of ulcerative colitis patients
SO INFLAMMATORY BOWEL DISEASES
LA English
DT Article
DE MAST3; inflammatory bowel disease; NF-kappa B
ID NECROSIS-FACTOR-ALPHA; ZINC-FINGER PROTEIN; KAPPA-B ACTIVATION;
CROHNS-DISEASE; BOWEL-DISEASE; TH17 CELLS; INFLIXIMAB; BIOINFORMATICS;
SUSCEPTIBILITY; PATHOGENESIS
AB Background: Crohn's disease (CD) and ulcerative colitis (UC) are inflammatory bowel diseases (IBDs) presumably caused by dysregulated immune responses to the gut microbiota. Genetic association studies have implicated dozens of chromosomal regions or loci in IBD susceptibility. The next challenge is to explain the individual role of each of these modest effect loci in the disease state. We have previously identified MAST3 as an IBD susceptibility gene through genetic fine-mapping of the 19p linkage region. Testing MAST3 in a reporter assay provided preliminary evidence that MAST3 modulates the activity of inflammation-related transcription factor nuclear factor kappa B. Methods: Here we characterized the function of MAST3 through an examination of the influence of the modulation of MAST3 expression on endogenous genome-wide expression patterns. More specifically, we looked at differential gene expression resulting from overexpression and knockdown of the MAST3 gene in epithelial and macrophage cell lines. From we highlight a group of genes whose expression is modulated by MAST3 and correlate their expression with NF-jB activity. Their expression was found to be enriched in inflamed mucosal tissue of UC patients, confirming the importance of these genes in IBD. Results: We highlight a group of genes whose expression is modulated by MAST3 and correlate their expression with NF-?B activity. Their expression was found to be enriched in inflamed mucosal tissue of UC patients, confirming the importance of these genes in IBD. These MAST3-regulated genes are central to mucosal immune responses. Among them are proinflammatory cytokines (e.g., CCL20, IL8), regulators of NF-?B (e.g., TNFAIP3, LY96, NFKBIA), genes involved in interferon-induced defense against pathogen invasion (e.g., IFIT1, ISG15), and genes involved in cell adhesion and/or migration (e.g., CD44, TMOD1). Conclusions: Taken together, these results confirm MAST3 as a modulator of the inflammatory response through regulation of immune gene expression in the gut of IBD patients. (Inflamm Bowel Dis 2012)
C1 [Labbe, Catherine; Boucher, Gabrielle; Foisy, Sylvain; Alikashani, Azadeh; Nkwimi, Herbert; David, Genevieve; Beaudoin, Melissa; Goyette, Philippe; Charron, Guy; Rioux, John D.] Montreal Heart Inst, Montreal, PQ H1T 1C8, Canada.
[Labbe, Catherine; David, Genevieve; Rioux, John D.] Univ Montreal, Dept Med, Montreal, PQ H3C 3J7, Canada.
[Labbe, Catherine; David, Genevieve; Rioux, John D.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Computat & Integrat Biol, Boston, MA USA.
[Labbe, Catherine; David, Genevieve; Rioux, John D.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Gastrointestinal Unit, Boston, MA USA.
[Xavier, Ramnik J.] Massachusetts Gen Hosp, Ctr Study Inflammatory Bowel Dis, Boston, MA 02114 USA.
RP Rioux, JD (reprint author), Montreal Heart Inst, 5000 Belanger St, Montreal, PQ H1T 1C8, Canada.
EM John.David.Rioux@umontreal.ca
RI Rioux, John/A-9599-2015
OI Rioux, John/0000-0001-7560-8326
FU U.S. National Institute of Diabetes and Digestive and Kidney Diseases
[DK062432]; Crohn's and Colitis Foundation of America [SRA512]; Fonds de
Recherche en Sante du Quebec
FX Funded by grants from the U.S. National Institute of Diabetes and
Digestive and Kidney Diseases (DK062432) and the Crohn's and Colitis
Foundation of America (SRA512) (to J.D.R.). C.L. holds a doctoral
training award from the Fonds de Recherche en Sante du Quebec.
NR 35
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U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1078-0998
J9 INFLAMM BOWEL DIS
JI Inflamm. Bowel Dis.
PD JUN
PY 2012
VL 18
IS 6
BP 1072
EP 1080
DI 10.1002/ibd.21887
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 943PR
UT WOS:000304137300011
PM 21994190
ER
PT J
AU Weaver, MJ
Harris, MB
Strom, AC
Smith, RM
Lhowe, D
Zurakowski, D
Vrahas, MS
AF Weaver, Michael J.
Harris, Mitchel B.
Strom, Adam C.
Smith, R. Malcolm
Lhowe, David
Zurakowski, David
Vrahas, Mark S.
TI Fracture pattern and fixation type related to loss of reduction in
bicondylar tibial plateau fractures
SO INJURY-INTERNATIONAL JOURNAL OF THE CARE OF THE INJURED
LA English
DT Article
DE Tibial plateau fractures; Fractures; Fracture fixation
AB Introduction: Bicondylar tibial plateau fractures can be treated with locked plating applied from the lateral side with or without additional application of a medial plate (dual plating). Recent studies demonstrate that these injuries can be sub-grouped based upon their morphology by computed tomography (CT). The purpose of this study is to evaluate the relationship between fracture pattern, method of fixation and loss of reduction in bicondylar tibial plateau fractures.
Patients and methods: Preoperative CT scans and postoperative plain films were evaluated on a consecutive series of bicondylar tibial plateau fractures. Fracture patterns were classified by CT. Angular alignment was measured immediately postoperatively and again at clinical and radiographic union to assess loss of reduction.
Results: A total of 140 patients were studied. Sixty-six (47%) had a single large medial fragment with the articular surface intact, 19 (14%) had a medial articular fracture line with a mainly sagittal component and 55 (39%) had a coronal fracture through the medial articular surface. A total of 129 patients had been treated with lateral locked plating alone whilst 11 patients (all with a coronal fracture of the medial condyle) underwent dual plating.
There was little loss of reduction (median subsidence 0.5 degrees) when lateral locked plating was employed alone in patients with a single medial fracture fragment or with a sagittal medial fracture line. When lateral locked plating was used in the presence of a medial coronal fracture line, there was a significantly higher rate of subsidence (median 2.0 degrees) compared to those with no medial fracture line (p = 0.002). Patients with coronal fracture lines treated with dual plating had significantly less loss of reduction that those treated with lateral locked plating (p = 0.01).
Conclusions: Most patients with bicondylar tibial plateau fractures do well when treated with lateral locked plating. However, those with a medial coronal fracture line tend to have a higher rate of subsidence and loss of reduction when lateral locked plating is employed alone. These fractures may be better treated with dual plating if the soft tissues allow. (c) 2011 Elsevier Ltd. All rights reserved.
C1 [Weaver, Michael J.; Harris, Mitchel B.] Harvard Univ, Brigham & Womens Hosp, Dept Orthopaed Surg, Sch Med, Boston, MA 02115 USA.
[Strom, Adam C.] Dartmouth Coll, Hanover, NH 03755 USA.
[Smith, R. Malcolm; Lhowe, David; Vrahas, Mark S.] Harvard Univ, Massachusetts Gen Hosp, Dept Orthopaed Surg, Sch Med, Boston, MA 02115 USA.
[Zurakowski, David] Harvard Univ, Childrens Hosp Boston, Dept Surg, Sch Med, Boston, MA 02115 USA.
RP Weaver, MJ (reprint author), Harvard Univ, Brigham & Womens Hosp, Dept Orthopaed Surg, Sch Med, 75 Francis St, Boston, MA 02115 USA.
EM mjweaver@partners.org
NR 14
TC 18
Z9 29
U1 0
U2 4
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0020-1383
J9 INJURY
JI Injury-Int. J. Care Inj.
PD JUN
PY 2012
VL 43
IS 6
BP 864
EP 869
DI 10.1016/j.injury.2011.10.035
PG 6
WC Critical Care Medicine; Emergency Medicine; Orthopedics; Surgery
SC General & Internal Medicine; Emergency Medicine; Orthopedics; Surgery
GA 942LI
UT WOS:000304045100033
PM 22169068
ER
PT J
AU Zhu, JY
Li, LP
Li, YX
Shi, MY
Lu, HY
Garnick, DW
Weingart, SN
AF Zhu, Junya
Li, Liping
Li, Yuxia
Shi, Meiyu
Lu, Haiying
Garnick, Deborah W.
Weingart, Saul N.
TI What constitutes patient safety culture in Chinese hospitals?
SO INTERNATIONAL JOURNAL FOR QUALITY IN HEALTH CARE
LA English
DT Article
DE patient safety; quality culture; focus groups; China; hospital
ID PSYCHOMETRIC PROPERTIES; HEALTH-CARE; ADVERSE EVENTS; CLIMATE;
PERCEPTIONS; INSTRUMENTS; TAIWAN; JAPAN
AB To develop a patient safety culture instrument for use in Chinese hospitals, we assessed the appropriateness of existing safety culture questionnaires used in the USA and Japan for Chinese respondents and identified new items and domains suitable to Chinese hospitals.
Focus group study.
Twenty-four physicians, nurses and other health-care workers from 11 hospitals in three Chinese cities.
Three focus groups were conducted in 2010 to elicit information from hospital workers about their perceptions of the appropriateness and importance of each of 97 questionnaire items, derived from a literature review and an expert panel, characterizing hospital safety culture.
Participants understood the concepts of patient safety and safety culture and identified features associated with safe care. They judged that numerous questions from existing surveys were inappropriate, including 39 items that were dropped because they were judged unimportant, semantically redundant, confusing, ambiguous or inapplicable in Chinese settings. Participants endorsed eight new items and three additional dimensions addressing staff training, mentoring of new hires, compliance with rules and procedures, equipment availability and leadership walk-rounds they judged appropriate to assessing safety culture in Chinese hospitals. This process resulted in a 66-item instrument for testing in cognitive interviews, the next stage of survey development.
Focus group participants provided important insights into the refinement of existing items and the construction of new items for measuring patient safety culture in Chinese hospitals. This is a necessary first step in producing a culturally appropriate instrument applicable to specific local contexts.
C1 [Zhu, Junya; Weingart, Saul N.] Dana Farber Canc Inst, Ctr Patient Safety, Boston, MA 02215 USA.
[Zhu, Junya; Garnick, Deborah W.] Brandeis Univ, Heller Sch Social Policy & Management, Waltham, MA USA.
[Zhu, Junya; Li, Liping; Li, Yuxia; Shi, Meiyu; Lu, Haiying] Shanghai Univ Tradit Chinese Med, Sch Nursing, Shanghai, Peoples R China.
[Weingart, Saul N.] Harvard Univ, Sch Med, Boston, MA USA.
RP Zhu, JY (reprint author), Dana Farber Canc Inst, Ctr Patient Safety, 450 Brookline Ave, Boston, MA 02215 USA.
EM junya_zhu@dfci.harvard.edu
RI Garnick, Deborah/I-9009-2012; Davis, Mark/J-5101-2015
FU World Health Organization (WHO) [PS08212]
FX We gratefully acknowledge the World Health Organization (WHO) Patient
Safety Research Small Grants (grant no. PS08212) for the funding support
and guidance. All views expressed in this manuscript are those of the
authors and do not necessarily reflect the view of the WHO.
NR 43
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U1 4
U2 17
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1353-4505
J9 INT J QUAL HEALTH C
JI Int. J. Qual. Health Care
PD JUN
PY 2012
VL 24
IS 3
BP 250
EP 257
DI 10.1093/intqhc/mzs010
PG 8
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 944KA
UT WOS:000304198700008
PM 22461205
ER
PT J
AU Moffat, KA
Timleck, M
Spitzer, E
Plumhoff, E
Van Cott, E
Hayward, CPM
AF Moffat, Karen A.
Timleck, Marilyn
Spitzer, Ernie
Plumhoff, Elizabeth
Van Cott, Elizabeth
Hayward, Catherine P. M.
TI ORAL ABSTRACT: EXTERNAL PROFICIENCY TESTING ASSESSMENT - RESULTS OF
SURVEYS ON DENSE GRANULE DEFICIENCY
SO INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY
LA English
DT Meeting Abstract
C1 [Moffat, Karen A.; Spitzer, Ernie; Hayward, Catherine P. M.] Hamilton Reg Lab Med Program, Hamilton, ON, Canada.
[Moffat, Karen A.; Hayward, Catherine P. M.] McMaster Univ, Dept Med, Hamilton, ON, Canada.
[Moffat, Karen A.; Plumhoff, Elizabeth; Van Cott, Elizabeth; Hayward, Catherine P. M.] N Amer Specialized Coagulat Lab Assoc, Rochester, MN USA.
[Timleck, Marilyn; Hayward, Catherine P. M.] McMaster Univ, Dept Pathol & Mol Med, Hamilton, ON, Canada.
[Plumhoff, Elizabeth] Mayo Clin, Rochester, MN USA.
[Van Cott, Elizabeth] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1751-5521
J9 INT J LAB HEMATOL
JI Int. J. Lab. Hematol.
PD JUN
PY 2012
VL 34
SU 1
SI SI
BP 41
EP 42
PG 2
WC Hematology
SC Hematology
GA 942YH
UT WOS:000304087100048
ER
PT J
AU Timur, AA
Murugesan, G
Zhang, L
Aung, PP
Barnard, J
Wang, QK
Gaussem, P
Silverstein, RL
Bhatt, DL
Kottke-Marchant, K
AF Timur, Ayse Anil
Murugesan, Gurunathan
Zhang, Li
Phyu Phyu Aung
Barnard, John
Wang, Qing K.
Gaussem, Pasacale
Silverstein, Roy L.
Bhatt, Deepak L.
Kottke-Marchant, Kandice
TI P2RY1 AND P2RY12 POLYMORPHISMS AND RESIDUAL PLATELET REACTIVITY IN
CORONARY ARTERY DISEASE PATIENTS ON ASPIRIN
SO INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY
LA English
DT Meeting Abstract
C1 [Timur, Ayse Anil; Murugesan, Gurunathan; Phyu Phyu Aung; Kottke-Marchant, Kandice] Pathol & Lab Med Inst Cleveland, Cleveland, OH USA.
[Wang, Qing K.] Cleveland Clin Cleveland, Ctr Cardiovasc Genet, Cleveland, OH USA.
[Wang, Qing K.] Cleveland Clin Cleveland, Dept Mol Cardiol, Cleveland, OH USA.
[Gaussem, Pasacale] Univ Paris 05, Inserm U765, AP HP Hop Europeen Georges Pompidou Paris, Paris, France.
[Silverstein, Roy L.] Med Coll Wisconsin Milwaukee, Dept Med, Milwaukee, WI USA.
[Bhatt, Deepak L.] Brigham & Womens Hosp, VA Boston Healthcare Syst, Boston, MA 02115 USA.
[Bhatt, Deepak L.] Harvard Univ, Med Sch Boston, Cambridge, MA 02138 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1751-5521
J9 INT J LAB HEMATOL
JI Int. J. Lab. Hematol.
PD JUN
PY 2012
VL 34
SU 1
SI SI
BP 90
EP 90
PG 1
WC Hematology
SC Hematology
GA 942YH
UT WOS:000304087100141
ER
PT J
AU Thompson, GR
Wiederhold, NP
Najvar, LK
Bocanegra, R
Kirkpatrick, WR
Graybill, JR
Patterson, TF
AF Thompson, George R., III
Wiederhold, Nathan P.
Najvar, Laura K.
Bocanegra, Rosie
Kirkpatrick, William R.
Graybill, John R.
Patterson, Thomas F.
TI A murine model of Cryptococcus gattii meningoencephalitis
SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY
LA English
DT Article
DE cryptococcal meningoencephalitis; C; gattii; Cryptococcus neoformans;
posaconazole; fluconazole
ID NEOFORMANS; MENINGITIS; OUTBREAK; FLUCONAZOLE; FLUCYTOSINE; GENOTYPE;
VARIETY
AB Meningoencephalitis caused by Cryptococcus gattii is associated with significant morbidity and the need for aggressive therapy, and often necessitates neurosurgical intervention. We adapted a previously described murine model of cryptococcal meningoencephalitis due to Cryptococcus neoformans to that caused by C. gattii.
Mice were inoculated intracranially with either C. gattii (genotype VGIIa) or C. neoformans. In virulence studies, different C. gattii infecting inocula were compared with a fixed inoculum of C. neoformans, and differences were assessed by survival, brain tissue fungal burden, serum antigen titres and histopathological changes within brain tissue. For treatment, fluconazole or posaconazole (10 mg/kg orally twice daily) was initiated 24 h post-inoculation.
C. gattii was more virulent than C. neoformans, as evident by shorter median survival, earlier histopathological changes and higher serum antigen titres. However, no differences in fungal burden or dissemination to other organs were observed among the various groups. In treatment studies, both fluconazole and posaconazole improved the median survival of mice infected with either species. However, neither regimen improved the percentage of animals surviving to the predetermined study endpoint.
These results demonstrate the virulence of C. gattii meningoencephalitis and the potential of this model for the assessment of new treatment strategies.
C1 [Thompson, George R., III] Univ Calif Davis, Div Infect Dis, Dept Med Microbiol & Immunol, Davis, CA 95616 USA.
[Thompson, George R., III] Univ Calif Davis, Div Infect Dis, Dept Internal Med, Davis, CA 95616 USA.
[Wiederhold, Nathan P.; Najvar, Laura K.; Bocanegra, Rosie; Kirkpatrick, William R.; Graybill, John R.; Patterson, Thomas F.] Univ Texas Hlth Sci Ctr San Antonio, Div Infect Dis, Dept Internal Med, San Antonio, TX 78229 USA.
[Wiederhold, Nathan P.] Univ Texas Austin, Coll Pharm, Austin, TX 78712 USA.
[Patterson, Thomas F.] S Texas Vet Hlth Care Syst, Div Infect Dis, Dept Internal Med, San Antonio, TX USA.
RP Thompson, GR (reprint author), Univ Calif Davis, Div Infect Dis, Dept Med Microbiol & Immunol, Davis, CA 95616 USA.
EM grthompson@ucdavis.edu
OI Wiederhold, Nathan/0000-0002-2225-5122
FU National Institutes of Health/National Institute of Allergy and
Infectious Diseases [N01-AI-25475]; Pfizer; Schering-Plough; Merck;
Basilea; Astellas
FX This work was supported by a contract from the National Institutes of
Health/National Institute of Allergy and Infectious Diseases
(N01-AI-25475) to J. R. G. and T. F. P.; G. R. T. has received research
support from Pfizer. N. P. W. has received research support from Pfizer,
Schering-Plough, Merck, Basilea and Astellas. J. R. G. has received
research support from Pfizer, Merck and Astellas, and has been paid to
act as a consultant for Merck. T. F. P. has received research grants
from Astellas, Basilea, Merck and Pfizer (to the University of Texas
Health Science Center at San Antonio), and has been paid to act as a
consultant for Astellas, Basilea, Merck, Pfizer and Toyoma. All other
authors: none to declare.
NR 19
TC 13
Z9 13
U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-7453
J9 J ANTIMICROB CHEMOTH
JI J. Antimicrob. Chemother.
PD JUN
PY 2012
VL 67
IS 6
BP 1432
EP 1438
DI 10.1093/jac/dks060
PG 7
WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy
SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy
GA 942RJ
UT WOS:000304064400020
PM 22378683
ER
PT J
AU Huttner, B
Jones, M
Rubin, MA
Madaras-Kelly, K
Nielson, C
Goetz, MB
Neuhauser, MM
Samore, MH
AF Huttner, Benedikt
Jones, Makoto
Rubin, Michael A.
Madaras-Kelly, Karl
Nielson, Christopher
Goetz, Matthew Bidwell
Neuhauser, Melinda M.
Samore, Matthew H.
TI Double trouble: how big a problem is redundant anaerobic antibiotic
coverage in Veterans Affairs medical centres?
SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY
LA English
DT Article
DE antibiotic stewardship; anaerobes; metronidazole; inappropriate
antibiotic use
ID METRONIDAZOLE; THERAPY
AB Objectives: To assess the prevalence of, and the variation in, avoidable use of metronidazole in the Veterans Affairs (VA) healthcare system
Methods: Barcode Medication Administration (BCMA) data were retrospectively assessed for all patients hospitalized between January 2006 and December 2010 in acute-care wards of all VA medical centres (VAMCs) with complete BCMA data and at least 10 acute-care non-intensive care unit (ICU) beds. Potentially avoidable metronidazole days of therapy (DOT) were defined as the administration of metronidazole with anotheranti-anaerobic antibiotic on the same day for at least two consecutive days during the same hospitalization. Metronidazole was not considered redundant in combination with another anti-anaerobic agent within 28 days after a positive test for Clostridium difficile and during hospitalizations associated with discharge diagnosis codes for cholecystitis or cholangitis.
Results: A total of 128 VAMCs satisfied the inclusion criteria. Over the study period there were a total of 782821 DOT of metronidazole (57.4 DOT per 1000 patient-days), of which 183267 (23.4%) fulfilled the criteria for avoidable metronidazole DOT. The percentage of avoidable metronidazole DOT remained stable over the study period (22.8% in 2006 and 22.9% in 2010) despite a decrease in overall metronidazole use. There was wide variation in the percentage of avoidable metronidazole DOT among facilities (2010: median 20.3%, IQR 15.3%-29.4%). Piperacillin/tazobactam was the most commonly administered drug on avoidable metronidazole DOT (56.8%).
Conclusions: Potentially avoidable use of metronidazole affected about a quarter of all days when metronidazole was given. The combination of metronidazole with piperacillin/tazobactam was particularly common and represents a possible target for antibiotic stewardship interventions.
C1 [Huttner, Benedikt; Jones, Makoto; Rubin, Michael A.; Samore, Matthew H.] VA Salt Lake City Hlth Care Syst, IDEAS Ctr, Salt Lake City, UT 84148 USA.
[Huttner, Benedikt; Jones, Makoto; Rubin, Michael A.; Samore, Matthew H.] Univ Utah, Div Epidemiol, Salt Lake City, UT 84132 USA.
[Madaras-Kelly, Karl] Boise VA Med Ctr, Boise, ID 83702 USA.
[Madaras-Kelly, Karl] Idaho State Univ, Coll Pharm, Meridian, ID 83713 USA.
[Nielson, Christopher] VA Sierra Nevada Hlth Care Syst, Reno, NV 89502 USA.
[Goetz, Matthew Bidwell] VA Greater LA Healthcare Syst, Los Angeles, CA 90073 USA.
[Goetz, Matthew Bidwell] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90024 USA.
[Neuhauser, Melinda M.] Dept Vet Affairs Pharm Benefit Management Serv, Hines, IL USA.
RP Huttner, B (reprint author), VA Salt Lake City Hlth Care Syst, IDEAS Ctr, 500 Foothill Dr, Salt Lake City, UT 84148 USA.
EM huttner.benedikt@gmail.com
RI Huttner, Benedikt/M-5616-2014;
OI Huttner, Benedikt/0000-0002-1749-9464; Goetz,
Matthew/0000-0003-4542-992X
FU George E. Wahlen Department of Veterans Affairs Medical Center, Salt
Lake City, UT, USA [CDA 10-030-02]; Geneva University Hospitals,
Switzerland
FX This material is the result of work supported with resources and the use
of facilities at the George E. Wahlen Department of Veterans Affairs
Medical Center, Salt Lake City, UT, USA, a career development award (to
M. J., CDA 10-030-02) and a fellowship grant from Geneva University
Hospitals, Switzerland (to B. H.).
NR 10
TC 10
Z9 11
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-7453
J9 J ANTIMICROB CHEMOTH
JI J. Antimicrob. Chemother.
PD JUN
PY 2012
VL 67
IS 6
BP 1537
EP 1539
DI 10.1093/jac/dks074
PG 3
WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy
SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy
GA 942RJ
UT WOS:000304064400037
PM 22398652
ER
PT J
AU Chirinos, JA
AF Chirinos, Julio A.
TI Arterial Stiffness: Basic Concepts and Measurement Techniques
SO JOURNAL OF CARDIOVASCULAR TRANSLATIONAL RESEARCH
LA English
DT Article
DE Arterial stiffness; Compliance; Distensibility; Pulse wave velocity;
Elastic modulus
ID PRESSURE WAVE-FORMS; ALL-CAUSE MORTALITY; CAROTID-ARTERY;
CARDIOVASCULAR-DISEASE; AORTIC STIFFNESS; IN-VIVO; NONINVASIVE
EVALUATION; HYPERTENSIVE PATIENTS; CLINICAL-APPLICATIONS;
HEALTHY-INDIVIDUALS
AB Arterial stiffness is highly relevant to cardiovascular disease. Arterial stiffness is central to the pathogenesis of isolated systolic hypertension and directly impacts left ventricular afterload, pressure pulsatility in the arterial tree, and its penetration into the microvasculature of target organs such as the brain and kidney. Arterial stiffness is affected by various risk factors and biologic processes. Measurements of arterial stiffness may therefore not only provide information about prevalent processes, but also valuable information regarding the cumulative history of risk factor exposure. Available studies consistently demonstrate that large artery stiffness, measured via carotid-femoral pulse wave velocity, independently predicts the risk of incident cardiovascular events in clinical and community-based cohorts. Understanding the basic principles and definitions related to arterial stiffness is therefore desirable for cardiovascular clinicians and researchers. This introductory paper reviews basic physical principles and definitions regarding arterial stiffness and the most important non-invasive methods for its quantification in vivo.
C1 Univ Penn, Perelman Sch Med, Philadelphia VA Med Ctr, Philadelphia, PA 19104 USA.
RP Chirinos, JA (reprint author), Univ Penn, Perelman Sch Med, Philadelphia VA Med Ctr, Rm 8B111,Univ & Woodland Av, Philadelphia, PA 19104 USA.
EM julio.chirinos@uphs.upenn.edu
NR 56
TC 38
Z9 38
U1 1
U2 17
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1937-5387
J9 J CARDIOVASC TRANSL
JI J. Cardiovasc. Transl. Res.
PD JUN
PY 2012
VL 5
IS 3
SI SI
BP 243
EP 255
DI 10.1007/s12265-012-9359-6
PG 13
WC Cardiac & Cardiovascular Systems; Medicine, Research & Experimental
SC Cardiovascular System & Cardiology; Research & Experimental Medicine
GA 943HK
UT WOS:000304111300001
PM 22447229
ER
PT J
AU Agarwalla, P
Barnard, Z
Fecci, P
Dranoff, G
Curry, WT
AF Agarwalla, Pankaj
Barnard, Zachary
Fecci, Peter
Dranoff, Glenn
Curry, William T., Jr.
TI Sequential Immunotherapy by Vaccination With GM-CSF-expressing Glioma
Cells and CTLA-4 Blockade Effectively Treats Established Murine
Intracranial Tumors
SO JOURNAL OF IMMUNOTHERAPY
LA English
DT Article
DE glioma; vaccine; CTLA-4; GVAX; immunotherapy; GM-CSF
ID CENTRAL-NERVOUS-SYSTEM; BRAIN-TUMORS; COMBINATION IMMUNOTHERAPY;
CLINICAL ACTIVITY; GLIOBLASTOMA; VACCINES; GROWTH; MECHANISMS;
ANTIBODIES; RESPONSES
AB Malignant glioma is an incurable disease with a relatively short median survival. Several clinical trials have demonstrated that immunotherapy with vaccination is a safe and possibly effective way of prolonging survival. Antibody-based blockade of cytotoxic T-lymphocyte antigen 4 (CTLA-4) ligation on T lymphocytes is associated with enhanced antitumor immunity in animal models of cancer and in patients with advanced melanoma. We hypothesized that sequential therapy with granulocyte-macrophage-colony-stimulating factor (GM-CSF)-expressing whole-glioma-cell vaccination and CTLA-4 blockade is an effective strategy for treating established intracranial gliomas. GL261 glioma cells were injected into the right frontal lobes of syngeneic C57/BL6 mice. At days 3, 6, and 9 after tumor implantation, mice were treated with subcutaneous injection of irradiated GM-CSF-expressing GL261 cells. Mice were also treated with intraperitoneal injection of anti-CTLA-4 monoclonal antibodies (mAbs), either at days 3, 6, and 9 or days 12, 15, and 18. Animals were followed for survival. Splenocytes were harvested at day 22 for use in enzyme-linked immunosorbent spot assays. Early treatment of established intracranial gliomas with high-dose CTLA-4 blockade was associated with increased survival in GL261-bearing mice. Later treatment with anti-CTLA-4 monoclonal antibodies did not significantly improve survival compared with control-treated mice. Early vaccination followed by subsequent CTLA-4 blockade was associated with significantly improved survival versus either treatment alone and intensified tumor-specific immunity as measured by interferon-g enzyme-linked immunosorbent spot assay. Sequential immunotherapy with GM-CSF-expressing irradiated glioma cells and CTLA-4 blockade synergistically prolongs survival in mice bearing established intracranial gliomas.
C1 [Curry, William T., Jr.] Massachusetts Gen Hosp, Stephen E & Catherine Pappas Ctr Neurooncol, Dept Neurosurg, Boston, MA 02114 USA.
[Dranoff, Glenn] Dana Farber Canc Inst, Dept Med Oncol Hematol Neoplasia, Boston, MA 02115 USA.
RP Curry, WT (reprint author), Massachusetts Gen Hosp, Stephen E & Catherine Pappas Ctr Neurooncol, Dept Neurosurg, 55 Fruit St,Y9E,, Boston, MA 02114 USA.
EM wcurry@partners.org
FU Robert Wood Johnson Foundation; Executive Committee on Research,
Massachusetts General Hospital; NIH [CA143083]
FX W.T.C. was supported by Amos Medical Faculty Development Program of the
Robert Wood Johnson Foundation; Physician Scientist Development Award,
Executive Committee on Research, Massachusetts General Hospital and G.
D. was supported by NIH CA143083.
NR 25
TC 45
Z9 45
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1524-9557
J9 J IMMUNOTHER
JI J. Immunother.
PD JUN
PY 2012
VL 35
IS 5
BP 385
EP 389
DI 10.1097/CJI.0b013e3182562d59
PG 5
WC Oncology; Immunology; Medicine, Research & Experimental
SC Oncology; Immunology; Research & Experimental Medicine
GA 942LM
UT WOS:000304045500003
PM 22576343
ER
PT J
AU Mackay, G
House, MD
Bloch, E
Wolfberg, AJ
AF Mackay, Gillian
House, Michael D.
Bloch, Evan
Wolfberg, Adam J.
TI A GBS culture collected shortly after GBS prophylaxis may be inaccurate
SO JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE
LA English
DT Article
DE antibiotic prophylaxis; group B streptococcus (GBS); penicillin
ID B STREPTOCOCCAL DISEASE; INTRAPARTUM CHEMOPROPHYLAXIS; COLONIZATION;
DELIVERY; PREVENTION; TRANSMISSION; PENICILLIN; WOMEN
AB Objective: To determine whether a vaginal-rectal culture obtained after antibiotic therapy has begun accurately detects pre-existing colonization with group B streptococcus (GBS). Methods: A prospective cohort study of women presenting at in labor who were known to be colonized with GBS were recruited. A GBS culture was obtained prior to administration of intravenous penicillin prophylaxis and repeated 2 hours following the first dose of penicillin. The two results were compared. Results: Eighty subjects were recruited. Complete results were obtained for 61 (76 %) subjects. Of these, 47 (77 %) had a GBS positive on initial culture. Persistence of GBS 2 hours after antibiotic exposure was seen in 30/47 (64 %). Conversion from GBS positive to GBS negative status was seen in 17/47 (36%). Conclusions: A vaginal-rectal culture for GBS performed after antibiotic prophylaxis has commenced may not accurately reflect a patient's GBS colonization status.
C1 [Mackay, Gillian] Massachusetts Gen Hosp, Dept Obstet & Gynecol, Tufts Med Ctr, Div Maternal Fetal Med, Boston, MA 02114 USA.
RP Mackay, G (reprint author), Massachusetts Gen Hosp, Dept Obstet & Gynecol, Tufts Med Ctr, Div Maternal Fetal Med, Founders 4,55 Fruit St, Boston, MA 02114 USA.
EM gillmackay@yahoo.co.uk
FU George Mitchell Society at Tufts Medical Center
FX The authors report no declarations of interest. This study was funded by
financial support from The George Mitchell Society at Tufts Medical
Center.
NR 17
TC 1
Z9 1
U1 0
U2 0
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1476-7058
J9 J MATERN-FETAL NEO M
JI J. Matern.-Fetal Neonatal Med.
PD JUN
PY 2012
VL 25
IS 6
BP 736
EP 738
DI 10.3109/14767058.2011.596961
PG 3
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 943CH
UT WOS:000304097600036
PM 21801141
ER
PT J
AU Bianchi, MT
Eiseman, NA
Cash, SS
Mietus, J
Peng, CK
Thomas, RJ
AF Bianchi, Matt T.
Eiseman, Nathaniel A.
Cash, Sydney S.
Mietus, Joseph
Peng, Chung-Kang
Thomas, Robert J.
TI Probabilistic sleep architecture models in patients with and without
sleep apnea
SO JOURNAL OF SLEEP RESEARCH
LA English
DT Article
DE adult; biological rhythms; computational model; human; sleep disorders
ID HEART HEALTH; FRAGMENTATION; WAKEFULNESS; DYNAMICS; PATTERNS; AROUSALS;
SWITCH
AB Sleep fragmentation of any cause is disruptive to the rejuvenating value of sleep. However, methods to quantify sleep architecture remain limited. We have previously shown that human sleepwake stage distributions exhibit multi-exponential dynamics, which are fragmented by obstructive sleep apnea (OSA), suggesting that Markov models may be a useful method to quantify architecture in health and disease. Sleep stage data were obtained from two subsets of the Sleep Heart Health Study database: control subjects with no medications, no OSA, no medical co-morbidities and no sleepiness (n = 374); and subjects with severe OSA (n = 338). Sleep architecture was simplified into three stages: wake after sleep onset (WASO); non-rapid eye movement (NREM) sleep; and rapid eye movement (REM) sleep. The connectivity and transition rates among eight generator states of a first-order continuous-time Markov model were inferred from the observed (phenotypic) distributions: three exponentials each of NREM sleep and WASO; and two exponentials of REM sleep. Ultradian REM cycling was accomplished by imposing time-variation to REM state entry rates. Fragmentation in subjects with severe OSA involved faster transition probabilities as well as additional state transition paths within the model. The Markov models exhibit two important features of human sleep architecture: multi-exponential stage dynamics (accounting for observed bout distributions); and probabilistic transitions (an inherent source of variability). In addition, the model quantifies the fragmentation associated with severe OSA. Markov sleep models may prove important for quantifying sleep disruption to provide objective metrics to correlate with endpoints ranging from sleepiness to cardiovascular morbidity.
C1 [Bianchi, Matt T.; Eiseman, Nathaniel A.; Cash, Sydney S.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Bianchi, Matt T.] Harvard Univ, Sch Med, Div Sleep Med, Boston, MA USA.
[Mietus, Joseph; Peng, Chung-Kang] Beth Israel Deaconess Med Ctr, Div Interdisciplinary Med & Biotechnol, Boston, MA 02215 USA.
[Thomas, Robert J.] Beth Israel Deaconess Med Ctr, Dept Med, Div Pulm Crit Care & Sleep Med, Boston, MA 02215 USA.
RP Bianchi, MT (reprint author), Massachusetts Gen Hosp, Dept Neurol, Wang 7,55 Fruit St, Boston, MA 02114 USA.
EM mtbianchi@partners.org
RI Peng, Chung-Kang/E-1489-2011
OI Peng, Chung-Kang/0000-0003-3666-9833
FU Department of Neurology, Massachusetts General Hospital; Harvard/MIT
Health Sciences and Technology - Beth Israel Deaconess Medical Center;
Pfizer, Inc.; Merck Co
FX The authors thank Scott McKinney, and Drs Andrew Phillips, Elizabeth
Klerman and Catherine Chu-Shore for valuable discussions and comments on
the manuscript. Dr Bianchi receives funding from the Department of
Neurology, Massachusetts General Hospital, and the Clinical Investigator
Training Program: Harvard/MIT Health Sciences and Technology - Beth
Israel Deaconess Medical Center, in collaboration with Pfizer, Inc. and
Merck & Co. This funding source had no role in the design,
interpretation or publication of this study. This paper represents the
work of the authors, and not the Sleep Heart Health Study.
NR 33
TC 11
Z9 11
U1 1
U2 5
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0962-1105
J9 J SLEEP RES
JI J. Sleep Res.
PD JUN
PY 2012
VL 21
IS 3
BP 330
EP 341
DI 10.1111/j.1365-2869.2011.00937.x
PG 12
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 944IE
UT WOS:000304191900013
PM 21955148
ER
PT J
AU Fiorentino, L
Saxbe, D
Alessi, CA
Woods, DL
Martin, JL
AF Fiorentino, Lavinia
Saxbe, Darby
Alessi, Cathy A.
Woods, Diana Lynn
Martin, Jennifer L.
TI Diurnal Cortisol and Functional Outcomes in Post-Acute Rehabilitation
Patients
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Cortisol; Older adults; Rehabilitation; Inpatient; Functional Status
ID PITUITARY-ADRENAL AXIS; NURSING-HOME RESIDENTS; UNDER-THE-CURVE;
OLDER-PEOPLE; YOUNG-ADULTS; DEMENTIA; DECLINE; DISEASE; CARDIA; CLOCK
AB Background. Cortisol is a stress-related hormone with a robust circadian rhythm where levels typically peak in the morning hours and decline across the day. Although acute cortisol increases resulting from stressors are adaptive, chronic elevated cortisol levels are associated with poor functioning. Studies have shown age-related changes in cortisol levels. The present study investigated the relationship between salivary diurnal cortisol and functional outcomes among older adults undergoing inpatient post-acute rehabilitation.
Methods. Thirty-two older adults (mean age 78 years; 84% men) in a Veterans Administration inpatient post-acute rehabilitation unit were studied. Functional outcomes were assessed with the motor component of the Functional Independence Measure (mFIM; where mFIM change = discharge - admission score). Saliva samples were collected on 1 day at wake time, 45 minutes later, 11:30 am, 2 pm, 4:30 pm, and bedtime. We analyzed the relationship between cortisol measures and functional outcomes, demographics, and health measures.
Results. The analyses consistently showed that greater functional improvement (mFIM change) from admission to discharge was associated with lower comorbidity scores and higher cortisol levels at 2 pm, 4: 30 pm, and bedtime. A morning cortisol rise was also associated with greater mFIM change.
Conclusions. Measurement of cortisol in saliva may be a useful biological marker for identification of patients who are "at risk" of lower benefits from inpatient rehabilitation services and who may require additional assistance or intervention during their post-acute care stay.
C1 [Alessi, Cathy A.; Martin, Jennifer L.] VA Greater Los Angeles Healthcare Syst, Geriatr Res Educ & Clin Ctr, North Hills, CA 91343 USA.
[Fiorentino, Lavinia] Univ Calif San Diego, Sch Med, Dept Psychiat, San Diego, CA 92103 USA.
[Saxbe, Darby] Univ So Calif, Dept Psychol, Los Angeles, CA 90089 USA.
[Alessi, Cathy A.; Martin, Jennifer L.] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
[Woods, Diana Lynn] Univ Calif Los Angeles, Sch Nursing, Los Angeles, CA 90024 USA.
RP Martin, JL (reprint author), VA Greater Los Angeles Healthcare Syst, Geriatr Res Educ & Clin Ctr 11E, 16111 Plummer St,Bldg 25,Room B136, North Hills, CA 91343 USA.
EM jennifer.martin@va.gov
FU National Institute of Mental Health [T32 MH019934, MH080002, T32
MH019925-11]; National Institute on Aging at the National Institutes of
Health [K23 AG028452]; Veterans Administration Health Services Research
& Development Service [IIR 01-053-1, IIR 04-321-2, AIA 03-047]; Veterans
Affairs Greater Los Angeles Healthcare System, Geriatric Research,
Education and Clinical Center
FX This work was supported by the National Institute of Mental Health [T32
MH019934 (Jeste), MH080002 (Jeste), and T32 MH019925-11 (Irwin)] and the
National Institute on Aging [K23 AG028452 (J.L.M.)] at the National
Institutes of Health; Veterans Administration Health Services Research &
Development Service (IIR 01-053-1, C. A. A.; IIR 04-321-2, C. A. V.; and
AIA 03-047 J.L.M.); and the Veterans Affairs Greater Los Angeles
Healthcare System, Geriatric Research, Education and Clinical Center.
NR 22
TC 2
Z9 2
U1 1
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD JUN
PY 2012
VL 67
IS 6
BP 677
EP 682
DI 10.1093/gerona/glr230
PG 6
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 942OM
UT WOS:000304054700013
PM 22219521
ER
PT J
AU Hyman, BT
Yuan, JY
AF Hyman, Bradley T.
Yuan, Junying
TI Apoptotic and non-apoptotic roles of caspases in neuronal physiology and
pathophysiology
SO NATURE REVIEWS NEUROSCIENCE
LA English
DT Review
ID PROGRAMMED CELL-DEATH; LONG-TERM DEPRESSION; UBIQUITIN-PROTEASOME
SYSTEM; ALZHEIMERS-DISEASE; MOUSE MODEL; IN-VIVO; MITOCHONDRIAL
DYSFUNCTION; TAU PHOSPHORYLATION; PROTEIN-DEGRADATION; DECREASED
APOPTOSIS
AB Caspases are cysteine proteases that mediate apoptosis, which is a form of regulated cell death that effectively and efficiently removes extra and unnecessary cells during development. In the mature nervous system, caspases are not only involved in mediating cell death but also regulatory events that are important for neural functions, such as axon pruning and synapse elimination, which are necessary to refine mature neuronal circuits. Furthermore, caspases can be reactivated to cause cell death as well as non-lethal changes in neurons during numerous pathological processes. Thus, although a global activation of caspases leads to apoptosis, restricted and localized activation may control normal physiology and pathophysiology in living neurons. This Review explores the multiple roles of caspase activity in neurons.
C1 [Hyman, Bradley T.] Massachusetts Gen Hosp, Neurol Serv, Charlestown, MA 01029 USA.
[Yuan, Junying] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
RP Hyman, BT (reprint author), Massachusetts Gen Hosp, Neurol Serv, 114 16th St, Charlestown, MA 01029 USA.
EM bhyman@partners.org; jyuan@hms.harvard.edu
NR 99
TC 107
Z9 113
U1 3
U2 31
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-003X
J9 NAT REV NEUROSCI
JI Nat. Rev. Neurosci.
PD JUN
PY 2012
VL 13
IS 6
BP 395
EP 406
DI 10.1038/nrn3228
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 944JP
UT WOS:000304197000009
PM 22595785
ER
PT J
AU D'Souza, DC
Fridberg, DJ
Skosnik, PD
Williams, A
Roach, B
Singh, N
Carbuto, M
Elander, J
Schnakenberg, A
Pittman, B
Sewell, RA
Ranganathan, M
Mathalon, D
AF D'Souza, Deepak Cyril
Fridberg, Daniel J.
Skosnik, Patrick D.
Williams, Ashley
Roach, Brian
Singh, Nagendra
Carbuto, Michelle
Elander, Jacqueline
Schnakenberg, Ashley
Pittman, Brian
Sewell, R. Andrew
Ranganathan, Mohini
Mathalon, Daniel
TI Dose-Related Modulation of Event-Related Potentials to Novel and Target
Stimuli by Intravenous Delta(9)-THC in Humans
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE Delta(9)-THC; cannabinoids; cannabis; P300; perception; psychosis
ID CANNABINOID CB1 RECEPTOR; SELECTIVE ATTENTION; METABOTROPIC GLUTAMATE;
MEDIATED INHIBITION; MARIJUANA SMOKING; EVOKED-POTENTIALS; NOVELTY
DETECTION; AUDITORY-STIMULI; FREQUENT USERS; HUMAN BRAIN
AB Cannabinoids induce a host of perceptual alterations and cognitive deficits in humans. However, the neural correlates of these deficits have remained elusive. The current study examined the acute, dose-related effects of delta-9-tetrahydrocannabinol (Delta(9)-THC) on psychophysiological indices of information processing in humans. Healthy subjects (n = 26) completed three test days during which they received intravenous Delta(9)-THC (placebo, 0.015 and 0.03 mg/kg) in a within-subject, double-blind, randomized, cross-over, and counterbalanced design. Psychophysiological data (electroencephalography) were collected before and after drug administration while subjects engaged in an event-related potential (ERP) task known to be a valid index of attention and cognition (a three-stimulus auditory 'oddball' P300 task). Delta(9)-THC dose-dependently reduced the amplitude of both the target P300b and the novelty P300a. Delta(9)-THC did not have any effect on the latency of either the P300a or P300b, or on early sensory-evoked ERP components preceding the P300 (the N100). Concomitantly, Delta(9)-THC induced psychotomimetic effects, perceptual alterations, and subjective 'high' in a dose-dependent manner. Delta(9)-THC -induced reductions in P3b amplitude correlated with Delta(9)-THC-induced perceptual alterations. Lastly, exploratory analyses examining cannabis use status showed that whereas recent cannabis users had blunted behavioral effects to Delta(9)-THC, there were no dose-related effects of Delta(9)-THC on P300a/b amplitude between cannabis-free and recent cannabis users. Overall, these data suggest that at doses that produce behavioral and subjective effects consistent with the known properties of cannabis, Delta(9)-THC reduced P300a and P300b amplitudes without altering the latency of these ERPs. Cannabinoid agonists may therefore disrupt cortical processes responsible for context updating and the automatic orientation of attention, while leaving processing speed and earlier sensory ERP components intact. Collectively, the findings suggest that CB1R systems modulate top-down and bottom-up processing. Neuropsychopharmacology (2012) 37, 1632-1646; doi:10.1038/npp.2012.8; published online 15 February 2012
C1 [D'Souza, Deepak Cyril; Skosnik, Patrick D.; Williams, Ashley; Singh, Nagendra; Carbuto, Michelle; Elander, Jacqueline; Schnakenberg, Ashley; Pittman, Brian; Sewell, R. Andrew; Ranganathan, Mohini] Connecticut Mental Hlth Ctr, Abraham Ribicoff Res Facil, New Haven, CT 06519 USA.
[D'Souza, Deepak Cyril; Skosnik, Patrick D.; Williams, Ashley; Singh, Nagendra; Carbuto, Michelle; Elander, Jacqueline; Schnakenberg, Ashley; Pittman, Brian; Sewell, R. Andrew; Ranganathan, Mohini; Mathalon, Daniel] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA.
[Roach, Brian; Mathalon, Daniel] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA.
[Roach, Brian; Mathalon, Daniel] San Francisco VA Med Ctr, Mental Hlth Serv Line, San Francisco, CA USA.
[D'Souza, Deepak Cyril; Fridberg, Daniel J.; Skosnik, Patrick D.; Williams, Ashley; Singh, Nagendra; Carbuto, Michelle; Elander, Jacqueline; Schnakenberg, Ashley; Sewell, R. Andrew; Ranganathan, Mohini] VA Connecticut Healthcare Syst, Psychiat Serv, West Haven, CT 06516 USA.
RP D'Souza, DC (reprint author), VA Connecticut Healthcare Syst, Psychiat Serv, 116A,950 Campbell Ave, West Haven, CT 06516 USA.
EM deepak.dsouza@yale.edu
OI Mathalon, Daniel/0000-0001-6090-4974
FU Department of Veterans Affairs; National Institute of Mental Health;
National Institute of Drug Abuse [R21 DA020750]; National Institute of
Alcoholism and Alcohol Abuse (NIAAA); Yale Center for Clinical
Investigation (YCCI); NARSAD; AstraZeneca, Inc; Pfizer, Inc.; Abbott
Laboratories; Eli Lilly; Organon; Pfizer; Sanofi; Astra Zeneca
FX We acknowledge support from the (1) Department of Veterans Affairs, (2)
National Institute of Mental Health, (3) National Institute of Drug
Abuse, (4) National Institute of Alcoholism and Alcohol Abuse (NIAAA),
and (5) the Yale Center for Clinical Investigation (YCCI). This research
project was funded in part by grants from NIDA (R21 DA020750 to DCD) and
a NARSAD Young Investigator Award to PDS. We also thank Angelina
Genovese, RNC, MBA; Michelle San Pedro, RN; Elizabeth O'Donnell, RN;
Brenda Breault, RN, BSN; Sonah Yoo, RPh; Rachel Galvan, RPh; and Willie
Ford of the Neurobiological Studies Unit at the VA Connecticut
Healthcare System, West Haven Campus for their central contributions to
the success of this project.; Daniel Fridberg, Patrick Skosnik, Ashley
Williams, Brian Roach, Nagendra Singh, Michelle Carbuto, Jacqueline
Elander, Ashley Schnakenberg, Brian Pittman, and Andrew Sewell report no
financial relationships with commercial interests. Dr Mathalon reports
research funding from AstraZeneca, Inc, consulting fees from Pfizer,
Inc., and that his name is included under a provisional patent titled 'A
non-invasive biomarker of human cortical plasticity and cognition',
USPTO serial number 61/140 833. Mohini Ranganathan has in the past 3
years or currently receives research grant support administered through
Yale University School of Medicine from Eli Lilly. Deepak Cyril D'Souza
has in the past 3 years or currently receives research grant support
administered through Yale University School of Medicine from Astra
Zeneca, Abbott Laboratories, Eli Lilly, Organon, Pfizer, and Sanofi; he
is a consultant for Bristol Meyers Squibb.
NR 93
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PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD JUN
PY 2012
VL 37
IS 7
BP 1632
EP 1646
DI 10.1038/npp.2012.8
PG 15
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 942LO
UT WOS:000304045700008
PM 22334121
ER
PT J
AU Lotfipour, S
Mandelkern, M
Alvarez-Estrada, M
Brody, AL
AF Lotfipour, Shahrdad
Mandelkern, Mark
Alvarez-Estrada, Miguel
Brody, Arthur L.
TI A Single Administration of Low-Dose Varenicline Saturates alpha 4 beta
2* Nicotinic Acetylcholine Receptors in the Human Brain
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE cigarettes; nicotinic receptors; addiction; varenicline; withdrawal;
thalamus
ID PARTIAL AGONIST VARENICLINE; GENETICALLY-MODIFIED MICE; IN-VIVO;
WITHDRAWAL SYMPTOMS; TOBACCO WITHDRAWAL; BINDING-PROPERTIES;
SMOKING-CESSATION; PRENATAL-EXPOSURE; MATERNAL-SMOKING; DRUG-USE
AB The primary objective of this project was to determine the alpha 4 beta 2* nicotinic acetylcholine receptor (nAChR) occupancy in human brain of a single low dose of varenicline (0.5 mg), and to explore the relationship between receptor occupancy by varenicline and tobacco withdrawal symptoms (*denoting other putative nAChR subunits). Otherwise healthy smokers (n = 9) underwent two positron emission tomography (PET) sessions with the selective alpha 4 beta 2* radioligand 2-FA. For the PET sessions, participants received either a low dose of varenicline (0.5 mg) or matching placebo pill (double-blind, random order) before imaging. For both sessions, participants received bolus plus continuous infusions of 2-FA, were scanned for 1 h after allowing the radiotracer to reach a steady state, smoked to satiety, and were scanned for 2 more hours. We estimated the fractional receptor occupancy by a single dose of varenicline (0.5 mg) and the corresponding varenicline dissociation constant (K-V), along with the effect of low-dose varenicline, pill placebo, and smoking-to-satiety on withdrawal rating scales. The data are compatible with 100% occupancy of alpha 4 beta 2* nAChRs by a single dose of varenicline, with a 90% lower confidence limit of 89% occupancy for the thalamus and brainstem. The corresponding 90% upper limit on effective K-V with respect to plasma varenicline was 0.49 nM. Smoking to satiety, but not low-dose varenicline, significantly reduced withdrawal symptoms. Our findings demonstrate that low-dose varenicline results in saturation of alpha 4 beta 2* nAChRs in the thalamus and brainstem without reducing withdrawal symptoms. Neuropsychopharmacology (2012) 37, 1738-1748; doi:10.1038/npp.2012.20; published online 7 March 2012
C1 [Lotfipour, Shahrdad] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, MacDonald Res Labs, Los Angeles, CA 90095 USA.
[Lotfipour, Shahrdad; Brody, Arthur L.] Univ Calif Los Angeles, Hatos Ctr Neuropharmacol, Semel Inst, Los Angeles, CA 90095 USA.
[Lotfipour, Shahrdad; Mandelkern, Mark; Alvarez-Estrada, Miguel; Brody, Arthur L.] Vet Affairs Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Mandelkern, Mark] Univ Calif Irvine, Dept Phys, Irvine, CA 92717 USA.
RP Lotfipour, S (reprint author), Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, MacDonald Res Labs, 675 Charles E Young Dr S, Los Angeles, CA 90095 USA.
EM shahrdad@ucla.edu
RI Lotfipour, Shahrdad/K-8335-2014
OI Lotfipour, Shahrdad/0000-0002-2425-1096
FU Pfizer Pharmaceutical Corporation [WS653344]; NIMH [MH17140]; NIDA [R01
DA20872]; Richard Metzner Chair in Clinical Neuropharmacology
FX We thank Karen Ta, Jaime La Charite, Betram Nweke, Stuart Mirell, Van
Cayetano, Chien Nguyen, Judah Farahi, Andrew Leuchter, Hans Rollema,
Maziar Maghsoodnia, Alison Curtin, Ron Waldorf, Diep Seversen, and
Josephine Ribe for their assistance on the study. This work was funded
by Pfizer Pharmaceutical Corporation (Grant number: WS653344) (SL) and,
in part, by T-32 NIMH post-doctoral fellowship (MH17140) (SL), NIDA (R01
DA20872) (ALB), and the Richard Metzner Chair in Clinical
Neuropharmacology (ALB).
NR 52
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U2 8
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD JUN
PY 2012
VL 37
IS 7
BP 1738
EP 1748
DI 10.1038/npp.2012.20
PG 11
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 942LO
UT WOS:000304045700018
PM 22395733
ER
PT J
AU Paik, JM
Farwell, WR
Taylor, EN
AF Paik, J. M.
Farwell, W. R.
Taylor, E. N.
TI Demographic, dietary, and serum factors and parathyroid hormone in the
National Health and Nutrition Examination Survey
SO OSTEOPOROSIS INTERNATIONAL
LA English
DT Article
DE CDC; Centers for Disease Control and Prevention; National Health and
Nutrition Examination Survey; NHANES; Parathyroid hormone
ID AGE-RELATED-CHANGES; INTESTINAL CALCIUM-ABSORPTION; CHRONIC
KIDNEY-DISEASE; D-ENDOCRINE SYSTEM; VITAMIN-D; URIC-ACID; INCIDENT
HYPERTENSION; POSTMENOPAUSAL WOMEN; RACIAL-DIFFERENCES; BLOOD-PRESSURE
AB Many determinants of parathyroid hormone (PTH) are unknown. In the National Health and Nutrition Examination Survey (NHANES), numerous factors not classically associated with calcium-phosphorus homeostasis, such as uric acid and smoking, are independently associated with PTH in adults without chronic kidney disease. Associations between serum phosphorus and PTH may vary by race.
Although PTH may be an important biomarker for osteoporosis and cardiovascular disease, many determinants of PTH are unknown. We investigated associations between demographic, dietary, and serum factors and PTH level.
We studied 4,026 white, 1,792 black, and 1,834 Mexican-American adult participants without chronic kidney disease from the 2003-2004 and 2005-2006 NHANES.
The mean serum PTH level was 38.3 pg/ml for whites, 42.6 pg/ml for blacks, and 41.3 pg/ml for Mexican-Americans. After adjusting for diet, body mass index, serum levels of calcium, phosphorus, 25-hydroxyvitamin D, creatinine, and other factors, smokers compared to non-smokers had lower PTH, ranging from -4.2 pg/ml (95% confidence interval (CI) -7.3 to -1.1) in Mexican-Americans to -6.1 pg/ml (95% CI -8.7 to -3.5) in blacks. After multivariate adjustment, PTH was higher in females compared to males, ranging from 1.1 pg/ml (95% CI -1.2 to 3.4) in Mexican-Americans to 4.5 pg/ml (95% CI 1.9 to 7.0) in blacks, and in older (> 60 years) compared to younger participants (< 30 years), ranging from 3.7 pg/ml (95% CI 1.3 to 6.1) in Mexican-Americans to 8.0 pg/ml (95% CI 5.4 to 10.7) in blacks. Higher uric acid was associated with higher PTH. In whites only, lower serum phosphorus and lower serum retinol were associated with higher PTH.
Numerous factors not classically associated with calcium-phosphorus homeostasis are independently associated with PTH and should be considered in future studies of PTH and chronic disease. Additional research is needed to elucidate mechanisms underlying identified associations with PTH and to explore possible racial differences in phosphorus handling.
C1 [Paik, J. M.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Renal,Dept Med, Boston, MA 02115 USA.
[Paik, J. M.; Taylor, E. N.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Channing Lab,Dept Med, Boston, MA 02115 USA.
[Farwell, W. R.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Aging,Dept Med, Boston, MA 02115 USA.
[Farwell, W. R.] VA Boston Healthcare Syst, Massachusetts Vet Epidemiol Res & Informat Ctr, Boston, MA USA.
[Taylor, E. N.] Maine Med Ctr, Div Nephrol & Transplantat, Portland, ME 04102 USA.
RP Paik, JM (reprint author), Channing Lab 3rd Floor,181 Longwood Ave, Boston, MA 02115 USA.
EM jmpaik@partners.org
FU Department of Veterans Affairs Office of Research Development; National
Institutes of Health [DK084707, DK007527, R01 HL092947]
FX Work on this study was supported by the Cooperative Studies Program of
the Department of Veterans Affairs Office of Research Development.
Additional research support was obtained from grants DK084707, DK007527,
and R01 HL092947 from the National Institutes of Health.
NR 58
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U1 0
U2 7
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 JUN
PY 2012
VL 23
IS 6
BP 1727
EP 1736
DI 10.1007/s00198-011-1776-x
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 943ZN
UT WOS:000304167300010
PM 21932115
ER
PT J
AU Jung, M
AF Jung, Minsoo
TI Immigrant Workers' Knowledge of HIV/AIDS and Their Sexual Risk
Behaviors: A Respondent-Driven Sampling Survey in South Korea
SO SEXUALITY AND DISABILITY
LA English
DT Article
DE Sexual risk behavior; Immigrant groups; HIV knowledge; Respondent-driven
sampling; South Korea
ID HIV RISK; AIDS; MEN
AB As the labor market goes global, immigrant workers are becoming important around the world. However, little research has focused on the characteristics of their sex behaviors. This study examines foreign employees in Korea in order to investigate their understanding of HIV and sexual risk behaviors. The sample ( = 547) was formed from migrant workers in the industrial complex in Ansan district, which depends highly on foreigners as its labor source. Logistic regression, analysis revealed that 36.0% of the respondents were engaged in more than one sexual risk behavior. Those who knew someone infected with HIV (OR = 2.583) and Thai respondents (OR = 3.007) showed high sexual risk behaviors, while married (OR = 0.182) and Korean Chinese (OR = 0.280) workers showed low sexual risk behaviors. Those who had a wealth of knowledge about HIV took a less discriminatory position against the person who had infected them, but this had no statistical effects over the sexual risk behaviors.
C1 [Jung, Minsoo] Korea Univ, Dept Healthcare Management, Seoul 136703, South Korea.
[Jung, Minsoo] Korea Univ, Hlth Sci Res Inst, Seoul 136703, South Korea.
[Jung, Minsoo] Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Jung, M (reprint author), Korea Univ, Dept Healthcare Management, San 1, Seoul 136703, South Korea.
EM mins.jung@gmail.com
OI Jung, Minsoo/0000-0003-3317-6507
NR 25
TC 1
Z9 1
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0146-1044
J9 SEX DISABIL
JI Sex. Disabil.
PD JUN
PY 2012
VL 30
IS 2
BP 199
EP 208
DI 10.1007/s11195-011-9245-1
PG 10
WC Rehabilitation
SC Rehabilitation
GA 943VZ
UT WOS:000304155100008
ER
PT J
AU Zinzow, HM
Resnick, HS
McCauley, JL
Amstadter, AB
Ruggiero, KJ
Kilpatrick, DG
AF Zinzow, Heidi M.
Resnick, Heidi S.
McCauley, Jenna L.
Amstadter, Ananda B.
Ruggiero, Kenneth J.
Kilpatrick, Dean G.
TI Prevalence and risk of psychiatric disorders as a function of variant
rape histories: results from a national survey of women
SO SOCIAL PSYCHIATRY AND PSYCHIATRIC EPIDEMIOLOGY
LA English
DT Article
DE Rape; Sexual assault; Posttraumatic stress disorder; Depression; Alcohol
abuse; Drug abuse; Comorbidity
ID POSTTRAUMATIC-STRESS-DISORDER; SEXUAL ASSAULT; INCAPACITATED RAPE;
MENTAL-HEALTH; SUBSTANCE USE; ALCOHOL; SAMPLE; COMMUNITY; VIOLENCE;
COMORBIDITY
AB Rape is an established risk factor for mental health disorders, such as posttraumatic stress disorder (PTSD), major depressive episodes (MDE), and substance use disorders. The majority of studies have not differentiated substance-involved rape or examined comorbid diagnoses among victims. Therefore, the aim of the present study was to estimate the prevalence of common trauma-related psychiatric disorders (and their comorbidity) in a national sample of women, with an emphasis on distinguishing between rape tactics. A secondary objective was to estimate the risk for psychiatric disorders among victims of variant rape tactics, in comparison to non-victims.
A nationally representative population-based sample of 3,001 non-institutionalized, civilian, English or Spanish speaking women (aged 18-86 years) participated in a structured telephone interview assessing rape history and DSM-IV criteria for PTSD, MDE, alcohol abuse (AA), and drug abuse (DA). Descriptive statistics and multivariate logistic regression analyses were employed.
Women with rape histories involving both substance facilitation and forcible tactics reported the highest current prevalence of PTSD (36%), MDE (36%), and AA (20%). Multivariate models demonstrated that this victim group was also at highest risk for psychiatric disorders, after controlling for demographics and childhood and multiple victimization history. Women with substance-facilitated rapes reported higher prevalence of substance abuse in comparison to women with forcible rape histories. Comorbidity between PTSD and other psychiatric disorders was higher among rape victims in comparison to non-rape victims.
Researchers and clinicians should assess substance-facilitated rape tactics and attend to comorbidity among rape victims. Empirically supported treatments are needed to address the complex presentations observed among women with variant rape histories.
C1 [Zinzow, Heidi M.] Clemson Univ, Dept Psychol, Clemson, SC 29634 USA.
[Resnick, Heidi S.; McCauley, Jenna L.; Amstadter, Ananda B.; Ruggiero, Kenneth J.; Kilpatrick, Dean G.] Med Univ S Carolina, Dept Psychiat & Behav Sci, Natl Crime Victims Res & Treatment Ctr, Charleston, SC 29425 USA.
[Ruggiero, Kenneth J.] Ralph H Johnson VA Med Ctr, Charleston, SC USA.
RP Zinzow, HM (reprint author), Clemson Univ, Dept Psychol, 418 Brackett Hall, Clemson, SC 29634 USA.
EM hzinzow@clemson.edu
FU National Institute of Justice [2005-WG-BX-0006]; NIDA
[1R01DA023099-01A2]
FX The research design and data collection were supported by National
Institute of Justice Grant #2005-WG-BX-0006 (principal investigator:
Dean G. Kilpatrick). Support for manuscript preparation was provided by
NIDA 1R01DA023099-01A2 (principal investigator: Heidi Resnick). Views
expressed in this article do not necessarily represent those of the
agencies supporting this research.
NR 27
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U1 7
U2 23
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0933-7954
J9 SOC PSYCH PSYCH EPID
JI Soc. Psychiatry Psychiatr. Epidemiol.
PD JUN
PY 2012
VL 47
IS 6
BP 893
EP 902
DI 10.1007/s00127-011-0397-1
PG 10
WC Psychiatry
SC Psychiatry
GA 944AT
UT WOS:000304171300006
PM 21603967
ER
PT J
AU Lee, C
Fotovati, A
Triscott, J
Chen, J
Venugopal, C
Singhal, A
Dunham, C
Kerr, JM
Verreault, M
Yip, S
Wakimoto, H
Jones, C
Jayanthan, A
Narendran, A
Singh, SK
Dunn, SE
AF Lee, Cathy
Fotovati, Abbas
Triscott, Joanna
Chen, James
Venugopal, Chitra
Singhal, Ash
Dunham, Christopher
Kerr, John M.
Verreault, Maite
Yip, Stephen
Wakimoto, Hiroaki
Jones, Chris
Jayanthan, Aarthi
Narendran, Aru
Singh, Sheila K.
Dunn, Sandra E.
TI Polo-Like Kinase 1 Inhibition Kills Glioblastoma Multiforme Brain Tumor
Cells in Part Through Loss of SOX2 and Delays Tumor Progression in Mice
SO STEM CELLS
LA English
DT Article
DE Apoptosis; Cancer stem cells; Cancer; Glioma
ID HERPES-SIMPLEX-VIRUS; CANCER STEM-CELLS; BIPOLAR SPINDLE FORMATION;
ACUTE MYELOID-LEUKEMIA; ADVANCED SOLID TUMORS; INITIATING CELLS;
BREAST-CANCER; PHASE-I; GENE-EXPRESSION; PROGNOSTIC-SIGNIFICANCE
AB Glioblastoma multiforme (GBM) ranks among the deadliest types of cancer and given these new therapies are urgently needed. To identify molecular targets, we queried a microarray profiling 467 human GBMs and discovered that polo-like kinase 1 (PLK1) was highly expressed in these tumors and that it clustered with the proliferative subtype. Patients with PLK1-high tumors were more likely to die from their disease suggesting that current therapies are inactive against such tumors. This prompted us to examine its expression in brain tumor initiating cells (BTICs) given their association with treatment failure. BTICs isolated from patients expressed 110-470 times more PLK1 than normal human astrocytes. Moreover, BTICs rely on PLK1 for survival because the PLK1 inhibitor BI2536 inhibited their growth in tumorsphere cultures. PLK1 inhibition suppressed growth, caused G2/M arrest, induced apoptosis, and reduced the expression of SOX2, a marker of neural stem cells, in SF188 cells. Consistent with SOX2 inhibition, the loss of PLK1 activity caused the cells to differentiate based on elevated levels of glial fibrillary acidic protein and changes in cellular morphology. We then knocked glial fibrillary acidic protein (GFAP) down SOX2 with siRNA and showed that it too inhibited cell growth and induced cell death. Likewise, in U251 cells, PLK1 inhibition suppressed cell growth, downregulated SOX2, and induced cell death. Furthermore, BI2536 delayed tumor growth of U251 cells in an orthotopic brain tumor model, demonstrating that the drug is active against GBM. In conclusion, PLK1 level is elevated in GBM and its inhibition restricts the growth of brain cancer cells. STEM CELLS2012;30:10641075
C1 [Dunn, Sandra E.] Univ British Columbia, Dept Paediat, Dept Expt Med, Vancouver, BC V5Z 4H4, Canada.
[Venugopal, Chitra; Singh, Sheila K.] McMaster Univ, Dept Surg, Div Neurol Surg, Fac Hlth Sci, Hamilton, ON L8S 4L8, Canada.
[Singhal, Ash; Kerr, John M.] BC Childrens Hosp, Dept Surg, Div Pediat Neurosurg, Vancouver, BC, Canada.
[Dunham, Christopher] BC Childrens Hosp, Dept Pathol & Lab Med, Div Anat Patol, Vancouver, BC, Canada.
[Verreault, Maite] Univ British Columbia, Dept Expt Therapeut, Div Pharmacol & Toxicol, BC Canc Res Ctr, Vancouver, BC, Canada.
[Yip, Stephen] Ctr Translat & Appl Gen, BC Canc Agcy, Dept Pathol & Lab Med, Vancouver, BC, Canada.
[Wakimoto, Hiroaki] Massachusetts Gen Hosp, Brain Tumor Res Ctr, Simches Res Ctr, Boston, MA 02114 USA.
[Jones, Chris] Royal Marsden Hosp, Inst Canc Res, Surrey, England.
[Jayanthan, Aarthi; Narendran, Aru] Alberta Childrens Prov Gen Hosp, POETIC Lab Pre Clin & Drug Discovery Studies, Calgary, AB, Canada.
RP Dunn, SE (reprint author), Univ British Columbia, Dept Paediat, Dept Expt Med, Room 3082,950 W 28th Ave, Vancouver, BC V5Z 4H4, Canada.
EM sedunn@mail.ubc
OI Dunham, Christopher/0000-0002-6244-0584
FU Michael Smith Foundation for Health Research; Hannah's Heroes
Foundation; C17 Research Network; STEMCELL Technologies; NHS
FX This work was supported by the Michael Smith Foundation for Health
Research and Hannah's Heroes Foundation (SED and CL). It was also funded
by the C17 Research Network (SED and AN). We are also grateful to
STEMCELL Technologies for their kind support. CJ acknowledges NHS
funding to the NIHR Bio-medical Research Centre. We also thank our
collaborators Dr. Brent Reynolds as well as Dr. Paul Steinbok, Dr. Doug
Cochrane, Dr. Rod Rassekh, Dr. Vesna Popovska, and Dr. Glenda Hendson at
the B. C. Children's Hospital for helping us obtain patient tumor
specimens and for their contribution to the study.
NR 88
TC 31
Z9 31
U1 2
U2 16
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
EI 1549-4918
J9 STEM CELLS
JI Stem Cells
PD JUN
PY 2012
VL 30
IS 6
BP 1064
EP 1075
DI 10.1002/stem.1081
PG 12
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA 942YJ
UT WOS:000304087300004
PM 22415968
ER
PT J
AU Steere, A
AF Steere, A.
TI LYME DISEASE - OLD AND NEW INSIGHTS
SO ANNALS OF THE RHEUMATIC DISEASES
LA English
DT Meeting Abstract
C1 [Steere, A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Rheumatol Allergy & Immunol, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0003-4967
EI 1468-2060
J9 ANN RHEUM DIS
JI Ann. Rheum. Dis.
PD JUN
PY 2012
VL 71
SU 3
BP 43
EP 43
PG 1
WC Rheumatology
SC Rheumatology
GA V31QQ
UT WOS:000208898500178
ER
PT J
AU Rauen, T
Grammatikos, A
Hedrich, CM
Kyttaris, VC
Tenbrock, K
Raffetseder, U
Floege, J
Tsokos, GC
AF Rauen, T.
Grammatikos, A.
Hedrich, C. M.
Kyttaris, V. C.
Tenbrock, K.
Raffetseder, U.
Floege, J.
Tsokos, G. C.
TI CAMP RESPONSIVE ELEMENT MODULATOR (CREM) ALPHA CONTRIBUTES TO DECREASED
NOTCH-1 EXPRESSION IN T CELLS FROM PATIENTS WITH SYSTEMIC LUPUS
ERYTHEMATOSUS (SLE)
SO ANNALS OF THE RHEUMATIC DISEASES
LA English
DT Meeting Abstract
C1 [Rauen, T.; Raffetseder, U.; Floege, J.] Rhein Westfal TH Aachen, Dept Nephrol & Clin Immunol, Aachen, Germany.
[Grammatikos, A.; Hedrich, C. M.; Kyttaris, V. C.; Tsokos, G. C.] Harvard Univ, Sch Med, Bidmc, Div Rheumatol, Boston, MA USA.
[Tenbrock, K.] Rhein Westfal TH Aachen, Dept Pediat, Aachen, Germany.
NR 3
TC 0
Z9 0
U1 1
U2 1
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0003-4967
EI 1468-2060
J9 ANN RHEUM DIS
JI Ann. Rheum. Dis.
PD JUN
PY 2012
VL 71
SU 3
BP 155
EP 155
PG 1
WC Rheumatology
SC Rheumatology
GA V31QQ
UT WOS:000208898500493
ER
PT J
AU Krasoudaki, E
Stagakis, E
Loupasakis, K
Papagianni, A
Alexopoulos, E
Bertsias, G
Iliopoulos, D
Boumpas, D
AF Krasoudaki, E.
Stagakis, E.
Loupasakis, K.
Papagianni, A.
Alexopoulos, E.
Bertsias, G.
Iliopoulos, D.
Boumpas, D.
TI MICRORNA ANALYSIS OF HUMAN LUPUS NEPHRITIS: EVIDENCE FOR MODULATION OF
KALLIKREIN 4 BY MIR-422A
SO ANNALS OF THE RHEUMATIC DISEASES
LA English
DT Meeting Abstract
C1 [Krasoudaki, E.; Stagakis, E.; Bertsias, G.; Boumpas, D.] Univ Crete, Lab Autoimmun & Inflammat, Iraklion, Greece.
[Loupasakis, K.; Iliopoulos, D.] Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA.
[Papagianni, A.; Alexopoulos, E.] Aristotle Univ Thessaloniki, Dept Nephrol, GR-54006 Thessaloniki, Greece.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0003-4967
EI 1468-2060
J9 ANN RHEUM DIS
JI Ann. Rheum. Dis.
PD JUN
PY 2012
VL 71
SU 3
BP 472
EP 473
PG 2
WC Rheumatology
SC Rheumatology
GA V31QQ
UT WOS:000208898502356
ER
PT J
AU Singh, JA
Wells, GA
Christensen, R
Tanjong, E
MacDonald, J
Tugwell, P
Buchbinder, R
AF Singh, J. A.
Wells, G. A.
Christensen, R.
Tanjong, E.
MacDonald, J.
Tugwell, P.
Buchbinder, R.
CA Biol Safety Study Grp
TI ADVERSE EFFECTS OF BIOLOGICS: A NETWORK META-ANALYSIS AND COCHRANE
OVERVIEW
SO ANNALS OF THE RHEUMATIC DISEASES
LA English
DT Meeting Abstract
C1 [Singh, J. A.] Birmingham VA Med Ctr, Birmingham, AL USA.
[Singh, J. A.] Univ Alabama Birmingham, Birmingham, AL USA.
[Wells, G. A.] McMaster Univ, Ottawa, ON, Canada.
[Christensen, R.] Univ Denmark, Copenhagen, Denmark.
[Tanjong, E.; Tugwell, P.] Univ Ottawa, Montreal, PQ, Canada.
[MacDonald, J.] Univ Washington, Seattle, WA 98195 USA.
[Buchbinder, R.] Monash Univ, Monash, Australia.
NR 0
TC 0
Z9 0
U1 2
U2 3
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0003-4967
EI 1468-2060
J9 ANN RHEUM DIS
JI Ann. Rheum. Dis.
PD JUN
PY 2012
VL 71
SU 3
BP 628
EP 628
PG 1
WC Rheumatology
SC Rheumatology
GA V31QQ
UT WOS:000208898503315
ER
PT J
AU McDermott, S
Guimaraes, AR
AF McDermott, Shaunagh
Guimaraes, Alexander R.
TI Magnetic Nanoparticles in the Imaging of Tumor Angiogenesis
SO APPLIED SCIENCES-BASEL
LA English
DT Review
DE angiogenesis; ultrasmall superparamagnetic iron oxide; magnetic
resonance imaging
AB Angiogenesis, the growth of new capillary blood vessels, is central to the growth of tumors. Non-invasive imaging of tumor angiogenesis will allow for earlier detection of tumors and also the development of surrogate markers for assessing response to treatment. Steady state magnetic resonance imaging with magnetic nanoparticles is one method to assess angiogenesis. In this article we explain the theory behind steady state magnetic resonance imaging and review the available literature.
C1 [McDermott, Shaunagh; Guimaraes, Alexander R.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Guimaraes, Alexander R.] Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
RP McDermott, S (reprint author), Massachusetts Gen Hosp, 55 Fruit St, Boston, MA 02114 USA.
EM smcdermott1@partners.org; aguimaraes@mgh.harvard.edu
NR 42
TC 3
Z9 3
U1 0
U2 0
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 2076-3417
J9 APPL SCI-BASEL
JI Appl. Sci.-Basel
PD JUN
PY 2012
VL 2
IS 2
BP 525
EP 534
DI 10.3390/app2020525
PG 10
WC Chemistry, Multidisciplinary; Materials Science, Multidisciplinary;
Physics, Applied
SC Chemistry; Materials Science; Physics
GA V36XK
UT WOS:000209240800019
ER
PT J
AU von Recum, J
Matschke, S
Jupiter, JB
Ring, D
Souer, JS
Huber, M
Audige, L
AF von Recum, J.
Matschke, S.
Jupiter, J. B.
Ring, D.
Souer, J-S.
Huber, M.
Audige, L.
TI Characteristics of two different locking compression plates in the volar
fixation of complex articular distal radius fractures
SO BONE & JOINT RESEARCH
LA English
DT Article
DE Distal radius fracture; Open reduction and internal fixation; ORIF;
Locking compression plate; LCP; Comparative analysis
AB Objectives
To investigate the differences of open reduction and internal fixation (ORIF) of complex AO Type C distal radius fractures between two different models of a single implant type.
Methods
A total of 136 patients who received either a 2.4 mm (n = 61) or 3.5 mm (n = 75) distal radius locking compression plate (LCP DR) using a volar approach were followed over two years. The main outcome measurements included motion, grip strength, pain, and the scores of Gartland and Werley, the Short-Form 36 (SF-36) and the Disabilities of the Arm, Shoulder, and Hand (DASH). Differences between the treatment groups were evaluated using regression analysis and the likelihood ratio test with significance based on the Bonferroni corrected p-value of < 0.003.
Results
The groups were similar with respect to baseline and injury characteristics as well as general surgical details. The risk of experiencing a complication after ORIF with a LCP DR 2.4 mm was 18% (n = 11) compared with 11% (n = 8) after receiving a LCP DR 3.5 mm (p = 0.45). Wrist function was also similar between the cohorts based on the mean ranges of movement (all p > 0.052) and grip strength measurements relative to the contralateral healthy side (p = 0.583). In addition, DASH and SF-36 component scores as well as pain were not significantly different between the treatment groups throughout the two-year period (all p = 0.005). No patient from either treatment group had a step-off > 2 mm.
Conclusions
Differences in plate design do not influence the overall final outcome of fracture fixation using LCP.
C1 [Matschke, S.] BG Trauma Ctr Ludwigshafen, D-67071 Ludwigshafen, Germany.
[Jupiter, J. B.; Ring, D.; Souer, J-S.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Huber, M.; Audige, L.] AO Clin Invest & Documentat, CH-8600 Dubendorf, Switzerland.
RP von Recum, J (reprint author), Dept Knee Foot & Ankle Surg, Los Angeles, CA 90211 USA.
EM Jan.von-Recum@bgu-ludwigshafen.de
RI AOCID, AO Foundation/R-6455-2016
FU AO Foundation
FX The work presented in this manuscript was supported by the AO Foundation
NR 25
TC 4
Z9 4
U1 0
U2 1
PU BRITISH EDITORIAL SOC BONE JOINT SURGERY
PI LONDON
PA 22 BUCKINGHAM STREET, LONDON WC2N 6ET, ENGLAND
SN 2046-3758
J9 BONE JOINT RES
JI Bone Jt. Res.
PD JUN
PY 2012
VL 1
IS 6
BP 111
EP 117
DI 10.1302/2046-3758.16.2000008
PG 7
WC Cell & Tissue Engineering; Orthopedics
SC Cell Biology; Orthopedics
GA V35HA
UT WOS:000209139800003
PM 23610680
ER
PT J
AU Maleki, N
Becerra, L
Brawn, J
Bigal, M
Burstein, R
Borsook, D
AF Maleki, Nasim
Becerra, Lino
Brawn, Jennifer
Bigal, Marcelo
Burstein, Rami
Borsook, David
TI Concurrent functional and structural cortical alterations in migraine
SO CEPHALALGIA
LA English
DT Article
DE Headache; pain; fMRI; functional connectivity; morphometry;
somatosensory cortex; insula; cingulate cortex; temporal pole
ID HUMAN CEREBRAL-CORTEX; PRIMARY SOMATOSENSORY CORTEX; VOXEL-BASED
MORPHOMETRY; REGIONAL PAIN SYNDROME; GREY-MATTER CHANGES; HUMAN BRAIN;
GEOMETRICALLY ACCURATE; SYNAPTIC PLASTICITY; PREFRONTAL CORTEX;
NEUROPATHIC PAIN
AB Aim: Various animal and human studies have contributed to the idea of cortical structural-functional alterations in migraine. Defining concurrent cortical alterations may provide specific insights into the unfolding adaptive or maladaptive changes taking place in cortex in migraine.
Methods: From a group of 60 episodic migraineurs, 20 were recruited to the study. Using high-resolution magnetic resonance imaging, structural and functional cortical measures were compared in migraineurs who experienced increased frequency of attacks (HF; 8-14 days/month; n=10), to those who experienced less frequent migraine attacks (LF;<2 days/month; n=10), and to healthy controls (HC; n=20).
Results: Parallel structural and functional differences were found as follows: (i) HF patients showed higher thickness in the area representing the face in the post-central gyrus, which correlated with the observed stronger functional activation, suggesting adaptation to repeated sensory drive; (ii) smaller cortical volume was observed in the cingulate cortex that correlated with lower activation in the HF group; and (iii) similarly significant structural and functional differences (HF>LF) were observed in the insula that may reflect potential alteration in affective processing.
Conclusion: These results suggest differential response patterns in the sensory vs. affective processing regions in the brain that may be an adaptive response to repeated migraine attacks.
C1 [Becerra, Lino; Borsook, David] Harvard Univ, McLean Hosp, PAIN Grp, Brain Imaging Ctr,Med Sch,Dept Psychiat, Belmont, MA 02478 USA.
[Maleki, Nasim; Brawn, Jennifer] Harvard Univ, Sch Med, Dept Radiol, Childrens Hosp Boston, Belmont, MA 02478 USA.
[Becerra, Lino; Borsook, David] Harvard Univ, Sch Med, Dept Psychiat, Massachusetts Gen Hosp, Belmont, MA 02478 USA.
[Becerra, Lino; Borsook, David] Harvard Univ, Dept Radiol, Massachusetts Gen Hosp, Sch Med, Belmont, MA 02478 USA.
[Bigal, Marcelo] Merck & Co Inc, Merck Investigator Studies Program, Whitehouse Stn, NJ USA.
[Bigal, Marcelo] Merck & Co Inc, Sci Educ Grp, Merck Res Labs, Whitehouse Stn, NJ USA.
[Bigal, Marcelo] Albert Einstein Coll Med, Dept Neurol, New York, NY USA.
[Burstein, Rami] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Anesthesia & Crit Care, Belmont, MA 02478 USA.
RP Borsook, D (reprint author), Harvard Univ, McLean Hosp, PAIN Grp, Brain Imaging Ctr,Med Sch,Dept Psychiat, 115 Mill St, Belmont, MA 02478 USA.
EM dborsook@partners.org
FU NIH [K24 NS064050, R01 NS056195, R01-NS073997]; Merck and Co.
FX The work was supported by grants from NIH (K24 NS064050 (NINDS), R01
NS056195 (NINDS), and R01-NS073997 (NINDS) to DB) (data collection) and
an Investigator Initiated Grant from Merck and Co. (data analysis).
NR 68
TC 61
Z9 63
U1 1
U2 12
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0333-1024
EI 1468-2982
J9 CEPHALALGIA
JI Cephalalgia
PD JUN
PY 2012
VL 32
IS 8
BP 607
EP 620
DI 10.1177/0333102412445622
PG 14
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 959XS
UT WOS:000305352100005
PM 22623760
ER
PT J
AU Certain, L
Schuetz, P
AF Certain, Laura
Schuetz, Philipp
TI The Role of Procalcitonin in Respiratory Infections
SO CURRENT INFECTIOUS DISEASE REPORTS
LA English
DT Article
DE Procalcitonin; Respiratory infection; Antibiotic stewardship; Biomarker
ID COMMUNITY-ACQUIRED PNEUMONIA; C-REACTIVE PROTEIN; VENTILATOR-ASSOCIATED
PNEUMONIA; INTENSIVE-CARE-UNIT; OBSTRUCTIVE PULMONARY-DISEASE;
RANDOMIZED-CONTROLLED-TRIALS; CRITICALLY-ILL PATIENTS; SERUM
PROCALCITONIN; ANTIBIOTIC-THERAPY; TRACT INFECTIONS
AB Accurate diagnosis, risk stratification, and decisions about the need for and optimal duration of antibiotic therapy are cornerstones of the management of patients with respiratory infections. A growing body of evidence supports the use of procalcitonin, a marker of bacterial infection, in addition to conventional clinical parameters to improve diagnostic and prognostic assessment in patients with suspicion of respiratory infections. In addition, several randomized controlled trials indicate that procalcitonin may be used for clinical decision making about initiation and optimal duration of antibiotic therapy. For patients with respiratory infections, procalcitonin-guided antibiotic therapy resulted in less antibiotic use without any apparent adverse patient outcome. For other infections outcome studies are currently lacking. This review summarizes the results of recent investigations of procalcitonin in respiratory infections to provide physicians an overview of the utility and limitations of procalcitonin when used for bedside decision making.
C1 [Certain, Laura] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Schuetz, Philipp] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
RP Schuetz, P (reprint author), Harvard Univ, Sch Publ Hlth, 667 Huntington Ave, Boston, MA 02115 USA.
EM Schuetzph@gmail.com
OI schuetz, philipp/0000-0001-6400-4949
FU Swiss Foundation for Grants in Biology and Medicine (Schweizerische
Stiftung fur medizinisch-biologische Stipendien, SSMBS [PASMP3127684/1];
BRAHMS Inc and Biomerieux
FX Dr. Schuetz was supported by a research grant from the Swiss Foundation
for Grants in Biology and Medicine (Schweizerische Stiftung fur
medizinisch-biologische Stipendien, SSMBS, PASMP3127684/1) and reports
receiving support from BRAHMS Inc and Biomerieux to attend meetings and
fulfill speaking engagements. Dr. Certain reports no conflict of
interest.
NR 88
TC 1
Z9 1
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1523-3847
EI 1534-3146
J9 CURR INFECT DIS REP
JI Curr. Infect. Dis. Rep.
PD JUN
PY 2012
VL 14
IS 3
BP 308
EP 316
DI 10.1007/s11908-012-0249-5
PG 9
WC Infectious Diseases
SC Infectious Diseases
GA V32XE
UT WOS:000208983100011
PM 22382693
ER
PT J
AU El Nawawi, NM
Balboni, MJ
Balboni, TA
AF El Nawawi, Nora M.
Balboni, Michael J.
Balboni, Tracy A.
TI Palliative care and spiritual care: the crucial role of spiritual care
in the care of patients with advanced illness
SO CURRENT OPINION IN SUPPORTIVE AND PALLIATIVE CARE
LA English
DT Review
DE end of life; palliative care; religion; spiritual care; spirituality
AB Purpose of review
Within the hospice and palliative care movement, patients' religion/spirituality (R/S) has been a core component of care incorporated within international and US palliative care guidelines. However, as the discipline of palliative care has been incorporated into the larger biomedical community, the inclusion of spiritual care has become controversial. This review summarizes key empirical research at the intersection of palliative care and R/S in order to assess its validity as a domain of end-of-life care.
Recent findings
Recent research shows that R/S and spiritual care are important components to the care of patients facing advanced illness. Patients - particularly ethnic minorities - rely upon R/S as an important means to interpret and cope with illness. Studies suggest that R/S plays an important role in coping with disease-related symptoms, improves quality of life, and impacts medical decision-making near death. Patients largely desire medical caregivers to take an active role in providing spiritual care, and patients likewise frequently experience multiple spiritual needs arising in the face of life-threatening illness.
Summary
Despite an empirical evidence for spiritual care as part of palliative care, R/S remains insufficiently addressed by the medical system. Further research is required in order to more clearly identify the roles of healthcare providers and standardize the provision of spiritual care within palliative care.
C1 [El Nawawi, Nora M.; Balboni, Michael J.; Balboni, Tracy A.] Dana Farber Canc Inst, Ctr Psychosocial Oncol & Palliat Care Res, Boston, MA 02115 USA.
[Balboni, Michael J.; Balboni, Tracy A.] Dana Farber Canc Inst, Dept Psychosocial Oncol & Palliat Care, Boston, MA 02115 USA.
[Balboni, Michael J.] Harvard Univ, Sch Divin, Cambridge, MA 02138 USA.
[Balboni, Tracy A.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Balboni, Tracy A.] Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA.
RP Balboni, TA (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dana 1101,450 Brookline Ave, Boston, MA 02115 USA.
EM TBalboni@LROC.Harvard.edu
NR 33
TC 25
Z9 26
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1751-4258
EI 1751-4266
J9 CURR OPIN SUPPORT PA
JI Curr. Opin Support Palliat. Car.
PD JUN
PY 2012
VL 6
IS 2
BP 269
EP 274
DI 10.1097/SPC.0b013e3283530d13
PG 6
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA V32OR
UT WOS:000208961000024
PM 22469668
ER
PT J
AU Bikle, DD
AF Bikle, Daniel D.
TI Vitamin D and Bone
SO CURRENT OSTEOPOROSIS REPORTS
LA English
DT Article
DE Vitamin D; Vitamin D receptor; CYP27B1; 25hydroxyvitamin; 1,25
dihydroxyvitamin D; 24,25 dihydroxyvitamin D; Bone; Chondrocytes;
Osteoblasts; Osteoclasts
AB All cells comprising the skeleton-chondrocytes, osteoblasts, and osteoclasts-contain both the vitamin D receptor and the enzyme CYP27B1 required for producing the active metabolite of vitamin D, 1,25 dihydroxyvitamin D. Direct effects of 25 hydroxyvitamin D and 1,25 dihydroxyvitamin D on these bone cells have been demonstrated. However, the major skeletal manifestations of vitamin D deficiency or mutations in the vitamin D receptor and CYP27B1, namely rickets and osteomalacia, can be corrected by increasing the intestinal absorption of calcium and phosphate, indicating the importance of indirect effects. On the other hand, these dietary manipulations do not reverse defects in osteoblast or osteoclast function that lead to osteopenic bone. This review discusses the relative importance of the direct versus indirect actions of vitamin D on bone, and provides guidelines for the clinical use of vitamin D to prevent/treat bone loss and fractures.
C1 [Bikle, Daniel D.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RP Bikle, DD (reprint author), San Francisco VA Med Ctr, 4150 Clement St 111N, San Francisco, CA 94121 USA.
EM Daniel.bikle@ucsf.edu
FU National Institutes of Health [RO1 DK054793, AR055924, AR050023]
FX D.D. Bikle: has received grant support from the National Institutes of
Health (RO1 DK054793, AR055924, and AR050023); and receives loyalties
from Lange textbook chapter.
NR 86
TC 35
Z9 37
U1 0
U2 11
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
EI 1544-2241
J9 CURR OSTEOPOROS REP
JI Curr. Osteoporos. Rep.
PD JUN
PY 2012
VL 10
IS 2
BP 151
EP 159
DI 10.1007/s11914-012-0098-z
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA V35YS
UT WOS:000209181600007
PM 22544628
ER
PT J
AU Papisov, MI
Belov, V
Fischman, AJ
Belova, E
Titus, J
Gagne, M
Gillooly, C
AF Papisov, Mikhail I.
Belov, V.
Fischman, A. J.
Belova, E.
Titus, J.
Gagne, M.
Gillooly, C.
TI Delivery of proteins to CNS as seen and measured by positron emission
tomography
SO DRUG DELIVERY AND TRANSLATIONAL RESEARCH
LA English
DT Article
DE PET Imaging; Pharmacokinetics; Biopharmaceuticals; Macromolecules;
Brain; Central nervous system; Drug delivery; Iodine-124
AB Presently, there are no effective treatments for several diseases involving the central nervous system (CNS). While several novel molecular approaches are being developed, many of them require delivery of macromolecular or supramolecular agents to the CNS tissues protected by the blood-brain and blood-arachnoid barriers. A variety of approaches that are being developed for overcoming or bypassing the barriers are based on complex transfer processes. The delivery of biopharmaceuticals and other macromolecules and particulates to the CNS, especially through the leptomeningeal (intrathecal) route, includes a variety of stages, such as leptomeningeal propagation, drainage to the systemic circulation, and penetration into the CNS. The investigation of complex pharmacokinetics that includes convective, as well as diffusional and active transfer processes, greatly benefit from real-time non-invasive in vivo monitoring of the drug transport. Pharmacological positron emission tomography (PET) imaging, which enables such monitoring, plays an increasingly significant role in drug delivery and biopharmacology. PET is a powerful tool for quantitative in vivo tracking of molecules labeled with positron-emitting radionuclides. The high sensitivity, format, and accuracy of the data (similar to those of conventional tissue sampling biodistribution studies) make PET a readily adoptable pharmacological technique. In contrast to the conventional studies, PET also allows for longitudinal nonterminal same-animal studies. The latter may not only improve the data statistics, but also enable preclinical studies (especially in large and/or rare animals) not feasible under the conventional approach. This paper is intended to demonstrate the character of data that can be obtained by PET and to demonstrate how the main patterns of the leptomeningeal route pharmacokinetics can be investigated using this method. Examples of data processing are taken from our recent studies of five model proteins in rats and nonhuman primates.
C1 [Papisov, Mikhail I.; Belov, V.; Belova, E.; Titus, J.; Gagne, M.; Gillooly, C.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Papisov, Mikhail I.; Belov, V.; Fischman, A. J.; Belova, E.] Harvard Univ, Sch Med, Boston, MA USA.
[Papisov, Mikhail I.; Belov, V.; Fischman, A. J.; Belova, E.] Shriners Hosp Children, Boston, MA USA.
RP Papisov, MI (reprint author), Massachusetts Gen Hosp, Bartlett Hall 500R,55 Fruit St, Boston, MA 02114 USA.
EM papisov@helix.mgh.harvard.edu
OI Papisov, Mikhail/0000-0003-4716-2122
FU NIH [R21 CA152384]; DoD [BC100684]; Shire HGT
FX This work was supported by NIH grant R21 CA152384, DoD grant BC100684,
and grants from Shire HGT. Shire HGT also provided model proteins and
imaging equipment.
NR 16
TC 5
Z9 5
U1 0
U2 1
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 2190-393X
EI 2190-3948
J9 DRUG DELIV TRANSL RE
JI Drug Deliv. Transl. Res.
PD JUN
PY 2012
VL 2
IS 3
SI SI
BP 201
EP 209
DI 10.1007/s13346-012-0073-3
PG 9
WC Instruments & Instrumentation; Medicine, Research & Experimental;
Pharmacology & Pharmacy
SC Instruments & Instrumentation; Research & Experimental Medicine;
Pharmacology & Pharmacy
GA V39PW
UT WOS:000209423900007
PM 25786867
ER
PT J
AU Papisov, MI
Belov, V
Belova, E
Fischman, AJ
Fisher, R
Wright, JL
Gannon, KS
Titus, J
Gagne, M
Gillooly, CA
AF Papisov, Mikhail I.
Belov, V.
Belova, E.
Fischman, A. J.
Fisher, R.
Wright, J. L.
Gannon, K. S.
Titus, J.
Gagne, M.
Gillooly, C. A.
TI Investigation of intrathecal transport of NPT002, a prospective
therapeutic based on phage M13, in nonhuman primates
SO DRUG DELIVERY AND TRANSLATIONAL RESEARCH
LA English
DT Article
DE Bacteriophage M13, NPT002, PET imaging; Pharmacokinetics; Brain;
Iodine-124
AB Presently, there are no effective treatments for conditions characterized by protein misfolding, such as Alzheimer's, Parkinson's, and other diseases involving CNS. Since misfolding occurs at the earliest stage of the disease, it is likely to be involved in subsequent pathological developments. It has been found that NPT002 (bacteriophage M13) directly dissociates aggregates of misfolded proteins that form amyloid, including amyloid-beta, tau and alpha-synuclein. For CNS applications, NPT002 requires delivery to the brain parenchyma, the target tissue. NPT002 is an elongated similar to 950 nm particle that cannot penetrate into the brain from the blood. Furthermore, phage particles, due to their size, cannot be effectively transported in vivo by diffusion. Considering the physiology of the leptomeningeal space, intrathecal administration appears to be a promising convection-driven avenue for NPT002 delivery. In this paper, we use positron emission tomography to investigate the transport of NPT002 in Macaca fascicularis. The data suggest that approximately 50 % of the administered dose can reach the cerebral leptomeningeal space after a single lumbar intrathecal injection. A biologically significant fraction of the phage then enters the brain, resulting in potentially therapeutic cortical and subcortical exposure.
C1 [Papisov, Mikhail I.; Belov, V.; Belova, E.; Titus, J.; Gagne, M.; Gillooly, C. A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Papisov, Mikhail I.; Belov, V.; Belova, E.; Fischman, A. J.] Harvard Univ, Sch Med, Boston, MA USA.
[Papisov, Mikhail I.; Belov, V.; Belova, E.; Fischman, A. J.] Shriners Hosp Children, Boston, MA USA.
[Fisher, R.; Wright, J. L.; Gannon, K. S.] NeuroPhage Pharmaceut Inc, Cambridge, MA USA.
RP Papisov, MI (reprint author), Massachusetts Gen Hosp, Bartlett Hall 500R,55 Fruit St, Boston, MA 02114 USA.
EM papisov@helix.mgh.harvard.edu
OI Papisov, Mikhail/0000-0003-4716-2122
FU NeuroPhage Pharmaceuticals, Inc. [NPT001, NPT002]
FX This work was supported by a grant from NeuroPhage Pharmaceuticals, Inc.
NeuroPhage also provided the purified and formulated bacteriophage M13
preparations, NPT001 and NPT002.
NR 22
TC 2
Z9 2
U1 0
U2 0
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 2190-393X
EI 2190-3948
J9 DRUG DELIV TRANSL RE
JI Drug Deliv. Transl. Res.
PD JUN
PY 2012
VL 2
IS 3
SI SI
BP 210
EP 221
DI 10.1007/s13346-012-0074-2
PG 12
WC Instruments & Instrumentation; Medicine, Research & Experimental;
Pharmacology & Pharmacy
SC Instruments & Instrumentation; Research & Experimental Medicine;
Pharmacology & Pharmacy
GA V39PW
UT WOS:000209423900008
PM 25786868
ER
PT J
AU LeVarge, BL
Channick, RN
AF LeVarge, Barbara L.
Channick, Richard N.
TI Inhaled treprostinil for the treatment of pulmonary arterial
hypertension
SO EXPERT REVIEW OF RESPIRATORY MEDICINE
LA English
DT Article
DE administration; analogs and derivatives; epoprostenol; inhalation;
pulmonary arterial hypertension; pulmonary circulation; treprostinil
ID CONTINUOUS INTRAVENOUS PROSTACYCLIN; CONTINUOUS SUBCUTANEOUS INFUSION;
PLACEBO-CONTROLLED TRIAL; BLOOD-STREAM INFECTIONS; SMOOTH-MUSCLE-CELLS;
DOUBLE-BLIND; BERAPROST SODIUM; RANDOMIZED-TRIAL; IV TREPROSTINIL;
GAS-EXCHANGE
AB Treprostinil is a prostacyclin derivative approved for the treatment of pulmonary arterial hypertension by intravenous, subcutaneous and inhalational administration. Unlike its precursor epoprostenol, treprostinil is chemically stable at room temperature and neutral pH, and its plasma half-life is longer. In addition to promoting smooth muscle relaxation in the pulmonary vasculature, treprostinil has suppressive effects on platelet aggregation, smooth muscle proliferation and inflammation. A Phase III study, investigating the addition of inhaled treprostinil to oral bosentan or sildenafil, confirmed significant improvements in exercise capacity and quality of life. This review examines the pharmacodynamics, pharmacokinetics, clinical efficacy and safety of inhaled treprostinil for use in pulmonary arterial hypertension.
C1 [LeVarge, Barbara L.; Channick, Richard N.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP LeVarge, BL (reprint author), Massachusetts Gen Hosp, 55 Fruit St, Boston, MA 02114 USA.
EM blevarge@partners.org
FU Actelion; Bayer; Novartis; United Therapeutics
FX R Channick has consulted for and/or received research grants from
companies that produce treatments for pulmonary hypertension, including
Actelion, Bayer, Novartis and United Therapeutics. The authors have no
other relevant affiliations or financial involvement with any
organization or entity with a financial interest in or financial
conflict with the subject matter or materials discussed in the
manuscript apart from those disclosed.
NR 79
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U1 0
U2 2
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
ENGLAND
SN 1747-6348
J9 EXPERT REV RESP MED
JI Expert Rev. Respir. Med.
PD JUN
PY 2012
VL 6
IS 3
BP 255
EP 265
DI 10.1586/ERS.12.23
PG 11
WC Respiratory System
SC Respiratory System
GA 213LL
UT WOS:000324058600010
PM 22788940
ER
PT J
AU Papakostas, GI
AF Papakostas, G. I.
TI TRD: Pharmacotherapeutic strategies for adults with major depressive
disorder
SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
C1 [Papakostas, G. I.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1461-1457
EI 1469-5111
J9 INT J NEUROPSYCHOPH
JI Int. J. Neuropsychopharmacol.
PD JUN
PY 2012
VL 15
SU 1
MA S-02-001
BP 5
EP 5
PG 1
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA V34BS
UT WOS:000209062500014
ER
PT J
AU Patel, SG
Singh, B
Stambuk, HE
Carlson, D
Bridger, PG
Cantu, G
Cheesman, AD
Donald, P
Fliss, D
Gullane, P
Kamata, S
Janecka, I
Kowalski, LP
Kraus, DH
Levine, PA
Medina, LR
Pradhan, S
Schramm, V
Snyderman, C
Wei, WI
Shah, JP
AF Patel, Snehal G.
Singh, Bhuvanesh
Stambuk, Hilda E.
Carlson, Diane
Bridger, Patrick G.
Cantu, Giulio
Cheesman, Anthony D.
Donald, Paul
Fliss, Dan
Gullane, Patrick
Kamata, Shin-etsu
Janecka, Ivo
Kowalski, Luiz P.
Kraus, Dennis H.
Levine, Paul A.
Medina, Luiz R.
Pradhan, Sultan
Schramm, Victor
Snyderman, Carl
Wei, William I.
Shah, Jatin P.
TI Craniofacial Surgery for Esthesioneuroblastoma: Report of an
International Collaborative Study
SO JOURNAL OF NEUROLOGICAL SURGERY PART B-SKULL BASE
LA English
DT Article
DE nose neoplasms/mortality/pathology/surgery/*therapy;
esthesioneuroblastoma; olfactory/*therapy; combined modality therapy;
radiotherapy; adjuvant; survival analysis
ID SINONASAL UNDIFFERENTIATED CARCINOMA; OF-VIRGINIA EXPERIENCE; OLFACTORY
NEUROBLASTOMA; NEUROENDOCRINE CARCINOMAS; SURGICAL-MANAGEMENT;
RADIATION-THERAPY; SKULL BASE; TUMORS; RESECTION; PRESERVATION
AB Introduction Impact of treatment and prognostic indicators of outcome are relatively ill-defined in esthesioneuroblastomas (ENB) because of the rarity of these tumors. This study was undertaken to assess the impact of craniofacial resection (CFR) on outcome of ENB.
Patients and Methods Data on 151 patients who underwent CFR for ENB were collected from 17 institutions that participated in an international collaborative study. Patient, tumor, treatment, and outcome data were collected by questionnaires and variables were analyzed for prognostic impact on overall, disease-specific and recurrence-free survival. The majority of tumors were staged Kadish stage C (116 or 77%). Overall, 90 patients (60%) had received treatment before CFR, radiation therapy in 51 (34%), and chemotherapy in 23 (15%). The margins of surgical resection were reported positive in 23 (15%) patients. Adjuvant postoperative radiation therapy was used in 51 (34%) and chemotherapy in 9 (6%) patients.
Results Treatment-related complications were reported in 49 (32%) patients. With a median follow-up of 56 months, the 5-year overall, disease-specific, and recurrence-free survival rates were 78, 83, and 64%, respectively. Intracranial extension of the disease and positive surgical margins were independent predictors of worse overall, disease-specific, and recurrence-free survival on multivariate analysis.
Conclusion This collaborative study of patients treated at various institutions across the world demonstrates the efficacy of CFR for ENB. Intracranial extension of disease and complete surgical excision were independent prognostic predictors of outcome.
C1 [Patel, Snehal G.; Singh, Bhuvanesh; Kraus, Dennis H.; Shah, Jatin P.] Mem Sloan Kettering Canc Ctr, Dept Surg, New York, NY 10021 USA.
[Stambuk, Hilda E.] Mem Sloan Kettering Canc Ctr, Dept Radiol, New York, NY 10021 USA.
[Carlson, Diane] Cleveland Clin, Weston, FL USA.
[Bridger, Patrick G.] Prince Wales Hosp, Sydney, NSW, Australia.
[Cantu, Giulio] Inst Nazl, Milan, Italy.
[Cheesman, Anthony D.] Royal Natl Throat Nose & Ear Hosp, London WC1X 8DA, England.
[Donald, Paul] Univ Calif Davis, Davis, CA USA.
[Fliss, Dan] Tel Aviv Univ, Tel Aviv Sourasky Med Ctr, Dept Otolaryngol, IL-69978 Tel Aviv, Israel.
[Gullane, Patrick] Univ Toronto, Dept Otolaryngol Head & Neck Surg, Toronto, ON, Canada.
[Kamata, Shin-etsu] Canc Inst Hosp, Tokyo, Japan.
[Janecka, Ivo] Massachusetts Eye & Ear Infirm, Boston, MA USA.
[Kowalski, Luiz P.] Hosp Canc AC Camargo, Sao Paulo, Brazil.
[Levine, Paul A.] Univ Virginia Hlth Syst, Charlottesville, VA USA.
[Medina, Luiz R.] Hosp Clin Sao Paulo, Sao Paulo, Brazil.
[Pradhan, Sultan] Tata Mem Hosp, Bombay 400012, Maharashtra, India.
[Schramm, Victor] Ctr Head & Neck Surg, Denver, CO USA.
[Snyderman, Carl] Univ Pittsburgh, Pittsburgh, PA USA.
[Wei, William I.] Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China.
RP Shah, JP (reprint author), Mem Sloan Kettering Canc Ctr, Head & Neck Serv, 1275 York Ave, New York, NY 10021 USA.
EM shahj@mskcc.org
RI Kowalski, Luiz/D-1701-2012; Francisco, Suely/D-9065-2014;
OI Kowalski, Luiz/0000-0001-5865-9308; Kowalski, Luiz
Paulo/0000-0002-0481-156X
NR 46
TC 13
Z9 15
U1 1
U2 2
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 2193-6331
J9 J NEUROL SURG PART B
JI Journal of Neurol. Surg. Part B
PD JUN
PY 2012
VL 73
IS 3
BP 208
EP 220
DI 10.1055/s-0032-1311754
PG 13
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 175YB
UT WOS:000321268600009
PM 23730550
ER
PT J
AU Rapuano, BE
Hackshaw, K
MacDonald, DE
AF Rapuano, Bruce E.
Hackshaw, Kyle
MacDonald, Daniel E.
TI Heat or radiofrequency plasma glow discharge treatment of a titanium
alloy stimulates osteoblast gene expression in the MC3T3 osteoprogenitor
cell line
SO JOURNAL OF PERIODONTAL AND IMPLANT SCIENCE
LA English
DT Article
DE Cell differentiation; Dental implants; Fibronectins; Integrin
alpha5beta1; Osteoblasts
AB Purpose: The purpose of this study was to determine whether increasing the Ti6Al4V surface oxide negative charge through heat (600 degrees C) or radiofrequency plasma glow discharge (RFGD) pretreatment, with or without a subsequent coating with fibronectin, stimulated osteoblast gene marker expression in the MC3T3 osteoprogenitor cell line.
Methods: Quantitative real-time polymerase chain reaction was used to measure changes over time in the mRNA levels for osteoblast gene markers, including alkaline phosphatase, bone sialoprotein, collagen type I (alpha 1), osteocalcin, osteopontin and parathyroid hormone-related peptide (PTH-rP), and the osteoblast precursor genes Runx2 and osterix.
Results: Osteoprogenitors began to differentiate earlier on disks that were pretreated with heat or RFGD. The pretreatments increased gene marker expression in the absence of a fibronectin coating. However, pretreatments increased osteoblast gene expression for fibronectin-coated disks more than uncoated disks, suggesting a surface oxide-mediated specific enhancement of fibronectin's bioactivity. Heat pretreatment had greater effects on the mRNA expression of genes for PTH-rP, alkaline phosphatase and osteocalcin while RFGD pretreatment had greater effects on osteopontin and bone sialoprotein gene expression.
Conclusions: The results suggest that heat and RFGD pretreatments of the Ti6Al4V surface oxide stimulated osteoblast differentiation through an enhancement of (a) coated fibronectin's bioactivity and (b) the bioactivities of other serum or matrix proteins. The quantitative differences in the effects of the two pretreatments on osteoblast gene marker expression may have arisen from the unique physico-chemical characteristics of each resultant oxide surface. Therefore, engineering the Ti6Al4V surface oxide to become more negatively charged can be used to accelerate osteoblast differentiation through fibronectin-dependent and independent mechanisms.
C1 [Rapuano, Bruce E.; Hackshaw, Kyle; MacDonald, Daniel E.] Cornell Univ, Hosp Special Surg, Weill Med Coll, New York, NY 10021 USA.
[MacDonald, Daniel E.] James J Peters VA Med Ctr, Bronx, NY USA.
[MacDonald, Daniel E.] Columbia Univ, Langmuir Ctr Colloids & Interfaces, New York, NY 10027 USA.
RP MacDonald, DE (reprint author), Columbia Univ, Langmuir Ctr Colloids & Interfaces, 911 SW Mudd Bldg,500 West 120th St, New York, NY 10027 USA.
EM dem14@columbia.edu
FU National Center for Research Resources, NIH [C06-RR12538-01]; [NIH RO1
DE017695]
FX The project described was supported by Grant Number NIH RO1 DE017695
(Awarded to DEM). This material is also the result of work supported
with resources and the use of facilities at the James J. Peters VA
Medical Center, Bronx, New York. This investigation was also conducted
at the HSS research facility constructed with support of Grant
C06-RR12538-01 from the National Center for Research Resources, NIH. We
would like to acknowledge Dr. Xiaoyu Hu for technical advice with the
qRT-PCR analyses. Special thanks goes to Paul Lee, Carrie Guan, and Jani
Jae Eun Lee for the preparation and treatment of titanium alloy disks.
NR 38
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Z9 6
U1 3
U2 6
PU KOREAN ACAD PERIODONTOLOGY
PI SEOUL
PA OFFICIAL B-D 2212, 163 SINMUNRO 1-GA, JONGNO-GU, SEOUL, 110-990, SOUTH
KOREA
SN 2093-2278
EI 2093-2286
J9 J PERIODONTAL IMPLAN
JI J. Periodontal Implant Sci.
PD JUN
PY 2012
VL 42
IS 3
BP 95
EP 104
DI 10.5051/jpis.2012.42.3.95
PG 10
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA V34HG
UT WOS:000209076900006
PM 22803011
ER
PT J
AU Mifflin, J
AF Mifflin, Jeffrey
TI BLAZING A WAGON TRAIL TO OREGON: A Weekly Chronicle of the Great
Migration of 1843
SO JOURNAL OF THE WEST
LA English
DT Book Review
C1 [Mifflin, Jeffrey] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Mifflin, J (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU ABC-CLIO
PI SANTA BARBARA
PA 130 CREMONA DR, SANTA BARBARA, CA 93117 USA
SN 0022-5169
EI 1930-0115
J9 J WEST
JI J. West
PD SUM
PY 2012
VL 51
IS 3
BP 103
EP 104
PG 2
WC History
SC History
GA V31LQ
UT WOS:000208885500022
ER
PT J
AU Imielinski, M
Cha, SW
Rejtar, T
Richardson, EA
Karger, BL
Sgroi, DC
AF Imielinski, Marcin
Cha, Sangwon
Rejtar, Tomas
Richardson, Elizabeth A.
Karger, Barry L.
Sgroi, Dennis C.
TI Integrated Proteomic, Transcriptomic, and Biological Network Analysis of
Breast Carcinoma Reveals Molecular Features of Tumorigenesis and
Clinical Relapse
SO MOLECULAR & CELLULAR PROTEOMICS
LA English
DT Article
ID LASER CAPTURE MICRODISSECTION; GENE-EXPRESSION SIGNATURES; SET
ENRICHMENT ANALYSIS; HEAT-SHOCK PROTEINS; MASS-SPECTROMETRY; CANCER
PROGRESSION; INDUCED APOPTOSIS; HISTOLOGIC GRADE; BONE METASTASIS;
CELL-DEATH
AB Gene and protein expression changes observed with tumorigenesis are often interpreted independently of each other and out of context of biological networks. To address these limitations, this study examined several approaches to integrate transcriptomic and proteomic data with known protein-protein and signaling interactions in estrogen receptor positive (ER+) breast cancer tumors. An approach that built networks from differentially expressed proteins and identified among them networks enriched in differentially expressed genes yielded the greatest success. This method identified a set of genes and proteins linking pathways of cellular stress response, cancer metabolism, and tumor microenvironment. The proposed network underscores several biologically intriguing events not previously studied in the context of ER+ breast cancer, including the overexpression of p38 mitogen-activated protein kinase and the overexpression of poly(ADP-ribose) polymerase 1. A gene-based expression signature biomarker built from this network was significantly predictive of clinical relapse in multiple independent cohorts of ER+ breast cancer patients, even after correcting for standard clinicopathological variables. The results of this study demonstrate the utility and power of an integrated quantitative proteomic, transcriptomic, and network analysis approach to discover robust and clinically meaningful molecular changes in tumors. Molecular & Cellular Proteomics 11: 10.1074/mcp.M111.014910, 1-15, 2012.
C1 [Cha, Sangwon; Rejtar, Tomas; Karger, Barry L.] Northeastern Univ, Barnett Inst, Boston, MA 02115 USA.
[Imielinski, Marcin; Richardson, Elizabeth A.; Sgroi, Dennis C.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Karger, BL (reprint author), Northeastern Univ, Barnett Inst, Boston, MA 02115 USA.
EM b.karger@neu.edu; dsgroi@partners.org
FU National Institutes of Health [RO1GM15847, R01CA112021]; Susan G. Komen
Breast Cancer Foundation; NCI SPORE in breast cancer at Massachusetts
General Hospital; Avon Foundation
FX This work was supported by National Institutes of Health Grants
RO1GM15847 (to B. L. K.) and R01CA112021 (to D. C. S.) and funds from
the Susan G. Komen Breast Cancer Foundation (to B. L. K. and D. C. S.),
the NCI SPORE in breast cancer at Massachusetts General Hospital (to D.
C. S.), and the Avon Foundation (to D. C. S.). The costs of publication
of this article were defrayed in part by the payment of page charges.
This article must therefore be hereby marked "advertisement" in
accordance with 18 U. S. C. Section 1734 solely to indicate this fact.
NR 73
TC 5
Z9 6
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 1535-9476
EI 1535-9484
J9 MOL CELL PROTEOMICS
JI Mol. Cell. Proteomics
PD JUN
PY 2012
VL 11
IS 6
AR M111.014910
DI 10.1074/mcp.M111.014910
PG 15
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 974CX
UT WOS:000306408500014
PM 22240506
ER
PT J
AU Kuhn, E
Whiteaker, JR
Mani, DR
Jackson, AM
Zhao, L
Pope, ME
Smith, D
Rivera, KD
Anderson, NL
Skates, SJ
Pearson, TW
Paulovich, AG
Carr, SA
AF Kuhn, Eric
Whiteaker, Jeffrey R.
Mani, D. R.
Jackson, Angela M.
Zhao, Lei
Pope, Matthew E.
Smith, Derek
Rivera, Keith D.
Anderson, N. Leigh
Skates, Steven J.
Pearson, Terry W.
Paulovich, Amanda G.
Carr, Steven A.
TI Interlaboratory Evaluation of Automated, Multiplexed Peptide
Immunoaffinity Enrichment Coupled to Multiple Reaction Monitoring Mass
Spectrometry for Quantifying Proteins in Plasma
SO MOLECULAR & CELLULAR PROTEOMICS
LA English
DT Article
ID BIOMARKER DISCOVERY; QUANTIFICATION; ANTIBODIES; SERUM; PIPELINE;
ASSAYS; IMMUNOASSAYS; QUANTITATION; VALIDATION; VERIFICATION
AB The inability to quantify large numbers of proteins in tissues and biofluids with high precision, sensitivity, and throughput is a major bottleneck in biomarker studies. We previously demonstrated that coupling immunoaffinity enrichment using anti-peptide antibodies (SISCAPA) to multiple reaction monitoring mass spectrometry (MRM-MS) produces Immunoprecipitation MRM-MS (immuno-MRM-MS) assays that can be multiplexed to quantify proteins in plasma with high sensitivity, specificity, and precision. Here we report the first systematic evaluation of the interlaboratory performance of multiplexed (8-plex) immuno-MRM-MS in three independent labs. A staged study was carried out in which the effect of each processing and analysis step on assay coefficient of variance, limit of detection, limit of quantification, and recovery was evaluated. Limits of detection were at or below 1 ng/ml for the assayed proteins in 30 mu l of plasma. Assay reproducibility was acceptable for verification studies, with median intra-and interlaboratory coefficients of variance above the limit of quantification of 11% and <14%, respectively, for the entire immuno-MRM-MS assay process, including enzymatic digestion of plasma. Trypsin digestion and its requisite sample handling contributed the most to assay variability and reduced the recovery of target peptides from digested proteins. Using a stable isotope-labeled protein as an internal standard instead of stable isotope-labeled pep-tides to account for losses in the digestion process nearly doubled assay accuracy for this while improving assay precision 5%. Our results demonstrate that multiplexed immuno-MRM-MS can be made reproducible across independent laboratories and has the potential to be adopted widely for assaying proteins in matrices as complex as plasma. Molecular & Cellular Proteomics 11: 10.1074/mcp.M111.013854, 1-14, 2012.
C1 [Kuhn, Eric; Mani, D. R.; Carr, Steven A.] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Whiteaker, Jeffrey R.; Zhao, Lei; Paulovich, Amanda G.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Jackson, Angela M.; Smith, Derek] Univ Victoria, Genome British Columbia Prote Core Facil, Victoria, BC, Canada.
[Pearson, Terry W.] Univ Victoria, Dept Biochem & Microbiol, Victoria, BC, Canada.
[Rivera, Keith D.] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA.
[Anderson, N. Leigh] Plasma Proteome Inst, Washington, DC USA.
[Skates, Steven J.] Massachusetts Gen Hosp, Ctr Biostat, Boston, MA 02114 USA.
RP Carr, SA (reprint author), Broad Inst MIT & Harvard, Cambridge, MA USA.
EM scarr@Broad.MIT.edu
FU National Institutes of Health [1U24 CA126476-02, 1U24CA160034]; NCI as
part of the NCI Clinical Proteomic Technologies Initiative, National
Institutes of Health [R01HL096738-02, HHSN268201000033C]; National
Heart, Lung and Blood Institute; Genome Canada and Genome British
Columbia; Entertainment Industry Foundation
FX This work was supported by National Institutes of Health Grant 1U24
CA126476-02 and 1U24CA160034 (to S. A. C., N. L. A., and A. G. P.) from
the NCI as part of the NCI Clinical Proteomic Technologies Initiative,
National Institutes of Health Grant R01HL096738-02 and HHSN268201000033C
(to S. A. C.) from the National Heart, Lung and Blood Institute, and a
platform grant from Genome Canada and Genome British Columbia. This work
was also supported in part by funds from the Women's Cancer Research
Fund of the Entertainment Industry Foundation (to S. A. C. and A. G.
P.). The costs of publication of this article were defrayed in part by
the payment of page charges. This article must therefore be hereby
marked "advertisement" in accordance with 18 U. S. C. Section 1734
solely to indicate this fact.
NR 40
TC 12
Z9 12
U1 0
U2 3
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 1535-9476
EI 1535-9484
J9 MOL CELL PROTEOMICS
JI Mol. Cell. Proteomics
PD JUN
PY 2012
VL 11
IS 6
AR M111.013854
DI 10.1074/mcp.M111.013854
PG 14
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 974CX
UT WOS:000306408500037
PM 22199228
ER
PT J
AU Schlatzer, DM
Dazard, JE
Ewing, RM
Ilchenko, S
Tomcheko, SE
Eid, S
Ho, V
Yanik, G
Chance, MR
Cooke, KR
AF Schlatzer, Daniela M.
Dazard, Jean-Eudes
Ewing, Rob M.
Ilchenko, Serguei
Tomcheko, Sara E.
Eid, Saada
Ho, Vincent
Yanik, Greg
Chance, Mark R.
Cooke, Kenneth R.
TI Human Biomarker Discovery and Predictive Models for Disease Progression
for Idiopathic Pneumonia Syndrome Following Allogeneic Stem Cell
Transplantation
SO MOLECULAR & CELLULAR PROTEOMICS
LA English
DT Article
ID BONE-MARROW-TRANSPLANTATION; PEPTIDOGLYCAN RECOGNITION PROTEINS;
GRAM-NEGATIVE BACTERIA; VERSUS-HOST-DISEASE; MASS-SPECTROMETRY; LUNG
INJURY; PATHOGEN RECOGNITION; VARIABLE SELECTION; STATISTICAL-MODEL;
INNATE IMMUNITY
AB Allogeneic hematopoietic stem cell transplantation (SCT) is the only curative therapy for many malignant and non-malignant conditions. Idiopathic pneumonia syndrome (IPS) is a frequently fatal complication that limits successful outcomes. Preclinical models suggest that IPS represents an immune mediated attack on the lung involving elements of both the adaptive and the innate immune system. However, the etiology of IPS in humans is less well understood. To explore the disease pathway and uncover potential biomarkers of disease, we performed two separate label-free, proteomics experiments defining the plasma protein profiles of allogeneic SCT patients with IPS. Samples obtained from SCT recipients without complications served as controls. The initial discovery study, intended to explore the disease pathway in humans, identified a set of 81 IPS-associated proteins. These data revealed similarities between the known IPS pathways in mice and the condition in humans, in particular in the acute phase response. In addition, pattern recognition pathways were judged to be significant as a function of development of IPS, and from this pathway we chose the lipopolysaccaharide-binding protein (LBP) protein as a candidate molecular diagnostic for IPS, and verified its increase as a function of disease using an ELISA assay. In a separately designed study, we identified protein-based classifiers that could predict, at day 0 of SCT, patients who: 1) progress to IPS and 2) respond to cytokine neutralization therapy. Using cross-validation strategies, we built highly predictive classifier models of both disease progression and therapeutic response. In sum, data generated in this report confirm previous clinical and experimental findings, provide new insights into the pathophysiology of IPS, identify potential molecular classifiers of the condition, and uncover a set of markers potentially of interest for patient stratification as a basis for individualized therapy. Molecular & Cellular Proteomics 11: 10.1074/mcp.M111.015479, 1-15, 2012.
C1 [Schlatzer, Daniela M.; Dazard, Jean-Eudes; Ewing, Rob M.; Ilchenko, Serguei; Tomcheko, Sara E.; Chance, Mark R.] Case Western Reserve Univ, Sch Med, Ctr Prote & Bioinformat, Cleveland, OH 44106 USA.
[Ewing, Rob M.; Chance, Mark R.] Case Western Reserve Univ, Sch Med, Dept Genet, Cleveland, OH 44106 USA.
[Eid, Saada; Cooke, Kenneth R.] Case Western Reserve Univ, Sch Med, Dept Pediat, Cleveland, OH 44106 USA.
[Ho, Vincent] Univ Michigan, Dept Pediat, Blood & Marrow Transplantat Program, Ann Arbor, MI 48109 USA.
[Yanik, Greg] Dana Farber Canc Inst, Dept Med Oncol, Blood & Marrow Transplantat Program, Boston, MA 02115 USA.
RP Chance, MR (reprint author), Case Western Reserve Univ, Sch Med, Ctr Prote & Bioinformat, 10900 Euclid Ave,BRB 930, Cleveland, OH 44106 USA.
EM mark.chance@case.edu
OI Dazard, Jean-Eudes/0000-0003-4720-3684; Ewing, Rob/0000-0001-6510-4001
FU Burroughs Wellcome Fund; Leukemia and Lymphoma Society; Case Western
Reserve University/Cleveland Clinic CTSA from the National Center for
Research Resources (NCRR), National Institutes of Health and NIH Roadmap
for Medical Research [UL1 R024989]; Case Comprehensive Cancer Center
[P30-CA04370]
FX This work was supported by Burroughs Wellcome Fund, The Leukemia and
Lymphoma Society, and the Case Western Reserve University/Cleveland
Clinic CTSA (Grant Number UL1 R024989) from the National Center for
Research Resources (NCRR), a component of the National Institutes of
Health and NIH Roadmap for Medical Research. We also acknowledge support
from the Case Comprehensive Cancer Center Core Grant (P30-CA04370).
NR 73
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Z9 3
U1 0
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 1535-9476
EI 1535-9484
J9 MOL CELL PROTEOMICS
JI Mol. Cell. Proteomics
PD JUN
PY 2012
VL 11
IS 6
AR M111.015479
DI 10.1074/mcp.M111.015479
PG 15
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 974CX
UT WOS:000306408500033
PM 22337588
ER
PT J
AU Zhong, J
Kim, MS
Chaerkady, R
Wu, XY
Huang, TC
Getnet, D
Mitchell, CJ
Palapetta, SM
Sharma, J
O'Meally, RN
Cole, RN
Yoda, A
Moritz, A
Loriaux, MM
Rush, J
Weinstock, DM
Tyner, JW
Pandey, A
AF Zhong, Jun
Kim, Min-Sik
Chaerkady, Raghothama
Wu, Xinyan
Huang, Tai-Chung
Getnet, Derese
Mitchell, Christopher J.
Palapetta, Shyam M.
Sharma, Jyoti
O'Meally, Robert N.
Cole, Robert N.
Yoda, Akinori
Moritz, Albrecht
Loriaux, Marc M.
Rush, John
Weinstock, David M.
Tyner, Jeffrey W.
Pandey, Akhilesh
TI TSLP Signaling Network Revealed by SILAC-Based Phosphoproteomics
SO MOLECULAR & CELLULAR PROTEOMICS
LA English
DT Article
ID THYMIC STROMAL LYMPHOPOIETIN; ACUTE LYMPHOBLASTIC-LEUKEMIA;
PROTEIN-TYROSINE-PHOSPHATASE; CHRONIC LYMPHOCYTIC-LEUKEMIA; STEM-CELL
DIFFERENTIATION; BTK INHIBITOR PCI-32765; HUMAN EPITHELIAL-CELLS;
ABL-POSITIVE CELLS; N-TERMINAL KINASE; IGM(+) B-CELLS
AB Thymic stromal lymphopoietin (TSLP) is a cytokine that plays diverse roles in the regulation of immune responses. TSLP requires a heterodimeric receptor complex consisting of IL-7 receptor alpha subunit and its unique TSLP receptor (gene symbol CRLF2) to transmit signals in cells. Abnormal TSLP signaling (e. g. overexpression of TSLP or its unique receptor TSLPR) contributes to the development of a number of diseases including asthma and leukemia. However, a detailed understanding of the signaling pathways activated by TSLP remains elusive. In this study, we performed a global quantitative phosphoproteomic analysis of the TSLP signaling network using stable isotope labeling by amino acids in cell culture. By employing titanium dioxide in addition to antiphosphotyrosine antibodies as enrichment methods, we identified 4164 phosphopeptides on 1670 phosphoproteins. Using stable isotope labeling by amino acids in cell culture-based quantitation, we determined that the phosphorylation status of 226 proteins was modulated by TSLP stimulation. Our analysis identified activation of several members of the Src and Tec families of kinases including Btk, Lyn, and Tec by TSLP for the first time. In addition, we report TSLP-induced phosphorylation of protein phosphatases such as Ptpn6 (SHP-1) and Ptpn11 (Shp2), which has also not been reported previously. Co-immunoprecipitation assays showed that Shp2 binds to the adapter protein Gab2 in a TSLP-dependent manner. This is the first demonstration of an inducible protein complex in TSLP signaling. A kinase inhibitor screen revealed that pharmacological inhibition of PI-3 kinase, Jak family kinases, Src family kinases or Btk suppressed TSLP-dependent cellular proliferation making them candidate therapeutic targets in diseases resulting from aberrant TSLP signaling. Our study is the first phosphoproteomic analysis of the TSLP signaling pathway that greatly expands our understanding of TSLP signaling and provides novel therapeutic targets for TSLP/TSLPR-associated diseases in humans. Molecular & Cellular Proteomics 11: 10.1074/mcp.M112.017764, 1-22, 2012.
C1 [Zhong, Jun; Kim, Min-Sik; Chaerkady, Raghothama; Wu, Xinyan; Huang, Tai-Chung; Getnet, Derese; Mitchell, Christopher J.; Pandey, Akhilesh] Johns Hopkins Univ, Sch Med, McKusick Nathans Inst Genet Med, Baltimore, MD 21205 USA.
[Zhong, Jun; Kim, Min-Sik; Chaerkady, Raghothama; Wu, Xinyan; Huang, Tai-Chung; Getnet, Derese; Mitchell, Christopher J.; Pandey, Akhilesh] Johns Hopkins Univ, Sch Med, Dept Biol Chem, Baltimore, MD 21205 USA.
[Zhong, Jun; Kim, Min-Sik; Chaerkady, Raghothama; Wu, Xinyan; Huang, Tai-Chung; Getnet, Derese; Mitchell, Christopher J.; Pandey, Akhilesh] Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21205 USA.
[Zhong, Jun; Kim, Min-Sik; Chaerkady, Raghothama; Wu, Xinyan; Huang, Tai-Chung; Getnet, Derese; Mitchell, Christopher J.; Pandey, Akhilesh] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
[O'Meally, Robert N.; Cole, Robert N.] Johns Hopkins Univ, Sch Med, Inst Basic Biomed Sci, Mass Spectrometry & Prote Facil, Baltimore, MD 21205 USA.
[Mitchell, Christopher J.] Johns Hopkins Univ, Sch Med, Grad Program Biochem Cellular & Mol Biol, Baltimore, MD 21205 USA.
[Chaerkady, Raghothama; Palapetta, Shyam M.; Sharma, Jyoti] Inst Bioinformat, Bangalore 560066, Karnataka, India.
[Palapetta, Shyam M.] Pondicherry Univ, Sch Life Sci, Ctr Excellence Bioinformat, Pondicherry 605014, India.
[Sharma, Jyoti] Manipal Univ, Manipal 576104, Karnataka, India.
[Yoda, Akinori; Weinstock, David M.] Harvard Univ, Dana Farber Canc Inst, Sch Med, Dept Med Oncol, Boston, MA 02115 USA.
[Moritz, Albrecht; Rush, John] Cell Signaling Technol Inc, Danvers, MA 01923 USA.
[Loriaux, Marc M.] Oregon Hlth & Sci Univ, Dept Anat Pathol, Knight Canc Inst, Portland, OR 97239 USA.
[Tyner, Jeffrey W.] Oregon Hlth & Sci Univ, Div Hematol & Med Oncol, Knight Canc Inst, Portland, OR 97239 USA.
RP Pandey, A (reprint author), Johns Hopkins Univ, Sch Med, McKusick Nathans Inst Genet Med, 733 N Broadway,BRB Room 527, Baltimore, MD 21205 USA.
EM pandey@jhmi.edu
RI Zhong, Jun/D-1662-2010; Pandey, Akhilesh/B-4127-2009; Kim,
Min-Sik/M-3488-2016;
OI Zhong, Jun/0000-0003-3148-4143; Pandey, Akhilesh/0000-0001-9943-6127;
Kim, Min-Sik/0000-0001-7317-5360; Huang, Tai-Chung/0000-0002-1625-7295;
Tyner, Jeffrey/0000-0002-2133-0960; Palapetta, Shyam
Mohan/0000-0002-7674-1310
FU Department of Biotechnology, Government of India; Council of Scientific
and Industrial Research (CSIR), Government of India; National Heart Lung
and Blood Institute [HHSN268201000032C]; National Institutes of Health
(NIH) [S10RR023025]; NIH Roadmap grant "Technology Center for Networks
and Pathways" [U54 RR 020839]
FX We thank the Department of Biotechnology, Government of India for
research support to the Institute of Bioinformatics. Shyam M. Palapetta
and Jyoti Sharma are recipients of a Senior Research Fellowship from the
Council of Scientific and Industrial Research (CSIR), Government of
India. We thank Bernard Delanghe (Thermo Fisher Scientific (Bremen)
GmbH, Bremen, Germany) for providing access to the Proteome Discoverer
platform.; The work was supported by a contract HHSN268201000032C from
the National Heart Lung and Blood Institute (R. N. C. and A. P.) and by
a grant S10RR023025 from the High End Instrumentation Program of the
National Institutes of Health (NIH) (A. P.) and an NIH Roadmap grant
"Technology Center for Networks and Pathways" U54 RR 020839 (A. P.).
NR 142
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U1 0
U2 4
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 1535-9476
EI 1535-9484
J9 MOL CELL PROTEOMICS
JI Mol. Cell. Proteomics
PD JUN
PY 2012
VL 11
IS 6
AR M112.017764
DI 10.1074/mcp.M112.017764
PG 22
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 974CX
UT WOS:000306408500034
PM 22345495
ER
PT J
AU Oppenheim, CE
AF Oppenheim, Claire E.
TI Nelson Mandela and the Power of Ubuntu
SO RELIGIONS
LA English
DT Article
DE Ubuntu; botho; unity; community; Afro-communitarianism; humanity;
apartheid
AB Nelson Mandela dedicated his life to fighting for the freedom of his South African kin of all colors against the institution of apartheid. He spent twenty-seven years fighting from within prison, only gaining his freedom when his fellow South Africans could claim it as well. This article demonstrates how his faith, his spiritual development and his noble purpose can be conceptualized through the lens of Ubuntu: the African ethic of community, unity, humanity and harmony.
C1 Massachusetts Gen Hosp, Erich Lindemann Mental Hlth Ctr, Boston, MA 02114 USA.
RP Oppenheim, CE (reprint author), Massachusetts Gen Hosp, Erich Lindemann Mental Hlth Ctr, 25 Staniford St,2nd Floor, Boston, MA 02114 USA.
EM claireoppenheim@gmail.com
NR 4
TC 4
Z9 5
U1 0
U2 6
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 2077-1444
J9 RELIGIONS
JI Religions
PD JUN
PY 2012
VL 3
IS 2
BP 369
EP 388
DI 10.3390/rel3020369
PG 20
WC Religion
SC Religion
GA 175SR
UT WOS:000321253800014
ER
PT J
AU Guanci, MM
AF Guanci, Mary McKenna
TI Our hospital is new at using hypothermia following cardiac arrest and it
usually does not get started until the patient reaches the cardiac
intensive care unit. The doctors want to complete the cardiac
catheterization procedure first. Are there any suggestions for getting
hypothermia started sooner?
SO THERAPEUTIC HYPOTHERMIA AND TEMPERATURE MANAGEMENT
LA English
DT Letter
C1 Massachusetts Gen Hosp, Neurosci ICU, Boston, MA 02114 USA.
RP Guanci, MM (reprint author), Massachusetts Gen Hosp, Neurosci ICU, Boston, MA 02114 USA.
NR 5
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 2153-7658
EI 2153-7933
J9 THER HYPOTHERMIA TEM
JI Ther. Hypothermia Temp. Manag.
PD JUN 1
PY 2012
VL 2
IS 2
BP 99
EP 99
PG 1
WC Critical Care Medicine
SC General & Internal Medicine
GA V38PK
UT WOS:000209355100012
ER
PT J
AU Nakhlis, F
Golshan, M
AF Nakhlis, Faina
Golshan, Mehra
TI Bevacizumab: where do we go from here in breast cancer?
SO TRANSLATIONAL CANCER RESEARCH
LA English
DT Article
C1 Harvard Univ, Sch Med, Dept Surg, Brigham & Womens Faulkner Hosp, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Golshan, M (reprint author), Brigham & Womens Hosp, Dept Surg, 75 Francis St, Boston, MA 02115 USA.
EM mgolshan@partners.org
NR 2
TC 4
Z9 6
U1 0
U2 0
PU AME PUBL CO
PI SHEUNG WAN
PA ROOM 604 6-F HOLLYWOOD CENTER, 77-91, QUEENS ROAD, SHEUNG WAN, HONG KONG
00000, PEOPLES R CHINA
SN 2218-676X
EI 2219-6803
J9 TRANSL CANCER RES
JI Transl. Cancer Res.
PD JUN
PY 2012
VL 1
IS 1
BP 55
EP 56
DI 10.3978/j.issn.2218-676X.2012.03.01
PG 2
WC Oncology
SC Oncology
GA V42VY
UT WOS:000209642500009
ER
PT J
AU Yang, YR
Song, M
Lee, H
Jeon, Y
Choi, EJ
Jang, HJ
Moon, HY
Byun, HY
Kim, EK
Kim, DH
Lee, MN
Koh, A
Ghim, J
Choi, JH
Lee-Kwon, W
Kim, KT
Ryu, SH
Suh, PG
AF Yang, Yong Ryoul
Song, Minseok
Lee, Ho
Jeon, Yoon
Choi, Eun-Jeong
Jang, Hyun-Jun
Moon, Hyo Youl
Byun, Ha-Young
Kim, Eung-Kyun
Kim, Dae Hyun
Lee, Mi Nam
Koh, Ara
Ghim, Jaewang
Choi, Jang Hyun
Lee-Kwon, Whaseon
Kim, Kyong Tai
Ryu, Sung Ho
Suh, Pann-Ghill
TI O-GlcNAcase is essential for embryonic development and maintenance of
genomic stability
SO AGING CELL
LA English
DT Article
DE aging; genomic instability; O-GlcNAcase; O-GlcNAcylation; O-GlcNAc
transferase
ID BETA-N-ACETYLGLUCOSAMINE; RNA-POLYMERASE-II; DEPENDENT PHOSPHORYLATION;
MITOTIC PROGRESSION; TERMINAL DOMAIN; XENOPUS-LAEVIS; SPINDLE POLES;
X-CHROMOSOME; PROTEIN; TRANSFERASE
AB Dysregulation of O-GlcNAc modification catalyzed by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA) contributes to the etiology of chronic diseases of aging, including cancer, cardiovascular disease, type 2 diabetes, and Alzheimers disease. Here we found that natural aging in wild-type mice was marked by a decrease in OGA and OGT protein levels and an increase in O-GlcNAcylation in various tissues. Genetic disruption of OGA resulted in constitutively elevated O-GlcNAcylation in embryos and led to neonatal lethality with developmental delay. Importantly, we observed that serum-stimulated cell cycle entry induced increased O-GlcNAcylation and decreased its level after release from G2/M arrest, indicating that O-GlcNAc cycling by OGT and OGA is required for precise cell cycle control. Constitutively, elevated O-GlcNAcylation by OGA disruption impaired cell proliferation and resulted in mitotic defects with downregulation of mitotic regulators. OGA loss led to mitotic defects including cytokinesis failure and binucleation, increased lagging chromosomes, and micronuclei formation. These findings suggest an important role for O-GlcNAc cycling by OGA in embryonic development and the regulation of the maintenance of genomic stability linked to the aging process.
C1 [Yang, Yong Ryoul; Choi, Eun-Jeong; Jang, Hyun-Jun; Byun, Ha-Young; Kim, Eung-Kyun; Lee, Mi Nam; Koh, Ara; Ghim, Jaewang; Kim, Kyong Tai; Ryu, Sung Ho; Suh, Pann-Ghill] Pohang Univ Sci & Technol, Div Mol & Life Sci, Pohang 790784, Kyungbuk, South Korea.
[Yang, Yong Ryoul; Jang, Hyun-Jun; Moon, Hyo Youl; Byun, Ha-Young; Kim, Eung-Kyun; Kim, Dae Hyun; Lee-Kwon, Whaseon; Suh, Pann-Ghill] Ulsan Natl Inst Sci & Technol, Sch Nanobiotechnol & Chem Engn, Ulsan 689798, South Korea.
[Song, Minseok] Weill Cornell Med Coll, Dept Psychiat, New York, NY 10065 USA.
[Lee, Ho; Jeon, Yoon] Natl Canc Ctr, Canc Expt Resources Branch, Goyang Si 410769, Gyeonggi Do, South Korea.
[Moon, Hyo Youl] Pohang Univ Sci & Technol, Sch Interdisciplinary Biosci & Bioengn, Pohang 790784, South Korea.
[Choi, Jang Hyun] Dana Farber Canc Inst, Div Metab & Chron Dis, Boston, MA 02115 USA.
[Choi, Jang Hyun] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
RP Suh, PG (reprint author), Pohang Univ Sci & Technol, Div Mol & Life Sci, Pohang 790784, Kyungbuk, South Korea.
EM pgsuh@unist.ac.kr
RI Choi, Jang Hyun/B-3055-2012
FU National Research Foundation of Korea [PGB013]; Korean Government
[KRF-2007-341-C00027, 2010-0029434]; Korean Ministry of Education,
Science and Technology (Anti-aging and Well-being Research Center)
FX This work was supported by the National Research Foundation of Korea
Grant funded by the Korean Government (KRF-2007-341-C00027), a grant
from the Korean Ministry of Education, Science and Technology (The
Regional Core Research Program/Anti-aging and Well-being Research
Center), the National Research Foundation of Korea Grant funded by the
Korean government (no. 2010-0029434), and the Fusion Pioneer Project
(PGB013) from the National Research Foundation of Korea.
NR 43
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U1 0
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1474-9718
J9 AGING CELL
JI Aging Cell
PD JUN
PY 2012
VL 11
IS 3
BP 439
EP 448
DI 10.1111/j.1474-9726.2012.00801.x
PG 10
WC Cell Biology; Geriatrics & Gerontology
SC Cell Biology; Geriatrics & Gerontology
GA 940RG
UT WOS:000303910100009
PM 22314054
ER
PT J
AU Allen, NE
Javdani, S
Lehrner, AL
Walden, AL
AF Allen, Nicole E.
Javdani, Shabnam
Lehrner, Amy L.
Walden, Angela L.
TI "Changing the Text": Modeling Council Capacity to Produce
Institutionalized Change
SO AMERICAN JOURNAL OF COMMUNITY PSYCHOLOGY
LA English
DT Article
DE Councils; Institutionalized change; Coordinating councils; Coalitions;
Domestic violence; Intimate partner violence; Interagency coordination
ID VIOLENCE COORDINATING COUNCILS; COMMUNITY-HEALTH COALITIONS;
SUBSTANCE-ABUSE PREVENTION; GOVERNANCE PROCESSES; PARTICIPATION;
EMPOWERMENT; PARTNERSHIPS; OUTCOMES; IMPLEMENTATION; PERSPECTIVE
AB Collaboration is a ubiquitous approach to change, but is notoriously difficult and not definitively linked to desirable outcomes. Not surprisingly, the collaboration literature is replete with numerous facilitators and barriers to collaborative efforts. The current study aimed to develop a parsimonious model of factors influencing the success of collaborative efforts both internal and external to the council, including, (a) features of the council environment, (b) intermediate outcomes including the empowerment of members in the council context and the degree to which councils have generated social capital and (c) the extent to which collaborative efforts are occurring in a community context supportive of their aims. In particular, this study examines whether these factors affect the extent to which councils are positioned to achieve institutionalized change, or changes "in the text" that govern front line providers' (e.g., police, advocates) practices in the community response to intimate partner violence. Results suggest that perceived member empowerment, generation of social capital, and supportive community context are the most important predictors of the extent to which councils foster shifts in institutionalized change. Features of the council environment are only indirectly related to the degree to which institutionalized change is ultimately fostered as mediated by the generation of social capital. This suggests that the ability of members to act as change agents and the extent to which those in power support council efforts figure more prominently to facilitate or constrain council efforts than council functioning itself.
C1 [Allen, Nicole E.; Javdani, Shabnam; Walden, Angela L.] Univ Illinois, Dept Psychol, Champaign, IL 61820 USA.
[Lehrner, Amy L.] James J Peters VA Med Ctr, Traumat Stress Studies Div, Bronx, NY USA.
RP Allen, NE (reprint author), Univ Illinois, Dept Psychol, 603 E Daniel St, Champaign, IL 61820 USA.
EM allenne@illinois.edu
OI Javdani, Shabnam/0000-0003-3949-1970
NR 50
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U1 2
U2 11
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0091-0562
J9 AM J COMMUN PSYCHOL
JI Am. J. Community Psychol.
PD JUN
PY 2012
VL 49
IS 3-4
BP 317
EP 331
DI 10.1007/s10464-011-9460-z
PG 15
WC Public, Environmental & Occupational Health; Psychology,
Multidisciplinary; Social Work
SC Public, Environmental & Occupational Health; Psychology; Social Work
GA 939HR
UT WOS:000303800600002
PM 21842302
ER
PT J
AU Cashman, EC
Smyth, D
AF Cashman, Emma Catherine
Smyth, David
TI Primary headache syndromes and sinus headache: An approach to diagnosis
and management
SO AURIS NASUS LARYNX
LA English
DT Review
DE Headache; Migraine; Sinus; FESS
ID TRIGEMINAL-AUTONOMIC CEPHALALGIAS; TENSION-TYPE HEADACHE; CLUSTER
HEADACHE; MIGRAINE; PREVALENCE
AB Chronic rhinosinusitis (CRS) and primary headache syndromes are common disease entities and headache and facial pain are common reasons for referral to otolaryngology units. Because of an association of nasal symptoms with primary headache syndromes and considerable similarities in their clinical presentations, primary headache syndromes may be misdiagnosed as sinus disease and vice versa. In this review we examine the evidence on which otolaryngologists can base clinical diagnosis and management and offer an approach to distinguishing these common clinical entities. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
C1 [Cashman, Emma Catherine] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Smyth, David] Waterford Reg Hosp, Dept Otolaryngol, Waterford, Ireland.
RP Cashman, EC (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Longwood Ave, Boston, MA 02115 USA.
EM emma_cashman@dfci.harvard.ie
NR 28
TC 3
Z9 4
U1 0
U2 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0385-8146
J9 AURIS NASUS LARYNX
JI Auris Nasus Larynx
PD JUN
PY 2012
VL 39
IS 3
BP 257
EP 260
DI 10.1016/j.anl.2011.05.003
PG 4
WC Otorhinolaryngology
SC Otorhinolaryngology
GA 937WT
UT WOS:000303695200001
PM 21862253
ER
PT J
AU Gunduz-Bruce, H
Reinhart, RMG
Roach, BJ
Gueorguieva, R
Oliver, S
D'Souza, DC
Ford, JM
Krystal, JH
Mathalon, DH
AF Gunduz-Bruce, Handan
Reinhart, Robert M. G.
Roach, Brian J.
Gueorguieva, Ralitza
Oliver, Stephen
D'Souza, Deepak C.
Ford, Judith M.
Krystal, John H.
Mathalon, Daniel H.
TI Glutamatergic Modulation of Auditory Information Processing in the Human
Brain
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Glutamate; ketamine; MMN; N-acetylcysteine; NMDA; P300
ID MISMATCH NEGATIVITY MMN; HUMAN SELECTIVE ATTENTION; N-ACETYL-CYSTEINE;
HEALTHY-VOLUNTEERS; P300 AMPLITUDE; GLUTATHIONE PRECURSOR;
MENSTRUAL-CYCLE; SYSTEM X(C)(-); IN-VIVO; SCHIZOPHRENIA
AB Background: Auditory mismatch negativity (MMN) and P300 event-related potentials (ERPs) are reduced in schizophrenia patients and healthy volunteers administered the N-methyl-D-aspartate glutamate receptor antagonist, ketamine. In rodents, N-acetylcysteine (NAC), a stimulator of the cystine-glutamate exchanger, attenuates the cognitive and behavioral effects of N-methyl-D-aspartate receptor antagonists. On the basis of these findings, we tested whether NAC would reduce ketamine effects on behavior, MMN, and P300 in healthy humans.
Methods: This randomized, double-blind, placebo-controlled study consisted of 2 test days during which subjects (n = 16) were administered oral NAC (3000 mg in divided doses) or matching placebo 165 min before the infusion of saline and then ketamine (as a bolus of .23 mg/kg over 1 min followed by .58 mg/kg for 30 min, and then .29 mg/kg for 40 min) in a fixed order. Behavioral and ERP data including auditory MMN and P300 were collected during each test day.
Results: Ketamine produced psychotic-like positive symptoms, reductions in working memory and sustained attention performance, and amplitude reductions for the frequency- and intensity-deviant MMNs and P300. NAC pretreatment did not reduce the behavioral or ERP effects of ketamine. In addition, NAC reduced frequency-deviant MMN amplitude and increased target and novelty P3 amplitudes. The decrements in frequency-deviant MMN amplitude produced by ketamine and NAC were not additive.
Conclusions: NAC did not attenuate the effects of ketamine in humans, in contrast to previous studies in animals. NAC merits further investigation as a cognitive enhancing agent due to its ability to increase the P300 amplitude.
C1 [Gunduz-Bruce, Handan; D'Souza, Deepak C.; Krystal, John H.] VA Connecticut Healthcare Syst, West Haven, CT 06516 USA.
[Gunduz-Bruce, Handan; Gueorguieva, Ralitza; Oliver, Stephen; D'Souza, Deepak C.; Ford, Judith M.; Krystal, John H.; Mathalon, Daniel H.] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA.
[Reinhart, Robert M. G.] Vanderbilt Univ, Dept Psychol, Nashville, TN 37240 USA.
[Ford, Judith M.; Mathalon, Daniel H.] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA.
[Ford, Judith M.; Mathalon, Daniel H.] San Francisco Vet Adm Med Ctr, San Francisco, CA USA.
RP Gunduz-Bruce, H (reprint author), VA Connecticut Healthcare Syst, 116-A,950 Campbell Ave, West Haven, CT 06516 USA.
EM handan.gunduz-bruce@yale.edu
OI Roach, Brian/0000-0002-3264-1465; Mathalon, Daniel/0000-0001-6090-4974;
Gueorguieva, Ralitza/0000-0003-0944-5973
FU National Alliance for Research in Schizophrenia and Affective Disorders
(NARSAD); National Institute on Alcohol Abuse and Alcoholism [K05 AA
14906, 2P50 AA 012870]; US Department of Veterans Affairs Alcohol
Research Center, National Center Post Traumatic Stress Disorder,
Clinical Neurosciences Division, West Haven, Connecticut; VA
Schizophrenia Biological Research Center; National Institute of Mental
Health [MH40052, MH 58262, MH067967]; Astra Zeneca; Abbott Laboratories;
Eli Lilly; Organon; Pfizer; Sanofi; Department of Veterans Affairs;
Janssen Research Foundation; [R01 MH076989]
FX This study was supported by a National Alliance for Research in
Schizophrenia and Affective Disorders (NARSAD) Hammerschlag Young
Investigator Award to Dr. Gunduz-Bruce. Part of the data was previously
presented as a poster at the 2007 annual meeting of the American College
of Neuropsychopharmacology. We are thankful to the Biostudies Laboratory
Nursing Staff; Angelina M. Genovese, RNC, MBA; Elizabeth O'Donnell, RN;
Michelle Sanpedro, RN; and Brenda Breault, RN, BSN, for their
outstanding nursing; and Sonah Perry, R.Ph., for excellent Research
Pharmacy support. We also thank all the research participants. This
study was also partly supported by funding from the National Institute
on Alcohol Abuse and Alcoholism, K05 AA 14906, National Institute on
Alcohol Abuse and Alcoholism, 2P50 AA 012870, US Department of Veterans
Affairs Alcohol Research Center, National Center Post Traumatic Stress
Disorder, Clinical Neurosciences Division, West Haven, Connecticut, to
JHK; R01 MH076989 to DHM; VA Schizophrenia Biological Research Center,
and grants from the National Institute of Mental Health (MH40052, MH
58262, MH067967) and NARSAD to JMF.; Drs. Gunduz-Bruce, Gueorguieva,
Ford, and Mathalon and Mr. Reinhart, Mr. Roach, and Mr. Oliver report no
biomedical financial interests or potential conflict of interests. Dr.
D'Souza reports research grant support from Astra Zeneca, Abbott
Laboratories, Eli Lilly, Organon, Pfizer, and Sanofi. Dr. Krystal
reports serving as consultant for the following companies (the
Individual Consultant Agreements listed are <$10,000/year): Aisling
Capital, LLC, AstraZeneca Pharmaceuticals, Brintnall and Nicolini,
Easton Associates, Gilead Sciences, GlaxoSmith-Kline, Janssen
Pharmaceuticals, Lundbeck Research USA, Medivation, Merz
Pharmaceuticals, MK Medical Communications, F. Hoffmann-La Roche, SK
Holdings, Takeda Industries, and Teva Pharmaceutical Industries. Dr.
Krystal also serves for the Scientific Advisory Board of Abbott
Laboratories, Bristol-Myers Squibb, Eisai, Eli Lilly, Forest
Laboratories, Lohocla Research Corporation, Mnemosyne Pharmaceuticals,
Naurex, Pfizer Pharmaceuticals, and Shire Pharmaceuticals. Dr. Krystal
holds Exercisable Warrant Options that include Tetragenex
Pharmaceuticals (value <$150), and he serves as Board of Directors for
the Coalition for Translational Research in Alcohol and Substance Use
Disorders. Dr. Krystal is a President Elect for American College of
Neuropsychopharmacology and receives research support from Department of
Veterans Affairs and Janssen Research Foundation (provided drug and some
study support to the Department of Veterans Affairs). Dr. Krystal
receives >$10,000 as the Editor of Biological Psychiatry. Patents and
Inventions for Dr. Krystal include: 1) Seibyl JP, Krystal JH, Charney
DS. Dopamine and noradrenergic reuptake inhibitors in treatment of
schizophrenia. Patent #:5,447,948. September 5, 1995; 2) co-inventor
with Dr. Gerard Sanacora on a filed patent application by Yale
University related to targeting the glutamatergic system for the
treatment of neuropsychiatric disorders (PCTWO06108055A1); and 3)
Intranasal Administration of Ketamine to Treat Depression (pending).
NR 75
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U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD JUN 1
PY 2012
VL 71
IS 11
BP 969
EP 977
DI 10.1016/j.biopsych.2011.09.031
PG 9
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 939MH
UT WOS:000303814800009
PM 22036036
ER
PT J
AU Yomogida, K
Chou, Y
Pang, J
Baravati, B
Maniaci, BJ
Wu, S
Zhu, Y
Chu, CQ
AF Yomogida, Kentaro
Chou, Yuan
Pang, Jonathan
Baravati, Bobby
Maniaci, Brian J.
Wu, Shili
Zhu, Yong
Chu, Cong-Qiu
TI Streptavidin suppresses T cell activation and inhibits IL-2 production
and CD25 expression
SO CYTOKINE
LA English
DT Article
DE Streptavidin; Biotin; T Cell activation; Interleukin 2; Interleukin 2
receptor
ID JURKAT CELLS; PRETARGETED RADIOIMMUNOTHERAPY; RENAL-TRANSPLANTATION;
CHAIN IMMUNOTOXIN; BIOTIN DEFICIENCY; BINDING-PROTEIN; FUSION PROTEIN;
REJECTION; DIFFERENTIATION; BIOTINYLATION
AB Streptavidin is widely used as a detection tool in biology research because of its high affinity and specificity binding to biotin. Biotin-streptavidin system has also been explored for detection of infection and tumor in clinical medicine. Here, we show immunosuppressive property of streptavidin on T cell activation and proliferation. Upon CD3 and CD28 stimulation, CD4(+) T cells produce interleukin 2 (IL-2) and express IL-2 receptor alpha chain (CD25). Addition of streptavidin in T cell culture suppressed IL-2 synthesis and CD25 expression with no cytotoxicity. The immunosuppressive effect of streptavidin was reversed by excessive biotin. Conjugated to a single chain anti-CD7 variable fragment (scFvCD7), streptavidin was directly delivered to T cells and showed substantially more profound suppressive effect on T cell activation. These results suggest that streptavidin could potentially be used as a novel immunomodulator. Published by Elsevier Ltd.
C1 [Yomogida, Kentaro; Chou, Yuan; Chu, Cong-Qiu] Oregon Hlth & Sci Univ, Div Arthrit & Rheumat Dis, Portland, OR USA.
[Yomogida, Kentaro; Chou, Yuan; Chu, Cong-Qiu] Portland VA Med Ctr, Portland, OR USA.
[Pang, Jonathan; Baravati, Bobby; Maniaci, Brian J.; Wu, Shili; Zhu, Yong] VivoScript Inc, Costa Mesa, CA USA.
RP Chu, CQ (reprint author), 3181 SW Sam Jackson Pk Rd 0P09, Portland, OR 97239 USA.
EM chuc@ohsu.edu
FU NIH [AR055254]; Portland VA Medical Center
FX This work was supported by a Grant from NIH to C.Q.C. (AR055254) and
Portland VA Medical Center.
NR 46
TC 4
Z9 6
U1 0
U2 1
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD JUN
PY 2012
VL 58
IS 3
BP 431
EP 436
DI 10.1016/j.cyto.2012.02.007
PG 6
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 941FA
UT WOS:000303947900018
PM 22410319
ER
PT J
AU Walker, DD
Reeves, TD
de Costa, AM
Schuyler, C
Young, MRI
AF Walker, David D.
Reeves, Travis D.
de Costa, Anna-Maria
Schuyler, Corinne
Young, M. Rita I.
TI Immunological modulation by 1 alpha,25-dihydroxyvitamin D-3 in patients
with squamous cell carcinoma of the head and neck
SO CYTOKINE
LA English
DT Article
DE Cytokines; Head and neck cancer; HNSCC; Vitamin D
ID ENDOTHELIAL GROWTH-FACTOR; CANCER-PATIENTS; PERIPHERAL-BLOOD; CD34(+)
CELLS; DENDRITIC CELLS; VITAMIN-D; IMMUNITY; DIFFERENTIATION;
CARCINOGENESIS; IMMUNOTHERAPY
AB Prior studies showing that treatment of head and neck squamous cell carcinoma (HNSCC) patients with 1 alpha,25-dihydroxyvitamin D-3 [1,25(OH)(2)D-3] stimulated intratumoral immune infiltration were extended to analysis of cytokine profiles in the periphery and in oral tissues. Most prominent was the disparity between cytokine levels in plasma and in either pathologically normal oral tissue or HNSCC tissue from patients that were untreated or treated with 1,25(OH)(2)D-3. Levels of IL-6 and IL-10, but not IL-2, IFN-gamma or TNF-alpha, tended to be increased in the plasma of HNSCC patients and 1,25(OH)(2)D-3 further increased plasma levels of all of these cytokines. While these cytokines tended to be increased in HNSCC tissue, 1,25(OH)(2)D-3 resulted in variable cytokine responses that showed a general tendency toward further increased levels. Levels of IL-8 and VEGF were increased in plasma and tissue of untreated HNSCC patients, and were further increased in plasma, but not in tissues, of patients treated with 1,25(OH)(2)D-3. Levels of IL-1 alpha and IL-1 beta were similar in plasma of controls and HNSCC patients, but were increased in HNSCC tissues. In contrast to that seen in plasma where 1,25(OH)(2)D-3 increased levels of IL-1 alpha and IL-1 beta, this was not seen in tissue following 1,25(OH)(2)D-3 treatment. These results show a discordant relationship between systemic and intratumoral cytokine profiles and suggest a tendency of 1,25(OH)(2)D(3)to increase a multitude of cytokines within tumor tissue. Published by Elsevier Ltd.
C1 [Walker, David D.; Reeves, Travis D.; Young, M. Rita I.] Ralph H Johnson VA Med Ctr, Res Serv, Charleston, SC 29401 USA.
[de Costa, Anna-Maria] Med Univ S Carolina, Dept Otolaryngol, Charleston, SC USA.
Med Univ S Carolina, Dept Microbiol & Immunol, Charleston, SC USA.
[Young, M. Rita I.] Med Univ S Carolina, Dept Med, Charleston, SC USA.
RP Young, MRI (reprint author), Ralph H Johnson VA Med Ctr, Res Serv, 109 Bee St, Charleston, SC 29401 USA.
EM david.walker4@gmail.com; reevestd@musc.edu; clarkann@musc.edu;
schuylec@musc.edu; rita.young@va.gov
FU Biomedical Laboratory and Clinical Sciences of the Department of
Veterans Affairs; National Institute of Health [I01-CX000100,
R01-CA128837, R01-DE018268]
FX This work has been supported by awards from the Biomedical Laboratory
and Clinical Sciences Programs of the Department of Veterans Affairs and
by grants from the National Institute of Health (MRIY, I01-CX000100,
R01-CA128837 and R01-DE018268).
NR 28
TC 6
Z9 6
U1 0
U2 0
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD JUN
PY 2012
VL 58
IS 3
BP 448
EP 454
DI 10.1016/j.cyto.2012.03.002
PG 7
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 941FA
UT WOS:000303947900020
PM 22450225
ER
PT J
AU Zhang, HJ
Kim, A
Abraham, N
Khan, LA
Hall, DH
Fleming, JT
Gobel, V
AF Zhang, Hongjie
Kim, Ahlee
Abraham, Nessy
Khan, Liakot A.
Hall, David H.
Fleming, John T.
Gobel, Verena
TI Clathrin and AP-1 regulate apical polarity and lumen formation during C.
elegans tubulogenesis
SO DEVELOPMENT
LA English
DT Article
DE Caenorhabditis elegans; Polarity; Tubulogenesis; Clathrin; AP-1;
Sphingolipids
ID EPITHELIAL-CELL POLARITY; NEMATODE CAENORHABDITIS-ELEGANS; MICROVILLUS
INCLUSION DISEASE; RECEPTOR-MEDIATED ENDOCYTOSIS; MOLECULAR-MECHANISM;
COMPLEX; GENE; MORPHOGENESIS; MICROSCOPY; PHOSPHOINOSITIDES
AB Clathrin coats vesicles in all eukaryotic cells and has a well-defined role in endocytosis, moving molecules away from the plasma membrane. Its function on routes towards the plasma membrane was only recently appreciated and is thought to be limited to basolateral transport. Here, an unbiased RNAi-based tubulogenesis screen identifies a role of clathrin (CHC-1) and its AP-1 adaptor in apical polarity during de novo lumenal membrane biogenesis in the C. elegans intestine. We show that CHC-1/AP-1-mediated polarized transport intersects with a sphingolipid-dependent apical sorting process. Depleting each presumed trafficking component mislocalizes the same set of apical membrane molecules basolaterally, including the polarity regulator PAR-6, and generates ectopic lateral lumens. GFP::CHC-1 and BODIPY-ceramide vesicles associate perinuclearly and assemble asymmetrically at polarized plasma membrane domains in a co-dependent and AP-1-dependent manner. Based on these findings, we propose a trafficking pathway for apical membrane polarity and lumen morphogenesis that implies: (1) a clathrin/AP-1 function on an apically directed transport route; and (2) the convergence of this route with a sphingolipid-dependent apical trafficking path.
C1 [Zhang, Hongjie; Kim, Ahlee; Abraham, Nessy; Khan, Liakot A.; Fleming, John T.; Gobel, Verena] Massachusetts Gen Hosp, Dept Pediat, Boston, MA 02114 USA.
[Zhang, Hongjie; Kim, Ahlee; Abraham, Nessy; Khan, Liakot A.; Fleming, John T.; Gobel, Verena] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Hall, David H.] Yeshiva Univ Albert Einstein Coll Med, Dept Neurosci, Ctr C Elegans Anat, Bronx, NY 10461 USA.
RP Gobel, V (reprint author), Massachusetts Gen Hosp, Dept Pediat, Boston, MA 02114 USA.
EM gobel@helix.mgh.harvard.edu
FU National Institutes of Health [HD044589, GM078653]; Mattina R. Proctor
Award
FX This work was supported by the National Institutes of Health [grants
HD044589 and GM078653] and a Mattina R. Proctor Award to V.G. Deposited
in PMC for release after 12 months.
NR 55
TC 20
Z9 23
U1 0
U2 5
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0950-1991
J9 DEVELOPMENT
JI Development
PD JUN 1
PY 2012
VL 139
IS 11
BP 2071
EP 2083
DI 10.1242/dev.077347
PG 13
WC Developmental Biology
SC Developmental Biology
GA 940SV
UT WOS:000303914300023
PM 22535410
ER
PT J
AU Cortelli, JR
Fernandes, CB
Costa, FO
Cortelli, SC
Kajiya, M
Howell, SC
Kawai, T
AF Cortelli, J. R.
Fernandes, C. B.
Costa, F. O.
Cortelli, S. C.
Kajiya, M.
Howell, S. C.
Kawai, T.
TI Detection of periodontal pathogens in newborns and children with mixed
dentition
SO EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES
LA English
DT Article
ID POLYMERASE-CHAIN-REACTION; SUBGINGIVAL PLAQUE; HEALTHY-CHILDREN;
YOUNG-CHILDREN; MICROBIOTA; BACTERIA; COLONIZATION; GINGIVITIS;
PREVALENCE; SAMPLES
AB We report the age-related prevalence of red complex periodontal pathogens, , , and , along with four strains of orange complex pathogens. The bacteria present in samples isolated from tongue, cheek, and subgingival sulcus in edentulous newborns and children with mixed dentition were monitored by polymerase chain reaction (PCR). was not detected in any site of any subject in the two groups tested. However, was not only found in the 6-13 years age group, but also in edentulous newborns at a relatively high prevalence, indicating non-dentition-related colonization by . , , , , and were found in the oral cavity of most subjects belonging to the 6-13 years age group compared to newborns. This suggested a pronounced association between these colonizing bacteria and the presence of teeth. There was also a strong relation between and for their prevalence in the subgingival sulcus of the 6-13 years age group ( < 0.0001), but not in the other sites tested, suggesting that the colonization of dentition-related may be associated with the increased prevalence of non-dentition-related in the subgingival sulcus. Overall, these results suggest that dentition is a key determinant of bacterial colonization, especially orange complex bacteria and the red complex bacterium .
C1 [Cortelli, J. R.] Univ Taubate, Dept Periodontol & Prevent Dent, Dent Res Div, BR-12020040 Taubate, SP, Brazil.
[Fernandes, C. B.] Univ Taubate, Dept Periodontol, Dent Res Div, BR-12020040 Taubate, SP, Brazil.
[Costa, F. O.] Univ Fed Minas Gerais, Dept Periodontol, Sch Dent, BR-31270901 Belo Horizonte, MG, Brazil.
[Cortelli, S. C.] Univ Taubate, Nucleus Periodontolal Res, Dent Res Div, BR-12020040 Taubate, SP, Brazil.
[Kajiya, M.] Forsyth Inst, Dept Immunol, Cambridge, MA 02142 USA.
[Howell, S. C.] Harvard Univ, Dept Oral Med Infect & Immun, Sch Dent Med, Boston, MA 02115 USA.
[Kawai, T.] Harvard Univ, Div Endodont, Sch Dent Med, Boston, MA 02115 USA.
RP Cortelli, JR (reprint author), Univ Taubate, Dept Periodontol & Prevent Dent, Dent Res Div, 51 Visconde Rio Branco, BR-12020040 Taubate, SP, Brazil.
EM jrcortelli@uol.com.br
FU Sao Paulo Foundation for Research [04/00256-6]; National Council for
Scientific and Technological Development (CNPq); National Institutes of
Health [RO1 DE18499]; Harvard Catalyst Pilot Grant
FX The authors are grateful to the Sao Paulo Foundation for Research
(grant, 04/00256-6), the National Council for Scientific and
Technological Development (CNPq), the National Institutes of Health
(grant, RO1 DE18499), and the Harvard Catalyst Pilot Grant.
NR 26
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U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0934-9723
J9 EUR J CLIN MICROBIOL
JI Eur. J. Clin. Microbiol. Infect. Dis.
PD JUN
PY 2012
VL 31
IS 6
BP 1041
EP 1050
DI 10.1007/s10096-011-1405-9
PG 10
WC Infectious Diseases; Microbiology
SC Infectious Diseases; Microbiology
GA 940GQ
UT WOS:000303878400021
PM 21928086
ER
PT J
AU Liaw, JVP
Yun, CH
Walker, TG
Kalva, SP
d'Othee, BJ
AF Liaw, Jonathan V. P.
Yun, Chun-Ho
Walker, T. Gregory
Kalva, Sanjeeva P.
d'Othee, Bertrand Janne
TI Comparison of clinical and MR imaging outcomes after uterine fibroid
embolization with Bead Block and Embosphere
SO EUROPEAN JOURNAL OF RADIOLOGY
LA English
DT Article
DE Uterine fibroid embolization
ID TRIS-ACRYL GELATIN; POLYVINYL-ALCOHOL MICROSPHERES; ARTERY EMBOLIZATION;
PARTICLES; MODEL; LEIOMYOMAS; SHEEP; MULTICENTER
AB Purpose: To compare clinical and imaging outcomes after uterine fibroid embolization (UFE) with Embosphere versus Bead Block microspheres.
Materials and methods: Our institutional review board approved this HIPAA-compliant study. We conducted a retrospective review of all consecutive UFEs performed for symptomatic uterine fibroids at our academic institution from 2001 to 2008. UFE was performed using Embosphere (n = 70) or Bead Block (n = 55) microspheres. Patient symptoms and MR images were reviewed before and following UFE. The MR images were analyzed for changes in the size and contrast enhancement of the dominant fibroid and the uterus.
Results: 125 patients underwent UFE. Pre-treatment characteristics (patient age, presenting symptoms, fibroid location, and volume of the largest fibroid) were similar across groups. Procedure endpoint (near-stasis, reached in 94% of cases), duration, and sedation medication doses were also similar. Clinical follow-up was available in 69 (55%) patients (mean duration: 13.6 months). Of these, 92% had clinical improvement of their main presenting symptom(s) and 3% developed early menopause. MRI follow-up was available in 105 (84%) patients (mean 7.8 months). Mean volume reduction of the largest fibroid was similar after Embosphere (48%) and Bead Block (53%, p = NS). Residual enhancement >= 5% in the dominant fibroid was similarly uncommon after Bead Block (19%) or Embosphere (16%, p = NS). Mean uterine volume reduction was similar across groups (38%); no myometrial infarction occurred.
Conclusion: This retrospective study showed no superiority of Embosphere over Bead Block microspheres in terms of clinical and imaging outcomes after UFE. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
C1 [Liaw, Jonathan V. P.; Yun, Chun-Ho; Walker, T. Gregory; Kalva, Sanjeeva P.; d'Othee, Bertrand Janne] Massachusetts Gen Hosp, Dept Imaging, Div Cardiovasc Imaging & Intervent, Boston, MA 02114 USA.
RP Liaw, JVP (reprint author), Univ Texas Houston, Hlth Sci Ctr Houston, Houston, TX 77030 USA.
EM jvpliaw@hotmail.com
NR 22
TC 3
Z9 5
U1 0
U2 6
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0720-048X
J9 EUR J RADIOL
JI Eur. J. Radiol.
PD JUN
PY 2012
VL 81
IS 6
BP 1371
EP 1375
DI 10.1016/j.ejrad.2011.03.017
PG 5
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 939LT
UT WOS:000303813100050
PM 21439744
ER
PT J
AU Ananthakrishnan, AN
AF Ananthakrishnan, Ashwin N.
TI Detecting and Treating Clostridium Difficile Infections in Patients with
Inflammatory Bowel Disease
SO GASTROENTEROLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Inflammatory bowel disease; Clostridium difficile; Crohn disease;
Ulcerative colitis
ID ANTIBIOTIC-ASSOCIATED DIARRHEA; RISK-FACTORS; PSEUDOMEMBRANOUS
ENTERITIS; HYPERVIRULENT STRAIN; TREATMENT STRATEGIES; DIAGNOSTIC YIELD;
COLITIS; METRONIDAZOLE; EPIDEMIOLOGY; VANCOMYCIN
AB A cohort that appears to be at a higher risk for Clostridium difficile infection (CDI) and particularly vulnerable to the morbidity and mortality associated with it are patients with underlying inflammatory bowel diseases (IBD). Diagnosis requires demonstration of the toxin from a diarrhea stool sample. Mild CDI can be treated with oral metronidazole, whereas severe disease should be treated with oral vancomycin. Management of recurrent CDI remains challenging. Newer drugs are now available that appear to be effective with lower risk of disease recurrence. Specific treatment trials and prospective studies of CDI in patients with IBD are warranted.
C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA.
RP Ananthakrishnan, AN (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, 165 Cambridge St,9th Floor, Boston, MA 02114 USA.
EM aananthakrishnan@partners.org
NR 97
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Z9 13
U1 0
U2 4
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-8553
J9 GASTROENTEROL CLIN N
JI Gastroenterol. Clin. North Am.
PD JUN
PY 2012
VL 41
IS 2
BP 339
EP +
DI 10.1016/j.gtc.2012.01.003
PG 16
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 941HQ
UT WOS:000303954700007
PM 22500522
ER
PT J
AU Rose, DE
Tisnado, DM
Tao, ML
Malin, JL
Adams, JL
Ganz, PA
Kahn, KL
AF Rose, Danielle E.
Tisnado, Diana M.
Tao, May L.
Malin, Jennifer L.
Adams, John L.
Ganz, Patricia A.
Kahn, Katherine L.
TI Prevalence, Predictors, and Patient Outcomes Associated with Physician
Co-management: Findings from the Los Angeles Women's Health Study
SO HEALTH SERVICES RESEARCH
LA English
DT Article
DE Quality of care; physician practice style; physician co-management;
patient ratings of care; breast cancer care; provider network
restrictions
ID PRIMARY-CARE PHYSICIANS; BREAST-CANCER SURVIVORS; QUALITY-OF-CARE;
FINANCIAL INCENTIVES; SPECIALTY-CARE; SYSTEM; SATISFACTION; GENERALIST;
INTERFACE; PATTERNS
AB Background Physician co-management, representing joint participation in the planning, decision-making, and delivery of care, is often cited in association with coordination of care. Yet little is known about how physicians manage tasks and how their management style impacts patient outcomes. Objectives To describe physician practice style using breast cancer as a model. We characterize correlates and predictors of physician practice style for 10 clinical tasks, and then test for associations between physician practice style and patient ratings of care. Methods We queried 347 breast cancer physicians identified by a population-based cohort of women with incident breast cancer regarding care using a clinical vignette about a hypothetical 65-year-old diabetic woman with incident breast cancer. To test the association between physician practice style and patient outcomes, we linked medical oncologists responses to patient ratings of care (physician n = 111; patient n = 411). Results After adjusting for physician and practice setting characteristics, physician practice style varied by physician specialty, practice setting, financial incentives, and barriers to referrals. Patients with medical oncologists who co-managed tasks had higher patient ratings of care. Conclusion Physician practice style for breast cancer is influenced by provider and practice setting characteristics, and it is an important predictor of patient ratings. We identify physician and practice setting factors associated with physician practice style and found associations between physician co-management and patient outcomes (e.g., patient ratings of care).
C1 [Rose, Danielle E.] VA Greater Los Angeles Healthcare Syst, Ctr Study Healthcare Provider Behav, Sepulveda, CA 91343 USA.
[Tisnado, Diana M.; Kahn, Katherine L.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Gen Internal Med & Hlth Serv Res, Los Angeles, CA 90095 USA.
[Tao, May L.] Ctr Radiat Therapy Beverly Hills, Beverly Hills, CA USA.
[Adams, John L.] RAND Corp, Santa Monica, CA USA.
[Ganz, Patricia A.] Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA.
[Ganz, Patricia A.] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Sch Publ Hlth, Div Canc Prevent & Control Res, Los Angeles, CA 90024 USA.
RP Rose, DE (reprint author), VA Greater Los Angeles Healthcare Syst, Ctr Study Healthcare Provider Behav, 16111 Plummer St 152, Sepulveda, CA 91343 USA.
EM droseash@gmail.com
FU California Breast Cancer Research program [7PB-0126S]; National Cancer
Institute; Agency for Health Care Research and Quality
[1-R01-CA81338-01A1]; University of California, Los Angeles; Resource
Centers for Minority Aging Research Center for Health Improvement of
Minority Elderly (RCMAR/CHIME) under NIH/NIA [P30-AG021684]; UCLA;
National Cancer Institute [R25 CA087949]
FX This research was funded by the California Breast Cancer Research
program grant 7PB-0126S and the National Cancer Institute and the Agency
for Health Care Research and Quality grant 1-R01-CA81338-01A1. Dr.
Tisnado received support from the University of California, Los Angeles,
Resource Centers for Minority Aging Research Center for Health
Improvement of Minority Elderly (RCMAR/CHIME) under NIH/NIA Grant
P30-AG021684, and the content does not necessarily represent the
official views of the NIA or the NIH. Dr. Rose received support from the
UCLA Cancer Education and Career Development Program, National Cancer
Institute grant R25 CA087949. We thank the two anonymous referees for
suggestions that significantly strengthened the analyses. We acknowledge
Diane Fitzpatrick and Ann Zisser for their data collection efforts
(under supervision); Fang Ashlee Hu for programming and data management,
and Judith Magee for administrative support. The views expressed in this
article are those of the authors and do not necessarily reflect the
position or policy of the Department of Veterans Affairs or the United
States government.
NR 47
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U1 2
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0017-9124
J9 HEALTH SERV RES
JI Health Serv. Res.
PD JUN
PY 2012
VL 47
IS 3
BP 1091
EP 1116
DI 10.1111/j.1475-6773.2011.01359.x
PN 1
PG 26
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 939HN
UT WOS:000303800200012
PM 22171977
ER
PT J
AU Astrakas, LG
Naqvi, SHA
Kateb, B
Tzika, AA
AF Astrakas, Loukas G.
Naqvi, Syed Hassan Abbas
Kateb, Babak
Tzika, A. Aria
TI Functional MRI using robotic MRI compatible devices for monitoring
rehabilitation from chronic stroke in the molecular medicine era
(Review)
SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
LA English
DT Article
DE stroke; stroke biomarkers; rehabilitation; functional MR imaging;
robotic MRI compatible devices
ID INDUCED MOVEMENT THERAPY; CEREBRAL BLOOD-FLOW;
POSITRON-EMISSION-TOMOGRAPHY; CORTICOSPINAL TRACT INTEGRITY; RECOVERY
FOLLOWING STROKE; MAGNETIC-RESONANCE; MOTOR RECOVERY; UPPER-LIMB;
CORTICAL ACTIVATION; BRAIN PLASTICITY
AB The number of individuals suffering from stroke is increasing daily, and its consequences are a major contributor to invalidity in today's society. Stroke rehabilitation is relatively new, having been hampered from the longstanding view that lost functions were not recoverable. Nowadays, robotic devices, which aid by stimulating brain plasticity, can assist in restoring movement compromised by stroke-induced pathological changes in the brain which can be monitored by MRI. Multiparametric magnetic resonance imaging (MRI) of stroke patients participating in a training program with a novel Magnetic Resonance Compatible Hand-Induced Robotic Device (MR_CHIROD) could yield a promising biomarker that, ultimately, will enhance our ability to advance hand motor recovery following chronic stroke. Using state-of-the art MRI in conjunction with MR_CHIROD-assisted therapy can provide novel biomarkers for stroke patient rehabilitation extracted by a meta-analysis of data. Successful completion of such studies may provide a ground breaking method for the future evaluation of stroke rehabilitation therapies. Their results will attest to the effectiveness of using MR-compatible hand devices with MRI to provide accurate monitoring during rehabilitative therapy. Furthermore, such results may identify biomarkers of brain plasticity that can be monitored during stroke patient rehabilitation. The potential benefit for chronic stroke patients is that rehabilitation may become possible for a longer period of time after stroke than previously thought, unveiling motor skill improvements possible even after six months due to retained brain plasticity.
C1 [Astrakas, Loukas G.; Naqvi, Syed Hassan Abbas; Tzika, A. Aria] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Surg,NMR Surg Lab, Boston, MA 02114 USA.
[Astrakas, Loukas G.; Naqvi, Syed Hassan Abbas; Tzika, A. Aria] Harvard Univ, Sch Med, Shriners Burn Inst, Boston, MA 02114 USA.
[Astrakas, Loukas G.] Univ Ioannina, Dept Med Phys, GR-45110 Ioannina, Greece.
[Tzika, A. Aria] Massachusetts Gen Hosp, Dept Radiol, Athinoula A Martinos Ctr Biomed Imaging, Boston, MA 02114 USA.
[Kateb, Babak; Tzika, A. Aria] Brain Mapping Fdn, W Hollywood, CA 90046 USA.
[Naqvi, Syed Hassan Abbas] Dow Univ Hlth Sci, Dow Med Coll, Karachi 74200, Pakistan.
[Kateb, Babak] Soc Brain Mapping & Therapeut SBMT, W Hollywood, CA 90048 USA.
[Kateb, Babak] Natl Ctr Nanobioelect NCNBE, Moffett Field, CA 94035 USA.
[Kateb, Babak] Cedars Sinai Med Ctr, Dept Neurosurg, Maxine Dunitz Neurosurg Inst, Los Angeles, CA 90048 USA.
RP Tzika, AA (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Surg,NMR Surg Lab, 51 Blossom St,Room 261, Boston, MA 02114 USA.
EM atzika@hms.harvard.edu
RI Astrakas, Loukas/F-5918-2011
FU National Institute of Biomedical Imaging and Bioengineering of the
National Institutes of Health [R21 EB004665-01A2]
FX This study was supported in part by a grant from the National Institute
of Biomedical Imaging and Bioengineering of the National Institutes of
Health (Grant no. R21 EB004665-01A2) to T.A.A. We thank Dr C. Mavroidis
the principal investigator of the subcontract to Northeastern University
to build the MR_CHIROD. We thank Ann Power Smith, Ph.D. of Write Science
Right for editorial assistance. Finally, we thank the Brain Mapping
Foundation and Society for Brain Mapping and Therapeutics (SBMT) for
their contributions to this research.
NR 168
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Z9 5
U1 2
U2 9
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1107-3756
J9 INT J MOL MED
JI Int. J. Mol. Med.
PD JUN
PY 2012
VL 29
IS 6
BP 963
EP 973
DI 10.3892/ijmm.2012.942
PG 11
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 939CW
UT WOS:000303785700001
PM 22426741
ER
PT J
AU Nakamura-Palacios, EM
Benevides, MCD
Zago-Gomes, MD
de Oliveira, RWD
de Vasconcellos, VF
de Castro, LNP
da Silva, MC
Ramos, PA
Fregni, F
AF Nakamura-Palacios, Ester Miyuki
de Almeida Benevides, Marcelo Campos
Zago-Gomes, Maria da Penha
Dias de Oliveira, Roney Welinton
de Vasconcellos, Vitor Fiorin
Passos de Castro, Lais Norberto
da Silva, Morgana Croce
Ramos, Paula Amorim
Fregni, Felipe
TI Auditory event-related potentials (P3) and cognitive changes induced by
frontal direct current stimulation in alcoholics according to Lesch
alcoholism typology
SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE Alcoholism; FAB; Lesch's typology; P3; tDCS
ID PREFRONTAL CORTEX; DOUBLE-BLIND; PARKINSONS-DISEASE; BRAIN-STIMULATION;
CONTROLLED TRIAL; CEREBRAL CORTEX; WORKING-MEMORY; DRUG-ADDICTION; MOTOR
CORTEX; CONSUMPTION
AB Frontal lobe dysfunction is a hallmark of alcohol dependence. Recent studies have shown that a simple but powerful technique of cortical modulation - transcranial direct current stimulation (tDCS) - can induce significant cognitive changes. We therefore aimed to assess the clinical and electrophysiological (as indexed by P3) effects of tDCS of left dorsolateral prefrontal cortex (DLPFC) in different types of alcoholic patients according to Lesch's typology. We enrolled 49 alcoholic subjects, aged between 18 and 75 yr, during the subacute abstinence period to participate in this study. Subjects underwent event-related potential (ERP) registration of alcohol-related and neutral sounds before, during and after active tDCS (1 mA, 35 cm(2), during 10 min) or sham procedure in a counterbalanced and randomized order. Frontal assessment battery (FAB) and five items of the Obsessive Compulsive Drinking Scale were applied at the beginning and at the end of each experimental session. ERP analysis showed an increase in the mean amplitude of P3 associated with alcohol-related sounds after tDCS. This effect was not seen for neutral sounds. This change was more pronounced in Lesch IV alcoholics. Secondary exploratory analysis showed a significant improvement of FAB performance after active tDCS compared to sham tDCS in Lesch IV alcoholics only. We showed clinical and electrophysiological evidence of tDCS-induced frontal activity enhancement that was specific for Lesch IV alcoholics. Given that frontal dysfunction may contribute to the loss of control over drinking behaviour, local increase in frontal activity induced by tDCS might have a beneficial clinical impact in the future.
C1 [Nakamura-Palacios, Ester Miyuki] Univ Fed Espirito Santo, Lab Cognit Sci & Neuropsychopharmacol, Programa Posgrad Ciencias Fisiol, Ctr Ciencias Saude,Dept Physiol Sci, BR-29042755 Vitoria, ES, Brazil.
[Zago-Gomes, Maria da Penha; de Vasconcellos, Vitor Fiorin] Univ Fed Espirito Santo, Hlth Sci Ctr, Dept Internal Med, BR-29042755 Vitoria, ES, Brazil.
[Fregni, Felipe] Harvard Univ, Sch Med, Dept Phys Med & Rehabil, Lab Neuromodulat, Boston, MA USA.
[Fregni, Felipe] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Spauding Rehabil Hosp, Boston, MA USA.
[Fregni, Felipe] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Neurol, Boston, MA 02215 USA.
RP Nakamura-Palacios, EM (reprint author), Univ Fed Espirito Santo, Lab Cognit Sci & Neuropsychopharmacol, Programa Posgrad Ciencias Fisiol, Ctr Ciencias Saude,Dept Physiol Sci, Av Marechal Campos 1468, BR-29042755 Vitoria, ES, Brazil.
EM ester.palacios@terra.com.br
FU Fundacao de Apoio a Ciencia e Tecnologia do Espirito Santo (FAPES)
FX We are grateful to all patients and their relatives who agreed to
participate in this study. We thank the graduate students of the Medical
School of the Federal University of Espirito Santo for their help in
collecting data. Funding for this study was provided by Fundacao de
Apoio a Ciencia e Tecnologia do Espirito Santo (FAPES).
NR 52
TC 26
Z9 27
U1 2
U2 11
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1461-1457
J9 INT J NEUROPSYCHOPH
JI Int. J. Neuropsychopharmacol.
PD JUN
PY 2012
VL 15
IS 5
BP 601
EP 616
DI 10.1017/S1461145711001040
PG 16
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 940MZ
UT WOS:000303895000003
PM 21781352
ER
PT J
AU Song, JY
Jo, HH
Kim, MR
Lew, YO
Ryu, KS
Cha, JH
Kang, CS
Donahoe, PK
MacLaughlin, DT
Kim, JH
AF Song, Jae Yen
Jo, Hyun Hee
Kim, Mee Ran
Lew, Young Oak
Ryu, Ki Sung
Cha, Jung Ho
Kang, Chang Suk
Donahoe, Patricia K.
MacLaughlin, David T.
Kim, Jang Heub
TI Expression of Mullerian inhibiting substance type II receptor and
antiproliferative effects of MIS on human cervical cancer
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE Mullerian inhibiting substance; anti-Mullerian hormone; Mullerian
inhibiting substance type II receptor; cervical cancer;
immunohistochemistry; in situ hybridization
ID HUMAN OVARIAN-CANCER; TGF-BETA; CELL-GROWTH; IN-VIVO; TRANSDUCTION
PATHWAY; HORMONE; IMMUNOASSAY; MECHANISM; BOVINE; TARGET
AB This study aimed to analyze expression of Mullerian inhibiting substance type II receptor (MISRII) protein and mRNA in cervical neoplasia, to demonstrate the growth inhibition of cervical cancer cells by administration of highly purified recombinant human Mullerian inhibiting substance (MIS) and, furthermore, to evaluate the clinical significance of MIS as a biological modifier for MIS receptor expressing tumors. Reverse transcriptase polymerase chain reaction (RT-PCR) was used for MISRII mRNA expression, and in situ hybridization and immunohistochemistry were used to observe expression, location of MISRII mRNA and protein, respectively. To demonstrate the effect of MIS on the viability of cervical cancer cells, methyl thiazole tetrazolium (MTT) assay was performed. Flow cytometry was used to evaluate the cell cycle distribution after exposure to MIS in cervical cancer cells, and the annexin-V-FITC staining method was performed to demonstrate apoptosis by MIS in cervical cancer cells. Expression of MISRII protein and mRNA were observed in all normal cervical and cervical carcinoma tissues. There was no significant difference in expression of MISRII protein and MISRII mRNA between normal cervical and cervical carcinoma tissues. MTT assay showed negative correlation between MIS exposure time and the viability of cervical cells (P=0.008). The changes in cell cycle distribution after MIS exposure suggest that MIS plays an important role in inducing cellular apoptosis by causing arrest at the G, phase and increasing cells at sub-G(0)G(1) phase. Annexin-V-FITC staining methods showed that cellular apoptosis was, respectively, 10.44 and 12.89% after 24 and 48 h of MIS exposure in cervical carcinoma cells. There was a negative correlation between cellular survival and MIS exposure time. This study demonstrates that MISRII is present on normal cervical and cervical carcinoma tissues, and MIS shows receptor-mediated antiproliferative effect on cervical cells in vitro. These data suggest that MIS may be used as a biological modifier or therapeutic modulator on MISRII-expressing tumors in the future.
C1 [Song, Jae Yen; Jo, Hyun Hee; Kim, Mee Ran; Lew, Young Oak; Ryu, Ki Sung; Kim, Jang Heub] Catholic Univ Korea, Coll Med, Dept Obstet & Gynecol, Seoul 137701, South Korea.
[Cha, Jung Ho] Catholic Univ Korea, Coll Med, Dept Anat, Seoul 137701, South Korea.
[Kang, Chang Suk] Catholic Univ Korea, Coll Med, Dept Clin Pathol, Seoul 137701, South Korea.
[Donahoe, Patricia K.; MacLaughlin, David T.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Pediat Surg Res Labs, Boston, MA 02114 USA.
RP Kim, JH (reprint author), Catholic Univ Korea, Coll Med, Dept Obstet & Gynecol, 505 Banpo Dong, Seoul 137701, South Korea.
EM janghkim@catholic.ac.kr
NR 40
TC 1
Z9 3
U1 1
U2 3
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1019-6439
EI 1791-2423
J9 INT J ONCOL
JI Int. J. Oncol.
PD JUN
PY 2012
VL 40
IS 6
BP 2013
EP 2021
DI 10.3892/ijo.2012.1370
PG 9
WC Oncology
SC Oncology
GA 937YK
UT WOS:000303699900033
PM 22344630
ER
PT J
AU Hattangadi, JA
Chapman, PH
Bussiere, MR
Niemierko, A
Ogilvy, CS
Rowell, A
Daartz, J
Loeffler, JS
Shih, HA
AF Hattangadi, Jona A.
Chapman, Paul H.
Bussiere, Marc R.
Niemierko, Andrzej
Ogilvy, Christopher S.
Rowell, Alison
Daartz, Juliane
Loeffler, Jay S.
Shih, Helen A.
TI Planned Two-Fraction Proton Beam Stereotactic Radiosurgery for High-Risk
Inoperable Cerebral Arteriovenous Malformations
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE Cerebral arteriovenous malformation; Proton stereotactic radiosurgery;
AVM score; High-risk AVM
ID MOTOR CORTEX; BRAIN-STEM; RADIATION; OUTCOMES; THERAPY
AB Purpose: To evaluate patients with high-risk cerebral arteriovenous malformations (AVMs), based on eloquent brain location or large size, who underwent planned two-fraction proton stereotactic radiosurgery (PSRS).
Methods and Materials: From 1991 to 2009, 59 patients with high-risk cerebral AVMs received two-fraction PSRS. Median nidus volume was 23 cc (range, 1.4-58.1 cc), 70% of cases had nidus volume >= 14 cc, and 34% were in critical locations (brainstem, basal ganglia). Median AVM score based on age, AVM size, and location was 3.19 (range, 0.9-6.9). Many patients had prior surgery or embolization (40%) or prior PSRS (12%). The most common prescription was 16 Gy radiobiologic equivalent (RBE) in two fractions, prescribed to the 90% isodose.
Results: At a median follow-up of 56.1 months, 9 patients (15%) had total and 20 patients (34%) had partial obliteration. Patients with total obliteration received higher total dose than those with partial or no obliteration (mean dose, 17.6 vs. 15.5 Gy (RBE), p=0.01). Median time to total obliteration was 62 months (range, 23-109 months), and 5-year actuarial rate of partial or total obliteration was 33%. Five-year actuarial rate of hemorrhage was 22% (95% confidence interval, 12.5%-36.8%) and 14% (n=8) suffered fatal hemorrhage. Lesions with higher AVM scores were more likely to hemorrhage (p=0.024) and less responsive to radiation (p=0.026). The most common complication was Grade 1 headache acutely (14%) and long term (12%). One patient developed a Grade 2 generalized seizure disorder, and two had mild neurologic deficits.
Conclusions: High-risk AVMs can be safely treated with two-fraction PSRS, although total obliteration rate is low and patients remain at risk for future hemorrhage. Future studies should include higher doses or a multistaged PSRS approach for lesions more resistant to obliteration with radiation. (C) 2012 Elsevier Inc.
C1 [Chapman, Paul H.; Bussiere, Marc R.; Niemierko, Andrzej; Rowell, Alison; Daartz, Juliane; Loeffler, Jay S.; Shih, Helen A.] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
[Chapman, Paul H.; Ogilvy, Christopher S.] Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02114 USA.
[Hattangadi, Jona A.] Harvard Radiat Oncol Program, Boston, MA USA.
RP Shih, HA (reprint author), Massachusetts Gen Hosp, Dept Radiat Oncol, 100 Blossom St,Cox 3, Boston, MA 02114 USA.
EM hshih@partners.org
NR 20
TC 11
Z9 11
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD JUN 1
PY 2012
VL 83
IS 2
BP 533
EP 541
DI 10.1016/j.ijrobp.2011.08.003
PG 9
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 940VI
UT WOS:000303920800033
PM 22099050
ER
PT J
AU Lapusan, S
Vidriales, MB
Thomas, X
de Botton, S
Vekhoff, A
Tang, RP
Dumontet, C
Morariu-Zamfir, R
Lambert, JM
Ozoux, ML
Poncelet, P
San Miguel, JF
Legrand, O
DeAngelo, DJ
Giles, FJ
Marie, JP
AF Lapusan, Simona
Vidriales, Maria B.
Thomas, Xavier
de Botton, Stephane
Vekhoff, Anne
Tang, Ruoping
Dumontet, Charles
Morariu-Zamfir, Rodica
Lambert, John M.
Ozoux, Marie-Laure
Poncelet, Philippe
San Miguel, Jesus F.
Legrand, Ollivier
DeAngelo, Daniel J.
Giles, Francis J.
Marie, Jean-Pierre
TI Phase I studies of AVE9633, an anti-CD33 antibody-maytansinoid
conjugate, in adult patients with relapsed/refractory acute myeloid
leukemia
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE Acute myeloid leukemia; Antibody-drug conjugate; Maytansine;
Pharmacokinetic; Pharmacodynamic
ID CELLS
AB The efficacy of anti-CD33 immunoconjugates had been previously demonstrated for gemtuzumab-ozogamicin. AVE9633 is an anti-CD33-maytansine conjugate created by ImmunoGen Inc. Phase I trials of AVE9633 were performed in patients with AML to evaluate tolerability, pharmacokinetics and pharmacodynamics. Three phase I studies of AVE9633 were performed in 54 patients with refractory/relapsed AML, evaluating drug infusion on day 1 of a 21-day cycle (Day 1 study), day 1 and 8 (Day 1/8 study) and day 1, 4 and 7 (Day 1/4/7 study) of a 28-day cycle. Toxicity was mainly allergic reaction during infusion (3 grade 3 bronchospasms). DLT was reached for the D1-D7 schedule at 150 mg/sqm (1 keratitis, 1 liver toxicity), and the MTD was set at 130 mg/sqm for this schedule. In the two other phases I, the DLT was not reached. In the Day 1/8 study, CD33 on peripheral blasts was saturated and down-modulated for doses of 75 mg/m(2) x 2 or higher, which was correlated with WBC kinetics and plasma levels of AVE9633. Decrease of DM4/CD33 ratio on the blasts surface between day 1 and 8 was the rational for evaluating day 1/4/7 schedule. This induced relatively constant DM4/CD33 levels over the first 8 days, however no activity was noted. One CRp, one PR and biological activity in five other patients were observed in this study. The Day 1 and Day 1/4/7 studies were early discontinued because of drug inactivity at doses significantly higher than CD33 -saturating doses. No myelossuppression was observed at any trial of AVE9633. The pharmacokinetics/pharmacodynamics data obtained in these studies will provide very useful information for the design of the next generation of immunoconjugates.
C1 [Marie, Jean-Pierre] Hop St Antoine, Dept Hematol, F-75571 Paris 12, France.
[Lapusan, Simona; Vekhoff, Anne; Tang, Ruoping; Legrand, Ollivier; Marie, Jean-Pierre] St Antoine Hosp, AP HP, Dept Hematol & Oncol, Paris, France.
[Vidriales, Maria B.; San Miguel, Jesus F.] Hosp Univ Salamanca, Serv Haematol, Salamanca, Spain.
[Thomas, Xavier; Dumontet, Charles] Hop Edouard Herriot, Dept Hematol, Leukemia Unit, Lyon, France.
[de Botton, Stephane] Inst Gustave Roussy, Dept Hematol, Villejuif, France.
[Morariu-Zamfir, Rodica; Ozoux, Marie-Laure] Sanofi Aventis, Oncol, Paris, France.
[Lambert, John M.] ImmunoGen Inc, Cambridge, MA USA.
[Poncelet, Philippe] Biocytex, Marseille, France.
[Legrand, Ollivier; Marie, Jean-Pierre] Univ Paris 06, Paris, France.
[DeAngelo, Daniel J.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Giles, Francis J.] CTRC, San Antonio, TX USA.
RP Marie, JP (reprint author), Hop St Antoine, Dept Hematol, 184 Rue Faubourg St Antoine, F-75571 Paris 12, France.
EM jean-pierre.marie@sat.aphp.fr
OI SAN MIGUEL, JESUS/0000-0002-9183-4857; Vidriales,
Maria-Belen/0000-0001-5049-3673
NR 16
TC 35
Z9 37
U1 0
U2 3
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-6997
J9 INVEST NEW DRUG
JI Invest. New Drugs
PD JUN
PY 2012
VL 30
IS 3
BP 1121
EP 1131
DI 10.1007/s10637-011-9670-0
PG 11
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 940GT
UT WOS:000303878700028
PM 21519855
ER
PT J
AU Le Cesne, A
Yovine, A
Blay, JY
Delaloge, S
Maki, RG
Misset, JL
Frontelo, P
Nieto, A
Jiao, JJ
Demetri, GD
AF Le Cesne, Axel
Yovine, Alejandro
Blay, Jean-Yves
Delaloge, Suzette
Maki, Robert G.
Misset, Jean-Louis
Frontelo, Pilar
Nieto, Antonio
Jiao, Juhui James
Demetri, George D.
TI A retrospective pooled analysis of trabectedin safety in 1,132 patients
with solid tumors treated in phase II clinical trials
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE Trabectedin; Cancer; Safety; Phase II; Singleagent; Yondelis; ET-743
ID SOFT-TISSUE SARCOMAS; CONTINUOUS INTRAVENOUS-INFUSION; OVARIAN-CANCER;
ANTITUMOR-ACTIVITY; ADULT PATIENTS; ECTEINASCIDIN-743 ET-743; NUCLEOTIDE
EXCISION; PRETREATED PATIENTS; CHEMOTHERAPY; IFOSFAMIDE
AB Purpose To summarize the safety experience obtained from phase II clinical trials conducted with trabectedin as single-agent therapy in patients with advanced solid tumors. Methods This retrospective analysis includes 1,132 patients exposed to trabectedin in 19 phase II trials carried out between February 1999 and April 2008. Trabectedin was administered intravenously as 1 of 3 schedules: 24-hour infusion every 3 weeks (q3wk 24-h; n=570/2,818 cycles), 3-hour infusion every 3 weeks (q3wk 3-h; n=258/1,003 cycles), and 3-hour infusion for three consecutive weeks every 4 weeks (qwk 3-h; n=304/1,198 cycles). Results The majority of patients (90%) had received previous chemotherapy. Patients were given a median of three treatment cycles of trabectedin (range, 1-59). Nausea, fatigue and vomiting were the most common trabectedin-related adverse events, reported in >= 20% of patients. Reversible myelosuppression (mainly neutropenia) and transient reversible transaminase increases were the most common laboratory abnormalities seen with trabectedin, with a very low incidence of relevant clinical consequences. Deaths associated with drug-related adverse events were infrequent, occurring in 19 (1.7%) patients. Conclusion Single-agent trabectedin treatment was reasonably well tolerated. Trabectedin can be administered for prolonged periods to patients with sustained clinical benefit (induction of disease stability or shrinkage) without cumulative toxicities over time.
C1 [Le Cesne, Axel; Delaloge, Suzette] Inst Gustave Roussy, Dept Med, F-94805 Villejuif, France.
[Yovine, Alejandro; Misset, Jean-Louis] Hop St Louis, Paris, France.
[Blay, Jean-Yves] Ctr Leon Berard, F-69373 Lyon, France.
[Maki, Robert G.] Mem Sloan Kettering Canc Ctr, Sloan Kettering Inst, New York, NY 10021 USA.
[Frontelo, Pilar; Nieto, Antonio] PharmaMar Clin R&D, Madrid, Spain.
[Jiao, Juhui James] Johnson & Johnson Pharmaceut Res & Dev LLC, Raritan, NJ USA.
[Demetri, George D.] Dana Farber Canc Inst, Ludwig Ctr, Boston, MA 02115 USA.
[Demetri, George D.] Harvard Univ, Sch Med, Boston, MA USA.
RP Le Cesne, A (reprint author), Inst Gustave Roussy, Dept Med, F-94805 Villejuif, France.
EM lecesne@igr.fr
RI Blay, Jean-Yves/N-3966-2016
OI Blay, Jean-Yves/0000-0001-7190-120X
FU PharmaMar; Jonhson Johnson
FX A Le Cesne and JY Blay have received research support and honoraria from
PharmaMar and Jonhson & Johnson. S Delaloge has received honoraria from
PharmaMar. GD Demetri has served as scientific consultant for both
PharmaMar and Johnson & Johnson, and Dana-Farber/Harvard has received
research support for the conduct of clinical trials from both PharmaMar
and Johnson & Johnson. RG Maki has received research support from
PharmaMar. JL Misset has received research support and honoraria from
PharmaMar. A Yovine, P Frontelo and A Nieto are present or former
employees in PharmaMar and are stock owners. JJ Jiao is employee in
Johnson & Johnson.
NR 39
TC 42
Z9 44
U1 0
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-6997
EI 1573-0646
J9 INVEST NEW DRUG
JI Invest. New Drugs
PD JUN
PY 2012
VL 30
IS 3
BP 1193
EP 1202
DI 10.1007/s10637-011-9662-0
PG 10
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 940GT
UT WOS:000303878700037
PM 21484250
ER
PT J
AU Chung, M
Newberry, SJ
Ansari, MT
Yu, WW
Wu, H
Lee, J
Suttorp, M
Gaylor, JM
Motala, A
Moher, D
Balk, EM
Shekelle, PG
AF Chung, Mei
Newberry, Sydne J.
Ansari, Mohammed T.
Yu, Winifred W.
Wu, Helen
Lee, Jounghee
Suttorp, Marika
Gaylor, James M.
Motala, Aneesa
Moher, David
Balk, Ethan M.
Shekelle, Paul G.
TI Two methods provide similar signals for the need to update systematic
reviews
SO JOURNAL OF CLINICAL EPIDEMIOLOGY
LA English
DT Review
DE Evidence-based methodology; Systematic reviews; Comparative
effectiveness reviews; Omega-3 fatty acids; Cardiovascular disease risk
factors; Cancer; Cognitive function
ID OMEGA-3-FATTY-ACIDS; GUIDELINES
AB Objective: Apply and compare two methods that identify signals for the need to update systematic reviews, using three Evidence-based Practice Center reports on omega-3 fatty acids as test cases.
Study Design and Setting: We applied the RAND method, which uses domain (subject matter) expert guidance, and a modified Ottawa method, which uses quantitative and qualitative signals. For both methods, we conducted focused electronic literature searches of recent studies using the key terms from the original reports. We assessed the agreement between the methods and qualitatively assessed the merits of each system.
Results: Agreement between the two methods was "substantial" or better (kappa > 0.62) in three of the four systematic reviews. Overall agreement between the methods was "substantial" (kappa = 0.64, 95% confidence interval [Cl] 0.45-0.83).
Conclusion: The RAND and modified Ottawa methods appear to provide similar signals for the possible need to update systematic reviews in this pilot study. Future evaluation with a broader range of clinical topics and eventual comparisons between signals to update reports and the results of full evidence review updates will be needed. We propose a hybrid approach combining the best features of both methods, which should allow efficient review and assessment of the need to update. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Chung, Mei; Yu, Winifred W.; Lee, Jounghee; Gaylor, James M.; Balk, Ethan M.] Tufts Med Ctr, Inst Clin Res & Hlth Policy Studies, Tufts Evidence Based Practice Ctr, Boston, MA 02111 USA.
[Newberry, Sydne J.; Wu, Helen; Suttorp, Marika; Motala, Aneesa; Shekelle, Paul G.] So Calif Evidence Based Practice Ctr, RAND Hlth, Santa Monica, CA USA.
[Shekelle, Paul G.] W Los Angeles VA Med Ctr, Los Angeles, CA USA.
[Ansari, Mohammed T.; Moher, David] Univ Ottawa, Evidence Based Practice Ctr, Ottawa Methods Ctr, Clin Epidemiol Program,Ottawa Hosp Res Inst, Ottawa, ON, Canada.
RP Chung, M (reprint author), Tufts Med Ctr, Inst Clin Res & Hlth Policy Studies, Tufts Evidence Based Practice Ctr, Box 63,800 Washington St, Boston, MA 02111 USA.
EM mchung1@tuftsmedicalcenter.org
OI , /0000-0002-6834-7583; Wu, Helen/0000-0001-7775-5282; Moher , David
/0000-0003-2434-4206
FU NHLBI NIH HHS [T32 HL069772]
NR 16
TC 13
Z9 13
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0895-4356
J9 J CLIN EPIDEMIOL
JI J. Clin. Epidemiol.
PD JUN
PY 2012
VL 65
IS 6
BP 660
EP 668
DI 10.1016/j.jclinepi.2011.12.004
PG 9
WC Health Care Sciences & Services; Public, Environmental & Occupational
Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 940PA
UT WOS:000303904300011
PM 22464414
ER
PT J
AU Goodson, JM
Haffajee, AD
Socransky, SS
Kent, R
Teles, R
Hasturk, H
Bogren, A
Van Dyke, T
Wennstrom, J
Lindhe, J
AF Goodson, J. Max
Haffajee, Anne D.
Socransky, Sigmund S.
Kent, Ralph
Teles, Ricardo
Hasturk, Hatice
Bogren, Anna
Van Dyke, Thomas
Wennstrom, Jan
Lindhe, Jan
TI Control of periodontal infections: A randomized controlled trial I. The
primary outcome attachment gain and pocket depth reduction at treated
sites
SO JOURNAL OF CLINICAL PERIODONTOLOGY
LA English
DT Article
DE antibiotics; periodontal disease; periodontal surgery; randomized
controlled trial
ID GENERALIZED AGGRESSIVE PERIODONTITIS; SUBANTIMICROBIAL DOSE DOXYCYCLINE;
TETRACYCLINE FIBER THERAPY; REPOSITIONED FLAP SURGERY; CONTROLLED
CLINICAL-TRIAL; SUBGINGIVAL MICROBIOTA; NONSURGICAL TREATMENT; ADULT
PERIODONTITIS; MICROBIOLOGICAL PARAMETERS; MULTICENTER EVALUATION
AB Objective To compare the treatment outcome of scaling and root planing (SRP) in combination with systemic antibiotics, local antibiotic therapy and/or periodontal surgery. Material and Methods One hundred and eighty-seven patients were assigned to eight groups treated by SRP plus none, one, two or three adjunctive treatments and monitored for 24 similar to months in a randomized controlled clinical trial using a 2 similar to 2 similar to 2 factorial design. Systemic amoxicillin similar to metronidazole (SMA), local tetracycline delivery (LTC) and periodontal surgery (SURG) were evaluated as adjuncts. Changes in clinical attachment level (CAL) and probing pocket depth (PPD) were statistically evaluated by ancova of main effects. Results Effects of adjunctive therapy to SRP were minimal at 3 similar to months. Between 3 and 6 similar to months PPD reduction occurred particularly in patients receiving periodontal surgery. After 6 similar to months, both CAL gain and PPD reduction reached a plateau that was maintained at 24 similar to months in all groups. The 24-month CAL gain was improved by SMA (0.50 similar to mm) while PPD was reduced by SMA (0.51 similar to mm) and SURG (0.36 similar to mm). Smoking reduced CAL gain and PPD reduction. Conclusion Patients receiving adjunctive therapies generally exhibited improved CAL gain and/or PPD reduction when compared with the outcome of SRP alone. Only additive, not synergistic effects of the various adjunctive therapies were observed.
C1 [Goodson, J. Max; Haffajee, Anne D.; Socransky, Sigmund S.; Kent, Ralph; Teles, Ricardo] Forsyth Inst, Cambridge, MA USA.
[Hasturk, Hatice; Van Dyke, Thomas] Boston Univ, Sch Dent Med, Boston, MA 02215 USA.
[Bogren, Anna; Wennstrom, Jan; Lindhe, Jan] Univ Gothenburg, Sahlgrenska Acad, Dept Periodontol, Gothenburg, Sweden.
RP Goodson, JM (reprint author), Forsyth Inst, Boston, MA USA.
EM MGoodson@forsyth.org
FU National Institute of Dental and Craniofacial Research [DE12861,
RR025771]; GCRC [RR00533, RR01032]
FX J. M. Goodson developed the tetracycline fiber used in this study
between 1976 and 1994 when it was introduced. It has not been on the
market since 2003. No other participants have any conflict of interest
with any of the products tested in this study. This research was
supported by the National Institute of Dental and Craniofacial Research
grants DE12861 and RR025771, and GCRC funding from RR00533 and RR01032.
NR 44
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Z9 40
U1 0
U2 19
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0303-6979
J9 J CLIN PERIODONTOL
JI J. Clin. Periodontol.
PD JUN
PY 2012
VL 39
IS 6
BP 526
EP 536
DI 10.1111/j.1600-051X.2012.01870.x
PG 11
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 939XW
UT WOS:000303855200004
PM 22512461
ER
PT J
AU Matura, LA
McDonough, A
Carroll, DL
AF Matura, Lea Ann
McDonough, Annette
Carroll, Diane L.
TI Predictors of Health-Related Quality of Life in Patients With Idiopathic
Pulmonary Arterial Hypertension
SO JOURNAL OF HOSPICE & PALLIATIVE NURSING
LA English
DT Article
DE health status; idiopathic pulmonary arterial hypertension; quality of
life
ID REPORTED OUTCOMES; QUESTIONNAIRE; VALIDATION; EMPLOYMENT; GUIDELINES;
BOSENTAN; EXERCISE; THERAPY; DISEASE; CAMPHOR
AB Idiopathic pulmonary arterial hypertension is a debilitating disease that leads to right ventricular heart failure and death. There is limited research on how this disease affects patients. The purpose of this study was to describe differences in health status, health-related quality of life, and psychological states among functional classes along with predictors of health-related quality of life. A convenience sample of 104 participants with idiopathic pulmonary arterial hypertension was recruited. Participants completed a sociodemographic and clinical data form; Medical Outcomes Study Short-Form 36, US Cambridge Pulmonary Hypertension Outcome Review, and Profile of Mood States surveys. The mean age was 51.9 (SD, 16.6) years, and 81 (78%) were female. Patients with functional class IV had significantly worse self-reported physical health status, health-related quality of life, and psychological distress than the other functional classes. Predictors of health-related quality of life were role-emotional (Medical Outcomes Study Short-Form 36), symptoms and activity (US Cambridge Pulmonary Hypertension Outcome Review), depression (Profile of Mood States), employment, and diuretic and oxygen use, accounting for 86% of the variance. These factors need to be monitored and assessed with patients with idiopathic pulmonary arterial hypertension especially as functional class increases. Effective symptom management is necessary to reduce the negative impact on health-related quality of life. A case study is presented to illustrate these points.
C1 [Matura, Lea Ann] Univ Penn, Sch Nursing, Philadelphia, PA 19104 USA.
[McDonough, Annette] Univ Massachusetts, Lowell, MA USA.
[Carroll, Diane L.] Massachusetts Gen Hosp, Inst Patient Care, Munn Ctr Nursing Res, Boston, MA 02114 USA.
RP Matura, LA (reprint author), Univ Penn, Sch Nursing, Claire M Fagin Hall,418 Curie Blvd,Room 322, Philadelphia, PA 19104 USA.
EM matura@nursing.upenn.edu
FU Bouve College of Health Sciences; Sigma Theta Tau Epsilon Gamma Epsilon
FX This study was partially funded by the Bouve College of Health Sciences
and Sigma Theta Tau Epsilon Gamma Epsilon.
NR 36
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U1 1
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1522-2179
J9 J HOSP PALLIAT NURS
JI J. Hosp. Palliat. Nurs.
PD JUN
PY 2012
VL 14
IS 4
BP 283
EP 292
DI 10.1097/NJH.0b013e3182496c04
PG 10
WC Nursing
SC Nursing
GA 938YG
UT WOS:000303768900006
ER
PT J
AU Gandhi, RT
Sax, PE
Grinspoon, SK
AF Gandhi, Rajesh T.
Sax, Paul E.
Grinspoon, Steven K.
TI Metabolic and Cardiovascular Complications in HIV-Infected Patients: New
Challenges for a New Age
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID ANTIRETROVIRAL THERAPY; IMMUNODEFICIENCY
C1 [Gandhi, Rajesh T.] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
[Grinspoon, Steven K.] Massachusetts Gen Hosp, Program Nutr Metab, Dept Med, Boston, MA 02114 USA.
[Gandhi, Rajesh T.] Massachusetts Gen Hosp, Dept Med, Ragon Inst, Massachusetts Inst Technol & Harvard, Boston, MA 02114 USA.
[Sax, Paul E.] Brigham & Womens Hosp, Dept Med, Div Infect Dis, Boston, MA 02115 USA.
RP Gandhi, RT (reprint author), Massachusetts Gen Hosp, Div Infect Dis, GRJ 504,55 Fruit St, Boston, MA 02114 USA.
EM rgandhi@partners.org
FU National Institutes of Health [R01 AI066992-04A1, G08LM008830-01, NIH
U01 AI 694722, NIH 2P30 AI060354-06]; Harvard University Center for AIDS
Research; Bristol-Myers Squibb; Tibotec; Theratechnologies; Amgen
FX This work was supported in part by the National Institutes of Health
(grant numbers R01 AI066992-04A1 and G08LM008830-01 to R. T. G., NIH U01
AI 694722 to the AIDS Clinical Trials Group, and NIH 2P30 AI060354-06 to
the Harvard University Center for AIDS Research). This supplement was
supported by the Harvard University Center for AIDS Research and an
educational grant from Bristol-Myers Squibb.; R. T. G. has received
grant funding from and served on an advisory board for Gilead and has
received grant funding from Tibotec. P. E. S. has served as a consultant
for Bristol-Myers Squibb. S. G. has received research funding from
Theratechnologies, Amgen, and Bristol-Myers Squibb, and has served as a
consultant for EMD Serono and for Theratechnologies.
NR 8
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U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD JUN 1
PY 2012
VL 205
SU 3
BP S353
EP S354
DI 10.1093/infdis/jis202
PG 2
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 942BH
UT WOS:000304014000001
PM 22577207
ER
PT J
AU Lo, J
Plutzky, J
AF Lo, Janet
Plutzky, Jorge
TI The Biology of Atherosclerosis: General Paradigms and Distinct
Pathogenic Mechanisms Among HIV-Infected Patients
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID ANTIRETROVIRAL THERAPY; CORONARY ATHEROSCLEROSIS; ENDOTHELIAL
DYSFUNCTION; CARDIOVASCULAR-DISEASE; MYOCARDIAL-INFARCTION; PROTEASE
INHIBITORS; RISK; MACROPHAGES; OBESITY; IMMUNITY
AB Complications of atherosclerosis, including myocardial infarction and stroke, are the leading cause of death and disability worldwide. Recent data strongly implicate cardiovascular death as a contributor to mortality among patients with human immunodeficiency virus (HIV) infection, with evidence suggesting increased incidence of atherosclerosis among these patients. Therefore, greater understanding of atherosclerotic mechanisms and how these responses may be similar or distinct in HIV-infected patients is needed. Key concepts in atherosclerosis are reviewed, including the evidence that inflammation and abnormal metabolism are major drivers of atherosclerosis, and connected to the current literature regarding atherosclerosis in the context of HIV.
C1 [Plutzky, Jorge] Brigham & Womens Hosp, Vasc Dis Prevent Program, Div Cardiovasc Med, Boston, MA 02115 USA.
[Lo, Janet] Massachusetts Gen Hosp, Program Nutr Metab, Neuroendocrine Unit, Boston, MA 02114 USA.
[Lo, Janet; Plutzky, Jorge] Harvard Univ, Sch Med, Boston, MA USA.
RP Plutzky, J (reprint author), Brigham & Womens Hosp, Vasc Dis Prevent Program, Div Cardiovasc Med, 75 Francis St, Boston, MA 02115 USA.
EM jplutzky@rics.bwh.harvard.edu
FU National Institutes of Health [K23 HL092792, R01 HL048743]; Harvard
University Center for AIDS Research; Bristol-Myers Squibb
FX This work was supported by the National Institutes of Health (grant
numbers K23 HL092792 to J. L. and R01 HL048743 to J. P.). This
supplement was supported by the Harvard University Center for AIDS
Research and an educational grant from Bristol-Myers Squibb.
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U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD JUN 1
PY 2012
VL 205
SU 3
BP S368
EP S374
DI 10.1093/infdis/jis201
PG 7
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 942BH
UT WOS:000304014000004
PM 22577210
ER
PT J
AU Stanley, TL
Grinspoon, SK
AF Stanley, Takara L.
Grinspoon, Steven K.
TI Body Composition and Metabolic Changes in HIV-Infected Patients
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS INFECTION; REVERSE-TRANSCRIPTASE INHIBITOR;
ACTIVE ANTIRETROVIRAL THERAPY; MULTICENTER AIDS COHORT; REGIONAL
ADIPOSE-TISSUE; DISEASE RISK-FACTORS; PROTEASE INHIBITOR;
INSULIN-RESISTANCE; DIABETES-MELLITUS; FAT DEPOSITION
AB As antiretroviral therapy has decreased human immunodeficiency virus (HIV)-associated mortality, cardiometabolic abnormalities have become increasingly apparent in HIV-infected individuals. Many patients treated for HIV infection exhibit body composition changes, including peripheral fat atrophy and visceral lipohypertrophy. In addition, HIV-infected individuals demonstrate a higher prevalence of dyslipidemia, insulin resistance and diabetes, and cardiovascular risk, compared with the general population. Although antiretroviral therapy appears to contribute to some of the cardiometabolic abnormalities in HIV infection, HIV itself, immunologic factors, and lifestyle factors are also important mediators of cardiovascular risk. Treatment strategies for body composition changes and cardiometabolic abnormalities in HIV infection include lifestyle modification, lipid-lowering agents, insulin sensitizers, and treatments to reverse endocrine abnormalities in HIV, including growth hormone-releasing hormone. None of these strategies has comprehensively addressed the abnormalities experienced by this population, however, and further research is needed into combined strategies to improve body composition and ameliorate cardiovascular risk.
C1 [Grinspoon, Steven K.] Massachusetts Gen Hosp, Program Nutr Metab, Neuroendocrine Unit, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Grinspoon, SK (reprint author), Massachusetts Gen Hosp, Program Nutr Metab, Neuroendocrine Unit, LON5-207,55 Fruit St, Boston, MA 02114 USA.
EM sgrinspoon@partners.org
FU National Institute of Diabetes and Digestive and Kidney Diseases at the
National Institutes of Health [K24 DK064545, R01 DK063639, K23
DK089910]; Mary Fisher Clinical AIDS Research and Education Fund;
Harvard Center for AIDS Research; Bristol-Myers Squibb;
Theratechnologies; Amgen; Bristol Myers Squibb
FX This work was supported in part by the National Institute of Diabetes
and Digestive and Kidney Diseases at the National Institutes of Health
(grants K24 DK064545 and R01 DK063639 to S. G. and grant K23 DK089910 to
T. S.) and the Mary Fisher Clinical AIDS Research and Education Fund.
This supplement was supported by the Harvard Center for AIDS Research
and an educational grant from Bristol-Myers Squibb.; S. G. has received
research funding from Theratechnologies, Amgen, and Bristol Myers Squibb
and has served as a consultant for EMD Serono and for Theratechnologies.
T. S. certifies no potential conflicts of interest.
NR 50
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U1 1
U2 8
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD JUN 1
PY 2012
VL 205
SU 3
BP S383
EP S390
DI 10.1093/infdis/jis205
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 942BH
UT WOS:000304014000006
PM 22577212
ER
PT J
AU Triant, VA
AF Triant, Virginia A.
TI HIV Infection and Coronary Heart Disease: An Intersection of Epidemics
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS-INFECTION; ACTIVE ANTIRETROVIRAL THERAPY; ACUTE
MYOCARDIAL-INFARCTION; MULTICENTER AIDS COHORT; INTIMA-MEDIA THICKNESS;
RISK-FACTORS; CARDIOVASCULAR-DISEASE; PROTEASE INHIBITORS;
GENERAL-POPULATION; UNINFECTED INDIVIDUALS
AB Patients with human immunodeficiency virus (HIV) infection are at increased risk of developing coronary heart disease (CHD). Although factors potentially contributing to this elevated risk include traditional CHD risk factors and antiretroviral medications, more recent data support a role for inflammatory and immunologic factors as central to a complex mechanism. Decreasing CHD risk among HIV-infected patients is likely to involve modification of inflammatory and immunologic factors through antiretroviral therapy or other novel strategies as well as targeted treatment of traditional CHD risk factors. This review will highlight epidemiologic data investigating the association between HIV and CHD outcomes. An overview of potential mechanistic factors associated with CHD in HIV infection and of strategies for managing CHD risk in HIV-infected patients is also included. Specific cardiovascular and metabolic risk factors, CHD risk prediction, and the immunologic basis for CHD in HIV-infected patients will be discussed in separate reviews.
C1 [Triant, Virginia A.] Massachusetts Gen Hosp, Dept Med, Div Infect Dis, Boston, MA 02114 USA.
[Triant, Virginia A.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Triant, VA (reprint author), Massachusetts Gen Hosp, Dept Med, Div Infect Dis, 55 Fruit St,LON 207, Boston, MA 02114 USA.
EM vtriant@partners.org
FU National Institute of Allergy and Infectious Diseases at the National
Institutes of Health [K01AI073109]; Harvard Center for AIDS Research;
Bristol Myers-Squibb
FX This work was supported by the National Institute of Allergy and
Infectious Diseases at the National Institutes of Health (grant number
K01AI073109). This supplement was supported by the Harvard Center for
AIDS Research and an educational grant from Bristol Myers-Squibb.
NR 50
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U2 9
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD JUN 1
PY 2012
VL 205
SU 3
BP S355
EP S361
DI 10.1093/infdis/jis195
PG 7
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 942BH
UT WOS:000304014000002
PM 22577208
ER
PT J
AU Algamas-Dimantov, A
Davidovsky, D
Ben-Ari, J
Kang, JX
Peri, I
Hertz, R
Bar-Tana, J
Schwartz, B
AF Algamas-Dimantov, Anna
Davidovsky, Dana
Ben-Ari, Julius
Kang, Jing X.
Peri, Irena
Hertz, Rachel
Bar-Tana, Jacob
Schwartz, Betty
TI Amelioration of diabesity-induced colorectal ontogenesis by omega-3
fatty acids in mice
SO JOURNAL OF LIPID RESEARCH
LA English
DT Article
DE obesity; diabetes; epithelial cell growth; epithelial cell
differentiation; colorectal neoplasia
ID HEPATOCYTE NUCLEAR FACTOR-4-ALPHA; INFLAMMATORY-BOWEL-DISEASE; N-3
FATTY-ACIDS; TRANSCRIPTION FACTOR; METABOLIC SYNDROME; TRANSGENIC MICE;
GENE-EXPRESSION; LIGAND-BINDING; CELL-FUNCTION; CANCER
AB Postnatal intestinal ontogenesis in an animal model of diabesity may recapitulate morphological and transduction features of diabesity-induced intestinal dysplasia and its amelioration by endogenous (n-3) polyunsaturated fatty acids (PUFA). Proliferation, differentiation, and transduction aspects of intestinal ontogenesis have been studied here in obese, insulin-resistant db/db mice, in fat-1 transgene coding for desaturation of (n-6) PUFA into (n-3) PUFA, in db/db crossed with fat-1 mice, and in control mice. Diabesity resulted in increased colonic proliferation and dedifferentiation of epithelial colonocytes and goblet cells, with increased colonic beta-catenin and hepatocyte nuclear factor (HNF)-4 alpha transcriptional activities accompanied by enrichment in HNF-4 alpha-bound (n-6) PUFA. In contrast, in fat-1 mice, colonic proliferation was restrained, accompanied by differentiation of crypt stem cells into epithelial colonocytes and goblet cells and by decrease in colonic beta-catenin and HNF-4 alpha transcriptional activities, with concomitant enrichment in HNF-4 alpha-bound (n-3) PUFA at the expense of (n-6) PUFA. Colonic proliferation and differentiation, the profile of beta-catenin and HNF-4 alpha-responsive genes, and the composition of HNF-4 alpha-bound PUFA of db/db mice reverted to wild-type by introducing the fat-1 gene into the db/db context. Suppression of intestinal HNF-4 alpha activity by (n-3) PUFA may ameliorate diabesity-induced intestinal ontogenesis and offer an effective preventive modality for colorectal cancer. -Algamas-Dimantov, A., D. Davidovsky, J. Ben-Ari, J. X. Kang, I. Peri, R. Hertz, J. Bar-Tana, and B. Schwartz. Amelioration of diabesity-induced colorectal ontogenesis by omega-3 fatty acids in mice. J. Lipid Res. 2012. 53: 1056-1070.
C1 [Algamas-Dimantov, Anna; Davidovsky, Dana; Peri, Irena; Schwartz, Betty] Hebrew Univ Jerusalem, Robert H Smith Fac Agr Food & Environm, Inst Biochem Food Sci & Nutr, Jerusalem, Israel.
[Ben-Ari, Julius] Hebrew Univ Jerusalem, Robert H Smith Fac Agr Food & Environm, Interdept Equipment Facil, Jerusalem, Israel.
[Kang, Jing X.] Massachusetts Gen Hosp, Lab Lipid Med & Technol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
[Hertz, Rachel; Bar-Tana, Jacob] Hebrew Univ Jerusalem, Sch Med, Dept Human Nutr & Metab, IL-91010 Jerusalem, Israel.
RP Schwartz, B (reprint author), Hebrew Univ Jerusalem, Robert H Smith Fac Agr Food & Environm, Inst Biochem Food Sci & Nutr, Jerusalem, Israel.
EM bschwart@agri.huji.ac.il
FU Israel Science Foundation [134/06]
FX This work was supported by Israel Science Foundation Grant 134/06.
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U1 0
U2 6
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0022-2275
J9 J LIPID RES
JI J. Lipid Res.
PD JUN
PY 2012
VL 53
IS 6
BP 1056
EP 1070
DI 10.1194/jlr.M021949
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 940SK
UT WOS:000303913200003
PM 22357704
ER
PT J
AU Kopp, RP
Stroup, SP
Schroeck, FR
Freedland, SJ
Millard, F
Terris, MK
Aronson, WJ
Presti, JC
Amling, CL
Kane, CJ
AF Kopp, Ryan P.
Stroup, Sean P.
Schroeck, Florian R.
Freedland, Stephen J.
Millard, Frederick
Terris, Martha K.
Aronson, William J.
Presti, Joseph C., Jr.
Amling, Christopher L.
Kane, Christopher J.
TI Are Repeat Prostate Biopsies Safe? A Cohort Analysis From the SEARCH
Database
SO JOURNAL OF UROLOGY
LA English
DT Article
DE biopsy; prostatic neoplasms; prostatectomy; recurrence; diagnosis
ID INTRAEPITHELIAL NEOPLASIA; NEEDLE BIOPSIES; HIGH-GRADE; CANCER;
PROPHYLAXIS; INFECTION; TRENDS; MEN
AB Purpose: Patients question whether multiple biopsy sessions cause worse prostate cancer outcomes. Therefore, we investigated whether there is an association between the number of prior biopsy sessions and biochemical recurrence after radical prostatectomy.
Materials and Methods: Men in the SEARCH (Shared Equal Access Regional Cancer Hospital) database who underwent radical prostatectomy between 1988 and 2010 after a known number of prior biopsies were included in the analysis. Number of biopsy sessions (range 1 to 8) was examined as a continuous and categorical (1, 2 and 3 to 8) variable. Biochemical recurrence was defined as a prostate specific antigen greater than 0.2 ng/ml, 2 values at 0.2 ng/ml or secondary treatment for an increased prostate specific antigen. The association between number of prior biopsy sessions and biochemical recurrence was analyzed using the Cox proportional hazards model. Kaplan-Meier estimates of freedom from biochemical recurrence were compared among the groups.
Results: Of the 2,739 men in the SEARCH database who met the inclusion criteria 2,251 (82%) had only 1 biopsy, 365(13%) had 2 biopsies and 123 (5%) had 3 or more biopsies. More biopsy sessions were associated with higher prostate specific antigen (p < 0.001), greater prostate weight (p < 0.001), lower biopsy Gleason sum (p = 0.01) and more organ confined (pT2) disease (p = 0.017). The Cox proportional hazards model demonstrated no association between number of biopsy sessions as a continuous or categorical variable and biochemical recurrence. Kaplan-Meier estimates of freedom from biochemical recurrence were similar across biopsy groups (log rank p = 0.211).
Conclusions: Multiple biopsy sessions are not associated with an increased risk of biochemical recurrence in men undergoing radical prostatectomy. Multiple biopsy sessions appear to select for a low risk cohort.
C1 [Kopp, Ryan P.; Stroup, Sean P.; Kane, Christopher J.] Univ Calif San Diego, Div Urol, San Diego, CA 92103 USA.
[Stroup, Sean P.; Millard, Frederick; Kane, Christopher J.] Moores UCSD Canc Ctr, Sect Urol Oncol, La Jolla, CA USA.
[Stroup, Sean P.; Kane, Christopher J.] Vet Affairs San Diego Med Ctr, Urol Sect, La Jolla, CA USA.
[Aronson, William J.] Univ Calif Los Angeles, Sch Med, Dept Urol, Los Angeles, CA USA.
[Aronson, William J.] Vet Affairs Greater Los Angeles Healthcare Syst, Urol Sect, Los Angeles, CA USA.
[Presti, Joseph C., Jr.] Stanford Univ, Sch Med, Dept Urol, Palo Alto, CA 94304 USA.
[Presti, Joseph C., Jr.] Vet Affairs Med Ctr, Urol Sect, Palo Alto, CA 94304 USA.
[Schroeck, Florian R.; Freedland, Stephen J.] Duke Univ, Sch Med, Dept Surg, Div Urol Surg, Durham, NC USA.
[Freedland, Stephen J.] Duke Univ, Sch Med, Dept Pathol, Durham, NC 27706 USA.
[Freedland, Stephen J.] Duke Univ, Sch Med, Duke Prostate Ctr, Durham, NC USA.
[Freedland, Stephen J.] Vet Affairs Med Ctr, Urol Sect, Durham, NC USA.
[Terris, Martha K.] Vet Affairs Med Ctr, Urol Sect, Augusta, GA USA.
[Terris, Martha K.] Med Coll Georgia, Urol Sect, Augusta, GA 30912 USA.
[Amling, Christopher L.] Oregon Hlth & Sci Univ, Div Urol, Portland, OR 97201 USA.
RP Kane, CJ (reprint author), Univ Calif San Diego, Div Urol, 200 W Arbor Dr,8897, San Diego, CA 92103 USA.
EM ckane@ucsd.edu
OI Terris, Martha/0000-0002-3843-7270; Schroeck,
Florian/0000-0002-1860-2611
FU Department of Veterans Affairs; Department of Defense; Prostate Cancer
Research Program; NIH [R01CA100938, P50 CA92131-01A1]; Georgia Cancer
Coalition; American Urological Association Foundation
FX Supported by the Department of Veterans Affairs, the Department of
Defense, Prostate Cancer Research Program (SJF), NIH R01CA100938 (WJA),
NIH Specialized Programs of Research Excellence Grant P50 CA92131-01A1
(WJA), Georgia Cancer Coalition (MKT) and the American Urological
Association Foundation/Astellas Rising Star in Urology Award (SJF).
Views and opinions of and endorsements by the author(s) do not reflect
those of the U.S. Army, U.S. Navy or the Department of Defense.
NR 18
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U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5347
J9 J UROLOGY
JI J. Urol.
PD JUN
PY 2012
VL 187
IS 6
BP 2056
EP 2060
DI 10.1016/j.juro.2012.01.083
PG 5
WC Urology & Nephrology
SC Urology & Nephrology
GA 939OK
UT WOS:000303821300033
PM 22498218
ER
PT J
AU Tseng, YD
Chen, MH
Beard, CJ
Martin, NE
Orio, PF
Loffredo, M
Renshaw, AA
Choueiri, TK
Hu, JC
Kantoff, PW
D'Amico, AV
Nguyen, PL
AF Tseng, Yolanda D.
Chen, Ming-Hui
Beard, Clair J.
Martin, Neil E.
Orio, Peter F.
Loffredo, Marian
Renshaw, Andrew A.
Choueiri, Toni K.
Hu, Jim C.
Kantoff, Philip W.
D'Amico, Anthony V.
Nguyen, Paul L.
TI Posttreatment Prostate Specific Antigen Nadir Predicts Prostate Cancer
Specific and All Cause Mortality
SO JOURNAL OF UROLOGY
LA English
DT Article
DE prostate; prostatic neoplasms; prostate-specific antigen; radiotherapy;
mortality
ID EXTERNAL-BEAM RADIOTHERAPY; SURROGATE END-POINTS; RADIATION-THERAPY;
RADICAL PROSTATECTOMY; RANDOMIZED-TRIAL; SURVIVAL; DEATH
AB Purpose: We investigated whether the prostate specific antigen nadir predicts prostate cancer specific and all cause mortality in men treated in a randomized trial of radiation with or without 6 months of androgen deprivation therapy.
Materials and Methods: The study included 204 men with cT1b-T2bN0M0 prostate adenocarcinoma and at least 1 unfavorable factor, including prostate specific antigen less than 10 to 40 ng/ml, Gleason 7 or greater, or T3 on magnetic resonance imaging. We performed Fine and Gray regression, and Cox multivariable analysis to determine whether an increasing prostate specific antigen nadir was associated with prostate cancer specific and all cause mortality, adjusting for treatment, age, Adult Comorbidity Evaluation 27 score and cancer prognostic factors.
Results: At a 6.9-year median followup median prostate specific antigen nadir was 0.7 ng/ml for radiation alone and 0.1 ng/ml for radiation plus androgen deprivation therapy. The prostate specific antigen nadir (adjusted HR 1.18/ng/ml increase, 95% CI 1.07-1.31, p = 0.001) and Gleason 8 or greater (adjusted HR 8.05, 95% CI 1.01-64.05, p = 0.049) significantly predicted increased prostate cancer specific mortality. Moderate/severe comorbidity carried a decreased risk (adjusted HR 0.13, 95% CI 0.02-0.96, p = 0.045). Higher prostate specific antigen nadir (adjusted HR 1.10/ng/ml increase, 95% CI 1.04-1.17), older age (adjusted HR 1.10/year, 95% CI 1.04-1.15) and interaction between comorbidity score and randomization arm (each p < 0.001) increased the all cause mortality risk. Men who achieved a prostate specific antigen nadir of the median value or less had lower estimated prostate cancer specific and all cause mortality at 7 years (3.7% vs 18.3%, p = 0.0005 and 31.5% vs 55.0%, p = 0.002).
Conclusions: Posttreatment prostate specific antigen nadir is significantly associated with the risk of prostate cancer specific and all cause mortality after radiation with or without androgen deprivation therapy. A suboptimal prostate specific antigen nadir may identify candidates for earlier intervention to prolong survival.
C1 [Tseng, Yolanda D.] Dana Farber Canc Inst, Harvard Radiat Oncol Program, Boston, MA 02115 USA.
[Beard, Clair J.; Martin, Neil E.; Orio, Peter F.; Loffredo, Marian; D'Amico, Anthony V.; Nguyen, Paul L.] Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA.
[Choueiri, Toni K.; Kantoff, Philip W.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Hu, Jim C.] Dana Farber Canc Inst, Dept Urol, Boston, MA 02115 USA.
[Beard, Clair J.; Martin, Neil E.; Orio, Peter F.; Choueiri, Toni K.; Hu, Jim C.; Kantoff, Philip W.; D'Amico, Anthony V.; Nguyen, Paul L.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Beard, Clair J.; Martin, Neil E.; Orio, Peter F.; Choueiri, Toni K.; Hu, Jim C.; Kantoff, Philip W.; D'Amico, Anthony V.; Nguyen, Paul L.] Harvard Univ, Sch Med, Boston, MA USA.
[Chen, Ming-Hui] Univ Connecticut, Dept Stat, Storrs, CT 06269 USA.
[Renshaw, Andrew A.] Baptist Hosp Miami, Dept Pathol, Miami, FL USA.
RP Tseng, YD (reprint author), Dana Farber Canc Inst, Harvard Radiat Oncol Program, Boston, MA 02115 USA.
EM ydtseng@partners.org
RI Martin, Neil/E-2193-2014
OI Martin, Neil/0000-0002-8164-8516
FU Prostate Cancer Foundation
FX Supported by a Prostate Cancer Foundation Young Investigator Award,
David and Cynthia Chapin, and a grant from an anonymous family
foundation.
NR 17
TC 6
Z9 7
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5347
J9 J UROLOGY
JI J. Urol.
PD JUN
PY 2012
VL 187
IS 6
BP 2068
EP 2073
DI 10.1016/j.juro.2012.01.073
PG 6
WC Urology & Nephrology
SC Urology & Nephrology
GA 939OK
UT WOS:000303821300037
PM 22498212
ER
PT J
AU Hung, WW
Ross, JS
Boockvar, KS
Siu, AL
AF Hung, William W.
Ross, Joseph S.
Boockvar, Kenneth S.
Siu, Albert L.
TI Association of Chronic Diseases and Impairments With Disability in Older
Adults A Decade of Change?
SO MEDICAL CARE
LA English
DT Article
DE chronic disease; impairment; disability; prevalence trends
ID VISUAL FUNCTION QUESTIONNAIRE; LATE-LIFE DISABILITY; COGNITIVE
IMPAIRMENT; FUNCTIONAL DISABILITY; DIABETES-MELLITUS; WOMENS HEALTH;
UNITED-STATES; POPULATION; RETIREMENT; TRENDS
AB Background: Little is known about how the relationship between chronic disease, impairment, and disability has changed over time among older adults.
Objective: To examine how the associations of chronic disease and impairment with specific disability have changed over time.
Research Design: Repeated cross-sectional analysis, followed by examining the collated sample using time interaction variables, of 3 recent waves of the Health and Retirement Study.
Subjects: The subjects included 10,390, 10,621 and 10,557 community-dwelling adults aged 65 years and above in 1998, 2004, and 2008.
Measurements: Survey-based history of chronic diseases including hypertension, heart disease, heart failure, stroke, diabetes, cancer, chronic lung disease, and arthritis; impairments, including cognition, vision, and hearing; and disability, including mobility, complex activities of daily living (ADL), and self-care ADL.
Results: Over time, the relationship of chronic diseases and impairments with disability was largely unchanged; however, the association between hypertension and complex ADL disability weakened from 1998 to 2004 and 2008 [odds ratio (OR) = 1.24; 99% confidence interval (CI), 1.06-1.46; OR = 1.07; 99% CI, 0.90-1.27; OR = 1.00; 99% CI, 0.83-1.19, respectively], as it did for hypertension and self-care disability (OR = 1.32; 99% CI, 1.13-1.54; OR= 0.97; 99% CI, 0.82-1.14; OR = 0.99; 99% CI, 0.83-1.17). The association between diabetes and self-care disability strengthened from 1998 to 2004 and 2008 (OR = 1.21; 99% CI, 1.01-1.46; OR = 1.37; 99% CI, 1.15-1.64; OR = 1.52; 99% CI, 1.29-1.79), as it also did for lung disease and self-care disability (OR = 1.64; 99% CI, 1.33-2.03; OR = 1.63; 99% CI, 1.32-2.01; OR = 2.11; 99% CI, 1.73-2.57).
Conclusions: Although relationships between diseases, impairments, and disability were largely unchanged, disability became less associated with hypertension and more with diabetes and lung disease.
C1 [Hung, William W.; Boockvar, Kenneth S.; Siu, Albert L.] Mt Sinai Sch Med, Dept Geriatr & Palliat Med, New York, NY 10029 USA.
[Hung, William W.; Boockvar, Kenneth S.; Siu, Albert L.] James J Peters Vet Affairs Med Ctr, Geriatr Res Educ & Clin Ctr, Bronx, NY USA.
[Ross, Joseph S.] Yale Univ, Sch Med, Dept Med, Gen Internal Med Sect, New Haven, CT 06510 USA.
[Ross, Joseph S.] Yale New Haven Med Ctr, Ctr Outcomes Res & Evaluat, New Haven, CT 06504 USA.
[Boockvar, Kenneth S.] Jewish Home Lifecare, New York, NY USA.
[Hung, William W.; Boockvar, Kenneth S.; Siu, Albert L.] James J Peters VA Hlth Serv Res & Dev Res Enhance, Bronx, NY USA.
RP Hung, WW (reprint author), Mt Sinai Sch Med, Dept Geriatr & Palliat Med, 1 Gustave L Levy Pl,Box 1070, New York, NY 10029 USA.
EM william.hung@mssm.edu
OI Boockvar, Kenneth/0000-0003-1165-5558
FU John A Hartford Foundation Center of Excellence; New York Academy of
Medicine; National Institute on Aging [K08 AG032886, U01AG009740];
American Federation of Aging Research; Greenwall Foundation
FX W.W.H. is a John A Hartford Foundation Center of Excellence Scholar and
a New York Academy of Medicine Hoar Fellow. J.S.R. is currently
supported by the National Institute on Aging (K08 AG032886) and by the
American Federation of Aging Research through the Paul B. Beeson Career
Development Award Program. K. S. B. is supported by the Greenwall
Foundation. The Health and Retirement Study is sponsored by the National
Institute on Aging (grant number U01AG009740) and conducted by the
Institute for Social Research at the University of Michigan.
NR 35
TC 20
Z9 22
U1 2
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD JUN
PY 2012
VL 50
IS 6
BP 501
EP 507
DI 10.1097/MLR.0b013e318245a0e0
PG 7
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 941ST
UT WOS:000303985900006
PM 22584885
ER
PT J
AU Okunseri, C
Okunseri, E
Thorpe, JM
Xiang, Q
Szabo, A
AF Okunseri, Christopher
Okunseri, Elaye
Thorpe, Joshua M.
Xiang, Qun
Szabo, Aniko
TI Medications Prescribed in Emergency Departments for Nontraumatic Dental
Condition Visits in the United States
SO MEDICAL CARE
LA English
DT Article
DE dental care; dental service utilization; emergency service; medications
ID ETHNIC DISPARITIES; CARE; ANALGESIA; PAIN; MANAGEMENT; PATIENT
AB Background: Prior research has documented factors associated with nontraumatic dental condition (NTDC) visits to emergency departments (EDs), but little is known about the care received by patients in EDs for NTDC visits.
Objective: We examined national trends in prescription of analgesics and antibiotics in EDs for NTDC visits in the United States.
Research Design: We analyzed data from the National Hospital Ambulatory Medical Care survey from 1997 to 2007. We used a multivariable logistic regression model to examine factors associated with receiving analgesics and antibiotics for NTDC visits in EDs.
Results: Overall 74% received at least 1 analgesic, 56% received at least 1 antibiotic, and 13% received no medication at all during NTDC visits to EDs. The prescription of medications at EDs for NTDC visits steadily increased over time for analgesics (odds ratio = 1.11/y, P < 0.0001) and antibiotics (odds ratio = 1.06/y,P < 0.0001). In the multivariable analysis, self-pay patients had significantly higher adjusted odds of receiving antibiotics, whereas those with nondental reasons for visits and children (0-4 y) had significantly lower adjusted odds of receiving a prescription for antibiotics in EDs for NTDC visits. Children (0-4 y), adults (53-72 y), and older adults (73 y and older) had lower adjusted odds (P < 0.001) of receiving analgesics.
Conclusions: Nationally, analgesic and antibiotic prescriptions for NTDC visits to EDs have increased substantially over time. Selfpay patients had significantly higher odds of being prescribed antibiotics. Adults over 53 years and especially those 73 years and older had significantly lower odds of receiving analgesics in EDs for NTDC visits.
C1 [Okunseri, Christopher; Okunseri, Elaye] Marquette Univ, Dept Clin Serv, Sch Dent, Milwaukee, WI 53201 USA.
[Thorpe, Joshua M.] Univ Pittsburgh, Sch Pharm, Dept Pharm & Therapeut, VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Thorpe, Joshua M.] Ctr Hlth Equity Res & Promot, Pittsburgh, PA USA.
[Xiang, Qun; Szabo, Aniko] Med Coll Wisconsin, Div Biostat, Inst Hlth & Soc, Milwaukee, WI 53226 USA.
RP Okunseri, C (reprint author), Marquette Univ, Dept Clin Serv, Sch Dent, Room 356,POB 1881, Milwaukee, WI 53201 USA.
EM christopher.okunseri@mu.edu
RI Szabo, Aniko/F-9656-2012; Thorpe, Joshua/C-1188-2013
FU National Institute of Health [1R15DE021196-01]
FX Supported by the National Institute of Health Grant #1R15DE021196-01.
The authors declare no conflict of interest.
NR 25
TC 19
Z9 19
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD JUN
PY 2012
VL 50
IS 6
BP 508
EP 512
DI 10.1097/MLR.0b013e318245a575
PG 5
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 941ST
UT WOS:000303985900007
PM 22584886
ER
PT J
AU Kelly, PJ
Mannarino, E
Lewis, JH
Baldini, EH
Hacker, FL
AF Kelly, Paul J.
Mannarino, Edward
Lewis, John Henry
Baldini, Elizabeth H.
Hacker, Fred L.
TI Total dural irradiation: RapidArc versus static-field IMRT: A case study
SO MEDICAL DOSIMETRY
LA English
DT Article
DE IMRT; RapidArc; Dural irradiation; Scalp; Collimator angle
ID TOTAL SCALP IRRADIATION; HELICAL TOMOTHERAPY; RADIOTHERAPY; THERAPY;
CANCER; BRACHYTHERAPY
AB The purpose of this study was to compare conventional fixed-gantry angle intensity-modulated radiation therapy (IMRT) with RapidArc for total dural irradiation. We also hypothesize that target volume-individualized collimator angles may produce substantial normal tissue sparing when planning with RapidArc. Five-, 7-, and 9-field fixed-gantry angle sliding-window IMRT plans were generated for comparison with RapidArc plans. Optimization and normal tissue constraints were constant for all plans. All plans were normalized so that 95% of the planning target volume (PTV) received at least 100% of the dose. RapidArc was delivered using 350 clockwise and counterclockwise arcs. Conventional collimator angles of 45 and 315 were compared with 90 on both arcs. Dose prescription was 59.4 Gy in 33 fractions. PTV metrics used for comparison were coverage, V-107%, D1%, conformality index (CI95%), and heterogeneity index (D-5%-D-95%). Brain dose, the main challenge of this case, was compared using D-1%, Dmean, and V-5 Gy. Dose to optic chiasm, optic nerves, globes, and lenses was also compared. The use of unconventional collimator angles (90 on both arcs) substantially reduced dose to normal brain. All plans achieved acceptable target coverage. Homogeneity was similar for RapidArc and 9-field IMRT plans. However, heterogeneity increased with decreasing number of IMRT fields, resulting in unacceptable hotspots within the brain. Conformality was marginally better with RapidArc relative to IMRT. Low dose to brain, as indicated by V5Gy, was comparable in all plans. Doses to organs at risk (OARs) showed no clinically meaningful differences. The number of monitor units was lower and delivery time was reduced with RapidArc. The case-individualized RapidArc plan compared favorably with the 9-field conventional IMRT plan. In view of lower monitor unit requirements and shorter delivery time, RapidArc was selected as the optimal solution. Individualized collimator angle solutions should be considered by RapidArc dosimetrists for OARs dose reduction. RapidArc should be considered as a treatment modality for tumors that extensively involve in the skull, dura, or scalp. (C) 2012 Published by Elsevier Inc. on behalf of American Association of Medical Dosimetrists.
C1 [Kelly, Paul J.; Mannarino, Edward; Lewis, John Henry; Baldini, Elizabeth H.; Hacker, Fred L.] Harvard Univ, Sch Med, Dana Farber Brigham & Womens Canc Ctr, Dept Radiat Oncol, Boston, MA USA.
RP Kelly, PJ (reprint author), Cork Univ Hosp, Dept Radiotherapy, Cork, Cork, Ireland.
EM paulj.kelly@hse.ie
OI Hacker, Fred/0000-0001-7535-7598
NR 20
TC 5
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 0958-3947
J9 MED DOSIM
JI Med. Dosim.
PD SUM
PY 2012
VL 37
IS 2
BP 175
EP 181
DI 10.1016/j.meddos.2011.06.008
PG 7
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 941HV
UT WOS:000303955200012
PM 21862313
ER
PT J
AU Haas, NB
Lin, XY
Manola, J
Pins, M
Liu, G
McDermott, D
Nanus, D
Heath, E
Wilding, G
Dutcher, J
AF Haas, Naomi B.
Lin, Xinyi
Manola, Judith
Pins, Michael
Liu, Glenn
McDermott, David
Nanus, David
Heath, Elisabeth
Wilding, George
Dutcher, Janice
TI A phase II trial of doxorubicin and gemcitabine in renal cell carcinoma
with sarcomatoid features: ECOG 8802
SO MEDICAL ONCOLOGY
LA English
DT Article
DE Sarcomatoid; Gemcitabine; Doxorubicin; Renal cell cancer; Kidney cancer
ID HISTOLOGIC SUBTYPES; EXPRESSION; CANCER; CHEMOTHERAPY; EXPERIENCE;
TUMORS
AB Sarcomatoid features can arise in renal cell carcinoma of any subtype and are associated with a poor prognosis. Doxorubicin and gemcitabine in a limited series showed activity in aggressive renal tumors and we wished to formally assess the combination in patients with renal cell carcinoma specifically containing sarcomatoid features. The Eastern Cooperative Oncology Group (ECOG) conducted a phase II trial of doxorubicin 50 mg/m(2) IV push and gemcitabine 1,500 mg/m(2) IV over 30 min every 2 weeks in 39 patients with locally advanced or metastatic renal cell carcinoma with sarcomatoid features. Ten patients (26%) had grade 3 toxicity, and four patients (11%) had grade 4 toxicities. Although most toxicity was from myelosuppression, one patient died on study from cardiac dysfunction after a cumulative dose of 450 mg/m(2) doxorubicin. Six (16%) patients experienced responses (5 partial responses and 1 complete response), and ten (26%) patients had stable disease. In addition, another patient had an unconfirmed partial response and an additional patient experienced over 50% decrease in her tumor burden after an initial progression. The median overall survival was 8.8 months, and the median progression-free survival was 3.5 months. We conclude that the combination of doxorubicin and gemcitabine, inactive in patients with mostly clear cell histology, demonstrated responses in patients with RCC with sarcomatoid features. We acknowledge the toxicity of this combination but note that limited treatment options exist for this aggressive histology. Only through prospective multicenter trials with comprehensive central pathology review will better treatment options be identified.
C1 [Haas, Naomi B.] Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Lin, Xinyi] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Manola, Judith] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Pins, Michael] Univ Illinois, Chicago Coll Med, Advocate Lutheran Gen Hosp, Park Ridge, IL USA.
[Liu, Glenn; Wilding, George] Univ Wisconsin, Carbone Canc Ctr, Madison, WI 53706 USA.
[McDermott, David] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Nanus, David] New York Presbyterian Hosp, New York, NY USA.
[Heath, Elisabeth] Karmanos Canc Ctr Inst, Detroit, MI USA.
[Dutcher, Janice] St Lukes Roosevelt Hosp, Continuum Canc Ctr, Div Hematol Oncol, New York, NY USA.
RP Haas, NB (reprint author), Abramson Canc Ctr, 16 Penn Tower,3400 Spruce St, Philadelphia, PA 19104 USA.
EM naomi.haas@uphs.upenn.edu
FU NCI NIH HHS [U10 CA066636, U10 CA023318, U10 CA021076, U10 CA021115, U24
CA114737]
NR 29
TC 37
Z9 39
U1 1
U2 5
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1357-0560
J9 MED ONCOL
JI Med. Oncol.
PD JUN
PY 2012
VL 29
IS 2
BP 761
EP 767
DI 10.1007/s12032-011-9829-8
PG 7
WC Oncology
SC Oncology
GA 935RX
UT WOS:000303539000057
PM 21298497
ER
PT J
AU Ran, CZ
Moore, A
AF Ran, Chongzhao
Moore, Anna
TI Spectral Unmixing Imaging of Wavelength-Responsive Fluorescent Probes:
An Application for the Real-Time Report of Amyloid Beta Species in
Alzheimer's Disease
SO MOLECULAR IMAGING AND BIOLOGY
LA English
DT Article
DE Spectral unmixing; Alzheimer's disease; Wavelength-responsive
fluorescent probe
ID IN-VIVO; CELLS; OLIGOMERS; PEPTIDE; LIGHT; RED
AB The goal of the study was to investigate a method for the real-time assessment of a target concentration using a combination of a spectral unmixing technique and a fluorescent probe specific for amyloid beta (A beta) species, the biomarkers for Alzheimer's disease (AD).
The probe CRANAD-3 has a significant emission wavelength shift upon binding to A beta species. It was used to differentiate a bound probe from an unbound probe in a phantom, in brain slices and whole brain, and in a transgenic mouse model of AD.
The unmixing imaging of AD brain clearly showed differential distribution of the bound and unbound probes between the brain tissue and blood vessels. The unmixed signals of bound CRANAD-3 reached a plateau with increasing dosage, demonstrating that these signals correspond to A beta content, not probe injected dose.
This study provided evidence that signals processed by the spectral unmixing technique could be used as a real-time reporter of A beta species loading and .
C1 [Ran, Chongzhao; Moore, Anna] Harvard Univ, Massachusetts Gen Hosp, MGH MIT HMS Athinoula Martinos Ctr Biomed Imaging, Mol Imaging Lab Dept Radiol, Boston, MA 02129 USA.
RP Moore, A (reprint author), Harvard Univ, Massachusetts Gen Hosp, MGH MIT HMS Athinoula Martinos Ctr Biomed Imaging, Mol Imaging Lab Dept Radiol, Room 2301,Bldg 149, Boston, MA 02129 USA.
EM amoore@helix.mgh.harvard.edu
FU [K25AG036760]
FX This work was supported in part by K25AG036760 award to C. R. We would
like to thank Marytheresa Ifediba for proofreading this manuscript.
NR 20
TC 10
Z9 10
U1 3
U2 15
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1536-1632
J9 MOL IMAGING BIOL
JI Mol. Imaging. Biol.
PD JUN
PY 2012
VL 14
IS 3
BP 293
EP 300
DI 10.1007/s11307-011-0501-7
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 940IY
UT WOS:000303884400004
PM 21739354
ER
PT J
AU Sembajwe, G
Wahrendorf, M
Siegrist, J
Sitta, R
Zins, M
Goldberg, M
Berkman, L
AF Sembajwe, Grace
Wahrendorf, Morten
Siegrist, Johannes
Sitta, Remi
Zins, Marie
Goldberg, Marcel
Berkman, Lisa
TI Effects of job strain on fatigue: cross-sectional and prospective views
of the job content questionnaire and effort-reward imbalance in the
GAZEL cohort
SO OCCUPATIONAL AND ENVIRONMENTAL MEDICINE
LA English
DT Article
ID CORONARY-HEART-DISEASE; PSYCHOSOCIAL WORK-ENVIRONMENT; PSYCHOMETRIC
PROPERTIES; MYOCARDIAL-INFARCTION; DECISION LATITUDE; DEPRESSIVE
SYMPTOMS; VITAL EXHAUSTION; FRENCH VERSION; RISK-FACTORS; HEALTH
AB Objectives The objectives this study were (1) to investigate correlations between measures of psychosocial workplace stress as measured in separate years by the Job Content Questionnaire (JCQ) and Effort-Reward Imbalance (ERI) scales; (2) to establish a valid measure of psychosocial job stress with its components (by identifying the individual and interactive associations of job stress components) and (3) to use the component measures to assess the risk of psychosocial strain at work on fatigue.
Methods The JCQ and ERI from the annual survey of the GAZEL cohort established in 1989 initially with 20 624 respondents were used to investigate the associations of workplace stress on mental and physical fatigue in two separate years (1998 and 2006). First, the JCQ measures from separate years (1997 and 1999) were combined to create a measure for the same year as ERI (1998). The new measure was validated for internal and external consistency. Using logistic regression, the subcomponents of stress (upper tertiles of psychological demands, physical demands, decision latitude, social support, effort, reward, ERI and overcommitment) were tested for associations with the highest reporting of mental and physical fatigue.
Results By combining JCQ responses from 1997 to 1999, we were able to increase the amount of information available on psychosocial factors in 1998. Psychometric properties of the workplace stress scales also showed expected factor loadings. Workplace psychosocial factors had greater associations with fatigue among men than women. Although psychosocial factors became less predictive of fatigue at 8 years of follow-up, associations between fatigue and psychosocial components (overcommitment, social support and rewards) remained significant.
Conclusions These analyses continue to validate the various subcomponents scales of workplace stress as measured by the JCQ and effort-reward imbalance model in GAZEL. They also highlight the importance of psychosocial work factors in the experience of overall fatigue even after an 8-year follow-up.
C1 [Sembajwe, Grace; Berkman, Lisa] Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Boston, MA 02115 USA.
[Sembajwe, Grace] Dana Farber Canc Inst, Ctr Community Based Res, Boston, MA 02115 USA.
[Sembajwe, Grace; Sitta, Remi; Zins, Marie; Goldberg, Marcel] Ctr Res Epidemiol & Populat Hlth, INSERM, U1018, Villejuif, France.
[Wahrendorf, Morten; Siegrist, Johannes] Univ Dusseldorf, Inst Med Soziol, D-40225 Dusseldorf, Germany.
[Sitta, Remi; Zins, Marie; Goldberg, Marcel] Versailles St Quentin Univ, Versailles, France.
[Berkman, Lisa] Harvard Ctr Populat & Dev Studies, Cambridge, MA 02138 USA.
RP Sembajwe, G (reprint author), Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, 665 Huntington Ave, Boston, MA 02115 USA.
EM grace_sembajwe@dfci.harvard.edu
FU ANR; AFSSET; National Institute on Aging [5U01AG027669-06
/3U01AG027669-05S1]; National Institutes of Health; AFSSET, France;
EDF-GDF (Electricite de France-Gaz de France); INSERM (Institut National
de la Sante de de la Recherche Me dicale)
FX This study was supported by ANR and AFSSET Workage grants, and National
Institute on Aging grant #5U01AG027669-06 /3U01AG027669-05S1 for support
of LB during this period. Other Funders: National Institutes of Health;
l'Agence Nationale de la Recherche (ANR) and AFSSET, France. The GAZEL
cohort is funded by grants from EDF-GDF (Electricite de France-Gaz de
France) in association with INSERM (Institut National de la Sante de de
la Recherche Me dicale).
NR 53
TC 13
Z9 13
U1 4
U2 25
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1351-0711
J9 OCCUP ENVIRON MED
JI Occup. Environ. Med.
PD JUN
PY 2012
VL 69
IS 6
BP 377
EP 384
DI 10.1136/oem.2010.063503
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 940SH
UT WOS:000303912900002
PM 21849345
ER
PT J
AU Rush, AJ
Wisniewski, SR
Zisook, S
Fava, M
Sung, SC
Haley, CL
Chan, HN
Gilmer, WS
Warden, D
Nierenberg, AA
Balasubramani, GK
Gaynes, BN
Trivedi, MH
Hollon, SD
AF Rush, A. J.
Wisniewski, S. R.
Zisook, S.
Fava, M.
Sung, S. C.
Haley, C. L.
Chan, H. N.
Gilmer, W. S.
Warden, D.
Nierenberg, A. A.
Balasubramani, G. K.
Gaynes, B. N.
Trivedi, M. H.
Hollon, S. D.
TI Is prior course of illness relevant to acute or longer-term outcomes in
depressed out-patients? A STAR*D report
SO PSYCHOLOGICAL MEDICINE
LA English
DT Article
DE Chronic; course of illness; depression; outcomes; recurrent
ID SEQUENCED TREATMENT ALTERNATIVES; DIAGNOSTIC SCREENING QUESTIONNAIRE;
MEASUREMENT-BASED CARE; REPORT QIDS-SR; SELF-REPORT; RELIEVE DEPRESSION;
QUICK INVENTORY; RATING-SCALE; RECURRENT DEPRESSION; MAJOR DEPRESSION
AB Background. Major depressive disorder (MDD) is commonly chronic and/or recurrent. We aimed to determine whether a chronic and/or recurrent course of MDD is associated with acute and longer-term MDD treatment outcomes.
Method. This cohort study recruited out-patients aged 18-75 years with non-psychotic MDD from 18 primary and 23 psychiatric care clinics across the USA. Participants were grouped as : chronic (index episode >2 years) and recurrent (n=398); chronic non-recurrent (n=257); non-chronic recurrent (n=1614); and non-chronic non-recurrent (n=387). Acute treatment was up to 14 weeks of citalopram (<= 60 mg/day) with up to 12 months of follow-up treatment. The primary outcomes for this report were remission [16-item Quick Inventory of Depressive Symptomatology - Self-Rated (QIDS-SR16) <= 5] or response (>= 50% reduction from baseline in QIDS-SR16) and time to first relapse [first QIDS-SR16 by Interactive Voice Response (IVR) >= 11].
Results. Most participants (85%) had a chronic and/or recurrent course; 15% had both. Chronic index episode was associated with greater sociodemographic disadvantage. Recurrent course was associated with earlier age of onset and greater family histories of depression and substance abuse. Remission rates were lowest and slowest for those with chronic index episodes. For participants in remission entering follow-up, relapse was most likely for the chronic and recurrent group, and least likely for the non-chronic, non-recurrent group. For participants not in remission when entering follow-up, prior course was unrelated to relapse.
Conclusions. Recurrent MDD is the norm for out-patients, of whom 15% also have a chronic index episode. Chronic and recurrent course of MDD may be useful in predicting acute and long-term MDD treatment outcomes.
C1 [Rush, A. J.; Sung, S. C.; Haley, C. L.] Duke NUS Grad Med Sch Singapore, Off Clin Sci, Singapore, Singapore.
[Wisniewski, S. R.; Balasubramani, G. K.] Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA USA.
[Zisook, S.] Univ Calif San Diego, Dept Psychiat, San Diego VA Med Ctr, San Diego, CA 92103 USA.
[Fava, M.; Nierenberg, A. A.] Massachusetts Gen Hosp, Depress Clin & Res Program, Boston, MA 02114 USA.
[Chan, H. N.] Singapore Gen Hosp, Dept Psychiat, Singapore 0316, Singapore.
[Gilmer, W. S.; Trivedi, M. H.] Northwestern Univ, Dept Psychiat & Behav Sci, Feinberg Sch Med, Chicago, IL 60611 USA.
[Warden, D.] Univ Texas SW Med Ctr Dallas, Dept Psychiat, Dallas, TX 75390 USA.
[Gaynes, B. N.] Univ N Carolina, Sch Med, Dept Psychiat, Chapel Hill, NC USA.
[Hollon, S. D.] Vanderbilt Univ, Dept Psychol, Nashville, TN 37240 USA.
RP Trivedi, MH (reprint author), Univ Texas SW Med Ctr Dallas, Bass Ctr, 6363 Forest Pk Rd,13-354, Dallas, TX 75235 USA.
EM madhukar.trivedi@utsouthwestern.edu
OI Wisniewski, Stephen/0000-0002-3877-9860; Gaynes,
Bradley/0000-0002-8283-5030; Rush, Augustus/0000-0003-2004-2382;
Goundappa K, Balasubramani/0000-0001-7221-1825
FU NIMH [N01MH90003]; Bristol-Myers Squibb; Forest Laboratories;
GlaxoSmithKline; King Pharmaceuticals; Organon; Pfizer; Wyeth; Robert
Wood Johnson Foundation; NIMH; Stanley Medical Research Institute;
Aspect Medical; PamLab.; Abbott Laboratories; Alkermes; Aspect Medical
Systems; Astra-Zeneca; Bristol-Myers Squibb Company; Cephalon; Forest
Pharmaceuticals Inc.; J & J Pharmaceuticals; Lichtwer Pharma GmbH; Eli
Lilly Company; Lorex Pharmaceuticals; Novartis; Organon Inc.; LLC;
Pfizer Inc.; Pharmavite; Roche; Sanofi/Synthelabo; Solvay
Pharmaceuticals, Inc.; Wyeth-Ayerst Laboratories; Janssen Pharmaceutica;
Neuronetics; National Institute of Drug Abuse; NARSAD; Cederroth;
Cyberonics, Inc.; Lichtwer Pharma; National Alliance for Research in
Schizophrenia and Depression, Stanley Foundation; Agency for Healthcare
Research and Quality; M-3 Corporation; Ovation Pharmaceuticals;
Cephalon, Inc.; Corcept Therapeutics, Inc.; National Alliance for
Research in Schizophrenia and Depression; Predix Pharmaceuticals
FX This project was funded by the NIMH under Contract N01MH90003 to UT
Southwestern Medical Center at Dallas (PI: A.J. Rush). The content of
this publication does not necessarily reflect the views or policies of
the Department of Health and Human Services, nor does mention of trade
names, commercial products, or organizations imply endorsement by the
U.S. Government. We appreciate the support of Bristol-Myers Squibb,
Forest Laboratories, GlaxoSmithKline, King Pharmaceuticals, Organon,
Pfizer, and Wyeth for providing medications at no cost for this trial.
We also acknowledge the editorial support of J. Kilner. None of these
entities had a role in any part of the study (e.g. design, execution,
data collection, analysis, interpretation of the data, writing any
report, including this one). Drs Rush and Wisniewski had full access to
all of the data in the study and take responsibility for the integrity
of the data and the accuracy of the data analysis.; A.J. Rush: Research
support: Robert Wood Johnson Foundation; the NIMH; the Stanley Medical
Research Institute. Advisory/consulting: Advanced Neuronetic Systems,
Inc.; AstraZeneca; Best Practice Project Management, Inc.; Bristol-Myers
Squibb Company; Cyberonics, Inc.; Forest Pharmaceuticals, Inc.; Gerson
Lehman Group; GlaxoSmithKline; Healthcare Technology Systems, Inc.; Jazz
Pharmaceuticals; Eli Lilly & Company; Magellan Health Services; Merck &
Co., Inc.; Neuronetics; Ono Pharmaceutical; Organon USA Inc.;
Personality Disorder Research Corp.; Pfizer Inc.; The Urban Institute;
and Wyeth-Ayerst Laboratories Inc. Speaking : Cyberonics, Inc.; Forest
Pharmaceuticals, Inc.; GlaxoSmithKline; Eli Lilly & Company; and Merck &
Co., Inc. Equity holdings (exclude mutual funds/blinded trusts): Pfizer
Inc. Royalty/patent, other income: Guilford Publications; Healthcare
Technology Systems, Inc. S. R. Wisniewski: Research support: NIMH.
Advisory/consulting: Cyberonics, Inc. S. Zisook: Research support: NIMH;
Aspect Medical; PamLab. Advisory/consulting: GlaxoSmithKline. Speaking:
AstraZeneca Pharmaceuticals; Forest Pharmaceuticals, Inc.;
GlaxoSmithKline; Janssen Pharmaceutica Products, LP; Eli Lilly &
Company; Pfizer Inc.; Wyeth Pharmaceuticals. M. Fava: Research support:
Abbott Laboratories; Alkermes; Aspect Medical Systems; Astra-Zeneca;
Bristol-Myers Squibb Company; Cephalon; Forest Pharmaceuticals Inc.;
GlaxoSmithKline; J & J Pharmaceuticals; Lichtwer Pharma GmbH; Eli Lilly
& Company; Lorex Pharmaceuticals; Novartis; Organon Inc.; PamLab, LLC;
Pfizer Inc.; Pharmavite; Roche; Sanofi/Synthelabo; Solvay
Pharmaceuticals, Inc.; Wyeth-Ayerst Laboratories. Advisory/consulting:
Aspect Medical Systems; Astra-Zeneca; Bayer AG; Biovail Pharmaceuticals,
Inc.; BrainCells, Inc.; Bristol-Myers Squibb Company; Cephalon;
Compellis; Cypress Pharmaceuticals; Dov Pharmaceuticals; EPIX
Pharmaceuticals; Fabre-Kramer Pharmaceuticals, Inc.; Forest
Pharmaceuticals Inc.; GlaxoSmithKline; Grunenthal GmBH; J & J
Pharmaceuticals; Janssen Pharmaceutica; Jazz Pharmaceuticals; Knoll
Pharmaceutical Company; Eli Lilly & Company; Lundbeck; MedAvante, Inc.;
Novartis; Nutrition 21; Organon Inc.; PamLab, LLC; Pfizer Inc.;
PharmaStar; Pharmavite; Roche; Sanofi/Synthelabo; Sepracor; Solvay
Pharmaceuticals, Inc.; Somerset Pharmaceuticals; Wyeth-Ayerst
Laboratories. Speaking: Astra-Zeneca; Bristol-Myers Squibb Company;
Cephalon; Forest Pharmaceuticals Inc.; GlaxoSmithKline; Eli Lilly &
Company; Novartis; Organon Inc.; Pfizer Inc.; PharmaStar; Wyeth-Ayerst
Laboratories. Equity holdings (exclude mutual funds/blinded trusts):
Compellis, MedAvante. W. S. Gilmer: Research support: Abbott
Laboratories, Aspect Medical; Forest Pharmaceuticals Inc.; Janssen
Pharmaceutica; Neuronetics; Novartis; Pfizer Inc.; NIMH.
Advisory/consulting: Astra-Zeneca; Bristol-Myers Squibb Company; Eli
Lilly & Company; Forest Pharmaceuticals; GlaxoSmithKline; Pfizer, Inc.;
Shire. Speaking: Bristol-Myers Squibb Company; Forest Pharmaceuticals;
GlaxoSmithKline; Pfizer Inc.; Wyeth-Ayerst Laboratories. D. Warden:
Research Support: NIMH, National Institute of Drug Abuse, NARSAD; Equity
holdings: Pfizer, Bristol Myers Squib. A. A. Nierenberg: Research
support: Bristol-Myers Squibb Company; Cederroth; Cyberonics, Inc.;
Forest Pharmaceuticals Inc.; GlaxoSmithKline; Janssen Pharmaceutica;
Lichtwer Pharma; Eli Lilly & Company; Pfizer Inc.; NIMH; National
Alliance for Research in Schizophrenia and Depression, Stanley
Foundation; Wyeth-Ayerst Laboratories.; Advisory/consulting:
Bristol-Myers Squibb Company; Eli Lilly & Company; Genaissance;
GlaxoSmithKline; Innapharma; Neuronetics; Pfizer, Inc.; Sepracor; Shire.
Speaking: Eli Lilly & Company; GlaxoSmithKline; Organon, Inc.;
Wyeth-Ayerst Laboratories. B. N. Gaynes: Research support: NIMH; Agency
for Healthcare Research and Quality; Robert Wood Johnson Foundation; the
M-3 Corporation; Bristol-Myers Squibb Company; Novartis; Pfizer, Inc.;
and Ovation Pharmaceuticals. Advisory/consulting: Pfizer, Inc.; Shire
Pharmaceuticals; Wyeth-Ayerst. Speaking: GlaxoSmithKline. M. H. Trivedi:
Research support: Bristol-Myers Squibb Company; Cephalon, Inc.; Corcept
Therapeutics, Inc.; Eli Lilly & Company; GlaxoSmithKline; Janssen
Pharmaceutica; NIMH; National Alliance for Research in Schizophrenia and
Depression; Pfizer Inc.; Predix Pharmaceuticals; Wyeth-Ayerst
Laboratories. Advisory/consulting: Abbott Laboratories, Inc.; Akzo
(Organon Pharmaceuticals Inc.); Bayer; Bristol-Myers Squibb Company;
Cyberonics, Inc.; Forest Pharmaceuticals; GlaxoSmithKline; Janssen
Pharmaceutica Products, LP; Johnson & Johnson PRD; Eli Lilly & Company;
Meade Johnson; Parke-Davis Pharmaceuticals, Inc.; Pfizer, Inc.;
Pharmacia & Upjohn; Sepracor; Solvay Pharmaceuticals, Inc.; Wyeth-Ayerst
Laboratories. Speaking: Akzo (Organon Pharmaceuticals Inc.);
Bristol-Myers Squibb Company; Cyberonics, Inc.; Forest Pharmaceuticals;
Janssen Pharmaceutica Products, LP; Eli Lilly & Company; Pharmacia &
Upjohn; Solvay Pharmaceuticals, Inc.; Wyeth-Ayerst Laboratories. S. D.
Hollon: Research support: NIMH. Royalty/patent, other income: Guilford
Publications; Wiley.
NR 53
TC 20
Z9 20
U1 1
U2 5
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0033-2917
J9 PSYCHOL MED
JI Psychol. Med.
PD JUN
PY 2012
VL 42
IS 6
BP 1131
EP 1149
DI 10.1017/S0033291711002170
PG 19
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 939PV
UT WOS:000303825800002
PM 22008447
ER
PT J
AU Yu, DK
Shi, J
Sun, T
Du, XL
Liu, L
Zhang, XJ
Lu, C
Tang, XH
Li, M
Xiao, LC
Zhang, ZW
Yuan, QP
Yang, M
AF Yu, Dianke
Shi, Juan
Sun, Tong
Du, Xiaoli
Liu, Li
Zhang, Xiaojiao
Lu, Chao
Tang, Xiaohu
Li, Meng
Xiao, Lingchen
Zhang, Zhouwei
Yuan, Qipeng
Yang, Ming
TI Pharmacogenetic role of ERCC1 genetic variants in treatment response of
platinum-based chemotherapy among advanced non-small cell lung cancer
patients
SO TUMOR BIOLOGY
LA English
DT Article
DE Chemotherapy; ERCC1; Meta-analysis; Pharmacogenetics; Platinum
ID NUCLEOTIDE EXCISION-REPAIR; DNA-REPAIR; POLYMORPHISMS; CISPLATIN;
SURVIVAL; XPD; ENDONUCLEASE; METAANALYSIS; ASSOCIATION; EXPRESSION
AB The excision repair cross-complementation group 1 (ERCC1) plays an essential role in DNA repair and has been linked to resistance to platinum-based anticancer drugs among advanced non-small cell lung cancer (NSCLC) patients. We systematically evaluate whether ERCC1 Asn118Asn and C8092A genetic variants are associated with treatment response of platinum chemotherapy. We preformed a meta-analysis using ten eligible cohort studies (including 11 data-sets) with a total of 1,252 NSCLC patients to summarize the existing data on the association between the ERCC1 Asn118Asn and C8092A polymorphisms and response to platinum regiments. Odds ratio or hazard ratio with 95% confidence interval were calculated to estimate the correlation. We found that neither ERCC1 C8092A polymorphism nor Asn118Asn variant is associated with different response of platinum-based treatment among advanced NSCLC patients. Additionally, these two genetic variants are not related to treatment response in either Caucasian patients or Asian patients. Our meta-analysis indicates that the ERCC1 Asn118Asn and C8092A polymorphisms may not be good prognostic biomarkers for platinum-based chemotherapy in patients with stage III-IV NSCLC.
C1 [Yuan, Qipeng; Yang, Ming] Beijing Univ Chem Technol, Coll Life Sci & Technol, Beijing 100029, Peoples R China.
[Yu, Dianke] Chinese Acad Med Sci, State Key Lab Mol Oncol, Dept Etiol & Carcinogenesis, Canc Inst & Hosp, Beijing 100730, Peoples R China.
[Yu, Dianke] Peking Union Med Coll, Beijing 100021, Peoples R China.
[Shi, Juan; Liu, Li; Zhang, Xiaojiao; Lu, Chao; Tang, Xiaohu; Li, Meng; Xiao, Lingchen; Zhang, Zhouwei; Yuan, Qipeng; Yang, Ming] Beijing Univ Chem Technol, Coll Life Sci & Technol, Beijing, Peoples R China.
[Sun, Tong] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Sun, Tong] Harvard Univ, Sch Med, Boston, MA USA.
[Du, Xiaoli] NCI, Cellular Oncol Lab, NIH, Bethesda, MD 20892 USA.
RP Yuan, QP (reprint author), Beijing Univ Chem Technol, Coll Life Sci & Technol, POB 53, Beijing 100029, Peoples R China.
EM yuanqp@mail.buct.edu.cn; yangm@mail.buct.edu.cn
RI Yang, Ming/G-4705-2012
OI Yang, Ming/0000-0002-7722-7487
FU Beijing Nova Program [2010B013]; Fundamental Research Funds for the
Central Universities [ZZ1234]; National Natural Science Foundation of
China [30872968]
FX This work was supported by Beijing Nova Program (no. 2010B013 to M.
Yang), the Fundamental Research Funds for the Central Universities (no.
ZZ1234 to M. Yang) and National Natural Science Foundation of China (no.
30872968).
NR 29
TC 13
Z9 14
U1 0
U2 3
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1010-4283
J9 TUMOR BIOL
JI Tumor Biol.
PD JUN
PY 2012
VL 33
IS 3
SI SI
BP 877
EP 884
DI 10.1007/s13277-011-0314-y
PG 8
WC Oncology
SC Oncology
GA 935PA
UT WOS:000303530200033
PM 22249976
ER
PT J
AU Genta, RM
Sonnenberg, A
AF Genta, R. M.
Sonnenberg, A.
TI Non-Helicobacter pylori gastritis is common among paediatric patients
with inflammatory bowel disease
SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS
LA English
DT Article
ID FOCALLY ENHANCED GASTRITIS; CROHNS-DISEASE; ULCERATIVE-COLITIS;
PEPTIC-ULCER; INFECTION; MORTALITY; BIOPSIES; DUODENUM
AB Background
Helicobacter-negative gastritis and duodenitis occur more often in patients with inflammatory bowel disease (IBD) than in non-IBD controls. Preliminary evidence suggests that they are particularly common among children.
Aim
To study the age-specific occurrence of gastritis and duodenitis among paediatric IBD patients.
Methods
From a computerised database of surgical pathology reports, we selected 344 IBD patients and 4241 non-IBD controls between the age 0 and 21 years, who underwent colonoscopy and oesophago-gastro-duodenoscopy with biopsy results from both procedures.
Results
Helicobacter-negative chronic active gastritis was found in 2% of controls and 20% of IBD patients (Crohn's disease (CD) 26%, ulcerative colitis (UC) 13%). Duodenitis was found in 2% of controls and 17% of IBD patients (Crohn's disease 28%, UC 8%). Similar prevalence rates were observed in male and female patients. The most striking age-specific patterns were seen in Crohn's disease, with chronic active gastritis being highest in the 59 years age-group and declining in all subsequent age-groups. The age-specific rise and fall of duodenitis appeared more protracted, reaching a peak at age 1014 years and then gradually declining.
Conclusions
Helicobacter-negative gastritis and duodenitis occur significantly more often in paediatric IBD patients than in non-IBD controls, as well as in adult IBD patients. Such upper gastrointestinal inflammation appears to be particularly common in patients with Crohn's disease.
C1 [Genta, R. M.] Miraca Life Sci, Irving, TX USA.
[Genta, R. M.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Genta, R. M.] Dallas VA Med Ctr, Dallas, TX USA.
[Sonnenberg, A.] Portland VA Med Ctr, Portland, OR USA.
[Sonnenberg, A.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
RP Sonnenberg, A (reprint author), Portland VA Med Ctr P3 GI, 3710 SW US Vet Hosp Rd, Portland, OR 97239 USA.
EM sonnenbe@ohsu.edu
FU Takeda Pharmaceuticals
FX Declaration of personal interests: Robert M. Genta is employed by Miraca
Life Sciences, Irving, TX, USA. Amnon Sonnenberg is supported by a grant
from Takeda Pharmaceuticals.
NR 22
TC 12
Z9 13
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0269-2813
J9 ALIMENT PHARM THER
JI Aliment. Pharmacol. Ther.
PD JUN
PY 2012
VL 35
IS 11
BP 1310
EP 1316
DI 10.1111/j.1365-2036.2012.05090.x
PG 7
WC Gastroenterology & Hepatology; Pharmacology & Pharmacy
SC Gastroenterology & Hepatology; Pharmacology & Pharmacy
GA 934IF
UT WOS:000303437000007
PM 22486730
ER
PT J
AU Lee, YJ
Lee, HJ
Choi, SH
Jin, YB
An, HJ
Kang, JH
Yoon, SS
Lee, YS
AF Lee, Yoon-Jin
Lee, Hae-Jun
Choi, Seo-hyun
Jin, Yeung Bae
An, Ho Jung
Kang, Jin-Hyoung
Yoon, Sam S.
Lee, Yun-Sil
TI Soluble HSPB1 regulates VEGF-mediated angiogenesis through their direct
interaction
SO ANGIOGENESIS
LA English
DT Article
DE Heat shock protein 25/27 (HSPB1); Angiogenic balance; Vascular
endothelial growth (VEGF); Endothelial cell (EC)
ID ENDOTHELIAL GROWTH-FACTOR; ALPHA-B-CRYSTALLIN; HEAT-SHOCK PROTEINS;
TUMOR-GROWTH; CANCER; INHIBITION; KINASE; THROMBOSPONDIN-1;
PHOSPHORYLATION; EXPRESSION
AB Endothelial cell function is critical for angiogenic balance in both physiological and pathological conditions, such as wound healing and cancer, respectively. We report here that soluble heat shock protein beta-1 (HSPB1) is released primarily from endothelial cells (ECs), and plays a key role in regulating angiogenic balance via direct interaction with vascular endothelial growth factor (VEGF). VEGF-mediated phosphorylation of intracellular HSPB1 inhibited the secretion of HSPB1 and their binding activity in ECs. Interestingly, co-culture of tumor ECs with tumor cells decreased HSPB1 secretion from tumor ECs, suggesting that inhibition of HSPB1 secretion allows VEGF to promote angiogenesis. Additionally, neutralization of HSPB1 in a primary mouse sarcoma model promoted tumor growth, indicating the anti-angiogenic role of soluble HSPB1. Overexpression of HSPB1 by HSPB1 adenovirus was sufficient to suppress lung metastases of CT26 colon carcinoma in vivo, while neutralization of HSPB1 promoted in vivo wound healing. While VEGF-induced regulation of angiogenesis has been studied extensively, these findings illustrate the key contribution of HSPB1-VEGF interactions in the balance between physiological and pathological angiogenesis.
C1 [Lee, Yun-Sil] Ewha Womans Univ, Coll Pharm, Seoul 120750, South Korea.
[Lee, Yun-Sil] Ewha Womans Univ, Div Life & Pharmaceut Sci, Seoul 120750, South Korea.
[Lee, Yoon-Jin; Lee, Hae-Jun; Choi, Seo-hyun; Jin, Yeung Bae] Korea Inst Radiol & Med Sci, Div Radiat Effects, Seoul 139706, South Korea.
[Choi, Seo-hyun] Korea Univ, Sch Life Sci & Biotechnol, Seoul 136701, South Korea.
[An, Ho Jung; Kang, Jin-Hyoung] Catholic Univ, Div Med Oncol, Seoul St Marys Hosp, Seoul 137040, South Korea.
[Yoon, Sam S.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Yoon, Sam S.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Lee, YS (reprint author), Ewha Womans Univ, Coll Pharm, Seoul 120750, South Korea.
EM yslee0425@ewha.ac.kr
OI An, Ho Jung/0000-0003-0821-8365
FU Nuclear Research and Development Program [M2AMA006]; Basic Science
Research Program [R1A4A002]; National Research Foundation of Korea (NRF)
[2011-0013364]; Korean Ministry of Education, Science, and Technology
(MEST)
FX We thank Dr. Sandra Ryeom (University of Pennsylvania Medical School)
for helpful discussions and Dr. Christiana DelloRusso for assistance
editing the manuscript. This work was supported by the Nuclear Research
and Development Program (Grant No. M2AMA006), Basic Science Research
Program (Grant No. R1A4A002), and Mid-career Researcher Program (Grat
No. 2011-0013364) of the National Research Foundation of Korea (NRF)
funded by the Korean Ministry of Education, Science, and Technology
(MEST).
NR 42
TC 16
Z9 18
U1 1
U2 15
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0969-6970
J9 ANGIOGENESIS
JI Angiogenesis
PD JUN
PY 2012
VL 15
IS 2
BP 229
EP 242
DI 10.1007/s10456-012-9255-3
PG 14
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 934TU
UT WOS:000303470400005
PM 22350794
ER
PT J
AU Munshi, MN
Maguchi, M
Segal, AR
AF Munshi, Medha N.
Maguchi, Megumi
Segal, Alissa R.
TI Treatment of Type 2 Diabetes in the Elderly
SO CURRENT DIABETES REPORTS
LA English
DT Article
DE Diabetes; Elderly; Treatment, Type 2
ID COGNITIVE DYSFUNCTION; MEDICATION USE; OLDER-ADULTS; MELLITUS;
HYPOGLYCEMIA; PATIENT; POPULATION; MANAGEMENT; ADHERENCE; OUTCOMES
AB As the number of older adults increases in the United States and worldwide, management of patients with multiple coexisting chronic diseases has become a critical component in health care. Management of diabetes is particularly challenging in this population due to significant risks of microvascular and macrovascular diseases on the one hand, and complications of the treatment strategies (e.g., hypoglycemia) with intensive control on the other hand. To provide a balanced approach to diabetes in the elderly, a comprehensive and holistic strategy, with consideration of overall health, functional status, psychosocial environment, financial resources and, finally but most importantly, quality of life is needed. Understanding the unique challenges faced by older adults with diabetes and issues pertaining to antidiabetes medications with aging is an important first step in the direction of better and tailored care of this burgeoning population.
C1 [Munshi, Medha N.] Harvard Univ, Sch Med, Joslin Diabet Ctr, Div Geriatr,Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Segal, Alissa R.] Massachusetts Coll Pharm & Hlth Sci, Joslin Diabet Ctr, Dept Pharm Practice, Boston, MA 02215 USA.
RP Munshi, MN (reprint author), Harvard Univ, Sch Med, Joslin Diabet Ctr, Div Geriatr,Beth Israel Deaconess Med Ctr, 110 Francis St,LMOB 1B, Boston, MA 02215 USA.
EM mmunshi@bidmc.harvard.edu; mmaguchi@bidmc.harvard.edu;
alissa.segal@mcphs.edu
FU Sanofi-Aventis
FX M. Munshi: has received grant support from Sanofi-Aventis; M. Maguchi:
none; A. Segal: none.
NR 31
TC 8
Z9 10
U1 5
U2 15
PU CURRENT MEDICINE GROUP
PI PHILADELPHIA
PA 400 MARKET STREET, STE 700, PHILADELPHIA, PA 19106 USA
SN 1534-4827
J9 CURR DIABETES REP
JI Curr. Diabetes Rep.
PD JUN
PY 2012
VL 12
IS 3
BP 239
EP 245
DI 10.1007/s11892-012-0269-4
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 935JQ
UT WOS:000303515400005
PM 22484911
ER
PT J
AU Phipps, MS
Jastreboff, AM
Furie, K
Kernan, WN
AF Phipps, Michael S.
Jastreboff, Ania M.
Furie, Karen
Kernan, Walter N.
TI The Diagnosis and Management of Cerebrovascular Disease in Diabetes
SO CURRENT DIABETES REPORTS
LA English
DT Article
DE Cerebrovascular disorders; Stroke; Cerebral hemorrhage; Ischemic attack;
Transient; Diabetes mellitus; Diagnosis; Therapeutics; Cerebrovascular
disease
ID TRANSIENT ISCHEMIC ATTACK; ASSOCIATION/AMERICAN-STROKE-ASSOCIATION;
HEALTH-CARE PROFESSIONALS; SPONTANEOUS INTRACEREBRAL HEMORRHAGE;
AMERICAN-HEART-ASSOCIATION; MULTIPLE LACUNAR INFARCTS;
PLACEBO-CONTROLLED TRIAL; IN-HOSPITAL MORTALITY; BLOOD-GLUCOSE CONTROL;
HIGH-RISK PATIENTS
AB Cerebrovascular disease is a leading cause of morbidity and mortality in diabetes. Compared with nondiabetic patients, diabetic patients have at least twice the risk for stroke, earlier onset of symptoms, and worse functional outcomes. Approximately 20 % of diabetic patients will die from stroke, making it one of the leading causes of death in this population. Effective strategies for primary and secondary prevention of stroke have been developed in research cohorts that included both diabetic and nondiabetic patients. Nevertheless, prevention in diabetes has some specific considerations. In this paper, we summarize evidence to guide the diagnosis and management of stroke in diabetic patients. We propose that diabetic stroke patients should have a robust risk assessment to target interventions, like other patients with cerebrovascular disease, but with special attention to glycemic control and lifestyle modification.
C1 [Phipps, Michael S.] VA Connecticut Healthcare Syst, West Haven, CT 06519 USA.
[Phipps, Michael S.; Jastreboff, Ania M.] Yale Univ, Sch Med, New Haven, CT 06519 USA.
[Furie, Karen] Harvard Univ, Massachusetts Gen Hosp, Sch Med, J Philip Kistler MGH Stroke Res Ctr, Boston, MA 02114 USA.
[Kernan, Walter N.] Yale Univ, Sch Med, New Haven, CT 06525 USA.
RP Phipps, MS (reprint author), VA Connecticut Healthcare Syst, 950 Campbell Ave,Mail Code 11-ACSLG, West Haven, CT 06519 USA.
EM michael.phipps@yale.edu; ania.jastreboff@yale.edu; kfurie@partners.org;
walter.kernan@yale.edu
OI Phipps, Michael/0000-0001-8398-5404
FU Takeda Pharmaceuticals North America
FX M.S. Phipps: none; A. M. Jastreboff: has received payment for lectures
including service on speakers bureaus for Yale Affiliated Hospital
Program - providing medical education lectures to hospital in Southern
Connecticut; and is a contractor for Pfizer providing clinical services
for study volunteers; K. Furie: none; W.N. Kernan: has received grant
support from Takeda Pharmaceuticals North America.
NR 100
TC 6
Z9 8
U1 2
U2 2
PU CURRENT MEDICINE GROUP
PI PHILADELPHIA
PA 400 MARKET STREET, STE 700, PHILADELPHIA, PA 19106 USA
SN 1534-4827
J9 CURR DIABETES REP
JI Curr. Diabetes Rep.
PD JUN
PY 2012
VL 12
IS 3
BP 314
EP 323
DI 10.1007/s11892-012-0271-x
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 935JQ
UT WOS:000303515400014
PM 22492061
ER
PT J
AU Sprenger, T
Borsook, D
AF Sprenger, Till
Borsook, David
TI Migraine changes the brain: neuroimaging makes its mark
SO CURRENT OPINION IN NEUROLOGY
LA English
DT Review
DE functional MRI; migraine; magnetic resonance spectroscopy; PET;
voxel-based morphometry
ID PERIAQUEDUCTAL GRAY-MATTER; SPREADING DEPRESSION; HEMIPLEGIC MIGRAINE;
STEM ACTIVATION; BASAL GANGLIA; HEADACHE; PAIN; ATTACKS; AURA; CORTEX
AB Purpose of review
This review summarizes key findings of the current literature on functional neuroimaging in migraine and describes how these studies have changed our view of the disorder.
Recent findings
Recent studies have started not only to investigate the global cerebral activation pattern during migraine attacks, but to address specific aspects of migraine attacks such as photophobia, osmophobia as well as pain perception with the aim of disentangling the underlying mechanisms. There is also more and more evidence that the migraine brain is abnormal even outside of attacks and that repeated attacks are leading to functional and structural alterations in the brain, which may in turn drive the transformation of migraine to its chronic form. Some new results are pinpointing toward a potential role of interesting new brain areas in migraine pathophysiology such as the temporal cortex or the basal ganglia.
Summary
Neuroimaging studies are beginning to shed light on the mechanisms underlying the development and evolution of migraine and its specific symptoms. Future studies have the potential to also improve our understanding of established and upcoming treatment approaches and to monitor treatment effects in an objective and noninvasive way.
C1 [Sprenger, Till] Univ Basel Hosp, Dept Neurol, CH-4031 Basel, Switzerland.
[Sprenger, Till] Univ Basel Hosp, Div Neuroradiol, Dept Radiol & Nucl Med, CH-4031 Basel, Switzerland.
[Borsook, David] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Pain & Brain, Boston, MA USA.
[Borsook, David] Harvard Univ, Childrens Hosp, Sch Med, Ctr Pain & Brain, Boston, MA 02115 USA.
RP Borsook, D (reprint author), Harvard Univ, Ctr Pain & Brain, Sch Med, Brain Imaging Ctr, 115 Mill St, Belmont, MA 02478 USA.
EM dborsook@partners.org
FU NIH [K24 NS064050 (NINDS), R01 NS056195 (NINDS)]
FX We gratefully acknowledge Michaela Andelova, MUDr for help with Table 1.
The work was supported by grants from NIH (K24 NS064050 (NINDS) and R01
NS056195 (NINDS) to D.B.
NR 85
TC 34
Z9 34
U1 1
U2 14
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1350-7540
J9 CURR OPIN NEUROL
JI Curr. Opin. Neurol.
PD JUN
PY 2012
VL 25
IS 3
BP 252
EP 262
DI 10.1097/WCO.0b013e3283532ca3
PG 11
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 935UB
UT WOS:000303545600006
PM 22487570
ER
PT J
AU Hu, JC
Williams, SB
O'Malley, AJ
Smith, MR
Nguyen, PL
Keating, NL
AF Hu, Jim C.
Williams, Stephen B.
O'Malley, A. James
Smith, Matthew R.
Nguyen, Paul L.
Keating, Nancy L.
TI Androgen-Deprivation Therapy for Nonmetastatic Prostate Cancer Is
Associated With an Increased Risk of Peripheral Arterial Disease and
Venous Thromboembolism
SO EUROPEAN UROLOGY
LA English
DT Article
DE Hormonal/adverse effect; Prostatic neoplasms/drug therapy; Peripheral
vascular disease; Venous thromboembolism
ID CARDIOVASCULAR-DISEASE; BODY-COMPOSITION; SENSITIVITY; SUPPRESSION;
CONFOUNDERS; THROMBOSIS; STIFFNESS; HEALTH; MEN
AB Background: Previous studies demonstrate that androgen-deprivation therapy (ADT) with gonadotropin-releasing hormone (GnRH) agonists and orchiectomy for prostate cancer (PCa) is associated with cardiovascular disease. However, few studies have examined its effect on the peripheral vascular system.
Objective: To study the risk of peripheral artery disease (PAD) and venous thromboembolism associated with ADT for PCa.
Design, settings, and participants: This was a population-based observational study of 182 757 US men >= 66 yr of age who were diagnosed with nonmetastatic PCa from 1992 to 2007, with a median follow-up of 5.1 yr, of whom 47.8% received GnRH agonists and 2.2% orchiectomy.
Measurements: We used Cox proportional hazards models with time-varying treatment variables to adjust for demographic and tumor characteristics in assessing whether treatment with GnRH agonists or orchiectomy were associated with PAD and/or venous thromboembolism.
Results and limitations: GnRH agonist use was associated with an increased risk of incident PAD (adjusted hazard ratio [HR]: 1.16; 95% confidence interval [CI], 1.12-1.21) and incident venous thromboembolism (adjusted HR: 1.10; 95% CI, 1.04-1.15). In addition, orchiectomy was associated with an increased risk of peripheral arterial disease (adjusted HR: 1.13; 95% CI, 1.02-1.26) and venous thromboembolism (adjusted HR: 1.27; 95% CI, 1.11-1.45). Limitations include the observational study design and the inability to assess the use of oral antiandrogens.
Conclusions: ADT for nonmetastatic PCa is associated with an increased risk of PAD and venous thromboembolism. Additional research is needed to better understand the potential risks and benefits of ADT, so that this treatment can be targeted to patients for whom the benefits are clearest. (C) 2012 European Association of Urology. Published by Elsevier B.V. All rights reserved.
C1 [Hu, Jim C.] Univ Calif Los Angeles, Inst Urol Oncol, Dept Urol, David Geffen Sch Med, Los Angeles, CA 90024 USA.
[Williams, Stephen B.] Brigham & Womens Hosp, Div Urol, Ctr Surg & Publ Hlth, Boston, MA 02115 USA.
[O'Malley, A. James; Keating, Nancy L.] Harvard Univ, Dept Hlth Policy, Sch Med, Boston, MA USA.
[Smith, Matthew R.] Massachusetts Gen Hosp, Div Med Oncol, Boston, MA 02114 USA.
[Nguyen, Paul L.] Brigham & Womens Hosp, Dept Radiat Oncol, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Keating, Nancy L.] Brigham & Womens Hosp, Div Gen Internal Med, Boston, MA 02115 USA.
RP Hu, JC (reprint author), Univ Calif Los Angeles, Inst Urol Oncol, Dept Urol, David Geffen Sch Med, 924 Westwood BLVD,STE 1000, Los Angeles, CA 90024 USA.
EM jhu2@partners.org
FU Prostate Cancer Foundation
FX This study was funded by the Prostate Cancer Foundation.
NR 29
TC 34
Z9 34
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0302-2838
J9 EUR UROL
JI Eur. Urol.
PD JUN
PY 2012
VL 61
IS 6
BP 1119
EP 1128
DI 10.1016/j.eururo.2012.01.045
PG 10
WC Urology & Nephrology
SC Urology & Nephrology
GA 934PW
UT WOS:000303458000015
PM 22336376
ER
PT J
AU Konijeti, R
Kibel, AS
AF Konijeti, Ramdev
Kibel, Adam S.
TI Androgen Deprivation Therapy for Localized and Nonmetastatic Prostate
Cancer: Too Much of a Good Thing?
SO EUROPEAN UROLOGY
LA English
DT Editorial Material
C1 [Kibel, Adam S.] Harvard Univ, Div Urol, Dept Surg, Brigham & Womens Hosp,Med Sch, Boston, MA 02115 USA.
[Konijeti, Ramdev] Harvard Univ, Dept Med Oncol, Dana Farber Canc Inst, Sch Med, Boston, MA 02115 USA.
RP Kibel, AS (reprint author), Harvard Univ, Div Urol, Dept Surg, Brigham & Womens Hosp,Med Sch, 45 Francis St, Boston, MA 02115 USA.
EM akibel@partners.org
NR 10
TC 2
Z9 2
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0302-2838
J9 EUR UROL
JI Eur. Urol.
PD JUN
PY 2012
VL 61
IS 6
BP 1129
EP 1130
DI 10.1016/j.eururo.2012.03.002
PG 2
WC Urology & Nephrology
SC Urology & Nephrology
GA 934PW
UT WOS:000303458000016
PM 22445550
ER
PT J
AU Keating, NL
Smith, MR
Hu, JC
AF Keating, Nancy L.
Smith, Matthew R.
Hu, Jim C.
TI Reply from Authors re: Ramdev Konijeti, Adam S. Kibel. Androgen
Deprivation Therapy for Localized and Nonmetastatic Prostate Cancer: Too
Much of a Good Thing? Eur Urol 2012;61:1129-30 Still Much to Understand
About Androgen Deprivation Therapy and Cardiovascular Disease
SO EUROPEAN UROLOGY
LA English
DT Editorial Material
ID CLINICAL-TRIALS; PARTICIPATION; MEN; AGE
C1 [Keating, Nancy L.] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
[Keating, Nancy L.] Brigham & Womens Hosp, Div Gen Internal Med, Boston, MA 02115 USA.
[Smith, Matthew R.] Massachusetts Gen Hosp, Div Med Oncol, Boston, MA 02114 USA.
[Hu, Jim C.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Urol, Los Angeles, CA 90095 USA.
RP Keating, NL (reprint author), Harvard Univ, Sch Med, Dept Hlth Care Policy, 180 Longwood Ave, Boston, MA 02115 USA.
EM keating@hcp.med.harvard.edu
NR 11
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0302-2838
J9 EUR UROL
JI Eur. Urol.
PD JUN
PY 2012
VL 61
IS 6
BP 1131
EP 1131
DI 10.1016/j.eururo.2012.03.044
PG 1
WC Urology & Nephrology
SC Urology & Nephrology
GA 934PW
UT WOS:000303458000017
ER
PT J
AU Yu, HY
Hevelone, ND
Lipsitz, SR
Kowalczyk, KJ
Nguyen, PL
Choueiri, TK
Kibel, AS
Hu, JC
AF Yu, Hua-yin
Hevelone, Nathanael D.
Lipsitz, Stuart R.
Kowalczyk, Keith J.
Nguyen, Paul L.
Choueiri, Toni K.
Kibel, Adam S.
Hu, Jim C.
TI Comparative Analysis of Outcomes and Costs Following Open Radical
Cystectomy Versus Robot-Assisted Laparoscopic Radical Cystectomy:
Results From the US Nationwide Inpatient Sample
SO EUROPEAN UROLOGY
LA English
DT Article
DE Bladder cancer; Cost; Cystectomy; Outcomes; Robotic surgery
ID BLADDER-CANCER; PROSTATECTOMY; COMPLICATIONS; SURGERY; EMPHASIS
AB Background: Although robot-assisted laparoscopic radical cystectomy (RARC) was first reported in 2003 and has gained popularity, comparisons with open radical cystectomy (ORC) are limited to reports from high-volume referral centers.
Objective: To compare population-based perioperative outcomes and costs of ORC and RARC.
Design, setting, and participants: A retrospective observational cohort study using the US Nationwide Inpatient Sample to characterize 2009 RARC compared with ORC use and outcomes.
Outcome measurements and statistical analysis: Propensity score methods were used to compare inpatient morbidity and mortality, lengths of stay, and costs.
Results and limitations: We identified 1444 ORCs and 224 RARCs. Women were less likely to undergo RARC than ORC (9.8% compared with 15.5%, p = 0.048), and 95.7% of RARCs and 73.9% of ORCs were performed at teaching hospitals (p < 0.001). In adjusted analyses, subjects undergoing RARC compared with ORC experienced fewer inpatient complications (49.1% and 63.8%, p = 0.035) and fewer deaths (0% and 2.5%, p < 0.001). RARC compared with ORC was associated with lower parenteral nutrition use (6.4% and 13.3%, p = 0.046); however, there was no difference in length of stay. RARC compared with ORC was $3797 more costly (p = 0.023). Limitations include retrospective design, absence of tumor characteristics, and lack of outcomes beyond hospital discharge.
Conclusions: RARC is associated with lower parenteral nutrition use and fewer inpatient complications and deaths. However, lengths of stay are similar, and the robotic approach is significantly more costly. (C) 2012 European Association of Urology. Published by Elsevier B.V. All rights reserved.
C1 [Hu, Jim C.] Univ Calif Los Angeles, David Geffen Sch Med, Inst Urol Oncol, Dept Urol, Los Angeles, CA 90024 USA.
[Yu, Hua-yin; Kibel, Adam S.] Harvard Univ, Brigham & Womens Hosp, Div Urol, Sch Med, Boston, MA 02115 USA.
[Hevelone, Nathanael D.; Lipsitz, Stuart R.] Harvard Univ, Brigham & Womens Hosp, Ctr Surg & Publ Hlth, Sch Med, Boston, MA 02115 USA.
[Kowalczyk, Keith J.] Georgetown Univ Hosp, Dept Urol, Washington, DC 20007 USA.
[Nguyen, Paul L.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Radiat Oncol,Lank Ctr Genitourinary Oncol, Boston, MA 02115 USA.
[Choueiri, Toni K.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med,Lank Ctr Genitourinary Oncol, Boston, MA 02115 USA.
RP Hu, JC (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Inst Urol Oncol, Dept Urol, 924 Westwood Blvd,Suite 1000, Los Angeles, CA 90024 USA.
EM jimhumd@gmail.com
OI Hevelone, Nathanael/0000-0003-4740-2085
FU American Urological Association; Robert and Kathy Salipante
Minimally-Invasive Urologic Research Fellowship; US Department of
Defense [W81XWH-08-1-0283]
FX Jim C. Hu certifies that all conflicts of interest, including specific
financial interests and relationships and affiliations relevant to the
subject matter or materials discussed in the manuscript (eg,
employment/affiliation, grants or funding, consultancies, honoraria,
stock ownership or options, expert testimony, royalties, or patents
filed, received, or pending), are the following: Dr. Yu receives salary
support from the American Urological Association Foundation Research
Scholars Award and the Robert and Kathy Salipante Minimally-Invasive
Urologic Research Fellowship, and Dr. Hu receives salary support from
the US Department of Defense Physician Training Award W81XWH-08-1-0283.
NR 32
TC 53
Z9 53
U1 0
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0302-2838
J9 EUR UROL
JI Eur. Urol.
PD JUN
PY 2012
VL 61
IS 6
BP 1239
EP 1244
DI 10.1016/j.eururo.2012.03.032
PG 6
WC Urology & Nephrology
SC Urology & Nephrology
GA 934PW
UT WOS:000303458000040
PM 22482778
ER
PT J
AU Stephens, CE
Newcomer, R
Blegen, M
Miller, B
Harrington, C
AF Stephens, Caroline E.
Newcomer, Robert
Blegen, Mary
Miller, Bruce
Harrington, Charlene
TI Emergency Department Use by Nursing Home Residents: Effect of Severity
of Cognitive Impairment
SO GERONTOLOGIST
LA English
DT Article
DE cognitive impairment; nursing home; emergency department;
hospitalization; ambulatory care-sensitive condition
ID MINIMUM DATA SET; FACILITY RESIDENTS; TRANSITIONAL CARE; ADVANCED
DEMENTIA; AMBULATORY-CARE; OLDER-PEOPLE; HOSPITALIZATION; HEALTH;
DECISIONS; MDS
AB To examine the 1-year prevalence and risk of emergency department (ED) use and ambulatory care-sensitive (ACS) ED use by nursing home (NH) residents with different levels of severity of cognitive impairment (CI).
We used multinomial logistic regression to estimate the effect of CI severity on the odds of any ED visit and any ACS ED visit in a 2006 national random sample of NH residents, controlling for predisposing, enabling, and need characteristics.
Of 132,753 NH residents, 62% had at least one ED visit and approximately 24% had at least one ACS ED visit in 2006. The probability of any ED visit or any ACS ED visit varied with the severity of resident CI. Residents with mild CI had up to15% higher odds of any ED or any ACS ED visit and those with more moderate CI had 9% higher odds of an ACS ED visit compared with those without CI. The probability of any ED visit was negatively associated with advanced dementia (adjusted odds ratio = 0.60; 95% CI = 0.55-0.65).
Earlier identification of persons with mild CI may facilitate patient, family, and staff education, as well as advanced care planning to reduce ACS ED visits. Both ACS ED use and hospitalizations, adjusted for case mix, should be used as quality indicators to help ensure greater accountability for high-quality NH care and more appropriate utilization of ED resources.
C1 [Stephens, Caroline E.; Newcomer, Robert; Harrington, Charlene] Univ Calif San Francisco, Dept Social & Behav Sci, San Francisco, CA 94143 USA.
[Stephens, Caroline E.] San Francisco VA Med Ctr, Div Geriatr Palliat & Extended Care, San Francisco, CA USA.
[Blegen, Mary] Univ Calif San Francisco, Dept Neurol, San Francisco, CA USA.
[Miller, Bruce] Univ Calif San Francisco, Dept Community Hlth Syst, San Francisco, CA 94143 USA.
RP Stephens, CE (reprint author), Univ Calif San Francisco, Dept Social & Behav Sci, 3333 Calif St,Suite 455, San Francisco, CA 94143 USA.
EM caroline.stephens@ucsf.edu
NR 42
TC 11
Z9 11
U1 1
U2 8
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD JUN
PY 2012
VL 52
IS 3
BP 383
EP 393
DI 10.1093/geront/gnr109
PG 11
WC Gerontology
SC Geriatrics & Gerontology
GA 936OM
UT WOS:000303599900009
PM 22056961
ER
PT J
AU Menschikowski, M
Hagelgans, A
Fuessel, S
Mareninova, OA
Neumeister, V
Wirth, MP
Siegert, G
AF Menschikowski, Mario
Hagelgans, Albert
Fuessel, Susanne
Mareninova, Olga A.
Neumeister, Volker
Wirth, Manfred P.
Siegert, Gabriele
TI Serum Levels of Secreted Group IIA Phospholipase A(2) in Benign
Prostatic Hyperplasia and Prostate Cancer: A Biomarker for Inflammation
or Neoplasia?
SO INFLAMMATION
LA English
DT Article
DE prostate cancer; benign prostatic hyperplasia; secreted phospholipase
A(2); C-reactive protein; inflammation
ID C-REACTIVE PROTEIN; PROGNOSTIC MARKER; EXPRESSION; DISEASES; RISK;
ANTIGEN; INTERLEUKIN-6; ASSOCIATION; INCIDENT; ENZYMES
AB Secreted group IIA phospholipase A(2) (sPLA(2)-IIA) is markedly up-regulated in human prostate cancer (PCa) specimens and in some PCa-derived cell lines, indicating an important role of this enzyme in tumourigenesis. In this study, we measured levels of sPLA(2)-IIA, C-reactive protein (CRP), and prostate-specific antigen (PSA) in serum samples obtained from patients with benign prostatic hyperplasia (BPH) and with PCa of different stages. We found that serum levels of sPLA(2)-IIA and CRP in BPH and PCa patients were significantly elevated compared to those of healthy individuals, but the concentrations of these inflammatory biomarkers did not differ between patients with BPH or PCa. Furthermore, serum levels of sPLA(2)-IIA correlated with concentrations of CRP, but not with PSA, Gleason grade or tumour stage. In conclusion, these findings suggest that cancer-related changes are not exclusive factors contributing to elevated serum sPLA(2)-IIA levels and emphasize the utility of sPLA(2)-IIA as a circulating marker of inflammation in patients with BPH and PCa.
C1 [Menschikowski, Mario; Hagelgans, Albert; Neumeister, Volker; Siegert, Gabriele] Tech Univ Dresden, Med Fac Carl Gustav Carus, Inst Clin Chem & Lab Med, D-01307 Dresden, Germany.
[Fuessel, Susanne; Wirth, Manfred P.] Tech Univ Dresden, Med Fac Carl Gustav Carus, Dept Urol, D-01307 Dresden, Germany.
[Mareninova, Olga A.] Univ Calif Los Angeles, Vet Affairs Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
RP Menschikowski, M (reprint author), Tech Univ Dresden, Med Fac Carl Gustav Carus, Inst Clin Chem & Lab Med, Fetscherstr 74, D-01307 Dresden, Germany.
EM Mario.Menschikowski@uniklinikum-dresden.de
NR 40
TC 9
Z9 9
U1 0
U2 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0360-3997
EI 1573-2576
J9 INFLAMMATION
JI Inflammation
PD JUN
PY 2012
VL 35
IS 3
BP 1113
EP 1118
DI 10.1007/s10753-011-9418-1
PG 6
WC Cell Biology; Immunology
SC Cell Biology; Immunology
GA 933SI
UT WOS:000303382400041
PM 22189868
ER
PT J
AU Tan, NX
Tucker, JD
AF Tan, Nicholas X.
Tucker, Joseph D.
TI Inequality and infection in China
SO INTERNATIONAL JOURNAL OF INFECTIOUS DISEASES
LA English
DT Letter
ID INCOME INEQUALITY; HEALTH
C1 [Tan, Nicholas X.] Harvard Univ, Fac Arts & Sci, Boston, MA 02138 USA.
[Tucker, Joseph D.] Massachusetts Gen Hosp, Infect Dis Unit, Boston, MA 02114 USA.
RP Tan, NX (reprint author), Harvard Univ, Fac Arts & Sci, Boston, MA 02138 USA.
EM ntan@fas.harvard.edu
NR 7
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1201-9712
J9 INT J INFECT DIS
JI Int. J. Infect. Dis.
PD JUN
PY 2012
VL 16
IS 6
BP E468
EP E468
DI 10.1016/j.ijid.2012.02.008
PG 1
WC Infectious Diseases
SC Infectious Diseases
GA 934JN
UT WOS:000303440500011
PM 22486856
ER
PT J
AU Premereur, E
Vanduffel, W
Janssen, P
AF Premereur, Elsie
Vanduffel, Wim
Janssen, Peter
TI Local Field Potential Activity Associated with Temporal Expectations in
the Macaque Lateral Intraparietal Area
SO JOURNAL OF COGNITIVE NEUROSCIENCE
LA English
DT Article
ID POSTERIOR PARIETAL CORTEX; SELECTIVE VISUAL-ATTENTION; ALPHA
OSCILLATIONS; NEURONAL SYNCHRONIZATION; FREQUENCY OSCILLATIONS;
HEMODYNAMIC SIGNALS; OCCIPITAL CORTEX; REPRESENTATION; MODULATION;
MONKEY
AB Oscillatory brain activity is attracting increasing interest in cognitive neuroscience. Numerous EEG (magnetoencephalography) and local field potential (LFP) measurements have related cognitive functions to different types of brain oscillations, but the functional significance of these rhythms remains poorly understood. Despite its proven value, LFP activity has not been extensively tested in the macaque lateral intraparietal area (LIP), which has been implicated in a wide variety of cognitive control processes. We recorded action potentials and LFPs in area LIP during delayed eye movement tasks and during a passive fixation task, in which the time schedule was fixed so that temporal expectations about task-relevant cues could be formed. LFP responses in the gamma band discriminated reliably between saccade targets and distractors inside the receptive field (RF). Alpha and beta responses were much less strongly affected by the presence of a saccade target, however, but rose sharply in the waiting period before the go signal. Surprisingly, conditions without visual stimulation of the LIP-RF-evoked robust LFP responses in every frequency band-most prominently in those below 50 Hz-precisely time-locked to the expected time of stimulus onset in the RF. These results indicate that in area LIP, oscillations in the LFP, which reflect synaptic input and local network activity, are tightly coupled to the temporal expectation of task-relevant cues.
C1 [Premereur, Elsie] Katholieke Univ Leuven, Lab Neuro & Psychofysiol, B-3000 Louvain, Belgium.
[Vanduffel, Wim] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Vanduffel, Wim] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
RP Janssen, P (reprint author), Katholieke Univ Leuven, Lab Neuro & Psychofysiol, O&N 2,Herestr 49,Bus 1021, B-3000 Louvain, Belgium.
EM Peter.Janssen@med.kuleuven.be
FU Geneeskundige Stichting Koningin Elisabeth; Fonds voor Wetenschappelijk
Onderzoek [G.0713.09, G.0622.08, G.0831.11]; Interuniversity Attraction
Poles [P6/29]; Excellentie Financiering [EF/05/014]; National Science
Foundation [BCS-0745436]; Programma Financiering [PFV/10/008];
Geconcerteerde onderzoeksacties [GOA/10/19]
FX We thank Stijn Verstraeten, Piet Kayenbergh, Gerrit Meulemans, Marc De
Paep, Inez Puttemans, and Marjan Docx for assistance and Steve Raiguel
for comments on a previous version of this manuscript. This study was
supported by Geneeskundige Stichting Koningin Elisabeth, Fonds voor
Wetenschappelijk Onderzoek (G.0713.09, G.0622.08, and G.0831.11),
Interuniversity Attraction Poles (P6/29), Excellentie Financiering
(EF/05/014), National Science Foundation (BCS-0745436), Programma
Financiering (PFV/10/008), and Geconcerteerde onderzoeksacties
(GOA/10/19).
NR 53
TC 6
Z9 6
U1 0
U2 11
PU MIT PRESS
PI CAMBRIDGE
PA 55 HAYWARD STREET, CAMBRIDGE, MA 02142 USA
SN 0898-929X
J9 J COGNITIVE NEUROSCI
JI J. Cogn. Neurosci.
PD JUN
PY 2012
VL 24
IS 6
BP 1314
EP 1330
PG 17
WC Neurosciences; Psychology, Experimental
SC Neurosciences & Neurology; Psychology
GA 935EK
UT WOS:000303501600005
PM 22390466
ER
PT J
AU So, K
Ganguly, K
Jimenez, J
Gastpar, MC
Carmena, JM
AF So, Kelvin
Ganguly, Karunesh
Jimenez, Jessica
Gastpar, Michael C.
Carmena, Jose M.
TI Redundant information encoding in primary motor cortex during natural
and prosthetic motor control
SO JOURNAL OF COMPUTATIONAL NEUROSCIENCE
LA English
DT Article
DE Mutual information; Neural ensemble; Motor control; Brain-machine
interface; Electrophysiology; Primary motor cortex
ID CORTICAL-NEURONS; POPULATION CODES; MOVEMENT DIRECTION; ARM MOVEMENTS;
DISCHARGE; SYNERGY; REORGANIZATION; INDEPENDENCE; INTERFACE
AB Redundant encoding of information facilitates reliable distributed information processing. To explore this hypothesis in the motor system, we applied concepts from information theory to quantify the redundancy of movement-related information encoded in the macaque primary motor cortex (M1) during natural and neuroprosthetic control. Two macaque monkeys were trained to perform a delay center-out reaching task controlling a computer cursor under natural arm movement (manual control, 'MC'), and using a brain-machine interface (BMI) via volitional control of neural ensemble activity (brain control, 'BC'). During MC, we found neurons in contralateral M1 to contain higher and more redundant information about target direction than ipsilateral M1 neurons, consistent with the laterality of movement control. During BC, we found that the M1 neurons directly incorporated into the BMI ('direct' neurons) contained the highest and most redundant target information compared to neurons that were not incorporated into the BMI ('indirect' neurons). This effect was even more significant when comparing to M1 neurons of the opposite hemisphere. Interestingly, when we retrained the BMI to use ipsilateral M1 activity, we found that these neurons were more redundant and contained higher information than contralateral M1 neurons, even though ensembles from this hemisphere were previously less redundant during natural arm movement. These results indicate that ensembles most associated to movement contain highest redundancy and information encoding, which suggests a role for redundancy in proficient natural and prosthetic motor control.
C1 [So, Kelvin; Jimenez, Jessica; Gastpar, Michael C.; Carmena, Jose M.] Univ Calif Berkeley, Dept Elect Engn & Comp Sci, Berkeley, CA 94720 USA.
[Ganguly, Karunesh] San Francisco VA Med Ctr, San Francisco, CA USA.
[Ganguly, Karunesh] Univ Calif San Francisco, Dept Neurol, San Francisco, CA USA.
[Gastpar, Michael C.] Ecole Polytech Fed Lausanne, Sch Comp & Commun Sci, EPFL, Lausanne, Switzerland.
[Carmena, Jose M.] Univ Calif Berkeley, Helen Wills Neurosci Inst, Berkeley, CA 94720 USA.
[Carmena, Jose M.] Univ Calif Berkeley, UCB UCSF Joint Grad Grp Bioengn, Berkeley, CA 94720 USA.
[Carmena, Jose M.] Univ Calif Berkeley, Program Cognit Sci, Berkeley, CA 94720 USA.
RP Carmena, JM (reprint author), Univ Calif Berkeley, Dept Elect Engn & Comp Sci, 754 Sutardja Dai Hall, Berkeley, CA 94720 USA.
EM carmena@eecs.berkeley.edu
FU National Science Foundation CDI; Department of Veterans Affairs,
Veterans Health Administration, Rehabilitation Research and Development;
American Heart Association/American Stroke Association
FX The research reported here was supported by the National Science
Foundation CDI Type-I grant to M.C.G. and J.M.C., and the Department of
Veterans Affairs, Veterans Health Administration, Rehabilitation
Research and Development, and the American Heart Association/American
Stroke Association to K.G.
NR 26
TC 4
Z9 4
U1 2
U2 7
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0929-5313
J9 J COMPUT NEUROSCI
JI J. Comput. Neurosci.
PD JUN
PY 2012
VL 32
IS 3
BP 555
EP 561
DI 10.1007/s10827-011-0369-1
PG 7
WC Mathematical & Computational Biology; Neurosciences
SC Mathematical & Computational Biology; Neurosciences & Neurology
GA 936KO
UT WOS:000303589500011
PM 22042443
ER
PT J
AU Tolboom, H
Izamis, ML
Sharma, N
Milwid, JM
Uygun, B
Berthiaume, F
Uygun, K
Yarmush, ML
AF Tolboom, Herman
Izamis, Maria-Louisa
Sharma, Nripen
Milwid, Jack M.
Uygun, Basak
Berthiaume, Francois
Uygun, Korkut
Yarmush, Martin L.
TI Subnormothermic Machine Perfusion at Both 20 degrees C and 30 degrees C
Recovers Ischemic Rat Livers for Successful Transplantation
SO JOURNAL OF SURGICAL RESEARCH
LA English
DT Article
DE liver transplantation; reperfusion injury; sub-normothermic machine
perfusion
ID NORMOTHERMIC EXTRACORPOREAL PERFUSION; HEART-BEATING DONOR;
ORGAN-PRESERVATION; REPERFUSION INJURY; STEATOTIC LIVERS; TEMPERATURE;
GRAFTS; FUTURE; MODEL
AB Background. Utilizing livers from donors after cardiac death could significantly expand the donor pool. We have previously shown that normothermic (37 degrees C) extracorporeal liver perfusion significantly improves transplantation outcomes of ischemic rat livers. Here we investigate whether recovery of ischemic livers is possible using sub-normothermic machine perfusion at 20 degrees C and 30 degrees C.
Methods. Livers from male Lewis rats were divided into five groups after 1 h of warm ischemia (WI): (1) WI only, (2) 5 h of static cold storage (SCS), or 5 h of MP at (3) 20 degrees C, (4) 30 degrees C, and (5) 37 degrees C. Long-term graft performance was evaluated for 28 d post-transplantation. Acute graft performance was evaluated during a 2 h normothermic sanguineous reperfusion ex vivo. Fresh livers with 5 h of SCS were positive transplant controls while fresh livers were positive reperfusion controls.
Results. Following machine perfusion (MP) (Groups 3, 4, and 5), ischemically damaged livers could be ortho-topically transplanted into syngeneic recipients with 100% survival (N >= 4) after 4 wk. On the other hand, animals from WI only, or WI + SCS groups all died within 24 h of transplantation. Fresh livers preserved using SCS had the highest alanine aminotransferase (ALT), aspartate aminotransferase (AST), and the lowest bile production during reperfusion, while at 28 d post-transplantation, livers preserved at 20 degrees C and 30 degrees C had the highest total bilirubin values.
Conclusions. MP at both 20 degrees C and 30 degrees C eliminated temperature control in perfusion systems and recovered ischemically damaged rat livers. Postoperatively, low transaminases suggest a beneficial effect of sub-normothermic perfusion, while rising total bilirubin levels suggest inadequate prevention of ischemia-or hypothermia-induced biliary damage. (C) 2012 Elsevier Inc. All rights reserved.
C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Surg Serv,Ctr Engn Med, Boston, MA USA.
Shriners Burns Hosp, Boston, MA USA.
RP Yarmush, ML (reprint author), Shriners Hosp Children, 51 Blossom St, Boston, MA 02114 USA.
EM ireis@sbi.org
RI Uygun, Basak/I-1792-2012
OI Uygun, Basak/0000-0002-2600-7900
FU National Institutes of Health [R01DK59766, R00DK080942]; Shriners
Hospitals for Children
FX This work was supported by grants from the National Institutes of Health
(R01DK59766, R00DK080942) and the Shriners Hospitals for Children.
NR 36
TC 30
Z9 34
U1 1
U2 9
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0022-4804
J9 J SURG RES
JI J. Surg. Res.
PD JUN 1
PY 2012
VL 175
IS 1
BP 149
EP 156
DI 10.1016/j.jss.2011.03.003
PG 8
WC Surgery
SC Surgery
GA 934UP
UT WOS:000303472500029
PM 21550058
ER
PT J
AU Garrido, MM
Allison, KC
Bergeron, MJ
Dowd, B
AF Garrido, Melissa M.
Allison, Kirk C.
Bergeron, Mark J.
Dowd, Bryan
TI Hospital Religious Affiliation and Outcomes for High-Risk Infants
SO MEDICAL CARE RESEARCH AND REVIEW
LA English
DT Article
DE infant mortality; hospital ownership; religious affiliation
ID BIRTH-WEIGHT INFANTS; OF-LIFE; EMERGENCY CONTRACEPTION; MORTALITY-RATES;
INTENSIVE-CARE; NEONATAL CARE; UNITED-STATES; SERVICES; END; PROVISION
AB The effect of hospital organizational affiliation on perinatal outcomes is unknown. Using the 2004 American Hospital Association Annual Survey and Healthcare Cost and Utilization Project State Inpatient Databases, the authors examined relationships among organizational affiliation, equipment and service availability and provision, and in-hospital mortality for 5,133 infants across five states born with very low and extremely low birth weight and congenital anomalies. In adjusted bivariate probit selection models, the authors found that government hospitals had significantly higher mortality rates than not-for-profit nonreligious hospitals. Mortality differences among other types of affiliation (Catholic, not-for-profit religious, not-for-profit nonreligious, and for-profit) were not statistically significant. This is encouraging as health care reform efforts call for providers at facilities with different institutional values to coordinate care across facilities. Although there are anecdotes of facility religious affiliation being related to health care decisions, the authors did not find evidence of these relationships in their data.
C1 [Garrido, Melissa M.] James J Peters VA Med Ctr, Bronx, NY 10468 USA.
[Garrido, Melissa M.] Mt Sinai Sch Med, New York, NY USA.
[Allison, Kirk C.; Dowd, Bryan] Univ Minnesota, Sch Publ Hlth, Minneapolis, MN 55455 USA.
[Bergeron, Mark J.] Univ Minnesota, Sch Med, St Paul, MN 55108 USA.
RP Garrido, MM (reprint author), James J Peters VA Med Ctr, 130 W Kingsbridge Rd, Bronx, NY 10468 USA.
EM melissa.garrido@mssm.edu
OI Garrido, Melissa/0000-0002-8986-3536
FU Wessner Foundation; MacLaurinCSF
FX The author(s) disclosed receipt of the following financial support for
the research, authorship, and/or publication of this article: This grant
was supported in part by funding to Dr. Dowd from the Wessner Foundation
and MacLaurinCSF.
NR 52
TC 1
Z9 1
U1 1
U2 4
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1077-5587
J9 MED CARE RES REV
JI Med. Care Res. Rev.
PD JUN
PY 2012
VL 69
IS 3
BP 316
EP 338
DI 10.1177/1077558711432156
PG 23
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 933YB
UT WOS:000303401900004
PM 22203647
ER
PT J
AU Kahn, JM
Werner, RM
Carson, SS
Iwashyna, TJ
AF Kahn, Jeremy M.
Werner, Rachel M.
Carson, Shannon S.
Iwashyna, Theodore J.
TI Variation in Long-Term Acute Care Hospital Use After Intensive Care
SO MEDICAL CARE RESEARCH AND REVIEW
LA English
DT Article
DE mechanical ventilation; intensive care; long-term acute care; post-acute
care utilization; practice variation
ID PROLONGED MECHANICAL VENTILATION; MEDICARE; OUTCOMES; ILLNESS; TRIAL;
UNITS
AB Long-term acute care hospitals (LTACs) are an increasingly common discharge destination for patients recovering from intensive care. In this article the authors use U.S. Medicare claims data to examine regional- and hospital-level variation in LTAC utilization after intensive care to determine factors associated with their use. Using hierarchical regression models to control for patient characteristics, this study found wide variation in LTAC utilization across hospitals, even controlling for LTAC access within a region. Several hospital characteristics were independently associated with increasing LTAC utilization, including increasing hospital size, for-profit ownership, academic teaching status, and colocation of the LTAC within an acute care hospital. These findings highlight the need for research into LTAC admission criteria and the incentives driving variation in LTAC utilization across hospitals.
C1 [Kahn, Jeremy M.] Univ Pittsburgh, Dept Crit Med, Sch Med, Pittsburgh, PA 15261 USA.
[Kahn, Jeremy M.] Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA 15261 USA.
[Werner, Rachel M.] Philadelphia Vet Affairs Med Ctr, Philadelphia, PA USA.
Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Carson, Shannon S.] Univ N Carolina, Sch Med, Chapel Hill, NC USA.
[Iwashyna, Theodore J.] Univ Michigan, Sch Med, Ann Arbor, MI USA.
RP Kahn, JM (reprint author), Univ Pittsburgh, Dept Crit Med, Sch Med, Scaife Hall,Room 602-B,3550 Terrace St, Pittsburgh, PA 15261 USA.
EM kahnjm@upmc.edu
OI Iwashyna, Theodore/0000-0002-4226-9310
FU United States National Institutes of Health [R01HL096651]
FX This work was funded by the United States National Institutes of Health
(R01HL096651).
NR 20
TC 17
Z9 18
U1 1
U2 3
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1077-5587
J9 MED CARE RES REV
JI Med. Care Res. Rev.
PD JUN
PY 2012
VL 69
IS 3
BP 339
EP 350
DI 10.1177/1077558711432889
PG 12
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 933YB
UT WOS:000303401900005
PM 22311957
ER
PT J
AU Oh, B
Butow, PN
Mullan, BA
Clarke, SJ
Beale, PJ
Pavlakis, N
Lee, MS
Rosenthal, DS
Larkey, L
Vardy, J
AF Oh, Byeongsang
Butow, Phyllis N.
Mullan, Barbara A.
Clarke, Stephen J.
Beale, Philip J.
Pavlakis, Nick
Lee, Myeong Soo
Rosenthal, David S.
Larkey, Linda
Vardy, Janette
TI Effect of medical Qigong on cognitive function, quality of life, and a
biomarker of inflammation in cancer patients: a randomized controlled
trial
SO SUPPORTIVE CARE IN CANCER
LA English
DT Article
DE Cancer; Cognitive function; Quality of life; Inflammation; Medical
Qigong
ID STANDARD-DOSE CHEMOTHERAPY; C-REACTIVE PROTEIN; BREAST-CANCER; ADJUVANT
CHEMOTHERAPY; WOMEN; SURVIVORS; THERAPY; IMPAIRMENT; SYMPTOMS;
PERFORMANCE
AB Cancer patients often experience diminished cognitive function (CF) and quality of life (QOL) due to the side effects of treatment and the disease symptoms. This study evaluates the effects of medical Qigong (MQ; combination of gentle exercise and meditation) on CF, QOL, and inflammation in cancer patients.
Eighty-one cancer patients recruited between October 2007 and May 2008 were randomly assigned to two groups: a control group (n = 44) who received the usual health care and an intervention group (n = 37) who participated in a 10-week MQ program. Self-reported CF was measured by the European Organization for Research and Treatment of Cancer (EORTC-CF) and the Functional Assessment of Cancer Therapy-Cognitive (FACT-Cog). The Functional Assessment of Cancer Therapy-General (FACT-G) was used to measure QOL. C-reactive protein (CRP) was assessed as a biomarker of inflammation.
The MQ group self-reported significantly improved CF (mean difference (MD) = 7.78, t (51) = -2.532, p = 0.014) in the EORTC-CF and all the FACT-Cog subscales [perceived cognitive impairment (MD = 4.70, t (43) = -2.254, p = 0.029), impact of perceived cognitive impairment on QOL (MD = 1.64, t (45) = -2.377, p = 0.024), and perceived cognitive abilities (MD = 3.61, t (45) = -2.229, p = 0.031)] compared to controls. The MQ group also reported significantly improved QOL (MD = 12.66, t (45) = -5.715, p < 0.001) and had reduced CRP levels (MD = -0.72, t (45) = 2.092, p = 0.042) compared to controls.
Results suggest that MQ benefits cancer patients' self-reported CF, QOL, and inflammation. A larger randomized controlled trial including an objective assessment of CF is planned.
C1 [Oh, Byeongsang; Clarke, Stephen J.; Beale, Philip J.; Pavlakis, Nick] Royal N Shore Hosp, Dept Med Oncol, St Leonards, NSW 2065, Australia.
[Lee, Myeong Soo] Korea Inst Oriental Med, Brain Dis Res Ctr, Taejon 305811, South Korea.
[Rosenthal, David S.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Larkey, Linda] Arizona State Univ, Scottsdale Healthcare Chair Biobehav Oncol Res, Coll Nursing & Hlth Innovat, Tempe, AZ USA.
[Oh, Byeongsang; Clarke, Stephen J.; Beale, Philip J.; Vardy, Janette] Univ Sydney, Sydney Med Sch, Royal Prince Alfred Hosp, Sydney, NSW 2006, Australia.
[Oh, Byeongsang; Clarke, Stephen J.; Beale, Philip J.; Vardy, Janette] Concord Repatriat Gen Hosp, Sydney, NSW, Australia.
[Oh, Byeongsang; Butow, Phyllis N.; Mullan, Barbara A.; Vardy, Janette] Univ Sydney, Ctr Med Psychol & Evidence Based Decisionmaking C, Sch Psychol, Sydney, NSW 2006, Australia.
RP Oh, B (reprint author), Royal N Shore Hosp, Dept Med Oncol, St Leonards, NSW 2065, Australia.
EM byeong.oh@sydney.edu.au; phyllisb@psych.usyd.edu.au;
barbara@psych.usyd.edu.au; stephen.clarke@sydney.edu.au;
Philip.Beale@sswahs.nsw.gov.au; nick.pavlakis@sydney.edu.au;
drmslee@gmail.com; drose@uhs.harvard.edu; linda.larkey@asu.edu;
janette.vardy@sydney.edu.au
RI Lee, Myeong Soo/C-8147-2013;
OI Lee, Myeong Soo/0000-0001-6651-7641; Mullan,
Barbara/0000-0002-0177-8899; Vardy, Janette/0000-0002-5739-5790
FU University of Sydney; Royal Prince Alfred Hospital, Concord Hospital;
Royal North Shore Hospital
FX This study was supported by the University of Sydney Cancer Research
Fund. The authors would like to thank the support provided for the study
by the medical oncologists of Royal Prince Alfred Hospital, Concord
Hospital and Royal North Shore Hospital. The authors wish to acknowledge
the contribution of the biostatistician, Prof. Judy Simpson, who
provided statistical assistance and especially to thank the participants
who made this study possible.
NR 40
TC 58
Z9 60
U1 2
U2 25
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0941-4355
J9 SUPPORT CARE CANCER
JI Support. Care Cancer
PD JUN
PY 2012
VL 20
IS 6
BP 1235
EP 1242
DI 10.1007/s00520-011-1209-6
PG 8
WC Oncology; Health Care Sciences & Services; Rehabilitation
SC Oncology; Health Care Sciences & Services; Rehabilitation
GA 935PN
UT WOS:000303532000015
PM 21688163
ER
PT J
AU Tezil, T
Bodur, C
Kutuk, O
Basaga, H
AF Tezil, Tugsan
Bodur, Cagri
Kutuk, Ozgur
Basaga, Huveyda
TI IKK-beta mediates chemoresistance by sequestering FOXO3; A critical
factor for cell survival and death
SO CELLULAR SIGNALLING
LA English
DT Article
DE FOXO3; IKK; Chemoresistance; Cell death; Breast cancer
ID TRANSCRIPTION FACTOR FOXO3A; BREAST-CANCER CELLS; RECEPTOR-ALPHA
EXPRESSION; CISPLATIN RESISTANCE; PROMOTES TUMORIGENESIS; KINASE
INHIBITOR; GEFITINIB IRESSA; GENE-EXPRESSION; P53 MUTANTS; APOPTOSIS
AB Chemotherapeutic drugs proved only 50% successful in breast cancer because of cell type-dependent resistance mechanisms. FOXO3 is known to be involved in the regulation of several cell death-related genes; however, the extent of FOXO3 regulation in chemoresistance is still not fully understood. Here, we show that FOXO3 critically mediates cisplatin chemosensitivity of MCF-7 breast cancer cells which express higher levels of FOXO3 compared to resistant MDA-MB-231 cells. Administration of cisplatin induces apoptosis in MCF-7 cells in a FOXO3-dependent manner as indicated by RNA interference. On the other hand, IKK-beta (I kappa B kinase) appears to inhibit FOXO3 action after cisplatin treatment and promotes chemoresistance in MDA-MB-231 cells. IKK-p directly interacts and sequesters FOXO3 in the cytosol preventing its nuclear localization. Moreover, cisplatin treatment induces autophagosome formation through LC-3 conversion while inhibiting the cleavage of caspase 9 and caspase 3 in MDA-MB-231 cells manipulated to overexpress FOXO3. In brief, our findings demonstrate that in addition to cellular level of active FOXO3, cisplatin chemoresistance is also regulated by IKK-beta sequestration of FOXO3 in cytosol. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Tezil, Tugsan; Bodur, Cagri; Basaga, Huveyda] Sabanci Univ, Biol Sci & Bioengn Program, TR-34956 Istanbul, Turkey.
[Kutuk, Ozgur] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Basaga, H (reprint author), Sabanci Univ, Biol Sci & Bioengn Program, TR-34956 Istanbul, Turkey.
EM teziltugsan@su.sabanciuniv.edu; bodur@sabanciuniv.edu;
ozgur_kutuk@dfci.harvard.edu; huveyda@sabanciuniv.edu
RI Tezil, Tugsan/A-3909-2013
OI Tezil, Tugsan/0000-0003-0796-3718
FU TUBITAK [109S340]; Turkish Association for Cancer Research and Control;
Yousef Jameel Scholarship
FX We thank GJ Gores (Mayo Clinic, Minnesota) for pELE-HA-FOXO3(wt)
plasmid, MC Hung (MD Anderson Cancer Center, Texas) for
pEGFP-FOXO3(S644A) plasmid, RB Gaynor (Harold Simmons Cancer Center,
Texas) for pCMV-flag-IKK-beta plasmid and D Gozuacik (Sabanci
University, Turkey) for pEGFP-LC3 plasmid. This work was supported by
the grants from TUBITAK (SBAG#109S340) (HB), and Turkish Association for
Cancer Research and Control-Terry Fox Cancer Research Fund (TT). TT is
supported by Yousef Jameel Scholarship.
NR 46
TC 9
Z9 10
U1 0
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0898-6568
J9 CELL SIGNAL
JI Cell. Signal.
PD JUN
PY 2012
VL 24
IS 6
BP 1361
EP 1368
DI 10.1016/j.cellsig.2012.01.012
PG 8
WC Cell Biology
SC Cell Biology
GA 929WU
UT WOS:000303097200028
PM 22313691
ER
PT J
AU Bartzokis, G
AF Bartzokis, George
TI Neuroglialpharmacology: Myelination as a shared mechanism of action of
psychotropic treatments
SO NEUROPHARMACOLOGY
LA English
DT Review
DE White matter; Oligodendrocyte; Intracortical myelin; Medication; MRI;
NG2 cells; Neuregulin; ErbB; DISC1; IGF1; Reelin; Cdk; MAPK; mTOR;
Leptin
ID GROWTH-FACTOR-I; CENTRAL-NERVOUS-SYSTEM; GLYCOGEN-SYNTHASE KINASE-3;
WHITE-MATTER ABNORMALITIES; ACTIVATED PROTEIN-KINASE; NICOTINIC
ACETYLCHOLINE-RECEPTOR; OLIGODENDROCYTE PROGENITOR CELLS; DORSOLATERAL
PREFRONTAL CORTEX; SEIZURES INDUCE PROLIFERATION; NG2-EXPRESSING
GLIAL-CELLS
AB Current psychiatric diagnostic schema segregate symptom clusters into discrete entities, however, large proportions of patients suffer from comorbid conditions that fit neither diagnostic nor therapeutic schema. Similarly, psychotropic treatments ranging from lithium and antipsychotics to serotonin reuptake inhibitors (SSRIs) and acetylcholinesterase inhibitors have been shown to be efficacious in a wide spectrum of psychiatric disorders ranging from autism, schizophrenia (SZ), depression, and bipolar disorder (BD) to Alzheimer's disease (AD). This apparent lack of specificity suggests that psychiatric symptoms as well as treatments may share aspects of pathophysiology and mechanisms of action that defy current symptom-based diagnostic and neuron-based therapeutic schema.
A myelin-centered model of human brain function can help integrate these incongruities and provide novel insights into disease etiologies and treatment mechanisms. Available data are integrated herein to suggest that widely used psychotropic treatments ranging from antipsychotics and antidepressants to lithium and electroconvulsive therapy share complex signaling pathways such as Akt and glycogen synthase kinase-3 (GSK3) that affect myelination, its plasticity, and repair. These signaling pathways respond to neurotransmitters, neurotrophins, hormones, and nutrition, underlie intricate neuroglial communications, and may substantially contribute to the mechanisms of action and wide spectra of efficacy of current therapeutics by promoting myelination. Imaging and genetic technologies make it possible to safely and non-invasively test these hypotheses directly in humans and can help guide clinical trial efforts designed to correct myelination abnormalities. Such efforts may provide insights into novel avenues for treatment and prevention of some of the most prevalent and devastating human diseases. Published by Elsevier Ltd.
C1 [Bartzokis, George] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat, Los Angeles, CA 90095 USA.
[Bartzokis, George] Univ Calif Los Angeles, David Geffen Sch Med, Div Brain Mapping, Lab Neuroimaging,Dept Neurol, Los Angeles, CA 90095 USA.
[Bartzokis, George] Univ Calif Los Angeles, David Geffen Sch Med, Brain Res Inst, Los Angeles, CA 90095 USA.
[Bartzokis, George] Greater Los Angeles VA Healthcare Syst, Los Angeles, CA 90073 USA.
RP Bartzokis, G (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat, 300 UCLA Med Plaza,Suite 2200, Los Angeles, CA 90095 USA.
EM gbar@ucla.edu
RI Bartzokis, George/K-2409-2013
FU Pfizer; Janssen; Novartis; NIH [MH066029, AG027342]; Research and
Psychiatry Services of the Department of Veterans Affairs; RCS
Foundation
FX George Bartzokis has consulted for and received research funding from
Pfizer, Janssen, and Novartis, and consulted for Bristol-Myers Squibb
Company.; This work was supported in part by NIH grants (MH066029;
AG027342), Research and Psychiatry Services of the Department of
Veterans Affairs, and the RCS Foundation. The author thanks Lori L
Altshuler, M.D., and Keith H. Nuechterlein, Ph.D. for reading the
manuscript and providing helpful suggestions.
NR 271
TC 46
Z9 47
U1 2
U2 23
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3908
J9 NEUROPHARMACOLOGY
JI Neuropharmacology
PD JUN
PY 2012
VL 62
IS 7
BP 2137
EP 2153
DI 10.1016/j.neuropharm.2012.01.015
PG 17
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 931MG
UT WOS:000303223400001
PM 22306524
ER
PT J
AU Shabani, S
Dobbs, LK
Ford, MM
Mark, GP
Finn, DA
Phillips, TJ
AF Shabani, Shkelzen
Dobbs, Lauren K.
Ford, Matthew M.
Mark, Gregory P.
Finn, Deborah A.
Phillips, Tamara J.
TI A genetic animal model of differential sensitivity to methamphetamine
reinforcement
SO NEUROPHARMACOLOGY
LA English
DT Article
DE Methamphetamine; Addiction; Oral self-administration; Reinforcement;
Appetitive; Aversive
ID RECOMBINANT INBRED MICE; C57BL/6J MICE; D-AMPHETAMINE; BEHAVIORAL
SENSITIZATION; ETHANOL SEEKING; NATURAL REWARDS; DRUG; RATS; ALCOHOL;
COCAINE
AB Sensitivity to reinforcement from methamphetamine (MA) likely influences risk for MA addiction, and genetic differences are one source of individual variation. Generation of two sets of selectively bred mouse lines for high and low MA drinking has shown that genetic factors influence MA intake, and pronounced differences in sensitivity to rewarding and aversive effects of MA play a significant role. Further validation of these lines as a unique genetic model relevant to MA addiction was obtained using operant methods to study MA reinforcement High and low MA drinking line mice were used to test the hypotheses that: 1) oral and intracerebroventricular (ICV) MA serve as behavioral reinforcers, and 2) MA exhibits greater reinforcing efficacy in high than low MA drinking mice. Operant responses resulted in access to an MA or non-MA drinking tube or intracranial delivery of MA. Behavioral activation consequent to orally consumed MA was determined. MA available for consumption maintained higher levels of reinforced instrumental responding in high than low MA drinking line mice, and MA intake in the oral operant procedure was greater in high than low MA drinking line mice. Behavioral activation was associated with amount of MA consumed during operant sessions. High line mice delivered more MA via ICV infusion than did low line mice across a range of doses. Thus, genetic risk factors play a critical role in the reinforcing efficacy of MA and the oral self-administration procedure is suitable for delineating genetic contributions to MA reinforcement. Published by Elsevier Ltd.
C1 [Shabani, Shkelzen; Dobbs, Lauren K.; Ford, Matthew M.; Mark, Gregory P.; Finn, Deborah A.; Phillips, Tamara J.] Oregon Hlth & Sci Univ, Dept Behav Neurosci, Portland, OR 97239 USA.
[Shabani, Shkelzen; Dobbs, Lauren K.; Ford, Matthew M.; Mark, Gregory P.; Finn, Deborah A.; Phillips, Tamara J.] Oregon Hlth & Sci Univ, Methamphetamine Abuse Res Ctr, Portland, OR 97239 USA.
[Finn, Deborah A.; Phillips, Tamara J.] Portland VA Med Ctr, Portland, OR 97239 USA.
RP Phillips, TJ (reprint author), Portland VA Med Ctr VAMC, R&D 32,3710 SW US Vet Hosp Rd, Portland, OR 97239 USA.
EM shabanis@scripps.edu; dobbsl@ohsu.edu; fordma@ohsu.edu; markg@ohsu.edu;
finnd@ohsu.edu; phillipt@ohsu.edu
OI Ford, Matthew/0000-0002-1204-1980
FU Department of Veterans Affairs; NIDA [T32 DA07262]; NIDA Center [P50
DA018165]; NIAAA [K01 AA016849]
FX We thank Andrew Fredericks and Becca Rieger for their help collecting
oral operant self-administration data. We also thank Tammie Painter,
Marcia Ramaker and Nathan Klett for their help with ICV data collection.
This work was supported by the Department of Veterans Affairs, NIDA T32
DA07262, and NIDA Center grant P50 DA018165. In addition, NIAAA K01
AA016849 provided some salary support. The oral operant
self-administration and locomotor activity studies were in part
supported with resources and the use of facilities at the Portland VA
Medical Center.
NR 54
TC 14
Z9 15
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3908
J9 NEUROPHARMACOLOGY
JI Neuropharmacology
PD JUN
PY 2012
VL 62
IS 7
BP 2169
EP 2177
DI 10.1016/j.neuropharm.2012.01.002
PG 9
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 931MG
UT WOS:000303223400003
PM 22280875
ER
PT J
AU Cotter, SE
McBride, SM
Yock, TI
AF Cotter, Shane E.
McBride, Sean M.
Yock, Torunn I.
TI Proton Radiotherapy for Solid Tumors of Childhood
SO TECHNOLOGY IN CANCER RESEARCH & TREATMENT
LA English
DT Article
DE Protons; Radiation therapy; Pediatric cancer
ID CHILDRENS CANCER GROUP; GERM-CELL TUMORS; MODULATED RADIATION-THERAPY;
PRIOR CRANIAL IRRADIATION; PEDIATRIC BRAIN-TUMORS;
CENTRAL-NERVOUS-SYSTEM; LONG-TERM SURVIVORS; INDUCED 2ND CANCERS;
LOW-GRADE GLIOMAS; PHASE-II TRIAL
AB The increasing efficacy of pediatric cancer therapy over the past four decades has produced many long-term survivors that now struggle with serious treatment related morbidities affecting their quality of life. Radiation therapy is responsible for a significant proportion of these late effects, but a relatively new and emerging modality, proton radiotherapy hold great promise to drastically reduce these treatment related late effects in long term survivors by sparing dose to normal tissues. Dosimetric studies of proton radiotherapy compared with best available photon based treatment show significant dose sparing to developing normal tissues. Furthermore, clinical data are now emerging that begin to quantify the benefit in decreased late treatment effects while maintaining excellent cancer control rates.
C1 [Yock, Torunn I.] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
[Cotter, Shane E.] Brigham & Womens Hosp, Dept Radiat Oncol, Boston, MA 02115 USA.
[Cotter, Shane E.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[McBride, Sean M.] Harvard Radiat Oncol Program, Boston, MA 02115 USA.
RP Yock, TI (reprint author), Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
EM tyock@partners.org
NR 100
TC 7
Z9 7
U1 0
U2 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1533-0346
EI 1533-0338
J9 TECHNOL CANCER RES T
JI Technol. Cancer Res. Treat.
PD JUN
PY 2012
VL 11
IS 3
BP 267
EP 278
DI 10.7785/tcrt.2012.500295
PG 12
WC Oncology
SC Oncology
GA 926JK
UT WOS:000302827000008
PM 22417062
ER
PT J
AU Pedamallu, CS
Ozdamar, L
Kropat, E
Weber, GW
AF Pedamallu, Chandra Sekhar
Ozdamar, Linet
Kropat, Erik
Weber, Gerhard-Wilhelm
TI A system dynamics model for intentional transmission of HIV/AIDS using
cross impact analysis
SO CENTRAL EUROPEAN JOURNAL OF OPERATIONS RESEARCH
LA English
DT Article
DE HIV transmission by non-disclosure; Cross impact analysis; System
dynamics
ID HUMAN-IMMUNODEFICIENCY-VIRUS; SEXUALLY-TRANSMITTED-DISEASES;
SOUTH-AFRICA; HIV; SIMULATION; FUTURE; AIDS; INTERSECTIONS; PREVENTION;
DISCLOSURE
AB The system dynamics approach is a holistic way of solving problems in real-time scenarios. This is a powerful methodology and computer simulation modeling technique for framing, understanding, and discussing complex issues and problems. System dynamics modeling and simulation is often the background of a systemic thinking approach and has become a management and organizational development paradigm. This paper proposes a system dynamics approach for modeling the phenomenon of intentional transmission of HIV/AIDS by non-disclosure. The model is built using the Cross Impact Analysis (CIA) method of relating entities and attributes relevant to the risky conduct of HIV+ individuals in any given community. The proposed model uses a hypothetical cross impact matrix that relates pairs of attributes. The factors that impact non-disclosure are identified by simulating the model through dynamic difference equations. After the simulation results are reviewed, two policies are introduced and tested in order to observe the progress in the system state.
C1 [Weber, Gerhard-Wilhelm] Middle E Tech Univ, Dept Financial Math, Inst Appl Math, TR-06531 Ankara, Turkey.
[Weber, Gerhard-Wilhelm] Middle E Tech Univ, Dept Actuarial Sci, Inst Appl Math, TR-06531 Ankara, Turkey.
[Weber, Gerhard-Wilhelm] Middle E Tech Univ, Dept Comp Sci, Inst Appl Math, TR-06531 Ankara, Turkey.
[Pedamallu, Chandra Sekhar] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Pedamallu, Chandra Sekhar] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Ozdamar, Linet] Yeditepe Univ, Dept Syst Engn, TR-34755 Istanbul, Turkey.
[Kropat, Erik] Univ Bundeswehr Munchen, Dept Informat, Inst Theoret Comp Sci Math & Operat Res, D-85577 Neubiberg, Germany.
[Weber, Gerhard-Wilhelm] Univ Siegen, Fac Econ Business & Law, Siegen, Germany.
[Weber, Gerhard-Wilhelm] Univ Aveiro, Ctr Res Optimizat & Control, P-3800 Aveiro, Portugal.
[Weber, Gerhard-Wilhelm] Univ Teknol Malaysia, Skudai, Malaysia.
RP Weber, GW (reprint author), Middle E Tech Univ, Dept Financial Math, Inst Appl Math, TR-06531 Ankara, Turkey.
EM pcs.murali@gmail.com; ozdamar.linet@gmail.com;
kropat@am.uni-erlangen.de; gweber@metu.edu.tr
NR 48
TC 3
Z9 3
U1 1
U2 16
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1435-246X
EI 1613-9178
J9 CENT EUR J OPER RES
JI Cent. Europ. J. Oper. Res.
PD JUN
PY 2012
VL 20
IS 2
BP 319
EP 336
DI 10.1007/s10100-010-0183-2
PG 18
WC Operations Research & Management Science
SC Operations Research & Management Science
GA 921KU
UT WOS:000302477300006
ER
PT J
AU Forman, EM
Chapman, JE
Herbert, JD
Goetter, EM
Yuen, EK
Moitra, E
AF Forman, Evan M.
Chapman, Jason E.
Herbert, James D.
Goetter, Elizabeth M.
Yuen, Erica K.
Moitra, Ethan
TI Using Session-by-Session Measurement to Compare Mechanisms of Action for
Acceptance and Commitment Therapy and Cognitive Therapy
SO BEHAVIOR THERAPY
LA English
DT Article
DE ACT; CBT; psychotherapy mechanisms; mediation
ID BEHAVIORAL TREATMENT; CONFIDENCE-LIMITS; CONTROLLED TRIAL; DEPRESSION;
ANXIETY; MEDIATION; PREVENT; RELAPSE; QUESTIONNAIRE; RELIABILITY
AB Debate continues about the extent to which postulated mechanisms of action of cognitive behavior therapies (CBT), including standard CBT (i.e., Beckian cognitive therapy [CT]) and acceptance and commitment therapy (ACT) are supported by mediational analyses. Moreover, the distinctiveness of CT and ACT has been called into question. One contributor to ongoing uncertainty in this arena is the lack of time-varying process data. In this study, 174 patients presenting to a university clinic with anxiety or depression who had been randomly assigned to receive either ACT or CT completed an assessment of theorized mediators and outcomes before each session. Hierarchical linear modeling of session-by-session data revealed that increased utilization of cognitive and affective change strategies relative to utilization of psychological acceptance strategies mediated outcome for CT, whereas for ACT the mediation effect was in the opposite direction. Decreases in self-reported dysfunctional thinking, cognitive "defusion" (the ability to see one's thoughts as mental events rather than necessarily as representations of reality), and willingness to engage in behavioral activity despite unpleasant thoughts or emotions were equivalent mediators across treatments. These results have potential implications for the theoretical arguments behind, and distinctiveness of, CT and ACT.
C1 [Forman, Evan M.] Drexel Univ, Dept Psychol, Philadelphia, PA 19102 USA.
[Yuen, Erica K.] Med Univ S Carolina, Ralph H Johnson Vet Adm Med Ctr, Charleston, SC USA.
[Moitra, Ethan] Brown Univ, Providence, RI 02912 USA.
RP Forman, EM (reprint author), Drexel Univ, Dept Psychol, 245 N 15th St,MS 626, Philadelphia, PA 19102 USA.
EM evan.forman@drexel.edu
RI Forman, Evan/I-1042-2012
NR 61
TC 35
Z9 35
U1 7
U2 43
PU ASSOC ADV BEHAVIOR THERAPY
PI NEW YORK
PA 305 7TH AVE #16A, NEW YORK, NY 10001-6008 USA
SN 0005-7894
J9 BEHAV THER
JI Behav. Therapy
PD JUN
PY 2012
VL 43
IS 2
BP 341
EP 354
PG 14
WC Psychology, Clinical
SC Psychology
GA 920GZ
UT WOS:000302393600010
PM 22440070
ER
PT J
AU Gray, MJ
Schorr, Y
Nash, W
Lebowitz, L
Amidon, A
Lansing, A
Maglione, M
Lang, AJ
Litz, BT
AF Gray, Matt J.
Schorr, Yonit
Nash, William
Lebowitz, Leslie
Amidon, Amy
Lansing, Amy
Maglione, Melissa
Lang, Ariel J.
Litz, Brett T.
TI Adaptive Disclosure: An Open Trial of a Novel Exposure-Based
Intervention for Service Members With Combat-Related Psychological
Stress Injuries
SO BEHAVIOR THERAPY
LA English
DT Article
DE Combat; trauma; psychotherapy; moral injury; PTSD
ID MENTAL-HEALTH PROBLEMS; PSYCHOMETRIC PROPERTIES; PTSD CHECKLIST;
DISORDER; VETERANS; IRAQ; AFGHANISTAN; THERAPY; PSYCHOTHERAPY;
VALIDATION
AB We evaluated the preliminary effectiveness of a novel intervention that was developed to address combat stress injuries in active-duty military personnel. Adaptive disclosure (AD) is relatively brief to accommodate the busy schedules of active-duty service members while training for future deployments. Further, AD takes into account unique aspects of the phenomenology of military service in war in order to address difficulties such as moral injury and traumatic loss that may not receive adequate and explicit attention by conventional treatments that primarily address fear-inducing life-threatening experiences and sequelae. In this program development and evaluation open trial, 44 marines received AD while in garrison. It was well tolerated and, despite the brief treatment duration, promoted significant reductions in PTSD, depression, negative posttraumatic appraisals, and was also associated with increases in posttraumatic growth.
C1 [Gray, Matt J.] Univ Wyoming, Dept Psychol, Dept 3415, Laramie, WY 82070 USA.
[Schorr, Yonit; Litz, Brett T.] VA Boston Healthcare Syst, Boston, MA USA.
[Nash, William] Def Ctr Excellence, Arlington, VA USA.
[Amidon, Amy; Lansing, Amy; Maglione, Melissa; Lang, Ariel J.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Amidon, Amy; Lansing, Amy; Maglione, Melissa; Lang, Ariel J.] VA San Diego Healthcare Syst, San Diego, CA USA.
[Litz, Brett T.] Boston Univ, Boston, MA 02215 USA.
[Litz, Brett T.] Massachusetts Vet Epidemiol Res & Informat Ctr, Natl Ctr PTSD, Bedford, MA USA.
RP Gray, MJ (reprint author), Univ Wyoming, Dept Psychol, Dept 3415, 1000 E Univ Ave, Laramie, WY 82070 USA.
EM gray@uwyo.edu
NR 26
TC 30
Z9 30
U1 0
U2 16
PU ASSOC ADV BEHAVIOR THERAPY
PI NEW YORK
PA 305 7TH AVE #16A, NEW YORK, NY 10001-6008 USA
SN 0005-7894
J9 BEHAV THER
JI Behav. Therapy
PD JUN
PY 2012
VL 43
IS 2
BP 407
EP 415
PG 9
WC Psychology, Clinical
SC Psychology
GA 920GZ
UT WOS:000302393600015
PM 22440075
ER
PT J
AU Cohen, LE
Gordon, JH
Popovsky, EY
Sainath, NN
Feldman, HA
Kieran, MW
Gordon, CM
AF Cohen, Laurie E.
Gordon, Joshua H.
Popovsky, Erica Y.
Sainath, Nina N.
Feldman, Henry A.
Kieran, Mark W.
Gordon, Catherine M.
TI Bone density in post-pubertal adolescent survivors of childhood brain
tumors
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE bone mineral density; brain tumors; growth hormone deficiency; fracture
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; YOUNG-ADULT SURVIVORS; QUALITY-OF-LIFE;
MINERAL DENSITY; GROWTH-HORMONE; PHYSICAL-ACTIVITY; RADIATION-THERAPY;
CANCER; CHILDREN; MASS
AB Background Childhood cancer survivors are at high risk for reduced bone mineral density (BMD). Our objective was to determine whether post-pubertal adolescent survivors of brain tumors, whose tumor or treatments placed them at risk for pituitary hormone deficiencies, have low BMD near time of peak bone mass accrual, and to assess risk factors for decreased BMD. Procedure. Chart review of 36 post-pubertal adolescents with history of tumor or radiation therapy (RT) of the hypothalamicpituitary area who had undergone BMD screening via dual-energy X-ray absorptiometry (DXA). Results. Age at DXA was 16.9 +/- 1.9 years (mean +/- SD). Time since diagnosis was 8.5 +/- 3.6 years. Median BMD Z scores were -0.95 (range -2.7 to 1.7) at the femoral neck, -1.20 (-3.6 to 1.8) at the hip, and -0.90 (-3.7 to 1.8) at the spine. Bone mineral apparent density (BMAD) Z scores were -0.23 (-2.7 to 1.9) at the femoral neck and -0.45 (-3.0 to 2.3) at the spine. Those with history of >= 1 fracture had lower BMD Z scores of the femoral neck, total hip, and spine (P < 0.05). Those with treated GH deficiency (GHD) had a higher BMD Z-score at the femoral neck, total hip, and spine (P < 0.05) than those not treated. There was no difference in BMD with respect to treatment with chemotherapy, cranial or spinal RT, or hypogonadism. Spontaneous menarche and regular periods did not correlate with BMD. Conclusions. In post-pubertal adolescent survivors of childhood brain tumors, fracture history and untreated GHD are risk factors for decreased BMD. Pediatr Blood Cancer 2012; 58: 959-963. (C) 2011 Wiley Periodicals, Inc.
C1 [Cohen, Laurie E.; Gordon, Joshua H.; Popovsky, Erica Y.; Gordon, Catherine M.] Childrens Hosp Boston, Div Endocrinol, Boston, MA 02115 USA.
[Sainath, Nina N.] NYU, Sch Med, New York, NY USA.
[Feldman, Henry A.] Childrens Hosp Boston, Clin Res Program, Boston, MA 02115 USA.
[Kieran, Mark W.] Childrens Hosp Boston, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Cohen, LE (reprint author), Childrens Hosp Boston, Div Endocrinol, 300 Longwood Ave, Boston, MA 02115 USA.
EM laurie.cohen@childrens.harvard.edu
OI Kieran, Mark/0000-0003-2184-7692
FU Harvard Clinical and Translational Science Center [NIH UL1 RR-025758]
FX Grant sponsor: Harvard Clinical and Translational Science Center; Grant
number: NIH UL1 RR-025758.
NR 41
TC 2
Z9 2
U1 0
U2 2
PU WILEY PERIODICALS, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN STREET, MALDEN, MA 02148-529 USA
SN 1545-5009
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD JUN
PY 2012
VL 58
IS 6
BP 959
EP 963
DI 10.1002/pbc.23300
PG 5
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA 910QQ
UT WOS:000301656300024
PM 22431246
ER
PT J
AU Bymaster, FP
Golembiowska, K
Kowalska, M
Choi, YK
Tarazi, FI
AF Bymaster, Frank P.
Golembiowska, Krystyna
Kowalska, Magdalena
Choi, Yong Kee
Tarazi, Frank I.
TI Pharmacological characterization of the norepinephrine and dopamine
reuptake inhibitor EB-1020: Implications for treatment of
attention-deficit hyperactivity disorder
SO SYNAPSE
LA English
DT Article
DE norepinephrine transporter; dopamine transporter; ADHD; microdialysis;
locomotor activity
ID ADJUNCT OROS-METHYLPHENIDATE; RAT PREFRONTAL CORTEX;
DEFICIT/HYPERACTIVITY DISORDER; EXTRACELLULAR DOPAMINE; MOTOR
HYPERACTIVITY; SEROTONIN UPTAKE; ATOMOXETINE; ADULTS; ADHD; BRAIN
AB We report on the pharmacological, behavioral, and neurochemical characterization of a novel dual norepinephrine (NE)/dopamine (DA) transporter inhibitor EB-1020 (1R,5S)-1-(naphthalen-2-yl)-3-azabicyclo[3.1.0]hexane HCl). EB-1020 preferentially inhibited monoamine reuptake in cloned cell lines transfected with human transporters with IC50 values of 6 and 38, respectively, for NE and DA transporters. In microdialysis studies, EB-1020 markedly increased NE, and DA concentrations levels in rat prefrontal cortex in vivo with peak increases of 375 and 300%, respectively with the greatest effects on NE, and also increased DA extracellular concentrations in the striatum to 400% of baseline concentrations. Behavioral studies demonstrated that EB-1020 dose-dependently decreased immobility in the mouse tail suspension test of depression to 13% of control levels, and did not stimulate locomotor activity in adult rats in the optimal dose range. EB-1020 dose-dependently inhibited locomotor hyperactivity in juvenile rats lesioned with the neurotoxin 6-hydroxydopamine (100 mu g intracisternally) as neonates; a well-established animal model for attention-deficit hyperactivity disorder (ADHD). These data suggest that EB-1020 mediates its actions by stimulating NE and DA neurotransmission, which are typically impaired in ADHD. Synapse, 2012. (C) 2012 Wiley Periodicals, Inc.
C1 [Bymaster, Frank P.] Euthym Biosci Inc, Cambridge, MA 02141 USA.
[Golembiowska, Krystyna; Kowalska, Magdalena] Polish Acad Sci, Inst Pharmacol, Dept Pharmacol, PL-31343 Krakow, Poland.
[Choi, Yong Kee; Tarazi, Frank I.] Massachusetts Gen Hosp, McLean Div, Mailman Res Ctr, Belmont, MA USA.
[Choi, Yong Kee; Tarazi, Frank I.] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02478 USA.
[Choi, Yong Kee; Tarazi, Frank I.] Harvard Univ, Sch Med, Neurosci Program, Boston, MA 02478 USA.
RP Tarazi, FI (reprint author), Euthym Biosci Inc, 43 Thorndike St,Suite 1-3, Cambridge, MA 02141 USA.
EM fbymaster@euthymics.com
FU Euthymics Biosciences
FX Frank P. Bymaster is an employee, officer, and shareholder in Euthymics
Biosciences Inc. Drs. Krystyna Golembiowska and Frank Tarazi received
funding from Euthymics Biosciences to conduct the microdialysis studies
and ADHD model studies respectively.
NR 63
TC 8
Z9 8
U1 1
U2 12
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0887-4476
J9 SYNAPSE
JI Synapse
PD JUN
PY 2012
VL 66
IS 6
BP 522
EP 532
DI 10.1002/syn.21538
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 919AP
UT WOS:000302293300006
PM 22298359
ER
PT J
AU Fisher, MC
Furer, V
Hochberg, MC
Greenberg, JD
Kremer, JM
Curtis, JR
Reed, G
Harrold, L
Solomon, DH
AF Fisher, Mark C.
Furer, Victoria
Hochberg, Marc C.
Greenberg, Jeffrey D.
Kremer, Joel M.
Curtis, Jeff R.
Reed, George
Harrold, Leslie
Solomon, Daniel H.
TI Malignancy validation in a United States registry of rheumatoid
arthritis patients
SO BMC MUSCULOSKELETAL DISORDERS
LA English
DT Article
DE Malignancy; Rheumatoid arthritis; Registry; Validation
ID NECROSIS FACTOR THERAPY; FACTOR ANTAGONISTS; LUNG-CANCER; RISK;
LYMPHOMA; METHOTREXATE; DRUG; INCREASE; TRIALS; CLAIMS
AB Background: Physician reporting is commonly used to ascertain adverse events or outcomes measured in epidemiologic studies. However, little is known on the accuracy of physician reported malignancies compared to pertinent medical record review in large cohort studies.
Methods: The Consortium of Rheumatology Researchers of North America (CORRONA) registry gathers physician-completed questionnaires for rheumatoid arthritis (RA) patients, including request for information on incident malignancies, approximately every three months. For incident malignancies reported from October 1st, 2001, through December 31st, 2007, we retrospectively requested completion of a Targeted Adverse Event (TAE) form for additional information as well as primary source documents to adjudicate the malignancy reports. CORRONA has employed a prospective request for source documentation for these events since 2008. We classified each malignancy as definite, probable, possible, or not a malignancy.
Results: From 20,837 RA patients enrolled in CORRONA, 461 incident malignancies were initially reported on physician questionnaires. After review of returned source documents with adjudication, 234 were deemed definite, 69 probable, 101 possible, and 57 not an incident malignancy. The positive predictive value (PPV) of initial physician report of a malignancy versus "definite or probable" malignancy based on adjudication was 0.66 (95% CI 0.61 - 0.70). The PPV was 0.68 (95% CI 0.63 - 0.72) when the subsequent TAE form also confirmed the presence of malignancy. When possible malignancies were included, the PPV of physician-reported malignancies without a subsequent TAE form increased to 0.86 (0.83 - 0.89), and with a subsequent TAE form, 0.89 (0.85-0.91).
Conclusion: Twelve percent of initial physician reports of incident malignancy could not be confirmed with review of source documents. The most common reason for lack of confirmation was inability to obtain documents or insufficient data in source materials. These results suggest that timely collection of relevant medical records and an adjudication process are required to improve the accuracy of cancer reporting in epidemiologic studies.
C1 [Fisher, Mark C.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Furer, Victoria; Greenberg, Jeffrey D.] NYU, Hosp Joint Dis, Dept Rheumatol, New York, NY 10003 USA.
[Hochberg, Marc C.] Univ Maryland, Sch Med, Dept Med, Baltimore, MD 21201 USA.
[Hochberg, Marc C.] Univ Maryland, Sch Med, Dept Epidemiol & Prevent Med, Baltimore, MD 21201 USA.
[Kremer, Joel M.] SUNY Albany, Albany Med Coll, Ctr Rheumatol, Albany, NY 12206 USA.
[Curtis, Jeff R.] Univ Alabama Birmingham, Dept Med, Birmingham, AL 35294 USA.
[Reed, George] Univ Massachusetts, Sch Med, Div Prevent & Behav Med, Worcester, MA 01605 USA.
[Harrold, Leslie] Univ Massachusetts, Sch Med, Dept Med, Worcester, MA 01605 USA.
[Solomon, Daniel H.] Brigham & Womens Hosp, Div Rheumatol Immunol & Allergy, Boston, MA 02120 USA.
RP Fisher, MC (reprint author), Massachusetts Gen Hosp, 55 Fruit St, Boston, MA 02114 USA.
EM mfisher6@partners.org
FU NIH [K23AR054412, AR053351, K23AR053856, K24 AR 055989]; Arthritis
Foundation; National Arthritis Research Foundation; Amgen;
Roche/Genentech; Centecor; CORRONA; Abbott; Bristol Myers Squibb
FX Dr. Fisher has nothing to disclose. Dr. Furer has nothing to disclose.
Dr. Hochberg has consulted for Abbott Laboratories, Amgen, Bristol Myers
Squibb, Genentech, UCB Inc. Dr. Greenberg receives salary support from
research grants from the NIH (K23AR054412), the Arthritis Foundation and
the National Arthritis Research Foundation, serves as Chief Scientific
Officer for CORRONA and has served on Advisory Boards for Genentech and
Pfizer. Dr. Kremer is the President of CORRONA, receives salary support.
Dr. Curtis has consulted for or received honoraria from Roche/Genentech,
UCB, Centecor, CORRONA, Amgen, and Pfizer, and has received research
support from Amgen, Roche/Genentech, Centecor and CORRONA. Dr. Curtis
also receives salary support from the NIH (AR053351). Dr. Harrold
received support from the NIH (K23AR053856). She also has consulted for
CORRONA. Dr. Solomon has received research support from Amgen and Abbott
for rheumatoid arthritis research and has received support for an
educational course from Bristol Myers Squibb. Dr. Solomon also receives
salary support from the NIH for mentoring (K24 AR 055989).
NR 24
TC 2
Z9 2
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2474
J9 BMC MUSCULOSKEL DIS
JI BMC Musculoskelet. Disord.
PD MAY 31
PY 2012
VL 13
AR 85
DI 10.1186/1471-2474-13-85
PG 8
WC Orthopedics; Rheumatology
SC Orthopedics; Rheumatology
GA 978AW
UT WOS:000306712100001
PM 22651246
ER
PT J
AU Shanmugam, NKN
Ellenbogen, S
Trebicka, E
Wang, LJ
Mukhopadhyay, S
Lacy-Hulbert, A
Gallini, CA
Garrett, WS
Cherayil, BJ
AF Shanmugam, Nanda Kumar N.
Ellenbogen, Shiri
Trebicka, Estela
Wang, Lijian
Mukhopadhyay, Subhankar
Lacy-Hulbert, Adam
Gallini, Carey Ann
Garrett, Wendy S.
Cherayil, Bobby J.
TI Tumor Necrosis Factor alpha Inhibits Expression of the Iron Regulating
Hormone Hepcidin in Murine Models of Innate Colitis
SO PLOS ONE
LA English
DT Article
ID HEREDITARY HEMOCHROMATOSIS PROTEIN; ULCERATIVE-COLITIS; IN-VIVO;
INFLAMMATION; HFE; DISEASE; GROWTH; STAT3; MACROPHAGES; HOMEOSTASIS
AB Background: Abnormal expression of the liver peptide hormone hepcidin, a key regulator of iron homeostasis, contributes to the pathogenesis of anemia in conditions such as inflammatory bowel disease (IBD). Since little is known about the mechanisms that control hepcidin expression during states of intestinal inflammation, we sought to shed light on this issue using mouse models.
Methodology/Principal Findings: Hepcidin expression was evaluated in two types of intestinal inflammation caused by innate immune activation-dextran sulfate sodium (DSS)-induced colitis in wild-type mice and the spontaneous colitis occurring in T-bet/Rag2-deficient (TRUC) mice. The role of tumor necrosis factor (TNF) alpha was investigated by in vivo neutralization, and by treatment of a hepatocyte cell line, as well as mice, with the recombinant cytokine. Expression and activation of Smad1, a positive regulator of hepcidin transcription, were assessed during colitis and following administration or neutralization of TNF alpha. Hepcidin expression progressively decreased with time during DSS colitis, correlating with changes in systemic iron distribution. TNF alpha inhibited hepcidin expression in cultured hepatocytes and non-colitic mice, while TNF alpha neutralization during DSS colitis increased it. Similar results were obtained in TRUC mice. These effects involved a TNF alpha-dependent decrease in Smad1 protein but not mRNA.
Conclusions/Significance: TNF alpha inhibits hepcidin expression in two distinct types of innate colitis, with down-regulation of Smad1 protein playing an important role in this process. This inhibitory effect of TNF alpha may be superseded by other factors in the context of T cell-mediated colitis given that in the latter form of intestinal inflammation hepcidin is usually upregulated.
C1 [Shanmugam, Nanda Kumar N.; Ellenbogen, Shiri; Trebicka, Estela; Wang, Lijian; Cherayil, Bobby J.] Massachusetts Gen Hosp, Mucosal Immunol Lab, Boston, MA 02114 USA.
[Mukhopadhyay, Subhankar; Lacy-Hulbert, Adam] Massachusetts Gen Hosp, Dept Pediat, Dev Immunol Lab, Boston, MA 02114 USA.
[Mukhopadhyay, Subhankar] Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England.
[Lacy-Hulbert, Adam; Garrett, Wendy S.; Cherayil, Bobby J.] Harvard Univ, Sch Med, Boston, MA USA.
[Gallini, Carey Ann; Garrett, Wendy S.] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
[Gallini, Carey Ann; Garrett, Wendy S.] Harvard Univ, Sch Publ Hlth, Dept Genet & Complex Dis, Boston, MA 02115 USA.
[Garrett, Wendy S.] Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Shanmugam, NKN (reprint author), Massachusetts Gen Hosp, Mucosal Immunol Lab, Boston, MA 02114 USA.
EM cherayil@helix.mgh.harvard.edu
OI Lacy-Hulbert, Adam/0000-0003-2162-0156
FU National Institutes of Health [R56AI089700, R01AI089700, RO1CA154426,
K08AI078942]; Wellcome Trust Flexible Travel Award Fellowship
FX The work was supported by grants from the National Institutes of Health
to BJC (R56AI089700, R01AI089700) and to WSG (RO1CA154426, K08AI078942).
SM was supported by a Wellcome Trust Flexible Travel Award Fellowship.
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 41
TC 16
Z9 16
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAY 31
PY 2012
VL 7
IS 5
AR e38136
DI 10.1371/journal.pone.0038136
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 959TY
UT WOS:000305338500091
PM 22675442
ER
PT J
AU Ranieri, VM
Thompson, BT
Barie, PS
Dhainaut, JF
Douglas, IS
Finfer, S
Gardlund, B
Marshall, JC
Rhodes, A
Artigas, A
Payen, D
Tenhunen, J
Al-Khalidi, HR
Thompson, V
Janes, J
Macias, WL
Vangerow, B
Williams, MD
AF Ranieri, V. Marco
Thompson, B. Taylor
Barie, Philip S.
Dhainaut, Jean-Francois
Douglas, Ivor S.
Finfer, Simon
Gardlund, Bengt
Marshall, John C.
Rhodes, Andrew
Artigas, Antonio
Payen, Didier
Tenhunen, Jyrki
Al-Khalidi, Hussein R.
Thompson, Vivian
Janes, Jonathan
Macias, William L.
Vangerow, Burkhard
Williams, Mark D.
CA PROWESS-SHOCK Study Grp
TI Drotrecogin Alfa (Activated) in Adults with Septic Shock
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID MULTIPLE-ORGAN DYSFUNCTION; PLACEBO-CONTROLLED TRIAL; APACHE-II SCORE;
SEVERE SEPSIS; PROTEIN-C; SURGICAL-PATIENTS; PROWESS TRIAL;
UNITED-STATES; DEATH; CARE
AB BACKGROUND
There have been conflicting reports on the efficacy of recombinant human activated protein C, or drotrecogin alfa (activated) (DrotAA), for the treatment of patients with septic shock.
METHODS
In this randomized, double-blind, placebo-controlled, multicenter trial, we assigned 1697 patients with infection, systemic inflammation, and shock who were receiving fluids and vasopressors above a threshold dose for 4 hours to receive either DrotAA (at a dose of 24 mu g per kilogram of body weight per hour) or placebo for 96 hours. The primary outcome was death from any cause 28 days after randomization.
RESULTS
At 28 days, 223 of 846 patients (26.4%) in the DrotAA group and 202 of 834 (24.2%) in the placebo group had died (relative risk in the DrotAA group, 1.09; 95% confidence interval [CI], 0.92 to 1.28; P = 0.31). At 90 days, 287 of 842 patients (34.1%) in the DrotAA group and 269 of 822 (32.7%) in the placebo group had died (relative risk, 1.04; 95% CI, 0.90 to 1.19; P = 0.56). Among patients with severe protein C deficiency at baseline, 98 of 342 (28.7%) in the DrotAA group had died at 28 days, as compared with 102 of 331 (30.8%) in the placebo group (risk ratio, 0.93; 95% CI, 0.74 to 1.17; P = 0.54). Similarly, rates of death at 28 and 90 days were not significantly different in other predefined subgroups, including patients at increased risk for death. Serious bleeding during the treatment period occurred in 10 patients in the DrotAA group and 8 in the placebo group (P = 0.81).
CONCLUSIONS
DrotAA did not significantly reduce mortality at 28 or 90 days, as compared with placebo, in patients with septic shock. (Funded by Eli Lilly; PROWESS-SHOCK ClinicalTrials.gov number, NCT00604214.)
C1 [Ranieri, V. Marco] Univ Turin, Osped S Giovanni Battista Molinette, Turin, Italy.
[Thompson, B. Taylor] Massachusetts Gen Hosp, Pulm & Crit Care Unit, Boston, MA 02114 USA.
[Barie, Philip S.] Weill Cornell Med Coll, Dept Surg, New York, NY USA.
[Barie, Philip S.] Weill Cornell Med Coll, Dept Publ Hlth, New York, NY USA.
[Dhainaut, Jean-Francois] Paris Descartes Univ, Royal Hosp, Paris, France.
[Payen, Didier] Univ Paris Diderot, Paris, France.
[Payen, Didier] Hop Lariboisiere, AP HP, Dept Anesthesie Reanimat SMUR, F-75475 Paris, France.
[Douglas, Ivor S.] Univ Colorado, Sch Med, Denver, CO USA.
[Finfer, Simon] Univ Sydney, Royal N Shore Hosp, Sydney, NSW 2006, Australia.
[Finfer, Simon] Univ Sydney, George Inst Global Hlth, Sydney, NSW 2006, Australia.
[Gardlund, Bengt] Karolinska Univ Hosp, Dept Infect Dis, Stockholm, Sweden.
[Marshall, John C.] St Michaels Hosp, Li Ka Shing Knowledge Inst, Keenan Res Inst, Dept Surg, Toronto, ON M5B 1W8, Canada.
[Marshall, John C.] St Michaels Hosp, Li Ka Shing Knowledge Inst, Keenan Res Inst, Dept Crit Care Med, Toronto, ON M5B 1W8, Canada.
[Rhodes, Andrew] St Georges Healthcare NHS Trust, London, England.
[Artigas, Antonio] St Georges Univ, London, England.
[Artigas, Antonio] Univ Autonoma Barcelona, Univ Parc Tauli, CIBER Enfermedades Resp, Crit Care Ctr,Hosp Sabadell, Sabadell, Spain.
[Tenhunen, Jyrki] Uppsala Univ, Dept Surg Sci Anaesthesiol & Intens Care, Uppsala, Sweden.
[Al-Khalidi, Hussein R.; Thompson, Vivian] Duke Univ, Med Ctr, Duke Clin Res Inst, Durham, NC USA.
[Janes, Jonathan; Macias, William L.; Vangerow, Burkhard; Williams, Mark D.] Eli Lilly & Co, Lilly Res Labs, Indianapolis, IN 46285 USA.
RI Ruiz-Rodriguez, Juan Carlos/H-7703-2012; Pickkers, R.P./H-8080-2014;
Leditschke, Isabel/M-1186-2015; Asfar, Pierre/K-1402-2015; Sramek,
Vladimir/M-2152-2016; Betbese, Antoni/H-3419-2013; Malbrain,
Manu/B-3680-2017;
OI Ferguson, Niall/0000-0002-6213-5264; Rello, Jordi/0000-0003-0676-6210;
Van Haren, Frank/0000-0001-8037-4229; Leditschke,
Isabel/0000-0003-2212-2140; Betbese, Antoni/0000-0002-9059-4046;
Malbrain, Manu/0000-0002-1816-5255; Della Corte,
Francesco/0000-0003-1736-2318; , /0000-0002-4157-5148; Whitehouse,
Tony/0000-0002-4387-3421; Douglas, Ivor/0000-0002-4541-1431
FU Eli Lilly; Abbott; Sanofi-Aventis; Immunetrics; US Biotest; Sirius
Genomics; Eisai; Agennix; Idaho Technology; Roche Diagnostics; Bayer;
Vertex Technologies; Pfizer; Daiichi Sankyo; Hoffmann-La Roche;
BioMerieux; Edwards; LiDCO; Covidien; Brahms; Naturalia et Biologia
FX Dr. Ranieri reports serving as a member of a data and safety monitoring
board for Biotest and an advisory board member for Hemodec and Maquet;
Dr. Thompson, serving as the chair of a data and safety monitoring board
for AstraZeneca and as an advisory board member for Hemodec, receiving
consulting fees from Abbott, Sanofi-Aventis, Immunetrics, US Biotest,
Sirius Genomics, and Eli Lilly; Dr. Barie, receiving consulting fees
from Eisai and lecture fees from Eli Lilly; Dr. Douglas, receiving grant
support from Eli Lilly, Eisai, and Agennix and serving as cochair for
the International Guidelines Committee for the 2012 Surviving Sepsis
Campaign; Dr. Finfer, receiving consulting fees from Eisai, being a
member of the International Sepsis Forum (ISF), and receiving travel
support from ISF corporate sponsors; Dr. Marshall, receiving consulting
fees from Eisai, Idaho Technology, Roche Diagnostics, Bayer, Vertex
Technologies, Pfizer, Daiichi Sankyo, and Hoffmann-La Roche, receiving
grant support and travel expenses from BioMerieux, serving as a member
of the ISF and receiving travel support from ISF corporate sponsors,
serving as a member of the Center for Sepsis Control and Care at the
University of Jena and as a member of the data and safety monitoring
board for Artisan Pharma, Leo Pharma, Celgene Therapeutics, and
Therapeutic Monitoring Systems, and serving as a steering committee
member for Spectral Diagnostics and Eisai; Dr. Rhodes, serving on
advisory boards for LiDCO and BioMerieux and receiving lecture fees from
Edwards, LiDCO, and Covidien; all the preceding authors, or their
institutions, received financial support from Eli Lilly for time spent
performing committee activities and for travel; Dr. Artigas, receiving
travel support and lecture fees and grant support and support for
patient recruitment (through his institution) from Eli Lilly, serving on
advisory boards for Gambro and Hemodec, and receiving consulting fees
from Brahms; Dr. Payen, serving on an advisory board for Homeostasie
Consulting and receiving consulting and lecture fees from Homeostasie
Consulting and institutional grant support from Naturalia et Biologia;
Dr. Tenhunen, receiving institutional grant support for lectures, travel
expenses, and data analysis from Eli Lilly; Dr. Al-Khalidi and Ms.
Thompson, being employees of the Duke Clinical Research Institute, which
received financial support for statistical analysis, preparation of
study reports, manuscript review and writing, and travel from Eli Lilly;
and Drs. Janes, Macias, Vangerow, and Williams, being current or former
employees of and having an equity interest in Eli Lilly. No other
potential conflict of interest relevant to this article was reported.
NR 39
TC 437
Z9 459
U1 3
U2 48
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD MAY 31
PY 2012
VL 366
IS 22
BP 2055
EP 2064
DI 10.1056/NEJMoa1202290
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 949YE
UT WOS:000304613400005
PM 22616830
ER
PT J
AU Batchelor, TT
Sorensen, AG
Louis, DN
AF Batchelor, Tracy T.
Sorensen, A. Gregory
Louis, David N.
TI Case 17-2012: A 54-Year-Old Man with Visual-Field Loss and a Mass in the
Brain
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID NEWLY-DIAGNOSED GLIOBLASTOMA; PROMOTER METHYLATION STATUS; TEMOZOLOMIDE;
RADIOTHERAPY; CONCOMITANT; ADJUVANT; SURGERY; GLIOMAS; TRIAL
C1 [Batchelor, Tracy T.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Sorensen, A. Gregory] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Louis, David N.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Batchelor, Tracy T.] Harvard Univ, Sch Med, Dept Neurol, Boston, MA 02115 USA.
[Sorensen, A. Gregory] Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02115 USA.
[Louis, David N.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
RP Batchelor, TT (reprint author), Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
FU Millennium; Pfizer; AstraZeneca; Merck; Imedex; Educational Concepts
Group; Strategic Edge Communications; BayerScheringPharma; Bristol-Myers
Squibb; BiogenIdec; Merrimack Pharmaceuticals; Olea Medical; Mitsubishi
Pharma; GE Healthcare; Regeneron; Novartis; Roche; Siemens Healthcare;
Takeda; ACR-Image Metrix; Bayer
FX Dr. Batchelor reports receiving payment for advisory board membership
from Roche, Spectrum, and Amgen; consulting fees from Millennium; grant
support from Pfizer and AstraZeneca; lecture fees from Merck, Imedex,
Educational Concepts Group, and Strategic Edge Communications; and
payment for the development of educational presentations from UpToDate.
Dr. Sorensen reports being an employee of Siemens Healthcare; receiving
consulting fees from BayerScheringPharma, Bristol-Myers Squibb,
BiogenIdec, Merrimack Pharmaceuticals, Olea Medical, Mitsubishi Pharma,
GE Healthcare, Regeneron, Novartis, Roche, Siemens Healthcare, Takeda,
and AstraZeneca; receiving lecture fees from ACR-Image Metrix; receiving
income from patents (owned by Massachusetts General Hospital) for
neuroradiology-related image acquisition and analysis; receiving
royalties from Massachusetts General Hospital for licensure of brain
perfusion software; serving as an expert witness for Kit regarding the
imaging appearance of carbon monoxide poisoning; receiving payment from
the International Center for Postgraduate Medical Education for
preparation of an online course on the use of MRI contrast agents,
supported by a grant from Bayer; and owning stock in Catalyst Medical.
Dr. Louis reports receiving payment for expert opinion on the results of
genetic testing in brain tumors from Rohm and Haas. No other potential
conflict of interest relevant to this article was reported.
NR 13
TC 1
Z9 1
U1 0
U2 1
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD MAY 31
PY 2012
VL 366
IS 22
BP 2112
EP 2120
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 949YE
UT WOS:000304613400013
PM 22646634
ER
PT J
AU Janas, MM
Novina, CD
AF Janas, Maja M.
Novina, Carl D.
TI Not lost in translation: stepwise regulation of microRNA targets
SO EMBO JOURNAL
LA English
DT Editorial Material
ID MESSENGER-RNA; PROTEIN-SYNTHESIS; LET-7 MICRORNA; IN-VITRO; INITIATION;
DEADENYLATION; INHIBITION; ZEBRAFISH
AB MicroRNAs (miRNAs) are endogenous, similar to 22-nucleotide-long, noncoding RNAs that play critical roles in physiology and disease via mechanisms that remain obscure. Although numerous studies implicate miRNAs in repression of translation, more recent reports suggest that the major role of miRNAs is in reduction of target mRNA stability. Because mRNA translation and stability are intimately connected, it has been a challenge to establish whether miRNAs induce translational repression, mRNA decay, or both. If miRNAs reduce both mRNA translation and stability, the timing and contribution of each process to overall repression is unclear. Indeed, it has been debated whether mRNA decay is a cause or consequence of miRNA-mediated translational repression. On the other hand, if these events are mutually exclusive, what determines which mechanism is used? In a recent issue of Science, Bazzini et al (2012) use genome-wide ribosome footprinting and RNA sequencing (RNA-Seq) to demonstrate that in developing zebrafish embryos, miR-430 naturally represses translation initiation of target mRNAs, followed by their deadenylation and decay.
C1 [Janas, Maja M.; Novina, Carl D.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA.
[Janas, Maja M.; Novina, Carl D.] Harvard Univ, Sch Med, Dept Microbiol & Immunobiol, Boston, MA 02115 USA.
[Janas, Maja M.; Novina, Carl D.] Broad Inst MIT & Harvard, Cambridge, MA USA.
RP Novina, CD (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, 44 Binney St, Boston, MA 02115 USA.
EM carl_novina@dfci.harvard.edu
NR 13
TC 7
Z9 7
U1 1
U2 9
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0261-4189
J9 EMBO J
JI Embo J.
PD MAY 30
PY 2012
VL 31
IS 11
BP 2446
EP 2447
DI 10.1038/emboj.2012.119
PG 2
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 949UA
UT WOS:000304600300004
PM 22522704
ER
PT J
AU Moon, H
Park, HE
Kang, J
Lee, H
Cheong, C
Lim, YT
Ihm, SH
Seung, KB
Jaffer, FA
Narula, J
Chang, K
Hong, KS
AF Moon, Hyeyoung
Park, Hyo Eun
Kang, Jongeun
Lee, Hyunseung
Cheong, Chaejoon
Lim, Yong Taik
Ihm, Sang-Hyun
Seung, Ki-Bae
Jaffer, Farouc A.
Narula, Jagat
Chang, Kiyuk
Hong, Kwan Soo
TI Noninvasive Assessment of Myocardial Inflammation by Cardiovascular
Magnetic Resonance in a Rat Model of Experimental Autoimmune Myocarditis
SO CIRCULATION
LA English
DT Article
DE contrast media; inflammation; macrophage; magnetic resonance imaging;
myocarditis
ID VIRAL MYOCARDITIS; NANOPARTICLES; REJECTION; DIAGNOSIS; PLAQUE; DEATH;
CELLS
AB Background-Limited availability of noninvasive and biologically precise diagnostic tools poses a challenge for the evaluation and management of patients with myocarditis.
Methods and Results-The feasibility of cardiovascular magnetic resonance (CMR) imaging with magneto-fluorescent nanoparticles (MNPs) for detection of myocarditis and its effectiveness in discriminating inflammation grades were assessed in experimental autoimmune myocarditis (EAM) (n = 65) and control (n = 10) rats. After undergoing CMR, rats were administered with MNPs, followed by a second CMR 24 hours later. Head-to-head comparison of MNP-CMR with T-2-weighted, early and late gadolinium enhancement CMR was performed in additional EAM (n = 10) and control (n = 5) rats. Contrast-to-noise ratios were measured and compared between groups. Flow cytometry and microscopy demonstrated that infiltrating inflammatory cells engulfed MNPs, resulting in altered myocardial T-2* effect. Changes in contrast-to-noise ratio between pre- and post-MNP CMR were significantly greater in EAM rats (1.08 +/- 0.10 versus 0.48 +/- 0.20; P < 0.001). In addition, contrast-to-noise ratio measurement in MNP-CMR clearly detected the extent of inflammation (P < 0.001) except for mild inflammation. Compared with conventional CMR, MNP-CMR provided better image contrast (CNR change 8% versus 46%, P < 0.001) and detectability of focal myocardial inflammation. Notably, MNP-CMR successfully tracked the evolution of myocardial inflammation in the same EAM rats.
Conclusions-Magneto-fluorescent nanoparticle CMR permitted effective visualization of myocardial inflammatory cellular infiltrates and distinction of the extent of inflammation compared with conventional CMR in a preclinical model of EAM. Magneto-fluorescent nanoparticle CMR performs best in EAM rats with at least moderate inflammatory response. (Circulation. 2012; 125: 2603-2612.)
C1 [Moon, Hyeyoung; Kang, Jongeun; Lee, Hyunseung; Cheong, Chaejoon; Hong, Kwan Soo] Korea Basic Sci Inst, Div MR Res, Ochang Eup 363883, Cheongwon, South Korea.
[Moon, Hyeyoung; Hong, Kwan Soo] Univ Sci & Technol, Dept Bioanalyt Sci, Taejon, South Korea.
[Park, Hyo Eun; Ihm, Sang-Hyun; Seung, Ki-Bae; Chang, Kiyuk] Seoul St Marys Hosp, Ctr Cardiovasc, Seoul, South Korea.
[Chang, Kiyuk] Catholic Univ Korea, Coll Med, Dept Cardiovasc Med, Ctr Cardiovasc, Seoul 137701, South Korea.
[Kang, Jongeun; Lim, Yong Taik; Hong, Kwan Soo] Chungnam Natl Univ, Grad Sch Analyt Sci & Technol, Taejon, South Korea.
[Jaffer, Farouc A.] Harvard Univ, Sch Med, Div Cardiol, Cardiovasc Res Ctr,Massachusetts Gen Hosp, Charlestown, MA USA.
[Jaffer, Farouc A.] Harvard Univ, Sch Med, Ctr Mol Imaging Res, Massachusetts Gen Hosp, Charlestown, MA USA.
[Narula, Jagat] Mt Sinai Sch Med, Zena & Michael Wiener Cardiovasc Inst, New York, NY USA.
RP Hong, KS (reprint author), Korea Basic Sci Inst, Div MR Res, 804-1 Yangcheong Ri, Ochang Eup 363883, Cheongwon, South Korea.
EM kiyuk@catholic.ac.kr; kshong@kbsi.re.kr
OI Ihm, Sang Hyun/0000-0001-5017-5421; Jaffer, Farouc/0000-0001-7980-384X
FU National Research Foundation of Korea [2011-0029263, 2009-008146]; Korea
Basic Science Institute [T31403]; Ministry of Health and Welfare
[A090604, A092258]
FX This work was supported by grants from the National Research Foundation
of Korea (to Dr Hong, 2011-0029263 and 2009-008146), Korea Basic Science
Institute (to Dr Hong, T31403), and the Korea Health Technology R&D
Project, Ministry of Health and Welfare (to Dr Chang, A090604 and
A092258).
NR 35
TC 16
Z9 19
U1 1
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD MAY 29
PY 2012
VL 125
IS 21
BP 2603
EP U343
DI 10.1161/CIRCULATIONAHA.111.075283
PG 20
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 981MQ
UT WOS:000306972800017
PM 22550157
ER
PT J
AU Weiner, RB
Wang, F
Berkstresser, B
Kim, J
Wang, TJ
Lewis, GD
Hutter, AM
Picard, MH
Baggish, AL
AF Weiner, Rory B.
Wang, Francis
Berkstresser, Brant
Kim, Jonathan
Wang, Thomas J.
Lewis, Gregory D.
Hutter, Adolph M., Jr.
Picard, Michael H.
Baggish, Aaron L.
TI Regression of "Gray Zone" Exercise-Induced Concentric Left Ventricular
Hypertrophy During Prescribed Detraining
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Letter
ID DISEASE
C1 [Weiner, Rory B.; Wang, Francis; Berkstresser, Brant; Kim, Jonathan; Wang, Thomas J.; Lewis, Gregory D.; Hutter, Adolph M., Jr.; Picard, Michael H.; Baggish, Aaron L.] Massachusetts Gen Hosp, Cardiovasc Performance Program, Boston, MA 02114 USA.
RP Weiner, RB (reprint author), Massachusetts Gen Hosp, Cardiovasc Performance Program, Yawkey Suite 5B,55 Fruit St, Boston, MA 02114 USA.
EM rweiner@partners.org
OI Picard, Michael/0000-0002-9264-3243
FU NHLBI NIH HHS [K23 HL091106]
NR 5
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 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD MAY 29
PY 2012
VL 59
IS 22
BP 1992
EP 1994
DI 10.1016/j.jacc.2012.01.057
PG 3
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 949QR
UT WOS:000304591300014
PM 22624842
ER
PT J
AU Schumacher, J
Haslinger, R
Pipa, G
AF Schumacher, Johannes
Haslinger, Robert
Pipa, Gordon
TI Statistical modeling approach for detecting generalized synchronization
SO PHYSICAL REVIEW E
LA English
DT Article
ID SYSTEMS; PHASE; CHAOS
AB Detecting nonlinear correlations between time series presents a hard problem for data analysis. We present a generative statistical modeling method for detecting nonlinear generalized synchronization. Truncated Volterra series are used to approximate functional interactions. The Volterra kernels are modeled as linear combinations of basis splines, whose coefficients are estimated via l(1) and l(2) regularized maximum likelihood regression. The regularization manages the high number of kernel coefficients and allows feature selection strategies yielding sparse models. The method's performance is evaluated on different coupled chaotic systems in various synchronization regimes and analytical results for detecting m : n phase synchrony are presented. Experimental applicability is demonstrated by detecting nonlinear interactions between neuronal local field potentials recorded in different parts of macaque visual cortex.
C1 [Schumacher, Johannes; Haslinger, Robert; Pipa, Gordon] Univ Osnabruck, Inst Cognit Sci, D-4500 Osnabruck, Germany.
[Schumacher, Johannes; Haslinger, Robert; Pipa, Gordon] MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA.
[Schumacher, Johannes; Haslinger, Robert; Pipa, Gordon] Massachusetts Gen Hosp, Charlestown, MA USA.
[Schumacher, Johannes; Haslinger, Robert; Pipa, Gordon] Frankfurt Inst Adv Studies, Frankfurt, Germany.
RP Schumacher, J (reprint author), Univ Osnabruck, Inst Cognit Sci, D-4500 Osnabruck, Germany.
EM joschuma@uos.de; robhh@nmr.mgh.harvard.edu; gpipa@uos.de
RI Pipa, Gordon/M-1813-2014
OI Pipa, Gordon/0000-0002-3416-2652
FU EU [FET-Open 240763]; NIH [K25-NS052422-02]
FX We thank Sergio Neuenschwander for providing the local field potential
recordings. We thank Ingo Fischer and Miguel C. Soriano for providing
the simulated Mackey-Glass data. This work was partially supported by
the EU-project PHOCUS (FET-Open 240763) (J.S., G. P.) and the NIH Grant
No. K25-NS052422-02 (R.H.).
NR 21
TC 4
Z9 4
U1 0
U2 3
PU AMER PHYSICAL SOC
PI COLLEGE PK
PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA
SN 1539-3755
J9 PHYS REV E
JI Phys. Rev. E
PD MAY 29
PY 2012
VL 85
IS 5
AR 056215
DI 10.1103/PhysRevE.85.056215
PN 2
PG 7
WC Physics, Fluids & Plasmas; Physics, Mathematical
SC Physics
GA 948VG
UT WOS:000304530300005
PM 23004851
ER
PT J
AU Rajani, DK
Walch, M
Martinvalet, D
Thomas, MP
Lieberman, J
AF Rajani, Danielle K.
Walch, Michael
Martinvalet, Denis
Thomas, Marshall P.
Lieberman, Judy
TI Alterations in RNA processing during immune-mediated programmed cell
death
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE apoptosis; cytotoxic T lymphocyte
ID FAS-INDUCED APOPTOSIS; MESSENGER-RNA; HUMAN GRANZYME; PROTEOME ANALYSIS;
BINDING PROTEINS; HEAT-SHOCK; CLEAVAGE; IDENTIFICATION; COMPLEX; TARGETS
AB During immune-mediated death, death-inducing granzyme (Gzm) proteases concentrate in the nucleus of cells targeted for immune elimination, suggesting that nuclear processes are important targets. Here we used differential 2D proteomics of GzmA-treated nuclei to identify potential GzmA substrates. Of 44 candidates, 33 were RNA-binding proteins important in posttranscriptional RNA processing, including 14 heterogeneous nuclear ribonucleoproteins (hnRNP). Multiple hnRNPs were degraded in cells undergoing GzmA-, GzmB-, or caspase-mediated death. GzmA and caspase activation impaired nuclear export of newly synthesized RNA and disrupted pre-mRNA splicing. Expressing GzmA-resistant hnRNP A1 inhibited GzmA-mediated cell death and rescued pre-mRNA splicing, suggesting that hnRNP A1 is an important GzmA substrate. Cellular stresses are known to inhibit initiation of cap-dependent translation. Disrupting pre-mRNA processing should block further new protein synthesis and promote death by interfering with pathways induced to protect cells from death.
C1 [Rajani, Danielle K.; Walch, Michael; Martinvalet, Denis; Thomas, Marshall P.; Lieberman, Judy] Harvard Univ, Sch Med, Immune Dis Inst, Childrens Hosp Boston, Boston, MA 02115 USA.
[Rajani, Danielle K.; Walch, Michael; Martinvalet, Denis; Thomas, Marshall P.; Lieberman, Judy] Harvard Univ, Sch Med, Program Mol & Cellular Med, Childrens Hosp Boston, Boston, MA 02115 USA.
RP Lieberman, J (reprint author), Harvard Univ, Sch Med, Immune Dis Inst, Childrens Hosp Boston, Boston, MA 02115 USA.
EM lieberman@idi.harvard.edu
RI Lieberman, Judy/A-2717-2015
FU National Science Foundation; Kurt und Senta Herrmann-Foundation;
National Institutes of Health [AI45587]
FX We thank Gideon Dreyfuss for hnRNP antibodies and Arlene Sharpe, Paul
Anderson, Tom Kirchhausen, Melissa Moore and members of the J.L.
laboratory for helpful discussions. This work was supported by National
Science Foundation predoctoral fellowships (to D. K. R. and M. P. T.), a
Kurt und Senta Herrmann-Foundation fellowship (to M. W.), and National
Institutes of Health Grant AI45587 (to J.L.).
NR 29
TC 11
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U1 2
U2 6
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD MAY 29
PY 2012
VL 109
IS 22
BP 8688
EP 8693
DI 10.1073/pnas.1201327109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 953PD
UT WOS:000304881700067
PM 22589304
ER
PT J
AU Straume, O
Shimamura, T
Lampa, MJG
Carretero, J
Oyan, AM
Jia, D
Borgman, CL
Soucheray, M
Downing, SR
Short, SM
Kang, SY
Wang, SM
Chen, L
Collett, K
Bachmann, I
Wong, KK
Shapiro, GI
Kalland, KH
Folkman, J
Watnick, RS
Akslen, LA
Naumov, GN
AF Straume, Oddbjorn
Shimamura, Takeshi
Lampa, Michael J. G.
Carretero, Julian
Oyan, Anne M.
Jia, Di
Borgman, Christa L.
Soucheray, Margaret
Downing, Sean R.
Short, Sarah M.
Kang, Soo-Young
Wang, Souming
Chen, Liang
Collett, Karin
Bachmann, Ingeborg
Wong, Kwok-Kin
Shapiro, Geoffrey I.
Kalland, Karl Henning
Folkman, Judah
Watnick, Randolph S.
Akslen, Lars A.
Naumov, George N.
TI Suppression of heat shock protein 27 induces long-term dormancy in human
breast cancer
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE NF kappa B; STAT3
ID FIBROBLAST-GROWTH-FACTOR; HUMAN TUMOR DORMANCY; ENDOTHELIAL-CELLS;
ANGIOGENIC SWITCH; EXPRESSION SIGNATURE; HEAT-SHOCK-PROTEIN-27;
PROLIFERATION; MELANOCYTES; MECHANISMS; APOPTOSIS
AB The mechanisms underlying tumor dormancy have been elusive and not well characterized. We recently published an experimental model for the study of human tumor dormancy and the role of angiogenesis, and reported that the angiogenic switch was preceded by a local increase in VEGF-A and basic fibroblast growth factor. In this breast cancer xenograft model (MDA-MB-436 cells), analysis of differentially expressed genes revealed that heat shock protein 27 (HSP27) was significantly up-regulated in angiogenic cells compared with nonangiogenic cells. The effect of HSP27 down-regulation was further evaluated in cell lines, mouse models, and clinical datasets of human patients with breast cancer and melanoma. Stable down-regulation of HSP27 in angiogenic tumor cells was followed by long-term tumor dormancy in vivo. Strikingly, only 4 of 30 HSP27 knockdown xenograft tumors initiated rapid growth after day 70, in correlation with a regain of HSP27 protein expression. Significantly, no tumors escaped from dormancy without HSP27 expression. Down-regulation of HSP27 was associated with reduced endothelial cell proliferation and decreased secretion of VEGF-A, VEGF-C, and basic fibroblast growth factor. Conversely, overexpression of HSP27 in nonangiogenic cells resulted in expansive tumor growth in vivo. By clinical validation, strong HSP27 protein expression was associated with markers of aggressive tumors and decreased survival in patients with breast cancer and melanoma. An HSP27-associated gene expression signature was related to molecular subgroups and survival in breast cancer. Our findings suggest a role for HSP27 in the balance between tumor dormancy and tumor progression, mediated by tumor-vascular interactions. Targeting HSP27 might offer a useful strategy in cancer treatment.
C1 [Straume, Oddbjorn; Lampa, Michael J. G.; Jia, Di; Downing, Sean R.; Short, Sarah M.; Kang, Soo-Young; Wang, Souming; Folkman, Judah; Watnick, Randolph S.; Akslen, Lars A.; Naumov, George N.] Childrens Hosp, Vasc Biol Program, Boston, MA 02115 USA.
[Straume, Oddbjorn; Lampa, Michael J. G.; Jia, Di; Downing, Sean R.; Short, Sarah M.; Kang, Soo-Young; Wang, Souming; Folkman, Judah; Watnick, Randolph S.; Akslen, Lars A.; Naumov, George N.] Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA.
[Straume, Oddbjorn; Collett, Karin; Bachmann, Ingeborg; Kalland, Karl Henning; Akslen, Lars A.] Univ Bergen, Sect Pathol, Gade Inst, N-5021 Bergen, Norway.
[Shimamura, Takeshi; Carretero, Julian; Borgman, Christa L.; Chen, Liang; Wong, Kwok-Kin; Shapiro, Geoffrey I.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
[Shimamura, Takeshi; Carretero, Julian; Wong, Kwok-Kin; Shapiro, Geoffrey I.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Shimamura, Takeshi; Soucheray, Margaret] Loyola Univ Chicago, Stritch Sch Med, Dept Mol Pharmacol & Therapeut, Inst Oncol, Maywood, IL 60153 USA.
[Carretero, Julian] Univ Valencia, Dept Physiol, E-46100 Valencia, Spain.
[Oyan, Anne M.; Kalland, Karl Henning] Haukeland Hosp, Dept Microbiol & Immunol, N-5021 Bergen, Norway.
[Chen, Liang; Wong, Kwok-Kin] Dana Farber Harvard Canc Ctr, Ludwig Ctr, Boston, MA 02215 USA.
[Akslen, Lars A.] Haukeland Hosp, Dept Pathol, N-5021 Bergen, Norway.
RP Akslen, LA (reprint author), Childrens Hosp, Vasc Biol Program, 300 Longwood Ave, Boston, MA 02115 USA.
EM lars.akslen@gades.uib.no; george_naumov@merck.com
RI Jia, Di/E-6943-2013; Carretero, Julian/N-5214-2014; Kalland,
Karl-Henning/B-9445-2017; Akslen, Lars /C-1202-2017; Straume,
Oddbjorn/C-2186-2017;
OI Carretero, Julian/0000-0001-7269-8506; Kalland,
Karl-Henning/0000-0003-4486-2334; Akslen, Lars /0000-0003-2710-9543;
Straume, Oddbjorn/0000-0001-8867-3645; wong, kwok
kin/0000-0001-6323-235X
FU Helse Vest [911401, 911500, 15126600, 911403]; Norwegian Cancer Society
[HS02-2008-0188, 94070, 419328 71512-PR-2006-0356]; Unger Vetlesen
Foundation; Dana-Farber Cancer Institute; Dana-Farber/Harvard Cancer
Center, National Institutes of Health (NIH) [P50 CA090578]; Research
Council of Norway [185676/V40, 154942/310, 161231/V40, 163920/V50]; NIH
[P01CA045548]; Breast Cancer Research Foundation; Department of Defense
[W81XWH-04-1-0316]
FX We thank Gerd Lillian Hallseth, Hua My Hoang, and Bendik Nordanger for
excellent technical assistance and Marsha A. Moses and Alexis Mitsialis
of Children's Hospital Boston for helpful comments and experimental
support. The work of O.S. was supported by Helse Vest, the Norwegian
Cancer Society, and the Unger Vetlesen Foundation. T. S. was supported
by the Dana-Farber Cancer Institute Claudia Adams Barr Program in
Innovative Basic Cancer Research. G. I. S. was supported by
Dana-Farber/Harvard Cancer Center Specialized Program of Research
Excellence in Lung Cancer, National Institutes of Health (NIH) Grant P50
CA090578. The work of K. H. K. was supported by Research Council of
Norway Grant 185676/V40, Helse Vest Grants 911401 and 911500, and
Norwegian Cancer Society Grant HS02-2008-0188. The work of J.M.F. was
funded by NIH Grant P01CA045548, the Breast Cancer Research Foundation,
and Department of Defense Breast Cancer Innovator Award
W81XWH-04-1-0316. L. A. A. was supported by Research Council of Norway
Grants 154942/310, 161231/V40, and 163920/V50; Helse Vest Grants
15126600 and 911403; the Unger Vetlesen Foundation; and Norwegian Cancer
Society Grants 94070 and 419328 71512-PR-2006-0356.
NR 31
TC 50
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U1 1
U2 13
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD MAY 29
PY 2012
VL 109
IS 22
BP 8699
EP 8704
DI 10.1073/pnas.1017909109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 953PD
UT WOS:000304881700069
PM 22589302
ER
PT J
AU Seyedali, M
Czerniecki, JM
Morgenroth, DC
Hahn, ME
AF Seyedali, Mahyo
Czerniecki, Joseph M.
Morgenroth, David C.
Hahn, Michael E.
TI Co-contraction patterns of trans-tibial amputee ankle and knee
musculature during gait
SO JOURNAL OF NEUROENGINEERING AND REHABILITATION
LA English
DT Article
DE Electromyography; Myoelectric control; Trans-tibial amputees; Activation
patterns; Muscle amplitude
ID MUSCLE-ACTIVITY; WALKING SPEEDS; EMG PROFILES; CHILDREN; PROSTHESIS;
LOCOMOTION; INDEX; JOINT
AB Background: Myoelectric control of upper extremity powered prostheses has been used clinically for many years, however this approach has not been fully developed for lower extremity prosthetic devices. With the advent of powered lower extremity prosthetic components, the potential role of myoelectric control systems is of increasing importance. An understanding of muscle activation patterns and their relationship to functional ambulation is a vital step in the future development of myoelectric control. Unusual knee muscle co-contractions have been reported in both limbs of trans-tibial amputees. It is currently unknown what differences exist in co-contraction between trans-tibial amputees and controls. This study compares the activation and co-contraction patterns of the ankle and knee musculature of trans-tibial amputees (intact and residual limbs), and able-bodied control subjects during three speeds of gait. It was hypothesized that residual limbs would have greater ankle muscle co-contraction than intact and able-bodied control limbs and that knee muscle co-contraction would be different among all limbs. Lastly it was hypothesized that the extent of muscle co-contraction would increase with walking speed.
Methods: Nine unilateral traumatic trans-tibial amputees and five matched controls participated. Surface electromyography recorded activation from the Tibialis Anterior, Medial Gastrocnemius, Vastus Lateralis and Biceps Femoris of the residual, intact and control limbs. A series of filters were applied to the signal to obtain a linear envelope of the activation patterns. A co-contraction area (ratio of the integrated agonist and antagonist activity) was calculated during specific phases of gait.
Results: Co-contraction of the ankle muscles was greater in the residual limb than in the intact and control limbs during all phases of gait. Knee muscle co-contraction was greater in the residual limb than in the control limb during all phases of gait.
Conclusion: Co-contractions may represent a limb stiffening strategy to enhance stability during phases of initial foot-contact and single limb support. These strategies may be functionally necessary for amputee gait; however, the presence of co-contractions could confound future development of myoelectric controls and should thus be accounted for.
C1 [Seyedali, Mahyo; Czerniecki, Joseph M.; Morgenroth, David C.; Hahn, Michael E.] VA Puget Sound, Dept Vet Affairs VA, Rehabil Res & Dev Ctr Excellence Limb Loss Preven, Seattle, WA 98108 USA.
[Seyedali, Mahyo; Hahn, Michael E.] Univ Washington, Dept Mech Engn, Seattle, WA 98105 USA.
[Czerniecki, Joseph M.; Morgenroth, David C.] Univ Washington, Dept Rehabil Med, Seattle, WA 98195 USA.
RP Hahn, ME (reprint author), VA Puget Sound, Dept Vet Affairs VA, Rehabil Res & Dev Ctr Excellence Limb Loss Preven, 1660 S Columbian Way, Seattle, WA 98108 USA.
EM mhahn@uoregon.edu
OI Morgenroth, David/0000-0002-0226-7775
FU Department of Veterans Affairs, Veterans Health Administration,
Rehabilitation Research and Development Service; Department of Defense
[W81XWH-09-2-0142]
FX This research was supported by the Department of Veterans Affairs,
Veterans Health Administration, Rehabilitation Research and Development
Service. Additionally, this research was funded by a Department of
Defense grant (W81XWH-09-2-0142). We gratefully acknowledge the
supporting efforts of Janice Pecoraro and Elise Wright.
NR 35
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U1 0
U2 8
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1743-0003
J9 J NEUROENG REHABIL
JI J. NeuroEng. Rehabil.
PD MAY 28
PY 2012
VL 9
AR 29
DI 10.1186/1743-0003-9-29
PG 9
WC Engineering, Biomedical; Neurosciences; Rehabilitation
SC Engineering; Neurosciences & Neurology; Rehabilitation
GA 026IJ
UT WOS:000310268300001
PM 22640660
ER
PT J
AU Kumar, N
Bashar, Q
Reddy, N
Sengupta, J
Ananthakrishnan, A
Schroeder, A
Hogan, WJ
Venkatesan, T
AF Kumar, Nilay
Bashar, Qumseya
Reddy, Naveen
Sengupta, Jyotirmoy
Ananthakrishnan, Ashwin
Schroeder, Abigail
Hogan, Walter J.
Venkatesan, Thangam
TI Cyclic Vomiting Syndrome (CVS): is there a difference based on onset of
symptoms - pediatric versus adult?
SO BMC GASTROENTEROLOGY
LA English
DT Article
DE Motility; Cyclic vomiting; Nausea; Abdominal pain
ID CANNABINOID HYPEREMESIS; AMITRIPTYLINE; MANAGEMENT; DISORDERS; MIGRAINE;
THERAPY
AB Background: Cyclic Vomiting Syndrome (CVS) is a well-recognized functional gastrointestinal disorder in children but its presentation is poorly understood in adults. Genetic differences in pediatric-onset (presentation before age 18) and adult-onset CVS have been reported recently but their clinical features and possible differences in response to therapy have not been well studied.
Methods: This was a retrospective review of 101 CVS patients seen at the Medical College of Wisconsin between 2006 and 2008. Rome III criteria were utilized to make the diagnosis of CVS.
Results: Our study population comprised of 29(29%) pediatric-onset and 72 (71%) adult-onset CVS patients. Pediatric-onset CVS patients were more likely to be female (86% vs. 57%, p = 0.005) and had a higher prevalence of CVS plus (CVS + neurocognitive disorders) as compared to adult-onset CVS patients (14% vs. 3%, p = 0.05). There was a longer delay in diagnosis (10 +/- 7 years) in the pediatric-onset group when compared to (5 +/- 7 years) adultonset CVS group (p = 0.001). Chronic opiate use was less frequent in the pediatric-onset group compared to adultonset patients (0% vs. 23%, p = 0.004). Aside from these differences, the two groups were similar with regards to their clinical features and the time of onset of symptoms did not predict response to standard treatment. The majority of patients (86%) responded to treatment with tricyclic antidepressants, anticonvulsants (topiramate), coenzyme Q-10, and L-carnitine. Non-response to therapy was associated with coalescence of symptoms, chronic opiate use and more severe disease as characterized by longer episodes, greater number of emergency department visits in the year prior to presentation, presence of disability and non-compliance on univariate analysis. On multivariate analysis, only compliance to therapy was associated with a response. (88% vs. 38%, Odds Ratio, OR 9.6; 95% Confidence Interval [CI], 1.18-77.05).
Conclusion: Despite reported genetic differences, the clinical features and response to standard therapy in pediatric-and adult-onset CVS were mostly similar. Most patients (86%) responded to therapy and compliance was the only factor associated with a response.
C1 [Kumar, Nilay; Sengupta, Jyotirmoy; Schroeder, Abigail; Hogan, Walter J.; Venkatesan, Thangam] Med Coll Wisconsin, Dept Gastroenterol & Hepatol, Milwaukee, WI 53226 USA.
[Bashar, Qumseya] Mayo Clin Florida, Jacksonville, FL USA.
[Reddy, Naveen] Wayne State Univ, Detroit, MI USA.
[Ananthakrishnan, Ashwin] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Venkatesan, T (reprint author), Med Coll Wisconsin, Dept Gastroenterol & Hepatol, 4th Floor,Froedtert E Bldg,9200 W Wisconsin Ave, Milwaukee, WI 53226 USA.
EM tvenkate@mcw.edu
NR 24
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U1 0
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-230X
J9 BMC GASTROENTEROL
JI BMC Gastroenterol.
PD MAY 28
PY 2012
VL 12
AR 52
DI 10.1186/1471-230X-12-52
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 006MB
UT WOS:000308822200001
PM 22639867
ER
PT J
AU Zhou, C
Kirtane, T
Tsai, TH
Lee, HC
Adler, DC
Schmitt, JM
Huang, Q
Fujimoto, JG
Mashimo, H
AF Zhou, Chao
Kirtane, Tejas
Tsai, Tsung-Han
Lee, Hsiang-Chieh
Adler, Desmond C.
Schmitt, Joseph M.
Huang, Qin
Fujimoto, James G.
Mashimo, Hiroshi
TI Cervical inlet patch-optical coherence tomography imaging and clinical
significance
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Cervical inlet patch; Heterotopic gastric mucosa; Optical coherence
tomography; Optical biopsy; Barrett's esophagus
ID HETEROTOPIC GASTRIC-MUCOSA; HIGH-GRADE DYSPLASIA; UPPER ESOPHAGUS;
BARRETTS-ESOPHAGUS; 3-DIMENSIONAL ENDOMICROSCOPY; PRIMARY
ADENOCARCINOMA; INTESTINAL METAPLASIA; PROXIMAL ESOPHAGUS; GI TRACT;
PREVALENCE
AB AIM: To demonstrate the feasibility of optical coherence tomography (OCT) imaging in differentiating cervical inlet patch (UP) from normal esophagus, Barrett's esophagus (BE), normal stomach and duodenum.
METHODS: This study was conducted at the Veterans Affairs Boston Healthcare System (VABHS). Patients undergoing standard esophagogastroduodenoscopy at VABHS, including one patient with CIP, one representative patient with BE and three representative normal subjects were included. White light video endoscopy was performed and endoscopic 3D-OCT images were obtained in each patient using a prototype OCT system. The OCT imaging probe passes through the working channel of the endoscope to enable simultaneous video endoscopy and 3D-OCT examination of the human gastrointestinal (GI) tract. Standard hematoxylin and eosin (H and E) histology was performed on biopsy or endoscopic mucosal resection specimens in order to compare and validate the 3D-OCT data.
RESULTS: CIP was observed from a 68-year old male with gastroesophageal reflux disease. The CIP region appeared as a pink circular lesion in the upper esophagus under white light endoscopy. OCT imaging over the CIP region showed columnar epithelium structure, which clearly contrasted the squamous epithelium structure from adjacent normal esophagus. 3D-OCT images obtained from other representative patients demonstrated distinctive patterns of the normal esophagus, BE, normal stomach, and normal duodenum bulb. Microstructures, such as squamous epithelium, lamina propria, muscularis mucosa, muscularis propria, esophageal glands, Barrett's glands, gastric mucosa, gastric glands, and intestinal mucosal villi were clearly observed with OCT and matched with H and E histology. These results demonstrated the feasibility of using OCT to evaluate GI tissue morphology in situ and in real-time.
CONCLUSION: We demonstrate in situ evaluation of CIP microstructures using 3D-OCT, which may be a useful tool for future diagnosis and follow-up of patients with CIP. (C) 2012 Baishideng. All rights reserved.
C1 [Kirtane, Tejas; Huang, Qin; Mashimo, Hiroshi] Harvard Univ, Sch Med, Gastroenterol Sect, VA Boston Healthcare Syst, Boston, MA 02131 USA.
[Zhou, Chao; Tsai, Tsung-Han; Lee, Hsiang-Chieh; Fujimoto, James G.] MIT, Dept Elect Engn & Comp Sci, Elect Res Lab, Cambridge, MA 02139 USA.
[Adler, Desmond C.; Schmitt, Joseph M.] Light Lab Imaging St Jude Med Inc, Westford, MN 55117 USA.
RP Mashimo, H (reprint author), Harvard Univ, Sch Med, Gastroenterol Sect, VA Boston Healthcare Syst, 150 S Huntington Ave, Boston, MA 02131 USA.
EM hmashimo@hms.harvard.edu
RI Zhou, Chao/A-1327-2007;
OI Tsai, Tsung-Han/0000-0002-2306-2269
FU VA Boston Healthcare System; NIH [R01-CA75289-14, K99-EB010071-01A1];
Air Force Office of Scientific Research [FA9550-10-1-0063]; Medical Free
Electron Laser Program [FA9550-10-1-0551]; MIT/CIMIT
FX Supported by The VA Boston Healthcare System and NIH grants
R01-CA75289-14, to Fujimoto JG and Mashimo H; and K99-EB010071-01A1, to
Zhou C; Air Force Office of Scientific Research contract
FA9550-10-1-0063, to Fujimoto JG; Medical Free Electron Laser Program
contract FA9550-10-1-0551, to Fujimoto JG; and the MIT/CIMIT Medical
Engineering Fellowship, to Tsai TH
NR 57
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U1 1
U2 5
PU BAISHIDENG PUBL GRP CO LTD
PI BEIJING
PA RM 903, BLDG D, OCEAN INTERNATIONAL CTR, NO 62 DONGSIHUAN ZHONGLU,
BEIJING, CHAOYANG DISTRICT 100025, PEOPLES R CHINA
SN 1007-9327
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD MAY 28
PY 2012
VL 18
IS 20
BP 2502
EP 2510
DI 10.3748/wjg.v18.i20.2502
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 952HC
UT WOS:000304782100007
PM 22654447
ER
PT J
AU Nathan, DM
AF Nathan, David M.
TI Understanding the Long-term Benefits and Dangers of Intensive Therapy of
Diabetes
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Editorial Material
ID MICROVASCULAR COMPLICATIONS; GLUCOSE CONTROL; MELLITUS; RISK
C1 Harvard Univ, Diabet Unit, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA.
RP Nathan, DM (reprint author), Harvard Univ, Diabet Unit, Massachusetts Gen Hosp, Sch Med, 50 Staniford St,Ste 340, Boston, MA 02114 USA.
EM dnathan@partners.org
NR 10
TC 4
Z9 5
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9926
J9 ARCH INTERN MED
JI Arch. Intern. Med.
PD MAY 28
PY 2012
VL 172
IS 10
BP 769
EP 770
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 948FK
UT WOS:000304488800003
PM 22636821
ER
PT J
AU Pham-Kanter, G
Alexander, GC
Nair, K
AF Pham-Kanter, Genevieve
Alexander, G. Caleb
Nair, Kavita
TI Effect of Physician Payment Disclosure Laws on Prescribing
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Letter
C1 [Nair, Kavita] Univ Colorado, Dept Clin Pharm, Skaggs Sch Pharm & Pharmaceut Sci, Aurora, CO 80045 USA.
[Pham-Kanter, Genevieve] Harvard Univ, Edmond J Safra Ctr Eth, Cambridge, MA 02138 USA.
[Pham-Kanter, Genevieve] Massachusetts Gen Hosp, Mongan Inst Hlth Policy, Boston, MA 02114 USA.
[Pham-Kanter, Genevieve] Univ Colorado, Dept Hlth Syst Management & Policy, Colorado Sch Publ Hlth, Aurora, CO 80045 USA.
[Pham-Kanter, Genevieve] Univ Colorado, Dept Econ, Denver, CO 80202 USA.
[Alexander, G. Caleb] Johns Hopkins Univ, Dept Epidemiol, Baltimore, MD USA.
RP Nair, K (reprint author), Univ Colorado, Dept Clin Pharm, Skaggs Sch Pharm & Pharmaceut Sci, Anschutz Med Campus,Mail Stop C238,12850 E Montvi, Aurora, CO 80045 USA.
EM kavita.nair@ucdenver.edu
OI Pham-Kanter, Genevieve/0000-0002-3044-7829
FU AHRQ HHS [R01 HS0189960]; NCRR NIH HHS [UL1 RR025758]; NHLBI NIH HHS
[R01 HL 107345-01, R01 HL107345]; NICHD NIH HHS [P2C HD047879, T32
HD007163]
NR 4
TC 14
Z9 14
U1 0
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9926
J9 ARCH INTERN MED
JI Arch. Intern. Med.
PD MAY 28
PY 2012
VL 172
IS 10
BP 819
EP 821
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA 948FK
UT WOS:000304488800014
PM 22636826
ER
PT J
AU Grant, RW
Wexler, DJ
Ashburner, JM
Hong, CS
Atlas, SJ
AF Grant, Richard W.
Wexler, Deborah J.
Ashburner, Jeffrey M.
Hong, Clemens S.
Atlas, Steven J.
TI Characteristics of "Complex" Patients With Type 2 Diabetes Mellitus
According to Their Primary Care Physicians
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Letter
C1 [Grant, Richard W.] Kaiser Permanente No Calif, Div Res, Oakland, CA 94612 USA.
[Wexler, Deborah J.] Massachusetts Gen Hosp, Ctr Diabet, Boston, MA 02114 USA.
[Ashburner, Jeffrey M.; Hong, Clemens S.; Atlas, Steven J.] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[Wexler, Deborah J.; Hong, Clemens S.; Atlas, Steven J.] Harvard Univ, Sch Med, Boston, MA USA.
RP Grant, RW (reprint author), Kaiser Permanente No Calif, Div Res, 2101 Webster St, Oakland, CA 94612 USA.
EM Richard.W.Grant@kp.org
OI Grant, Richard/0000-0002-6164-8025
NR 4
TC 15
Z9 15
U1 1
U2 2
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9926
J9 ARCH INTERN MED
JI Arch. Intern. Med.
PD MAY 28
PY 2012
VL 172
IS 10
BP 821
EP 823
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA 948FK
UT WOS:000304488800015
PM 22636827
ER
PT J
AU Grady, D
Katz, MH
Berkowitz, SA
AF Grady, Deborah
Katz, Mitchell H.
Berkowitz, Seth A.
TI A Role for Opioids in Chronic Pain Management reply
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Letter
C1 [Grady, Deborah] Univ Calif San Francisco, Dept Med, San Francisco VA Med Ctr, San Francisco, CA 94115 USA.
[Katz, Mitchell H.] Los Angeles Cty Dept Hlth Serv, Los Angeles, CA USA.
RP Grady, D (reprint author), Univ Calif San Francisco, Dept Med, San Francisco VA Med Ctr, 1635 Divisadero St,Ste 600, San Francisco, CA 94115 USA.
EM Deborah.Grady@ucsf.edu
NR 2
TC 0
Z9 0
U1 0
U2 2
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9926
J9 ARCH INTERN MED
JI Arch. Intern. Med.
PD MAY 28
PY 2012
VL 172
IS 10
BP 824
EP 825
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 948FK
UT WOS:000304488800019
ER
PT J
AU Gabbita, SP
Srivastava, MK
Eslami, P
Johnson, MF
Kobritz, NK
Tweedie, D
Greig, NH
Zemlan, FP
Sharma, SP
Harris-White, ME
AF Gabbita, S. Prasad
Srivastava, Minu K.
Eslami, Pirooz
Johnson, Ming F.
Kobritz, Naomi K.
Tweedie, David
Greig, Nigel H.
Zemlan, Frank P.
Sharma, Sherven P.
Harris-White, Marni E.
TI Early intervention with a small molecule inhibitor for tumor necrosis
factor-alpha prevents cognitive deficits in a triple transgenic mouse
model of Alzheimer's disease
SO JOURNAL OF NEUROINFLAMMATION
LA English
DT Article
DE Alzheimer's disease; memory; neuroinflammation; thalidomide;
thiothalidomide; tumor necrosis factor-alpha
ID CENTRAL-NERVOUS-SYSTEM; BETA-AMYLOID STIMULATION; MARROW-DERIVED CELLS;
BLOOD-BRAIN-BARRIER; TNF-ALPHA; NEURODEGENERATIVE DISEASES; PERISPINAL
ETANERCEPT; SYNAPTIC PLASTICITY; HEMATOPOIETIC-CELLS; THERAPEUTIC TARGET
AB Background: Chronic neuroinflammation is an important component of Alzheimer's disease and could contribute to neuronal dysfunction, injury and loss that lead to disease progression. Multiple clinical studies implicate tumor necrosis factor-alpha as an inflammatory mediator of neurodegeneration in patients with Alzheimer's because of elevated levels of this cytokine in the cerebrospinal fluid, hippocampus and cortex. Current Alzheimer's disease interventions are symptomatic treatments with limited efficacy that do not address etiology. Thus, a critical need exists for novel treatments directed towards modifying the pathophysiology and progression.
Methods: To investigate the effect of early immune modulation on neuroinflammation and cognitive outcome, we treated triple transgenic Alzheimer's disease mice (harboring PS1(M146V), APP(Swe), and tau(P301L) transgenes) with the small molecule tumor necrosis factor-alpha inhibitors, 3,6'-dithiothalidomide and thalidomide, beginning at four months of age. At this young age, mice do not exhibit plaque or tau pathology but do show mild intraneuronal amyloid beta protein staining and a robust increase in tumor necrosis factor-alpha. After 10 weeks of treatment, cognitive performance was assessed using radial arm maze and neuroinflammation was assessed using biochemical, stereological and flow cytometric endpoints.
Results: 3,6'-dithiothalidomide reduced tumor necrosis factor-alpha mRNA and protein levels in the brain and improved working memory performance and the ratio of resting to reactive microglia in the hippocampus of triple transgenic mice.
In comparison to non-transgenic controls, triple transgenic Alzheimer's disease mice had increased total numbers of infiltrating peripheral monomyelocytic/granulocytic leukocytes with enhanced intracytoplasmic tumor necrosis factor-alpha, which was reduced after treatment with 3,6'-dithiothalidomide.
Conclusions: These results suggest that modulation of tumor necrosis factor-alpha with small molecule inhibitors is safe and effective with potential for the long-term prevention and treatment of Alzheimer's disease.
C1 [Srivastava, Minu K.; Eslami, Pirooz; Johnson, Ming F.; Kobritz, Naomi K.; Sharma, Sherven P.; Harris-White, Marni E.] Univ Calif Los Angeles, Vet Adm Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA.
[Srivastava, Minu K.; Eslami, Pirooz; Johnson, Ming F.; Kobritz, Naomi K.; Sharma, Sherven P.; Harris-White, Marni E.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90073 USA.
[Gabbita, S. Prasad; Zemlan, Frank P.] P2D Biosci, Cincinnati, OH 45242 USA.
[Tweedie, David; Greig, Nigel H.] NIA, NIH, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA.
RP Harris-White, ME (reprint author), Univ Calif Los Angeles, Vet Adm Greater Los Angeles Healthcare Syst, 11301 Wilshire Blvd 151, Los Angeles, CA 90073 USA.
EM marni@ucla.edu
FU Veterans Administration; Michael J. Fox Foundation; Alzheimer's Drug
Discovery Foundation; Intramural Research Program of NIA, NIH
FX The authors would like to thank Dr. Russell Brown at Eastern Tennessee
State University for assistance with the design and analysis of the
Radial Arm Maze experiments, Dr. Louis Hersh at the University of
Kentucky for providing breeding pairs of 3 x Tg mice and Dr. Kenneth
Hensley at the University of Toledo for assistance with data
interpretation and critical scientific review of the manuscript. This
work was supported by Veterans Administration Merit Funding (MEHW and
SPS), Michael J. Fox Foundation (SPG), Alzheimer's Drug Discovery
Foundation (MEHW and SPG) and the Intramural Research Program of NIA,
NIH (DT and NHG).
NR 81
TC 26
Z9 27
U1 2
U2 15
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-2094
J9 J NEUROINFLAMM
JI J. Neuroinflamm.
PD MAY 25
PY 2012
VL 9
AR 99
DI 10.1186/1742-2094-9-99
PG 16
WC Immunology; Neurosciences
SC Immunology; Neurosciences & Neurology
GA 976PV
UT WOS:000306597700001
PM 22632257
ER
PT J
AU Sung, RJ
Zhang, M
Qi, Y
Verdine, GL
AF Sung, Rou-Jia
Zhang, Michael
Qi, Yan
Verdine, Gregory L.
TI Sequence-dependent Structural Variation in DNA Undergoing Intrahelical
Inspection by the DNA glycosylase MutM
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID REPAIR ENZYME; CRYSTAL-STRUCTURE; BASE-EXCISION; LESION RECOGNITION;
ESCHERICHIA-COLI; DAMAGED DNA; 8-HYDROXYGUANINE
7,8-DIHYDRO-8-OXOGUANINE; MUTATIONAL HOTSPOT; PROTEIN-STRUCTURE; ABASIC
SITE
AB MutM, a bacterial DNA-glycosylase, plays a critical role in maintaining genome integrity by catalyzing glycosidic bond cleavage of 8-oxoguanine (oxoG) lesions to initiate base excision DNA repair. The task faced by MutM of locating rare oxoG residues embedded in an overwhelming excess of undamaged bases is especially challenging given the close structural similarity between oxoG and its normal progenitor, guanine (G). MutM actively interrogates the DNA to detect the presence of an intrahelical, fully base-paired oxoG, whereupon the enzyme promotes extrusion of the target nucleobase from the DNA duplex and insertion into the extrahelical active site. Recent structural studies have begun to provide the first glimpse into the protein DNA interactions that enable MutM to distinguish an intrahelical oxoG from G; however, these initial studies left open the important question of how MutM can recognize oxoG residues embedded in 16 different neighboring sequence contexts (considering only the 5'- and 3'-neighboring base pairs). In this study we set out to understand the manner and extent to which intrahelical lesion recognition varies as a function of the 5'-neighbor. Here we report a comprehensive, systematic structural analysis of the effect of the 5'-neighboring base pair on recognition of an intrahelical oxoG lesion. These structures reveal that MutM imposes the same extrusion-prone ("extrudogenic") backbone conformation on the oxoG lesion irrespective of its 5'-neighbor while leaving the rest of the DNA relatively free to adjust to the particular demands of individual sequences.
C1 [Sung, Rou-Jia; Verdine, Gregory L.] Harvard Univ, Dept Mol & Cell Biol, Cambridge, MA 02138 USA.
[Zhang, Michael; Verdine, Gregory L.] Harvard Univ, Dept Chem & Chem Biol, Cambridge, MA 02138 USA.
[Verdine, Gregory L.] Harvard Univ, Dept Stem Cell & Regenerat Biol, Cambridge, MA 02138 USA.
[Verdine, Gregory L.] Dana Farber Canc Inst, Chem Biol Initiat, Boston, MA 02115 USA.
[Qi, Yan] Harvard Univ, Sch Med, Grad Program Biophys, Boston, MA 02115 USA.
[Verdine, Gregory L.] Dana Farber Canc Inst, Program Canc Chem Biol, Boston, MA 02115 USA.
RP Verdine, GL (reprint author), 12 Oxford St, Cambridge, MA 02138 USA.
EM gregory_verdine@harvard.edu
FU National Institutes of Health [GM044853, CA100742]; Harvard College
Research Program; National Science Foundation
FX This work was supported, in whole or in part, by National Institutes of
Health Grants GM044853 and CA100742.; Supported by a grant by the
Harvard College Research Program.; Supported by a predoctoral fellowship
from the National Science Foundation.
NR 50
TC 10
Z9 10
U1 0
U2 3
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD MAY 25
PY 2012
VL 287
IS 22
BP 18044
EP 18054
DI 10.1074/jbc.M111.313635
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 974EC
UT WOS:000306411600014
PM 22465958
ER
PT J
AU Gude, L
Berkovitch, SS
Santos, WL
Kutchukian, PS
Pawloski, AR
Kuimelis, R
McGall, G
Verdine, GL
AF Gude, Lourdes
Berkovitch, Shaunna S.
Santos, Webster L.
Kutchukian, Peter S.
Pawloski, Adam R.
Kuimelis, Robert
McGall, Glenn
Verdine, Gregory L.
TI Mapping Targetable Sites on Human Telomerase RNA Pseudoknot/Template
Domain Using 2 '-OMe RNA-interacting Polynucleotide (RIPtide)
Microarrays
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID SECONDARY STRUCTURE; COMPLEMENTARY OLIGONUCLEOTIDES;
REVERSE-TRANSCRIPTASE; NUCLEIC-ACIDS; HUMAN-CELLS; IN-VIVO; INHIBITION;
ARRAYS; PROTEIN; CANCER
AB Most cellular RNAs engage in intrastrand base-pairing that gives rise to complex three-dimensional folds. This self-pairing presents an impediment toward binding of the RNA by nucleic acid-based ligands. An important step in the discovery of RNA-targeting ligands is therefore to identify those regions in a folded RNA that are accessible toward the nucleic acid-based ligand. Because the folding of RNA targets can involve interactions between nonadjacent regions and employ both Watson-Crick and non-Watson-Crick base-pairing, screening of candidate binder ensembles is typically necessary. Microarray-based screening approaches have shown great promise in this regard and have suggested that achieving complete sequence coverage would be a valuable attribute of a next generation system. Here, we report a custom microarray displaying a library of RNA-interacting polynucleotides comprising all possible 2'-OMe RNA sequences from 4- to 8-nucleotides in length. We demonstrate the utility of this array in identifying RNA-interacting polynucleotides that bind tightly and specifically to the highly conserved, functionally essential template/pseudoknot domain of human telomerase RNA and that inhibit telomerase function in vitro.
C1 [Gude, Lourdes; Kutchukian, Peter S.; Verdine, Gregory L.] Harvard Univ, Dept Chem & Chem Biol, Cambridge, MA 02138 USA.
[Berkovitch, Shaunna S.; Verdine, Gregory L.] Harvard Univ, Dept Mol & Cellular Biol, Cambridge, MA 02138 USA.
[Pawloski, Adam R.; Kuimelis, Robert; McGall, Glenn] Affymetrix Inc, Santa Clara, CA 95051 USA.
[Verdine, Gregory L.] Dana Farber Canc Inst, Program Canc Chem Biol, Boston, MA 02115 USA.
RP Verdine, GL (reprint author), 12 Oxford St, Cambridge, MA 02138 USA.
EM Gregory_verdine@harvard.edu
RI Gude, Lourdes/E-5860-2012; Kutchukian, Peter/A-9826-2016;
OI Gude, Lourdes/0000-0002-0220-3755; Kutchukian,
Peter/0000-0002-5684-1971; Santos, Webster/0000-0002-4731-8548
FU National Institutes of Health [R01 GM044853]; NRSA [F32 GM067380];
High-Tech Fund of the Dana-Farber Cancer Institute; Spanish Ministerio
de Educacion y Ciencia; National Science Foundation; [T32 GM007598]
FX This work was supported, in whole or in part, by National Institutes of
Health Grant R01 GM044853 (to G. L. V.), Grant F32 GM067380 from NRSA
(to W. L. S.), and Training Grant T32 GM007598 (to S. S. B.). This work
was also supported by the High-Tech Fund of the Dana-Farber Cancer
Institute, postdoctoral fellowships from the Spanish Ministerio de
Educacion y Ciencia (to L. G.), and a National Science Foundation
predoctoral fellowship (to P. S. K.). Affymetrix Inc. is a for-profit
entity. G. L. V. is a shareholder, consultant to, and corporate officer
of Ontorii, Inc., which has secured an option from Harvard University to
commercialize the RIPtide technology.
NR 55
TC 8
Z9 10
U1 0
U2 7
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD MAY 25
PY 2012
VL 287
IS 22
BP 18843
EP 18853
DI 10.1074/jbc.M111.316596
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 974EC
UT WOS:000306411600092
PM 22451672
ER
PT J
AU Ferrandiz, N
Caraballo, JM
Garcia-Gutierrez, L
Devgan, V
Rodriguez-Paredes, M
Lafita, MC
Bretones, G
Quintanilla, A
Munoz-Alonso, MJ
Blanco, R
Reyes, JC
Agell, N
Delgado, MD
Dotto, GP
Leon, J
AF Ferrandiz, Nuria
Caraballo, Juan M.
Garcia-Gutierrez, Lucia
Devgan, Vikram
Rodriguez-Paredes, Manuel
Carmen Lafita, M.
Bretones, Gabriel
Quintanilla, Andrea
Jose Munoz-Alonso, M.
Blanco, Rosa
Reyes, Jose C.
Agell, Neus
Dolores Delgado, M.
Dotto, G. Paolo
Leon, Javier
TI p21 as a Transcriptional Co-Repressor of S-Phase and Mitotic Control
Genes
SO PLOS ONE
LA English
DT Article
ID CELL-CYCLE INHIBITION; TUMOR SUPPRESSION; DNA-REPLICATION;
UP-REGULATION; P21(WAF1/CIP1); DIFFERENTIATION; EXPRESSION;
P21(CIP1/WAF1); ARREST; ENDOREDUPLICATION
AB It has been previously described that p21 functions not only as a CDK inhibitor but also as a transcriptional co-repressor in some systems. To investigate the roles of p21 in transcriptional control, we studied the gene expression changes in two human cell systems. Using a human leukemia cell line (K562) with inducible p21 expression and human primary keratinocytes with adenoviral-mediated p21 expression, we carried out microarray-based gene expression profiling. We found that p21 rapidly and strongly repressed the mRNA levels of a number of genes involved in cell cycle and mitosis. One of the most strongly down-regulated genes was CCNE2 (cyclin E2 gene). Mutational analysis in K562 cells showed that the N-terminal region of p21 is required for repression of gene expression of CCNE2 and other genes. Chromatin immunoprecipitation assays indicated that p21 was bound to human CCNE2 and other p21-repressed genes gene in the vicinity of the transcription start site. Moreover, p21 repressed human CCNE2 promoter-luciferase constructs in K562 cells. Bioinformatic analysis revealed that the CDE motif is present in most of the promoters of the p21-regulated genes. Altogether, the results suggest that p21 exerts a repressive effect on a relevant number of genes controlling S phase and mitosis. Thus, p21 activity as inhibitor of cell cycle progression would be mediated not only by the inhibition of CDKs but also by the transcriptional down-regulation of key genes.
C1 [Ferrandiz, Nuria; Caraballo, Juan M.; Garcia-Gutierrez, Lucia; Carmen Lafita, M.; Bretones, Gabriel; Quintanilla, Andrea; Jose Munoz-Alonso, M.; Blanco, Rosa; Dolores Delgado, M.; Leon, Javier] Univ Cantabria, CSIC, SODERCAN, Dept Biol Mol,Inst Biomed & Biotecnol Cantabria I, E-39005 Santander, Spain.
[Devgan, Vikram; Dotto, G. Paolo] Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA USA.
[Rodriguez-Paredes, Manuel; Reyes, Jose C.] CSIC, Ctr Andaluz Biol Mol & Med Regenerat CABIMER, E-41080 Seville, Spain.
[Jose Munoz-Alonso, M.] CSIC, Inst Invest Biomed Alberto Sols, Madrid, Spain.
[Agell, Neus] Univ Barcelona, Dept Biol Cellular Immunol & Neurociencies, Inst Invest Biomed August Pi & Sunyer IDIBAPS, Barcelona, Spain.
[Dotto, G. Paolo] Univ Lausanne, Dept Biochem, CH-1066 Epalinges, Switzerland.
RP Ferrandiz, N (reprint author), Univ London Imperial Coll Sci Technol & Med, MRC Clin Sci Ctr, Fac Med, Hammersmith Hosp Campus, London, England.
EM leonj@unican.es
RI Reyes, Jose/K-3699-2014; Agell, Neus/E-9640-2016;
OI Reyes, Jose/0000-0002-8042-5142; Agell, Neus/0000-0002-1205-6074
FU Spanish Ministerio de Ciencia e Innovacion (MICINN) [SAF08-01581,
ISCIII-RETIC RD06/0020/0017]; MICINN [BFU2008-00238, CSD2006-00049];
Junta de Andalucia [P06-CVI-4844]; postdoctoral fellowship of the
University of Cantabria; [FIS 08/0829]
FX This study was supported by grants SAF08-01581 and ISCIII-RETIC
RD06/0020/0017 from the Spanish Ministerio de Ciencia e Innovacion
(MICINN) to JL; FIS 08/0829 to MDD; BFU2008-00238 and CSD2006-00049 from
MICINN, and P06-CVI-4844 from Junta de Andalucia to JCR. NF was the
recipient of a postdoctoral fellowship of the University of Cantabria.
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of manuscript.
NR 48
TC 14
Z9 14
U1 0
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAY 25
PY 2012
VL 7
IS 5
AR e37759
DI 10.1371/journal.pone.0037759
PG 13
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 959UY
UT WOS:000305342300103
PM 22662213
ER
PT J
AU Kostopoulou, F
Gkretsi, V
Malizos, KN
Iliopoulos, D
Oikonomou, P
Poultsides, L
Tsezou, A
AF Kostopoulou, Fotini
Gkretsi, Vasiliki
Malizos, Konstantinos N.
Iliopoulos, Dimitrios
Oikonomou, Pagona
Poultsides, Lazaros
Tsezou, Aspasia
TI Central Role of SREBP-2 in the Pathogenesis of Osteoarthritis
SO PLOS ONE
LA English
DT Article
ID STEROL-REGULATORY ELEMENT; BINDING PROTEIN (SREBP)-2; LEUCINE ZIPPER
PROTEIN; EXPRESSION; GENE; TRANSCRIPTION; CHONDROCYTES; CHOLESTEROL;
IDENTIFICATION; POPULATION
AB Background: Recent studies have implied that osteoarthritis (OA) is a metabolic disease linked to deregulation of genes involved in lipid metabolism and cholesterol efflux. Sterol Regulatory Element Binding Proteins (SREBPs) are transcription factors regulating lipid metabolism with so far no association with OA. Our aim was to test the hypothesis that SREBP-2, a gene that plays a key role in cholesterol homeostasis, is crucially involved in OA pathogenesis and to identify possible mechanisms of action.
Methodology/Principal Findings: We performed a genetic association analysis using a cohort of 1,410 Greek OA patients and healthy controls and found significant association between single nucleotide polymorphism (SNP) 1784G>C in SREBP-2 gene and OA development. Moreover, the above SNP was functionally active, as normal chondrocytes' transfection with SREBP-2-G/C plasmid resulted in interleukin-1 beta and metalloproteinase-13 (MMP-13) upregulation. We also evaluated SREBP-2, its target gene 3-hydroxy-3-methylglutaryl-coenzymeA reductase (HMGCR), phospho-phosphoinositide3-kinase (PI3K), phospho-Akt, integrin-alphaV (ITGAV) and transforming growth factor-beta (TGF-beta) mRNA and protein expression levels in osteoarthritic and normal chondrocytes and found that they were all significantly elevated in OA chondrocytes. To test whether TGF-beta alone can induce SREBP-2, we treated normal chondrocytes with TGF-beta and found significant upregulation of SREBP-2, HMGCR, phospho-PI3K and MMP-13. We also showed that TGF-beta activated aggrecan (ACAN) in chondrocytes only through Smad3, which interacts with SREBP-2. Finally, we examined the effect of an integrin inhibitor, cyclo-RGDFV peptide, on osteoarthritic chondrocytes, and found that it resulted in significant upregulation of ACAN and downregulation of SREBP-2, HMGCR, phospho-PI3K and MMP-13 expression levels.
Conclusions/Significance: We demonstrated, for the first time, the association of SREBP-2 with OA pathogenesis and provided evidence on the molecular mechanism involved. We suggest that TGF-beta induces SREBP-2 pathway activation through ITGAV and PI3K playing a key role in OA and that integrin blockage may be a potential molecular target for OA treatment.
C1 [Kostopoulou, Fotini; Tsezou, Aspasia] Univ Thessaly, Dept Cytogenet & Mol Genet, Sch Med, Larisa, Greece.
[Kostopoulou, Fotini; Gkretsi, Vasiliki; Malizos, Konstantinos N.; Oikonomou, Pagona; Tsezou, Aspasia] Ctr Res & Technol Thessaly, Inst Biomed Res & Technol, Larisa, Greece.
[Malizos, Konstantinos N.; Poultsides, Lazaros] Univ Thessaly, Dept Orthopaed, Sch Med, Larisa, Greece.
[Iliopoulos, Dimitrios] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Iliopoulos, Dimitrios] Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA.
[Tsezou, Aspasia] Univ Thessaly, Dept Biol, Sch Med, Larisa, Greece.
RP Kostopoulou, F (reprint author), Univ Thessaly, Dept Cytogenet & Mol Genet, Sch Med, Larisa, Greece.
EM atsezou@med.uth.gr
OI Gkretsi, Vasiliki/0000-0002-3671-4078
FU Hellenic Society of Orthopaedic Surgery and Traumatology
FX The present study was financed by the Hellenic Society of Orthopaedic
Surgery and Traumatology. No additional external funding was received.
The funders had no role in study design, data collection and analysis,
decision to publish or preparation of the manuscript.
NR 38
TC 21
Z9 23
U1 1
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAY 25
PY 2012
VL 7
IS 5
AR e35753
DI 10.1371/journal.pone.0035753
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 959UY
UT WOS:000305342300005
PM 22662110
ER
PT J
AU Makino, CL
Wen, XH
Michaud, NA
Covington, HI
DiBenedetto, E
Hamm, HE
Lem, J
Caruso, G
AF Makino, Clint L.
Wen, Xiao-Hong
Michaud, Norman A.
Covington, Henry I.
DiBenedetto, Emmanuele
Hamm, Heidi E.
Lem, Janis
Caruso, Giovanni
TI Rhodopsin Expression Level Affects Rod Outer Segment Morphology and
Photoresponse Kinetics
SO PLOS ONE
LA English
DT Article
ID PHOTORECEPTOR MEMBRANE; LATERAL DIFFUSION; TRANSGENIC MICE; DISK
MEMBRANES; FINE STRUCTURE; KNOCKOUT MICE; MOUSE RETINA;
PHOTOTRANSDUCTION; ORGANIZATION; TRANSPORT
AB Background: The retinal rod outer segment is a sensory cilium that is specialized for the conversion of light into an electrical signal. Within the cilium, up to several thousand membranous disks contain as many as a billion copies of rhodopsin for efficient photon capture. Disks are continually turned over, requiring the daily synthesis of a prodigious amount of rhodopsin. To promote axial diffusion in the aqueous cytoplasm, the disks have one or more incisures. Across vertebrates, the range of disk diameters spans an order of magnitude, and the number and length of the incisures vary considerably, but the mechanisms controlling disk architecture are not well understood. The finding that transgenic mice overexpressing rhodopsin have enlarged disks lacking an incisure prompted us to test whether lowered rhodopsin levels constrain disk assembly.
Methodology/Principal Findings: The structure and function of rods from hemizygous rhodopsin knockout (R+/-) mice with decreased rhodopsin expression were analyzed by transmission electron microscopy and single cell recording. R+/- rods were structurally altered in three ways: disk shape changed from circular to elliptical, disk surface area decreased, and the single incisure lengthened to divide the disk into two sections. Photocurrent responses to flashes recovered more rapidly than normal. A spatially resolved model of phototransduction indicated that changes in the packing densities of rhodopsin and other transduction proteins were responsible. The decrease in aqueous outer segment volume and the lengthened incisure had only minor effects on photon response amplitude and kinetics.
Conclusions/Significance: Rhodopsin availability limits disk assembly and outer segment girth in normal rods. The incisure may buffer the supply of structural proteins needed to form larger disks. Decreased rhodopsin level accelerated photoresponse kinetics by increasing the rates of molecular collisions on the membrane. Faster responses, together with fewer rhodopsins, combine to lower overall sensitivity of R+/- rods to light.
C1 [Makino, Clint L.; Wen, Xiao-Hong; Michaud, Norman A.; Covington, Henry I.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol, Boston, MA 02115 USA.
[DiBenedetto, Emmanuele] Vanderbilt Univ, Dept Math, Nashville, TN USA.
[Hamm, Heidi E.] Vanderbilt Univ, Dept Pharmacol, Nashville, TN USA.
[Lem, Janis] Tufts Univ, Sch Med, Dept Ophthalmol, Program Genet,Program Neurosci,Program Cell Mol &, Boston, MA 02111 USA.
[Caruso, Giovanni] CNR, Construct Technol Inst, Rome, Italy.
RP Makino, CL (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol, Boston, MA 02115 USA.
EM cmakino@meei.harvard.edu
OI Makino, Clint/0000-0002-6005-9069
FU National Eye Institute [EY006062, EY011358, EY014104, EY12008]; National
Institute of General Medical Sciences [GM068953]; National Science
Foundation [DMS 0652385, DMS 0970008]; Lions of Massachusetts
FX This work was supported by grants from the National Eye Institute
(EY006062, EY011358, EY014104, EY12008), National Institute of General
Medical Sciences (GM068953), National Science Foundation (DMS 0652385,
DMS 0970008), and Lions of Massachusetts. The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 50
TC 15
Z9 15
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAY 25
PY 2012
VL 7
IS 5
AR e37832
DI 10.1371/journal.pone.0037832
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 959UY
UT WOS:000305342300124
PM 22662234
ER
PT J
AU Mathalon, DH
Ford, JM
AF Mathalon, Daniel H.
Ford, Judith M.
TI Neurobiology of schizophrenia: search for the elusive correlation with
symptoms
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE schizophrenia; positive symptoms; negative symptoms; neurobiology;
correlation; reliability; validity; rating scales
ID TRANSCRANIAL MAGNETIC STIMULATION; PSYCHIATRIC RATING-SCALE;
HEALTHY-VOLUNTEERS; WORKING-MEMORY; KETAMINE; DYSFUNCTION; NEGATIVITY;
ANTAGONIST; PSYCHOSIS; DEFICITS
AB In the last half-century, human neuro science methods provided a way to study schizophrenia in vivo, and established that it is associated with subtle abnormalities in brain structure and function. However, efforts to understand the neurobiological bases of the clinical symptoms that the diagnosis is based on have been largely unsuccessful. In this paper, we provide an overview of the conceptual and methodological obstacles that undermine efforts to link the severity of specific symptoms to specific neurobiological measures. These obstacles include small samples, questionable reliability and validity of measurements, medication confounds, failure to distinguish state and trait effects, correlation-causation ambiguity, and the absence of compelling animal models of specific symptoms to test mechanistic hypotheses derived from brain-symptom correlations. We conclude with recommendations to promote progress in establishing brain-symptom relationships.
C1 [Mathalon, Daniel H.; Ford, Judith M.] San Francisco VA Med Ctr, Psychiat Serv, San Francisco, CA 94121 USA.
[Mathalon, Daniel H.; Ford, Judith M.] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA.
RP Mathalon, DH (reprint author), San Francisco VA Med Ctr, Psychiat Serv 116D, 4150 Clement St, San Francisco, CA 94121 USA.
EM daniel.mathalon@ucsf.edu
OI Mathalon, Daniel/0000-0001-6090-4974
FU CSRD VA [I01 CX000497]; NIMH NIH HHS [R01 MH076989]
NR 43
TC 16
Z9 16
U1 2
U2 14
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD MAY 25
PY 2012
VL 6
AR 136
DI 10.3389/fnhum.2012.00136
PG 6
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 953HT
UT WOS:000304858500001
PM 22654745
ER
PT J
AU Mantegazza, AR
Guttentag, SH
El-Benna, J
Sasai, M
Iwasaki, A
Shen, H
Laufer, TM
Marks, MS
AF Mantegazza, Adriana R.
Guttentag, Susan H.
El-Benna, Jamel
Sasai, Miwa
Iwasaki, Akiko
Shen, Hao
Laufer, Terri M.
Marks, Michael S.
TI Adaptor Protein-3 in Dendritic Cells Facilitates Phagosomal Toll-like
Receptor Signaling and Antigen Presentation to CD4(+) T Cells
SO IMMUNITY
LA English
DT Article
ID HERMANSKY-PUDLAK-SYNDROME; MHC CLASS-II; AP-3 ADAPTER;
CROSS-PRESENTATION; BETA-3A SUBUNIT; SORTING SIGNALS; IMMUNE-RESPONSE;
SYNDROME TYPE-2; TRAFFICKING; MUTATIONS
AB Effective major histocompatibility complex-II (MHC-II) antigen presentation from phagocytosed particles requires phagosome-intrinsic Toll-like receptor (TLR) signaling, but the molecular mechanisms underlying TLR delivery to phagosomes and how signaling regulates antigen presentation are incompletely understood. We show a requirement in dendritic cells (DCs) for adaptor protein-3 (AP-3) in efficient TLR recruitment to phagosomes and MHC-II presentation of antigens internalized by phagocytosis but not receptor-mediated endocytosis. DCs from AP-3-deficient pearl mice elicited impaired CD4(+) T cell activation and Th1 effector cell function to particulate antigen in vitro and to recombinant Listeria monocytogenes infection in vivo. Whereas phagolysosome maturation and peptide:MHC-II complex assembly proceeded normally in pearl DCs, peptide:MHC-II export to the cell surface was impeded. This correlated with reduced TLR4 recruitment and proinflammatory signaling from phagosomes by particulate TLR ligands. We propose that AP-3-dependent TLR delivery from endosomes to phagosomes and subsequent signaling mobilize peptide:MHC-II export from intracellular stores.
C1 [Mantegazza, Adriana R.; Marks, Michael S.] Univ Penn, Perelman Sch Med, Dept Pathol, Philadelphia, PA 19104 USA.
[Mantegazza, Adriana R.; Marks, Michael S.] Univ Penn, Perelman Sch Med, Dept Lab Med, Philadelphia, PA 19104 USA.
[Mantegazza, Adriana R.; Marks, Michael S.] Univ Penn, Perelman Sch Med, Dept Physiol, Philadelphia, PA 19104 USA.
[Shen, Hao] Univ Penn, Perelman Sch Med, Dept Microbiol, Philadelphia, PA 19104 USA.
[Laufer, Terri M.] Univ Penn, Perelman Sch Med, Dept Med, Philadelphia, PA 19104 USA.
[Guttentag, Susan H.] Childrens Hosp Philadelphia, Dept Pediat, Philadelphia, PA 19104 USA.
[El-Benna, Jamel] Univ Paris 07, INSERM, U773, Fac Med, F-75018 Paris, France.
[Sasai, Miwa; Iwasaki, Akiko] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT 06520 USA.
[Laufer, Terri M.] Philadelphia Vet Affairs Med Ctr, Philadelphia, PA 19104 USA.
RP Marks, MS (reprint author), Univ Penn, Perelman Sch Med, Dept Pathol, Philadelphia, PA 19104 USA.
EM marksm@mail.med.upenn.edu
RI Guttentag, Susan/D-8705-2013;
OI Guttentag, Susan/0000-0003-4420-5879; Marks, Michael/0000-0001-7435-7262
FU National Institutes of Health [R01 EY015625, R21 AI092398, R21 AI079724,
R01 AI081884, R01 AI064705]; University Research Foundation from the
University of Pennsylvania; HPS Network; United States Veterans
Administration
FX We thank R. Steinman, M. Pepper Pew, M. Jenkins, A. Rudensky, J. Liboon,
S. Chatterjee, A. Fisher, S. Ross, S. Akira, P. Oliver, L. Eisenlohr, M.
Chou, and C. Lopez for generous gifts of reagents; A. Stout, P. Zhang,
S. Leach, A. Sitaram, and C. Lopez Haber for technical assistance; and
the Amigorena laboratory for experimental protocols. This work was
supported by National Institutes of Health grants R01 EY015625 (to
M.S.M.), R21 AI092398 (to A.R.M. and M.S.M.), R21 AI079724 (to H.S.),
and R01 AI081884 and R01 AI064705 (to A.I); a University Research
Foundation grant from the University of Pennsylvania (to M.S.M.); Donna
and Richard Appel and the HPS Network (to S.H.G.); and a research grant
from the United States Veterans Administration (to T.M.L.).
NR 57
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U1 1
U2 12
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PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
J9 IMMUNITY
JI Immunity
PD MAY 25
PY 2012
VL 36
IS 5
BP 782
EP 794
DI 10.1016/j.immuni.2012.02.018
PG 13
WC Immunology
SC Immunology
GA 954VL
UT WOS:000304976000012
PM 22560444
ER
PT J
AU Nik-Zainal, S
Alexandrov, LB
Wedge, DC
Van Loo, P
Greenman, CD
Raine, K
Jones, D
Hinton, J
Marshall, J
Stebbings, LA
Menzies, A
Martin, S
Leung, K
Chen, L
Leroy, C
Ramakrishna, M
Rance, R
Lau, KW
Mudie, LJ
Varela, I
McBride, DJ
Bignell, GR
Cooke, SL
Shlien, A
Gamble, J
Whitmore, I
Maddison, M
Tarpey, PS
Davies, HR
Papaemmanuil, E
Stephens, PJ
McLaren, S
Butler, AP
Teague, JW
Jonsson, G
Garber, JE
Silver, D
Miron, P
Fatima, A
Boyault, S
Langerod, A
Tutt, A
Martens, JWM
Aparicio, SAJR
Borg, A
Salomon, AV
Thomas, G
Borresen-Dale, AL
Richardson, AL
Neuberger, MS
Futreal, PA
Campbell, PJ
Stratton, MR
AF Nik-Zainal, Serena
Alexandrov, Ludmil B.
Wedge, David C.
Van Loo, Peter
Greenman, Christopher D.
Raine, Keiran
Jones, David
Hinton, Jonathan
Marshall, John
Stebbings, Lucy A.
Menzies, Andrew
Martin, Sancha
Leung, Kenric
Chen, Lina
Leroy, Catherine
Ramakrishna, Manasa
Rance, Richard
Lau, King Wai
Mudie, Laura J.
Varela, Ignacio
McBride, David J.
Bignell, Graham R.
Cooke, Susanna L.
Shlien, Adam
Gamble, John
Whitmore, Ian
Maddison, Mark
Tarpey, Patrick S.
Davies, Helen R.
Papaemmanuil, Elli
Stephens, Philip J.
McLaren, Stuart
Butler, Adam P.
Teague, Jon W.
Jonsson, Goran
Garber, Judy E.
Silver, Daniel
Miron, Penelope
Fatima, Aquila
Boyault, Sandrine
Langerod, Anita
Tutt, Andrew
Martens, John W. M.
Aparicio, Samuel A. J. R.
Borg, Ake
Salomon, Anne Vincent
Thomas, Gilles
Borresen-Dale, Anne-Lise
Richardson, Andrea L.
Neuberger, Michael S.
Futreal, P. Andrew
Campbell, Peter J.
Stratton, Michael R.
CA Int Canc Genome Consortium
TI Mutational Processes Molding the Genomes of 21 Breast Cancers
SO CELL
LA English
DT Article
ID NONNEGATIVE MATRIX FACTORIZATION; RNA-EDITING PROTEIN; DNA-DAMAGE;
SOMATIC HYPERMUTATION; HEPATOCELLULAR-CARCINOMA; TOBACCO-SMOKE; P53
MUTATIONS; GENE; PATTERNS; TUMORS
AB All cancers carry somatic mutations. The patterns of mutation in cancer genomes reflect the DNA damage and repair processes to which cancer cells and their precursors have been exposed. To explore these mechanisms further, we generated catalogs of somatic mutation from 21 breast cancers and applied mathematical methods to extract mutational signatures of the underlying processes. Multiple distinct single- and double-nucleotide substitution signatures were discernible. Cancers with BRCA1 or BRCA2 mutations exhibited a characteristic combination of substitution mutation signatures and a distinctive profile of deletions. Complex relationships between somatic mutation prevalence and transcription were detected. A remarkable phenomenon of localized hypermutation, termed "kataegis,'' was observed. Regions of kataegis differed between cancers but usually colocalized with somatic rearrangements. Base substitutions in these regions were almost exclusively of cytosine at TpC dinucleotides. The mechanisms underlying most of these mutational signatures are unknown. However, a role for the APOBEC family of cytidine deaminases is proposed.
C1 [Nik-Zainal, Serena; Alexandrov, Ludmil B.; Wedge, David C.; Van Loo, Peter; Greenman, Christopher D.; Raine, Keiran; Jones, David; Hinton, Jonathan; Marshall, John; Stebbings, Lucy A.; Menzies, Andrew; Martin, Sancha; Leung, Kenric; Chen, Lina; Leroy, Catherine; Ramakrishna, Manasa; Rance, Richard; Lau, King Wai; Mudie, Laura J.; Varela, Ignacio; McBride, David J.; Bignell, Graham R.; Cooke, Susanna L.; Shlien, Adam; Gamble, John; Whitmore, Ian; Maddison, Mark; Tarpey, Patrick S.; Davies, Helen R.; Papaemmanuil, Elli; Stephens, Philip J.; McLaren, Stuart; Butler, Adam P.; Teague, Jon W.; Futreal, P. Andrew; Campbell, Peter J.; Stratton, Michael R.] Wellcome Trust Sanger Inst, Canc Genome Project, Hinxton CB10 1SA, England.
[Van Loo, Peter] VIB, Ctr Biol Dis, B-3000 Louvain, Belgium.
[Van Loo, Peter] Katholieke Univ Leuven, Dept Human Genet, B-3000 Louvain, Belgium.
[Greenman, Christopher D.] Univ E Anglia, Dept Comp, Norwich NR4 7TJ, Norfolk, England.
[Greenman, Christopher D.] Genome Anal Ctr, Norwich NR4 7UH, Norfolk, England.
[Aparicio, Samuel A. J. R.] Univ British Columbia, Dept Pathol & Lab Med, Vancouver, BC V6T 2B5, Canada.
[Garber, Judy E.; Silver, Daniel; Miron, Penelope; Fatima, Aquila; Richardson, Andrea L.] Dana Farber Canc Inst, Boston, MA 02215 USA.
[Boyault, Sandrine; Thomas, Gilles] Ctr Leon Berard, INCa Synergie, Fac Med, Lyon 08, France.
[Langerod, Anita; Borresen-Dale, Anne-Lise] Norwegian Radium Hosp, Oslo Univ Hosp, Inst Canc Res, Dept Genet, N-0310 Oslo, Norway.
[Tutt, Andrew] Kings Coll London, Breakthrough Breast Canc Res Unit, London SE1 9RT, England.
[Martens, John W. M.] Erasmus MC, Dept Med Oncol, NL-3000 CA Rotterdam, Netherlands.
[Aparicio, Samuel A. J. R.] British Columbia Canc Res Ctr, Vancouver, BC V5Z 1L3, Canada.
[Jonsson, Goran; Borg, Ake] Lund Univ, Dept Oncol, SE-22184 Lund, Sweden.
[Salomon, Anne Vincent] Inst Curie, Dept Pathol, F-75248 Paris 05, France.
[Salomon, Anne Vincent] INSERM, U830, F-75248 Paris 05, France.
[Borresen-Dale, Anne-Lise] Univ Oslo, KG Jebsen Ctr Breast Canc Res, Inst Clin Med, Fac Med, N-0310 Oslo, Norway.
[Richardson, Andrea L.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Neuberger, Michael S.] MRC Lab Mol Biol, Cambridge CB2 0QH, England.
[Campbell, Peter J.] Addenbrookes Hosp, Dept Haematol, Cambridge CB2 0QQ, England.
[Campbell, Peter J.] Univ Cambridge, Dept Haematol, Cambridge CB2 2XY, England.
RP Stratton, MR (reprint author), Wellcome Trust Sanger Inst, Canc Genome Project, Hinxton CB10 1SA, England.
EM mrs@sanger.ac.uk
RI Van Loo, Peter/A-3287-2012; Jonsson, Goran/D-1212-2014; Alexandrov,
Ludmil/B-6582-2014; Varela, Ignacio/G-1699-2016;
OI Alexandrov, Ludmil/0000-0003-3596-4515; Varela,
Ignacio/0000-0002-0969-506X; Van Loo, Peter/0000-0003-0292-1949; Wedge,
David/0000-0002-7572-3196; Martin, Sancha/0000-0001-6213-5259
FU Wellcome Trust [098051]; Breakthrough Breast Cancer Research [ICGC
08/09]; Wellcome Trust Clinical Research; Wellcome Trust Senior Clinical
Research [WT088340MA]; Research Foundation - Flanders [FWO]; National
Research Council Canada; EMBO; International Human Frontier Science
Program Organization; Netherlands Genomics Initiative (NGI)/Netherlands
Organization for Scientific Research; Norwegian Research Council; The
Norwegian Cancer Society; The Radium Hospital Foundation; Health Region
South-East; European Community [242006]; Breast Cancer Somatic Genetics
Study [BASIS]; Wellcome Trust Sanger Institute; Breakthrough Breast
Cancer Unit; ICGC Breast Cancer Working Group; Oslo University Hospital;
United States National Cancer Institute Specialized Program Of Research
Excellence [CA089393]; Centre for Translational Genomics (CTAG);
Department of Health via NIHR comprehensive Biomedical Research Centre;
NHS Foundation Trust, King's College London; King's College Hospital NHS
Foundation Trust
FX This work was supported by the Wellcome Trust (grant reference 098051)
and Breakthrough Breast Cancer Research (ICGC 08/09). Individual
support: S.N.Z. (Wellcome Trust Clinical Research Training Fellow);
P.J.C. (Wellcome Trust Senior Clinical Research Fellow grant reference
WT088340MA); P.V.L. (Research Foundation - Flanders [FWO]); A.S.
(National Research Council Canada [HL Holmes Award] and EMBO); I.V.
(International Human Frontier Science Program Organization); J.W.M.M.
(Netherlands Genomics Initiative (NGI)/Netherlands Organization for
Scientific Research); A.L.B.D. and A.L. (Norwegian Research Council, The
Norwegian Cancer Society, The Radium Hospital Foundation and Health
Region South-East); S.M (European Community's Seventh Framework
Programme [FP7/2010-2014] grant reference 242006 Breast Cancer Somatic
Genetics Study [BASIS]). We thank Nancy Miller for her activities
related to the curation and collection of the clinical data associated
with this study. We acknowledge the Core Sequencing Facility and IT
groups of the Wellcome Trust Sanger Institute, the Breakthrough Breast
Cancer Unit, members of the ICGC Breast Cancer Working Group, the
OSBREAC Consortium of Oslo University Hospital, the United States
National Cancer Institute Specialized Program Of Research Excellence
(grant reference CA089393) and Dr. Peter Watson of the BCCA Tumour
Tissue Repository and the Centre for Translational Genomics (CTAG). The
authors acknowledge financial support from the Department of Health via
NIHR comprehensive Biomedical Research Centre award to Guy's and St
Thomas' NHS Foundation Trust, King's College London, and King's College
Hospital NHS Foundation Trust. We thank George Vassiliou for pointing us
to the term "kataegis.'' J.E.G. is a consultant for Generation Health.
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PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD MAY 25
PY 2012
VL 149
IS 5
BP 979
EP 993
DI 10.1016/j.cell.2012.04.024
PG 15
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 947TN
UT WOS:000304453900006
PM 22608084
ER
PT J
AU Nik-Zainal, S
Van Loo, P
Wedge, DC
Alexandrov, LB
Greenman, CD
Lau, KW
Raine, K
Jones, D
Marshall, J
Ramakrishna, M
Shlien, A
Cooke, SL
Hinton, J
Menzies, A
Stebbings, LA
Leroy, C
Jia, MM
Rance, R
Mudie, LJ
Gamble, SJ
Stephens, PJ
McLaren, S
Tarpey, PS
Papaemmanuil, E
Davies, HR
Varela, I
McBride, DJ
Bignell, GR
Leung, K
Butler, AP
Teague, JW
Martin, S
Jonsson, G
Mariani, O
Boyault, S
Miron, P
Fatima, A
Langerod, A
Aparicio, SAJR
Tutt, A
Sieuwerts, AM
Borg, A
Thomas, G
Salomon, AV
Richardson, AL
Borresen-Dale, AL
Futreal, PA
Stratton, MR
Campbell, PJ
AF Nik-Zainal, Serena
Van Loo, Peter
Wedge, David C.
Alexandrov, Ludmil B.
Greenman, Christopher D.
Lau, King Wai
Raine, Keiran
Jones, David
Marshall, John
Ramakrishna, Manasa
Shlien, Adam
Cooke, Susanna L.
Hinton, Jonathan
Menzies, Andrew
Stebbings, Lucy A.
Leroy, Catherine
Jia, Mingming
Rance, Richard
Mudie, Laura J.
Gamble, Stephen J.
Stephens, Philip J.
McLaren, Stuart
Tarpey, Patrick S.
Papaemmanuil, Elli
Davies, Helen R.
Varela, Ignacio
McBride, David J.
Bignell, Graham R.
Leung, Kenric
Butler, Adam P.
Teague, Jon W.
Martin, Sancha
Joensson, Goran
Mariani, Odette
Boyault, Sandrine
Miron, Penelope
Fatima, Aquila
Langerod, Anita
Aparicio, Samuel A. J. R.
Tutt, Andrew
Sieuwerts, Anieta M.
Borg, Ake
Thomas, Gilles
Salomon, Anne Vincent
Richardson, Andrea L.
Borresen-Dale, Anne-Lise
Futreal, P. Andrew
Stratton, Michael R.
Campbell, Peter J.
CA Int Canc Genome Consortium
TI The Life History of 21 Breast Cancers
SO CELL
LA English
DT Article
ID ACUTE MYELOID-LEUKEMIA; GENOMIC REARRANGEMENT; PANCREATIC-CANCER;
EVOLUTION; MUTATIONS; PATTERNS; INSTABILITY; METASTASIS; SIGNATURES;
RESOLUTION
AB Cancer evolves dynamically as clonal expansions supersede one another driven by shifting selective pressures, mutational processes, and disrupted cancer genes. These processes mark the genome, such that a cancer's life history is encrypted in the somatic mutations present. We developed algorithms to decipher this narrative and applied them to 21 breast cancers. Mutational processes evolve across a cancer's lifespan, with many emerging late but contributing extensive genetic variation. Subclonal diversification is prominent, and most mutations are found in just a fraction of tumor cells. Every tumor has a dominant subclonal lineage, representing more than 50% of tumor cells. Minimal expansion of these subclones occurs until many hundreds to thousands of mutations have accumulated, implying the existence of long-lived, quiescent cell lineages capable of substantial proliferation upon acquisition of enabling genomic changes. Expansion of the dominant subclone to an appreciable mass may therefore represent the final rate-limiting step in a breast cancer's development, triggering diagnosis.
C1 [Nik-Zainal, Serena; Van Loo, Peter; Wedge, David C.; Alexandrov, Ludmil B.; Greenman, Christopher D.; Lau, King Wai; Raine, Keiran; Jones, David; Marshall, John; Ramakrishna, Manasa; Shlien, Adam; Cooke, Susanna L.; Hinton, Jonathan; Menzies, Andrew; Stebbings, Lucy A.; Leroy, Catherine; Jia, Mingming; Rance, Richard; Mudie, Laura J.; Gamble, Stephen J.; Stephens, Philip J.; McLaren, Stuart; Tarpey, Patrick S.; Papaemmanuil, Elli; Davies, Helen R.; Varela, Ignacio; McBride, David J.; Bignell, Graham R.; Leung, Kenric; Butler, Adam P.; Teague, Jon W.; Martin, Sancha; Futreal, P. Andrew; Stratton, Michael R.; Campbell, Peter J.] Wellcome Trust Sanger Inst, Canc Genome Project, Hinxton CB10 1SA, England.
[Van Loo, Peter] VIB, Ctr Biol Dis, B-3000 Louvain, Belgium.
[Van Loo, Peter] Katholieke Univ Leuven, Dept Human Genet, B-3000 Louvain, Belgium.
[Greenman, Christopher D.] Univ E Anglia, Dept Comp, Norwich NR4 7TJ, Norfolk, England.
[Greenman, Christopher D.] Genome Anal Ctr, Norwich NR4 7UH, Norfolk, England.
[Joensson, Goran; Tutt, Andrew] Kings Coll London, Breakthrough Breast Canc Res Unit, London SE1 9RT, England.
[Mariani, Odette; Salomon, Anne Vincent] Inst Curie, Dept Tumor Biol, F-75248 Paris 05, France.
[Boyault, Sandrine; Thomas, Gilles] Univ Lyon 1, Ctr Leon Berard, INCa Synergie, Lyon 08, France.
[Miron, Penelope; Fatima, Aquila; Richardson, Andrea L.] Dana Farber Canc Inst, Boston, MA 02215 USA.
[Langerod, Anita; Borresen-Dale, Anne-Lise] Norwegian Radium Hosp, Oslo Univ Hosp, Inst Canc Res, Dept Genet, N-0310 Oslo, Norway.
[Aparicio, Samuel A. J. R.] Univ British Columbia, Dept Pathol & Lab Med, Vancouver, BC V6T 2B5, Canada.
[Aparicio, Samuel A. J. R.] British Columbia Canc Res Ctr, Vancouver, BC V5Z 1L3, Canada.
[Sieuwerts, Anieta M.] Erasmus MC, NL-3000 CA Rotterdam, Netherlands.
[Borg, Ake] Lund Univ, Dept Oncol, SE-22184 Lund, Sweden.
[Richardson, Andrea L.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Borresen-Dale, Anne-Lise] Univ Oslo, Fac Med, Inst Clin Med, KG Jebsen Ctr Breast Canc Res, N-0310 Oslo, Norway.
[Campbell, Peter J.] Addenbrookes Hosp, Dept Haematol, Cambridge CB2 0QQ, England.
[Campbell, Peter J.] Univ Cambridge, Dept Haematol, Cambridge CB2 2XY, England.
RP Campbell, PJ (reprint author), Wellcome Trust Sanger Inst, Canc Genome Project, Hinxton CB10 1SA, England.
EM pc8@sanger.ac.uk
RI Van Loo, Peter/A-3287-2012; Gamble, Stephen/D-1417-2011; Jonsson,
Goran/D-1212-2014; Alexandrov, Ludmil/B-6582-2014; Varela,
Ignacio/G-1699-2016
OI Van Loo, Peter/0000-0003-0292-1949; Gamble, Stephen/0000-0002-0867-3723;
Wedge, David/0000-0002-7572-3196; Martin, Sancha/0000-0001-6213-5259;
Alexandrov, Ludmil/0000-0003-3596-4515; Varela,
Ignacio/0000-0002-0969-506X
FU Wellcome Trust [098051]; Breakthrough Breast Cancer Research [ICGC
08/09]; National Research Council Canada; EMBO; International Human
Frontier Science Program Organization; Netherlands Genomics Initiative
(NGI)/Netherlands Organization for Scientific Research (NWO); Norwegian
Research Council; Norwegian Cancer Society; Radium Hospital Foundation;
Health Region South-East; European Community [242006]; National Cancer
Institute Specialized Program Of Research Excellence [CA089393];
Department of Health via the National Institute for Health Research
comprehensive Biomedical Research Centre; St Thomas' NHS Foundation
Trust
FX This work was supported by the Wellcome Trust (grant reference 098051)
and Breakthrough Breast Cancer Research (ICGC 08/09). S. N.-Z. is a
Wellcome Trust Clinical Research Training Fellow. P.J.C. is a Wellcome
Trust Senior Clinical Research Fellow (WT088340MA). P.V.L. is a
postdoctoral researcher of the Research Foundation-Flanders. A.S. is
supported by the HL Holmes Award from the National Research Council
Canada and a Fellowship from EMBO. I.V. is supported by a fellowship
from the International Human Frontier Science Program Organization.
J.W.M.M. is funded in part by a research grant from the Netherlands
Genomics Initiative (NGI)/Netherlands Organization for Scientific
Research (NWO). A.-L.B.-D. and A.L. are funded by the Norwegian Research
Council, Norwegian Cancer Society, Radium Hospital Foundation and Health
Region South-East. S. M. is funded by the BASIS project through the
European Community's FP7/2010-2014 under grant agreement 242006. We
acknowledge the Core Sequencing Facility and IT groups of the Wellcome
Trust Sanger Institute, support for samples, sample banking, and
processing from the Breakthrough Breast Cancer Unit, members of the ICGC
Breast Cancer Working Group, the Pathology Review subgroup of the Breast
Cancer Working Group, the OSBREAC Consortium of The Oslo University
Hospital and the National Cancer Institute Specialized Program Of
Research Excellence (grant reference CA089393). We also acknowledge Dr.
Peter Watson, the BCCA Tumour Tissue Repository, and the Centre for
Translational Genomics. The authors acknowledge financial support from
the Department of Health via the National Institute for Health Research
comprehensive Biomedical Research Centre award to Guy's and St Thomas'
NHS Foundation Trust.
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PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD MAY 25
PY 2012
VL 149
IS 5
DI 10.1016/j.cell.2012.04.023
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 947TN
UT WOS:000304453900007
PM 22608083
ER
PT J
AU Jain, M
Nilsson, R
Sharma, S
Madhusudhan, N
Kitami, T
Souza, AL
Kafri, R
Kirschner, MW
Clish, CB
Mootha, VK
AF Jain, Mohit
Nilsson, Roland
Sharma, Sonia
Madhusudhan, Nikhil
Kitami, Toshimori
Souza, Amanda L.
Kafri, Ran
Kirschner, Marc W.
Clish, Clary B.
Mootha, Vamsi K.
TI Metabolite Profiling Identifies a Key Role for Glycine in Rapid Cancer
Cell Proliferation
SO SCIENCE
LA English
DT Article
ID ANTICANCER DRUG SCREEN; ONE-CARBON METABOLISM; BREAST-CANCER; SERINE
HYDROXYMETHYLTRANSFERASE; EXPRESSION SIGNATURE; DEPENDENCE; SURVIVAL;
MUTANTS; PATHWAY; NMR
AB Metabolic reprogramming has been proposed to be a hallmark of cancer, yet a systematic characterization of the metabolic pathways active in transformed cells is currently lacking. Using mass spectrometry, we measured the consumption and release ( CORE) profiles of 219 metabolites from media across the NCI-60 cancer cell lines, and integrated these data with a preexisting atlas of gene expression. This analysis identified glycine consumption and expression of the mitochondrial glycine biosynthetic pathway as strongly correlated with rates of proliferation across cancer cells. Antagonizing glycine uptake and its mitochondrial biosynthesis preferentially impaired rapidly proliferating cells. Moreover, higher expression of this pathway was associated with greater mortality in breast cancer patients. Increased reliance on glycine may represent a metabolic vulnerability for selectively targeting rapid cancer cell proliferation.
C1 [Jain, Mohit; Nilsson, Roland; Madhusudhan, Nikhil; Kitami, Toshimori; Souza, Amanda L.; Clish, Clary B.; Mootha, Vamsi K.] Broad Inst, Cambridge, MA 02142 USA.
[Jain, Mohit; Nilsson, Roland; Madhusudhan, Nikhil; Kitami, Toshimori; Kafri, Ran; Kirschner, Marc W.; Mootha, Vamsi K.] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA.
[Jain, Mohit; Nilsson, Roland; Madhusudhan, Nikhil; Kitami, Toshimori; Mootha, Vamsi K.] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
[Jain, Mohit; Nilsson, Roland; Madhusudhan, Nikhil; Kitami, Toshimori; Mootha, Vamsi K.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Jain, Mohit] Brigham & Womens Hosp, Dept Med, Div Cardiovasc Med, Boston, MA 02115 USA.
[Nilsson, Roland] Karolinska Inst, Dept Med, Unit Computat Med, S-17176 Stockholm, Sweden.
[Sharma, Sonia] La Jolla Inst Allergy & Immunol, La Jolla, CA 92037 USA.
RP Mootha, VK (reprint author), Broad Inst, Cambridge, MA 02142 USA.
EM vamsi@hms.harvard.edu
FU NIH [K08HL107451, R01DK081457]; Knut & Alice Wallenberg Foundation;
Stockholm County (SLL) [01626-2009]; Leukemia & Lymphoma Society
FX We thank T. R. Golub, O. Shaham, S. B. Vafai, and L. Strittmatter for
scientific discussions and feedback; X. Cao for assistance with glucose
and lactate measurements; the Broad Institute RNAi Platform for shRNA
reagents; D. Gomez-Cabrero for assistance with multidimensional scaling;
A. Ploner and P. Dickman for assistance with survival analysis; W. C.
Kopp, S. L. Holbeck, K. Gill, and P. Sellers of the Developmental
Therapeutics Program, National Cancer Institute, for reagents and
assistance with cell culture; and T. Hasaka of the Broad Institute for
assistance with imaging studies. Supported by NIH grant K08HL107451
(M.J.), a postdoctoral scholarship from the Knut & Alice Wallenberg
Foundation and Stockholm County (SLL) grant 01626-2009 (R.N.), a Special
Fellow award from the Leukemia & Lymphoma Society (S. S.), and NIH grant
R01DK081457 and a gift from the Nestle Research Center (V. K. M.). The
full metabolite CORE profiling data set is available in the
supplementary materials as well as through the NCI Molecular Targets
data repository (http://dtp.nci.nih.gov/mtargets/download.html). M.J.
and R.N. conceived and performed all experiments, collected and analyzed
experimental data, and prepared the manuscript. S. S. assisted with cell
culture, RNAi, and T lymphocyte experiments. N.M. and T. K. assisted
with cell culture and imaging-based experiments. A. L. S. and C. B. C.
performed LC-MS/MS profiling experiments and provided experimental
feedback. R. K. and M. W. K. performed cell cycle studies. V. K. M.
conceived all experiments, reviewed all experimental data, and prepared
the manuscript. All authors have discussed the results and reviewed the
manuscript. All authors declare no competing financial interests.
NR 29
TC 367
Z9 383
U1 27
U2 169
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD MAY 25
PY 2012
VL 336
IS 6084
BP 1040
EP 1044
DI 10.1126/science.1218595
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 947DK
UT WOS:000304406800047
PM 22628656
ER
PT J
AU Ma, TZ
Su, ZJ
Chen, L
Liu, SY
Zhu, NX
Wen, LF
Yuan, Y
Lv, LL
Chen, XC
Huang, JM
Chen, HB
AF Ma, Tianzhong
Su, Zhongjing
Chen, Ling
Liu, Shuyan
Zhu, Ningxia
Wen, Lifeng
Yuan, Yan
Lv, Leili
Chen, Xiancai
Huang, Jianmin
Chen, Haibin
TI Human Papillomavirus Type 18 E6 and E7 Genes Integrate into Human
Hepatoma Derived Cell Line Hep G2
SO PLOS ONE
LA English
DT Article
ID HEPATOCELLULAR-CARCINOMA; CERVICAL-CANCER; LIVER; TRANSFORMATION;
INFECTION; APOPTOSIS; BIOLOGY; PROTEIN; HPV-18; HBV
AB Background and Objectives: Human papillomaviruses have been linked causally to some human cancers such as cervical carcinoma, but there is very little research addressing the effect of HPV infection on human liver cells. We chose the human hepatoma derived cell line Hep G2 to investigate whether HPV gene integration took place in liver cells as well.
Methods: We applied PCR to detect the possible integration of HPV genes in Hep G2 cells. We also investigated the expression of the integrated E6 and E7 genes by using RT-PCR and Western blotting. Then, we silenced E6 and E7 expression and checked the cell proliferation and apoptosis in Hep G2 cells. Furthermore, we analyzed the potential genes involved in cell cycle and apoptosis regulatory pathways. Finally, we used in situ hybridization to detect HPV 16/18 in hepatocellular carcinoma samples.
Results: Hep G2 cell line contains integrated HPV 18 DNA, leading to the expression of the E6 and E7 oncogenic proteins. Knockdown of the E7 and E6 genes expression reduced cell proliferation, caused the cell cycle arrest at the S phase, and increased apoptosis. The human cell cycle and apoptosis real-time PCR arrays analysis demonstrated E6 and E7-mediated regulation of some genes such as Cyclin H, UBA1, E2F4, p53, p107, FASLG, NOL3 and CASP14. HPV16/18 was found in only 9% (9/100) of patients with hepatocellular carcinoma.
Conclusion: Our investigations showed that HPV 18 E6 and E7 genes can be integrated into the Hep G2, and we observed a low prevalence of HPV 16/18 in hepatocellular carcinoma samples. However, the precise risk of HPV as causative agent of hepatocellular carcinoma needs further study.
C1 [Ma, Tianzhong; Su, Zhongjing; Liu, Shuyan; Zhu, Ningxia; Wen, Lifeng; Yuan, Yan; Lv, Leili; Chen, Xiancai; Chen, Haibin] Shantou Univ, Dept Histol & Embryol, Coll Med, Shantou, Guangdong, Peoples R China.
[Chen, Ling] Shantou Univ, Dept Biochem & Mol Biol, Coll Med, Shantou, Guangdong, Peoples R China.
[Huang, Jianmin] Harvard Univ, Sch Med, Boston, MA USA.
[Huang, Jianmin] Massachusetts Gen Hosp, Pediat Endocrine Unit, Boston, MA 02114 USA.
RP Ma, TZ (reprint author), Shantou Univ, Dept Histol & Embryol, Coll Med, Shantou, Guangdong, Peoples R China.
EM chenhb@stu.edu.cn
FU Natural Science Foundation of Guangdong Province, China
[10151503102000034]; Research Foundation of Shantou University Medical
College [LC0401]
FX This study was supported by Natural Science Foundation of Guangdong
Province, China (Grant No. 10151503102000034) and Research Foundation of
Shantou University Medical College (Grant No. LC0401). The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 18
TC 0
Z9 2
U1 2
U2 8
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAY 24
PY 2012
VL 7
IS 5
AR e37964
DI 10.1371/journal.pone.0037964
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 959UB
UT WOS:000305338900065
PM 22655088
ER
PT J
AU Moore, FE
Reyon, D
Sander, JD
Martinez, SA
Blackburn, JS
Khayter, C
Ramirez, CL
Joung, JK
Langenau, DM
AF Moore, Finola E.
Reyon, Deepak
Sander, Jeffry D.
Martinez, Sarah A.
Blackburn, Jessica S.
Khayter, Cyd
Ramirez, Cherie L.
Joung, J. Keith
Langenau, David M.
TI Improved Somatic Mutagenesis in Zebrafish Using Transcription
Activator-Like Effector Nucleases (TALENs)
SO PLOS ONE
LA English
DT Article
ID ZINC-FINGER NUCLEASES; TARGETED GENE DISRUPTION; POOL ENGINEERING OPEN;
MICROINJECTION; KNOCKOUT
AB Zinc Finger Nucleases (ZFNs) made by Context-Dependent Assembly (CoDA) and Transcription Activator-Like Effector Nucleases (TALENs) provide robust and user-friendly technologies for efficiently inactivating genes in zebrafish. These designer nucleases bind to and cleave DNA at particular target sites, inducing error-prone repair that can result in insertion or deletion mutations. Here, we assess the relative efficiencies of these technologies for inducing somatic DNA mutations in mosaic zebrafish. We find that TALENs exhibited a higher success rate for obtaining active nucleases capable of inducing mutations than compared with CoDA ZFNs. For example, all six TALENs tested induced DNA mutations at genomic target sites while only a subset of CoDA ZFNs exhibited detectable rates of mutagenesis. TALENs also exhibited higher mutation rates than CoDA ZFNs that had not been pre-screened using a bacterial two-hybrid assay, with DNA mutation rates ranging from 20%-76.8% compared to 1.1%-3.3%. Furthermore, the broader targeting range of TALENs enabled us to induce mutations at the methionine translation start site, sequences that were not targetable using the CoDA ZFN platform. TALENs exhibited similar toxicity to CoDA ZFNs, with >50% of injected animals surviving to 3 days of life. Taken together, our results suggest that TALEN technology provides a robust alternative to CoDA ZFNs for inducing targeted gene-inactivation in zebrafish, making it a preferred technology for creating targeted knockout mutants in zebrafish.
C1 [Moore, Finola E.; Reyon, Deepak; Sander, Jeffry D.; Martinez, Sarah A.; Blackburn, Jessica S.; Khayter, Cyd; Ramirez, Cherie L.; Joung, J. Keith; Langenau, David M.] Massachusetts Gen Hosp, Mol Pathol Unit, Charlestown, MA USA.
[Moore, Finola E.; Reyon, Deepak; Sander, Jeffry D.; Martinez, Sarah A.; Blackburn, Jessica S.; Khayter, Cyd; Ramirez, Cherie L.; Joung, J. Keith; Langenau, David M.] Massachusetts Gen Hosp, Ctr Canc Res, Charlestown, MA USA.
[Moore, Finola E.; Martinez, Sarah A.; Blackburn, Jessica S.; Langenau, David M.] Harvard Stem Cell Inst, Boston, MA USA.
[Moore, Finola E.; Reyon, Deepak; Sander, Jeffry D.; Martinez, Sarah A.; Blackburn, Jessica S.; Khayter, Cyd; Ramirez, Cherie L.; Joung, J. Keith; Langenau, David M.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Reyon, Deepak; Sander, Jeffry D.; Khayter, Cyd; Ramirez, Cherie L.; Joung, J. Keith] Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Charlestown, MA USA.
RP Moore, FE (reprint author), Massachusetts Gen Hosp, Mol Pathol Unit, Charlestown, MA USA.
EM dlangenau@partners.org
FU Alex's Lemonade Stand Foundation; American Cancer Society; Harvard Stem
Cell Institute; NIH [K01 AR055619, RO1 CA154923, R21 CA156056, DP1
OD006862, R01 GM088040, T32 CA009216]; Jim and Ann Orr MGH Research
Scholar Award; National Science Foundation [DBI-0923827]
FX D.M.L. is supported by NIH grants K01 AR055619, RO1 CA154923, and R21
CA156056, the Alex's Lemonade Stand Foundation, the American Cancer
Society, and the Harvard Stem Cell Institute. J.K.J. is supported by an
NIH Director's Pioneer Award (DP1 OD006862), NIH R01 GM088040, and the
Jim and Ann Orr MGH Research Scholar Award. J.D.S. is supported by NIH
T32 CA009216. D. R. is supported by National Science Foundation award
DBI-0923827. The funders had no role in study design, data collection
and analysis, decision to publish, or preparation of the manuscript.
NR 32
TC 88
Z9 96
U1 1
U2 49
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAY 24
PY 2012
VL 7
IS 5
AR e37877
DI 10.1371/journal.pone.0037877
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 959UB
UT WOS:000305338900052
PM 22655075
ER
PT J
AU Koleva, RI
Ficarro, SB
Radomska, HS
Carrasco-Alfonso, MJ
Alberta, JA
Webber, JT
Luckey, CJ
Marcucci, G
Tenen, DG
Marto, JA
AF Koleva, Rositsa I.
Ficarro, Scott B.
Radomska, Hanna S.
Carrasco-Alfonso, Marlene J.
Alberta, John A.
Webber, James T.
Luckey, C. John
Marcucci, Guido
Tenen, Daniel G.
Marto, Jarrod A.
TI C/EBP alpha and DEK coordinately regulate myeloid differentiation
SO BLOOD
LA English
DT Article
ID BINDING PROTEIN-ALPHA; ACUTE MYELOGENOUS LEUKEMIA; GENE-EXPRESSION;
TRANSCRIPTIONAL ACTIVATION; PROTEOMIC IDENTIFICATION; NEUTROPHIL
DEVELOPMENT; CD34(+) CELLS; SELF-RENEWAL; IN-VIVO; PHOSPHORYLATION
AB The transcription factor C/EBP alpha is a critical mediator of myeloid differentiation and is often functionally impaired in acute myeloid leukemia. Recent studies have suggested that oncogenic FLT3 activity disrupts wild-type C/EBP alpha function via phosphorylation on serine 21 (S21). Despite the apparent role of pS21 as a negative regulator of C/EBP alpha transcription activity, the mechanism by which phosphorylation tips the balance between transcriptionally competent and inhibited forms remains unresolved. In the present study, we used immuno-affinity purification combined with quantitative mass spectrometry to delineate the proteins associated with C/EBP alpha on chromatin. We identified DEK, a protein with genetic links to leukemia, as a member of the C/EBP alpha complexes, and demonstrate that this association is disrupted by S21 phosphorylation. We confirmed that DEK is recruited specifically to chromatin with C/EBP alpha to enhance GCSFR3 promoter activation. In addition, we demonstrated that genetic depletion of DEK reduces the ability of C/EBP alpha to drive the expression of granulocytic target genes in vitro and disrupts G-CSF-mediated granulocytic differentiation of fresh human BM-derived CD34(+) cells. Our data suggest that C/EBP alpha and DEK coordinately activate myeloid gene expression and that S21 phosphorylation on wild-type C/EBP alpha mediates protein interactions that regulate the differentiation capacity of hematopoietic progenitors. (Blood. 2012;119(21): 4878-4888)
C1 [Koleva, Rositsa I.; Ficarro, Scott B.; Alberta, John A.; Webber, James T.; Marto, Jarrod A.] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02215 USA.
[Koleva, Rositsa I.; Ficarro, Scott B.; Webber, James T.; Marto, Jarrod A.] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Ficarro, Scott B.; Marto, Jarrod A.] Dana Farber Canc Inst, Blais Prote Ctr, Boston, MA 02115 USA.
[Radomska, Hanna S.; Tenen, Daniel G.] Beth Israel Deaconess Med Ctr, Div Hematol Oncol, Boston, MA 02215 USA.
[Radomska, Hanna S.; Tenen, Daniel G.] Harvard Univ, Stem Cell Inst, Ctr Life Sci, Boston, MA 02115 USA.
[Carrasco-Alfonso, Marlene J.; Luckey, C. John] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Marcucci, Guido] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
[Tenen, Daniel G.] Natl Univ Singapore, Canc Sci Inst, Singapore 117548, Singapore.
RP Marto, JA (reprint author), Dana Farber Canc Inst, Dept Canc Biol, 450 Brookline Ave,Smith 1158A, Boston, MA 02215 USA.
EM jarrod_marto@dfci.harvard.edu
FU Dana-Farber Cancer Institute; National Institutes of Health
[P01NS047572, P30 CA016058, CA118316, DK080665]
FX This work was supported by the Dana-Farber Cancer Institute, and the
National Institutes of Health (P01NS047572 to J.M., P30 CA016058 to G.
M., and CA118316 and DK080665 to D.T.).
NR 49
TC 22
Z9 22
U1 2
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD MAY 24
PY 2012
VL 119
IS 21
BP 4878
EP 4888
DI 10.1182/blood-2011-10-383083
PG 11
WC Hematology
SC Hematology
GA 959CZ
UT WOS:000305290400014
PM 22474248
ER
PT J
AU Arnason, JE
Campigotto, F
Neuberg, D
Bussel, JB
AF Arnason, Jon E.
Campigotto, Federico
Neuberg, Donna
Bussel, James B.
TI Abnormalities in IgA and IgM are associated with treatment-resistant ITP
SO BLOOD
LA English
DT Article
ID THROMBOCYTOPENIC PURPURA; IMMUNE THROMBOCYTOPENIA
AB We hypothesized that immune dysregulation, as represented by abnormal immunoglobulin (Ig) levels, may increase immune thrombocytopenia (ITP) severity. A cross-sectional analysis was performed encompassing patients with ITP seen at the New York Presbyterian Platelet Disorder Center in the past 10 years. The subjects' Ig levels were measured, and subjects were analyzed for differences in treatment response. Subjects with an IgA level greater than median had a significantly increased chance of failing to respond to standard treatment (steroids, intravenous Ig, and intravenous anti-D) than did subjects with an IgA level lower than median (37 of 271, 14%; vs 22 of 281, 8%; P = .03) and an increased risk for bleeding (36 of 378, 10%; vs 19 of 386, 5%; P = .02). Subjects with an IgM less than 56 (lower limit of normal) failed to respond to standard treatment more often than patients with a normal IgM (12 of 67, 18%; vs 44 of 467, 9%; P = .05) with a trend toward worsened response to splenectomy (3 of 18, 17%; vs 36 of 86, 42%; P = .06). These observations suggest that immune dysregulation, as represented by elevations in IgA or decreased levels of IgM, are associated with ITP that is more resistant to treatment. (Blood. 2012;119(21):5016-5020)
C1 [Arnason, Jon E.] Harvard Univ, Hematol Malignancy & Bone Marrow Transplantat Pro, Beth Israel Deaconess Med Ctr, Sch Med, Boston, MA 02215 USA.
[Campigotto, Federico; Neuberg, Donna] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Bussel, James B.] Weill Cornell Med Ctr, New York, NY USA.
RP Arnason, JE (reprint author), Harvard Univ, Hematol Malignancy & Bone Marrow Transplantat Pro, Beth Israel Deaconess Med Ctr, Sch Med, 330 Brookline Ave, Boston, MA 02215 USA.
EM jarnason@bidmc.harvard.edu
FU Amgen; Cangene; GlaxoSmithKline; Genzyme; IgG of America; Immunomedics;
Ligand; Eisai Inc; Shionogi; Sysmex
FX J.B.B. currently receives clinical research support from the following
companies: Amgen, Cangene, GlaxoSmithKline, Genzyme, IgG of America,
Immunomedics, Ligand, Eisai Inc, Shionogi, and Sysmex. His family owns
stock in Amgen and GlaxoSmithKline. He has participated in Advisory
Boards for Amgen, GlaxoSmithKline, Ligand, Shionogi, and Eisai Inc. He
also had a 1-day consult with Portola. The remaining authors declare no
competing financial interests.
NR 9
TC 4
Z9 5
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD MAY 24
PY 2012
VL 119
IS 21
BP 5016
EP 5020
DI 10.1182/blood-2011-09-381020
PG 5
WC Hematology
SC Hematology
GA 959CZ
UT WOS:000305290400028
PM 22490683
ER
PT J
AU Lee, JS
FitzGibbon, EJ
Chen, YR
Kim, HJ
Lustig, LR
Akintoye, SO
Collins, MT
Kaban, LB
AF Lee, J. S.
FitzGibbon, E. J.
Chen, Y. R.
Kim, H. J.
Lustig, L. R.
Akintoye, S. O.
Collins, M. T.
Kaban, L. B.
TI Clinical guidelines for the management of craniofacial fibrous dysplasia
SO ORPHANET JOURNAL OF RARE DISEASES
LA English
DT Article
ID MCCUNE-ALBRIGHT-SYNDROME; OPTICAL COHERENCE TOMOGRAPHY; STIMULATORY
G-PROTEIN; ANTERIOR SKULL BASE; TEMPORAL BONE; PARANASAL SINUSES;
PAMIDRONATE TREATMENT; MALIGNANT TRANSFORMATION; ACTIVATING MUTATIONS;
FIBROOSSEOUS LESIONS
AB Fibrous dysplasia (FD) is a non-malignant condition caused by post-zygotic, activating mutations of the GNAS gene that results in inhibition of the differentiation and proliferation of bone-forming stromal cells and leads to the replacement of normal bone and marrow by fibrous tissue and woven bone. The phenotype is variable and may be isolated to a single skeletal site or multiple sites and sometimes is associated with extraskeletal manifestations in the skin and/or endocrine organs (McCune-Albright syndrome). The clinical behavior and progression of FD may also vary, thereby making the management of this condition difficult with few established clinical guidelines. This paper provides a clinically-focused comprehensive description of craniofacial FD, its natural progression, the components of the diagnostic evaluation and the multi-disciplinary management, and considerations for future research.
C1 [Lee, J. S.] Univ Calif San Francisco, Dept Oral & Maxillofacial Surg, San Francisco, CA 94143 USA.
[FitzGibbon, E. J.] NEI, Sensorimotor Res Lab, NIH, Bethesda, MD 20892 USA.
[Chen, Y. R.] Chang Gung Univ, Chang Gung Mem Hosp, Chang Gung Craniofacial Ctr, Tao Yuan, Taiwan.
[Kim, H. J.] Natl Inst Deafness & Other Commun Disorders, Head & Neck Surg Branch, NIH, Bethesda, MD USA.
[Kim, H. J.] Georgetown Univ, Med Ctr, Dept Otolaryngol Head & Neck Surg, Washington, DC 20007 USA.
[Lustig, L. R.] Univ Calif San Francisco, Dept Otolaryngol Head & Neck Surg, San Francisco, CA USA.
[Akintoye, S. O.] Univ Penn, Sch Dent Med, Dept Oral Med, Philadelphia, PA 19104 USA.
[Collins, M. T.] Natl Inst Dent & Craniofacial Res, Skeletal Clin Studies Unit, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD USA.
[Kaban, L. B.] Harvard Univ, Sch Dent Med, Massachusetts Gen Hosp, Walter C Guralnick Prof & Chairman Dept Oral & Ma, Boston, MA 02115 USA.
RP Lee, JS (reprint author), Univ Calif San Francisco, Dept Oral & Maxillofacial Surg, San Francisco, CA 94143 USA.
FU Fibrous Dysplasia Foundation; Zimmer
FX This article has been published as part of Orphanet Journal of Rare
Diseases Volume 7 Supplement 1, 2012: Proceedings of the International
Meeting on McCune-Albright Syndrome and Cherubism. The full contents of
the supplement are available online at
http://www.ojrd.com/supplements/7/S1. Publication of the proceedings was
funded by the Fibrous Dysplasia Foundation and an unrestricted grant
from Zimmer.
NR 100
TC 26
Z9 27
U1 1
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1750-1172
J9 ORPHANET J RARE DIS
JI Orphanet J. Rare Dis.
PD MAY 24
PY 2012
VL 7
SU 1
AR S2
DI 10.1186/1750-1172-7-S1-S2
PG 19
WC Genetics & Heredity; Medicine, Research & Experimental
SC Genetics & Heredity; Research & Experimental Medicine
GA 951YJ
UT WOS:000304756300002
PM 22640797
ER
PT J
AU Papadaki, ME
Lietman, SA
Levine, MA
Olsen, BR
Kaban, LB
Reichenberger, EJ
AF Papadaki, Maria E.
Lietman, Steven A.
Levine, Michael A.
Olsen, Bjorn R.
Kaban, Leonard B.
Reichenberger, Ernst J.
TI Cherubism: best clinical practice
SO ORPHANET JOURNAL OF RARE DISEASES
LA English
DT Article
ID GIANT-CELL LESIONS; ADAPTER PROTEIN 3BP2; TNF-ALPHA BLOCKADE; JAW TUMOR
SYNDROME; TERM-FOLLOW-UP; NOONAN-SYNDROME; GINGIVAL FIBROMATOSIS;
AGGRESSIVE-BEHAVIOR; ORBITAL INVOLVEMENT; CYTOLOGIC FEATURES
AB Cherubism is a skeletal dysplasia characterized by bilateral and symmetric fibro-osseous lesions limited to the mandible and maxilla. In most patients, cherubism is due to dominant mutations in the SH3BP2 gene on chromosome 4p16.3. Affected children appear normal at birth. Swelling of the jaws usually appears between 2 and 7 years of age, after which, lesions proliferate and increase in size until puberty. The lesions subsequently begin to regress, fill with bone and remodel until age 30, when they are frequently not detectable.
Fibro-osseous lesions, including those in cherubism have been classified as quiescent, non-aggressive and aggressive on the basis of clinical behavior and radiographic findings. Quiescent cherubic lesions are usually seen in older patients and do not demonstrate progressive growth. Non-aggressive lesions are most frequently present in teenagers. Lesions in the aggressive form of cherubism occur in young children and are large, rapidly growing and may cause tooth displacement, root resorption, thinning and perforation of cortical bone.
Because cherubism is usually self-limiting, operative treatment may not be necessary. Longitudinal observation and follow-up is the initial management in most cases. Surgical intervention with curettage, contouring or resection may be indicated for functional or aesthetic reasons. Surgical procedures are usually performed when the disease becomes quiescent. Aggressive lesions that cause severe functional problems such as airway obstruction justify early surgical intervention.
C1 [Reichenberger, Ernst J.] Univ Connecticut, Ctr Hlth, Dept Reconstruct Sci, Ctr Regenerat Med & Skeletal Dev, Farmington, CT USA.
[Papadaki, Maria E.; Kaban, Leonard B.] Harvard Univ, Sch Dent Med, Massachusetts Gen Hosp, Dept Oral & Maxillofacial Surg, Boston, MA 02115 USA.
[Lietman, Steven A.] Cleveland Clin, Lerner Res Inst, Dept Orthopaed Surg, Cleveland, OH 44106 USA.
[Lietman, Steven A.] Cleveland Clin, Lerner Res Inst, Dept Biomed Engn, Cleveland, OH 44106 USA.
[Levine, Michael A.] Childrens Hosp Philadelphia, Div Endocrinol & Diabet, Philadelphia, PA 19104 USA.
[Levine, Michael A.] Univ Penn, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA.
[Olsen, Bjorn R.] Harvard Univ, Sch Dent Med, Dept Dev Biol, Boston, MA 02115 USA.
RP Reichenberger, EJ (reprint author), Univ Connecticut, Ctr Hlth, Dept Reconstruct Sci, Ctr Regenerat Med & Skeletal Dev, Farmington, CT USA.
EM reichenberger@uchc.edu
OI Levine, Michael/0000-0003-0036-7809
FU Fibrous Dysplasia Foundation; NIH (National Institutes of Dental and
Craniofacial Research); NIH (Office of Rare Diseases); Zimmer
FX Written consent for publication was obtained from patients or their
relatives. This study was supported by funding from the Fibrous
Dysplasia Foundation and the NIH (National Institutes of Dental and
Craniofacial Research and the Office of Rare Diseases).; This article
has been published as part of Orphanet Journal of Rare Diseases Volume 7
Supplement 1, 2012: International Meeting on Fibrous
Dysplasia/McCune-Albright Syndrome and Cherubism. The full contents of
the supplement are available online at
http://www.ojrd.com/supplements/7/S1. Publication of the proceedings was
funded by the Fibrous Dysplasia Foundation and an unrestricted grant
from Zimmer.
NR 99
TC 25
Z9 25
U1 0
U2 4
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1750-1172
J9 ORPHANET J RARE DIS
JI Orphanet J. Rare Dis.
PD MAY 24
PY 2012
VL 7
SU 1
AR S6
DI 10.1186/1750-1172-7-S1-S6
PG 14
WC Genetics & Heredity; Medicine, Research & Experimental
SC Genetics & Heredity; Research & Experimental Medicine
GA 951YJ
UT WOS:000304756300006
PM 22640403
ER
PT J
AU Reichenberger, EJ
Levine, MA
Olsen, BR
Papadaki, ME
Lietman, SA
AF Reichenberger, Ernst J.
Levine, Michael A.
Olsen, Bjorn R.
Papadaki, Maria E.
Lietman, Steven A.
TI The role of SH3BP2 in the pathophysiology of cherubism
SO ORPHANET JOURNAL OF RARE DISEASES
LA English
DT Article
ID ADAPTER PROTEIN 3BP2; WOLF-HIRSCHHORN-SYNDROME; CELL LESION SYNDROME;
PHOSPHOLIPASE-C-GAMMA; NEUROFIBROMATOSIS-NOONAN-SYNDROME; ANTIGEN
RECEPTOR; T-CELLS; REGULATES OSTEOCLASTOGENESIS; TRANSCRIPTION FACTOR;
PTPN11 MUTATIONS
AB Cherubism is a rare bone dysplasia that is characterized by symmetrical bone resorption limited to the jaws. Bone lesions are filled with soft fibrous giant cell-rich tissue that can expand and cause severe facial deformity. The disorder typically begins in children at ages of 2-5 years and the bone resorption and facial swelling continues until puberty; in most cases the lesions regress spontaneously thereafter. Most patients with cherubism have germline mutations in the gene encoding SH3BP2, an adapter protein involved in adaptive and innate immune response signaling. A mouse model carrying a Pro416Arg mutation in SH3BP2 develops osteopenia and expansile lytic lesions in bone and some soft tissue organs. In this review we discuss the genetics of cherubism, the biological functions of SH3BP2 and the analysis of the mouse model. The data suggest that the underlying cause for cherubism is a systemic autoinflammatory response to physiologic challenges despite the localized appearance of bone resorption and fibrous expansion to the jaws in humans.
C1 [Reichenberger, Ernst J.] Univ Connecticut, Ctr Hlth, Dept Reconstruct Sci, Ctr Regenerat Med & Skeletal Dev, Farmington, CT USA.
[Levine, Michael A.] Univ Penn, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA.
[Levine, Michael A.] Univ Penn, Childrens Hosp Philadelphia, Sch Med, Div Endocrinol & Diabet, Philadelphia, PA 19104 USA.
[Olsen, Bjorn R.] Harvard Univ, Sch Dent Med, Dept Dev Biol, Boston, MA 02115 USA.
[Papadaki, Maria E.] Harvard Univ, Sch Dent Med, Massachusetts Gen Hosp, Dept Oral & Maxillofacial Surg, Boston, MA 02115 USA.
[Lietman, Steven A.] Cleveland Clin, Lerner Res Inst, Dept Orthopaed Surg, Cleveland, OH 44106 USA.
[Lietman, Steven A.] Cleveland Clin, Lerner Res Inst, Dept Biomed Engn, Cleveland, OH 44106 USA.
RP Reichenberger, EJ (reprint author), Univ Connecticut, Ctr Hlth, Dept Reconstruct Sci, Ctr Regenerat Med & Skeletal Dev, Farmington, CT USA.
EM reichenberger@uchc.edu
OI Levine, Michael/0000-0003-0036-7809
FU National Institute of Dental and Craniofacial Research; Office of Rare
Diseases; NIH; Fibrous Dysplasia Foundation; Zimmer, Inc.; Zimmer
FX This article was developed as part of the Proceedings of the
International Meeting on Fibrous Dysplasia/McCune-Albright Syndrome and
Cherubism that took place at the National Institutes of Health,
Bethesda, MD, October 3-5, 2010. The meeting was supported by funding
from the National Institute of Dental and Craniofacial Research and
Office of Rare Diseases, NIH, and the Fibrous Dysplasia Foundation. The
publication of this manuscript was supported by the Fibrous Dysplasia
Foundation and an unrestricted grant from Zimmer, Inc.; This article has
been published as part of Orphanet Journal of Rare Diseases Volume 7
Supplement 1, 2012: International Meeting on Fibrous
Dysplasia/McCune-Albright Syndrome and Cherubism. The full contents of
the supplement are available online at
http://www.ojrd.com/supplements/7/S1. Publication of the proceedings was
funded by the Fibrous Dysplasia Foundation and an unrestricted grant
from Zimmer.
NR 102
TC 26
Z9 27
U1 0
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1750-1172
J9 ORPHANET J RARE DIS
JI Orphanet J. Rare Dis.
PD MAY 24
PY 2012
VL 7
SU 1
AR S5
DI 10.1186/1750-1172-7-S1-S5
PG 12
WC Genetics & Heredity; Medicine, Research & Experimental
SC Genetics & Heredity; Research & Experimental Medicine
GA 951YJ
UT WOS:000304756300005
PM 22640988
ER
PT J
AU Stanton, RP
Ippolito, E
Springfield, D
Lindaman, L
Wientroub, S
Leet, A
AF Stanton, Robert P.
Ippolito, Ernesto
Springfield, Dempsey
Lindaman, Lynn
Wientroub, Shlomo
Leet, Arabella
TI The surgical management of fibrous dysplasia of bone
SO ORPHANET JOURNAL OF RARE DISEASES
LA English
DT Article
ID SKELETAL LESIONS; PAMIDRONATE
AB The surgical management of Polyostotic Fibrous Dysplasia (FD) of bone is technically demanding. The most effective methods to manage the associated bone deformity remain unclear. The marked variation in the degree and pattern of bone involvement has made it difficult to acquire data to guide the surgeon's approach to these patients. In light of the paucity of data, but need for guidance, recognized experts in the management of these patients came together at the National Institutes of Health in Bethesda, Maryland as part of an International meeting to address issues related to fibrous dysplasia of bone to discuss and refine their recommendations regarding the surgical indications and preferred methods for the management of these challenging patients. The specific challenges, recommended approaches, and "lessons learned" are presented in hopes that surgeons faced with typical deformities can be guided in the surgical reconstruction of both children and adults with FD.
C1 [Stanton, Robert P.] Nemours Childrens Clin, Pensacola, FL USA.
[Ippolito, Ernesto] Univ Roma Tor Vergata, Dept Orthoped Surg, Rome, Italy.
[Springfield, Dempsey] Harvard Univ, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Lindaman, Lynn] Lindaman Orthoped, Des Moines, IA USA.
[Wientroub, Shlomo] Tel Aviv Univ, Dana Childrens Hosp, IL-69978 Tel Aviv, Israel.
[Leet, Arabella] Johns Hopkins Univ, Baltimore, MD USA.
RP Stanton, RP (reprint author), Nemours Childrens Clin, Pensacola, FL USA.
FU National Institute of Dental and Craniofacial Research; Fibrous
Dysplasia Foundation; Zimmer, Inc.; Zimmer; Office of Rare Diseases; NIH
FX This article was developed as part of the Proceedings of the
International Meeting on Fibrous Dysplasia/McCune-Albright Syndrome and
Cherubism that took place at the National Institutes of Health,
Bethesda, MD, October 3-5, 2010. The meeting was supported by funding
from the National Institute of Dental and Craniofacial Research and
Office of Rare Diseases, NIH, and the Fibrous Dysplasia Foundation. The
publication of this manuscript was supported by the Fibrous Dysplasia
Foundation and an unrestricted grant from Zimmer, Inc.; This article has
been published as part of Orphanet Journal of Rare Diseases Volume 7
Supplement 1, 2012: International Meeting on Fibrous
Dysplasia/McCune-Albright Syndrome and Cherubism. The full contents of
the supplement are available online at
http://www.ojrd.com/supplements/7/S1. Publication of the proceedings was
funded by the Fibrous Dysplasia Foundation and an unrestricted grant
from Zimmer.
NR 16
TC 19
Z9 23
U1 0
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1750-1172
J9 ORPHANET J RARE DIS
JI Orphanet J. Rare Dis.
PD MAY 24
PY 2012
VL 7
SU 1
AR S1
DI 10.1186/1750-1172-7-S1-S1
PG 9
WC Genetics & Heredity; Medicine, Research & Experimental
SC Genetics & Heredity; Research & Experimental Medicine
GA 951YJ
UT WOS:000304756300001
PM 22640754
ER
PT J
AU Gimenez-Cassina, A
Martinez-Francois, JR
Fisher, JK
Szlyk, B
Polak, K
Wiwczar, J
Tanner, GR
Lutas, A
Yellen, G
Danial, NN
AF Gimenez-Cassina, Alfredo
Martinez-Francois, Juan Ramon
Fisher, Jill K.
Szlyk, Benjamin
Polak, Klaudia
Wiwczar, Jessica
Tanner, Geoffrey R.
Lutas, Andrew
Yellen, Gary
Danial, Nika N.
TI BAD-Dependent Regulation of Fuel Metabolism and K-ATP Channel Activity
Confers Resistance to Epileptic Seizures
SO NEURON
LA English
DT Article
ID KETOGENIC DIET INCREASES; GLYCEMIC-INDEX TREATMENT; KAINIC ACID;
DEFICIENT MICE; CELL-DEATH; SYNAPTIC-TRANSMISSION; INSULIN-SECRETION;
DENTATE GYRUS; DUAL ROLE; BRAIN
AB Neuronal excitation can be substantially modulated by alterations in metabolism, as evident from the anticonvulsant effect of diets that reduce glucose utilization and promote ketone body metabolism. We provide genetic evidence that BAD, a protein with dual functions in apoptosis and glucose metabolism, imparts reciprocal effects on metabolism of glucose and ketone bodies in brain cells. These effects involve phosphoregulation of BAD and are independent of its apoptotic function. BAD modifications that reduce glucose metabolism produce a marked increase in the activity of metabolically sensitive K-ATP channels in neurons, as well as resistance to behavioral and electrographic seizures in vivo. Seizure resistance is reversed by genetic ablation of the K-ATP channel, implicating the BAD-K-ATP axis in metabolic control of neuronal excitation and seizure responses.
C1 [Martinez-Francois, Juan Ramon; Tanner, Geoffrey R.; Lutas, Andrew; Yellen, Gary] Harvard Univ, Sch Med, Dept Neurobiol, Boston, MA 02115 USA.
[Gimenez-Cassina, Alfredo; Danial, Nika N.] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
[Gimenez-Cassina, Alfredo; Fisher, Jill K.; Szlyk, Benjamin; Polak, Klaudia; Wiwczar, Jessica; Danial, Nika N.] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02215 USA.
RP Yellen, G (reprint author), Harvard Univ, Sch Med, Dept Neurobiol, Boston, MA 02115 USA.
EM gary_yellen@hms.harvard.edu; nika_danial@dfci.harvard.edu
OI Lutas, Andrew/0000-0002-6991-2898; Gimenez-Cassina,
Alfredo/0000-0002-2768-2350; Yellen, Gary/0000-0003-4228-7866
FU Ministerio de Educacion y Ciencia (MEC, Spain); Burroughs Wellcome Fund
Career Award in Biomedical Sciences; U.S. National Institutes of Health
[K01CA106596, R01 NS055031, R56 NS072142]; NIH [UL1 RR025758]; CURE
FX We thank Marina Godes and Juan Quijada for technical assistance and
animal husbandry; Gregory Holmes for advice on EEG acquisition and
analysis; Rosalind Segal, Bernardo Sabatini, Qiufu Ma, S. Robert Datta,
and members of the Danial and Yellen laboratories for critical reading
of this manuscript and valuable discussions; and E. Smith for manuscript
preparation. A.G.C. was supported by a postdoctoral fellowship from the
Ministerio de Educacion y Ciencia (MEC, Spain). N.N.D. is a recipient of
the Burroughs Wellcome Fund Career Award in Biomedical Sciences. This
work was supported by the U.S. National Institutes of Health grants
(K01CA106596 to N.N.D., R01 NS055031 to G.Y., and R56 NS072142 to N.N.D.
and G.Y.), Harvard Catalyst Pilot Award (based on NIH UL1 RR025758 to
N.N.D. and G.Y.), and a CURE Epilepsy Challenge Award (G.Y. and N.N.D.).
NR 66
TC 52
Z9 52
U1 0
U2 16
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
J9 NEURON
JI Neuron
PD MAY 24
PY 2012
VL 74
IS 4
BP 719
EP 730
DI 10.1016/j.neuron.2012.03.032
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 951VD
UT WOS:000304747200015
PM 22632729
ER
PT J
AU Zeigerer, A
Gilleron, J
Bogorad, RL
Marsico, G
Nonaka, H
Seifert, S
Epstein-Barash, H
Kuchimanchi, S
Peng, CG
Ruda, VM
Del Conte-Zerial, P
Hengstler, JG
Kalaidzidis, Y
Koteliansky, V
Zerial, M
AF Zeigerer, Anja
Gilleron, Jerome
Bogorad, Roman L.
Marsico, Giovanni
Nonaka, Hidenori
Seifert, Sarah
Epstein-Barash, Hila
Kuchimanchi, Satya
Peng, Chang Geng
Ruda, Vera M.
Del Conte-Zerial, Perla
Hengstler, Jan G.
Kalaidzidis, Yannis
Koteliansky, Victor
Zerial, Marino
TI Rab5 is necessary for the biogenesis of the endolysosomal system in vivo
SO NATURE
LA English
DT Article
ID POLARIZED EPITHELIAL-CELLS; LIPID-LIKE MATERIALS; RECYCLING ENDOSOMES;
MEMBRANE-FUSION; PLASMA-MEMBRANE; RNAI THERAPEUTICS; ENDOCYTIC PATHWAY;
TRAFFICKING; PROTEINS; TRANSPORT
AB An outstanding question is how cells control the number and size of membrane organelles. The small GTPase Rab5 has been proposed to be a master regulator of endosome biogenesis. Here, to test this hypothesis, we developed a mathematical model of endosome dependency on Rab5 and validated it by titrating down all three Rab5 isoforms in adult mouse liver using state-of-the-art RNA interference technology. Unexpectedly, the endocytic system was resilient to depletion of Rab5 and collapsed only when Rab5 decreased to a critical level. Loss of Rab5 below this threshold caused a marked reduction in the number of early endosomes, late endosomes and lysosomes, associated with a block of low-density lipoprotein endocytosis. Loss of endosomes caused failure to deliver apical proteins to the bile canaliculi, suggesting a requirement for polarized cargo sorting. Our results demonstrate for the first time, to our knowledge, the role of Rab5 as an endosome organizer in vivo and reveal the resilience mechanisms of the endocytic system.
C1 [Zeigerer, Anja; Gilleron, Jerome; Marsico, Giovanni; Nonaka, Hidenori; Seifert, Sarah; Del Conte-Zerial, Perla; Kalaidzidis, Yannis; Zerial, Marino] Max Planck Inst Mol Cell Biol & Genet, D-01307 Dresden, Germany.
[Bogorad, Roman L.; Koteliansky, Victor] MIT, Koch Inst Integrat Canc Res, Cambridge, MA 02139 USA.
[Epstein-Barash, Hila; Kuchimanchi, Satya; Peng, Chang Geng; Koteliansky, Victor] Alnylam Pharmaceut Inc, Cambridge, MA 02142 USA.
[Ruda, Vera M.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Ruda, Vera M.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Ruda, Vera M.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Hengstler, Jan G.] Leibniz Res Ctr Working Environm & Human Factors, D-44139 Dortmund, Germany.
[Kalaidzidis, Yannis] Moscow MV Lomonosov State Univ, Belozersky Inst Physicochem Biol, Moscow 119899, Russia.
RP Zerial, M (reprint author), Max Planck Inst Mol Cell Biol & Genet, D-01307 Dresden, Germany.
EM zerial@mpi-cbg.de
RI Bogorad, Roman/G-2609-2011; Hengstler, Jan/O-1415-2013; Kalaidzidis,
Yannis/H-3094-2016;
OI Kalaidzidis, Yannis/0000-0002-6137-1193; Zeigerer,
Anja/0000-0003-4072-0566; Gilleron, Jerome/0000-0002-6389-8685
FU Virtual Liver initiative; German Federal Ministry of Research and
Education (BMBF); Max Planck Society (MPG); DFG; Marie Curie Action,
Intra-European Fellowship [fp7-people-ief-2008]; EMBO
FX We acknowledge K. Simons, E. Knust, C. Fetzer, T. Galvez, G. O'Sullivan
and M. P. McShane for discussions and comments on the manuscript. We
thank W. John and A. Muench-Wuttke from the Biomedical Services Facility
for mouse care and injections. We acknowledge J. Peychl for the
management of the Light Microscopy Facility and K. Manygoats as well as
J.-M. Verbavatz for their support. We thank B. Bettencourt and J.
Hettinger for siRNA design and serum biochemistry assays, respectively.
This work was financially supported by the Virtual Liver initiative
(http://www.virtual-liver.de), funded by the German Federal Ministry of
Research and Education (BMBF), the Max Planck Society (MPG) and the DFG.
A.Z. was supported by a grant from Marie Curie Action, Intra-European
Fellowship (fp7-people-ief-2008) and J. G. from an EMBO long-term
fellowship.
NR 49
TC 119
Z9 122
U1 1
U2 34
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD MAY 24
PY 2012
VL 485
IS 7399
BP 465
EP 470
DI 10.1038/nature11133
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 946IH
UT WOS:000304344500035
PM 22622570
ER
PT J
AU Berger, MF
Hodis, E
Heffernan, TP
Deribe, YL
Lawrence, MS
Protopopov, A
Ivanova, E
Watson, IR
Nickerson, E
Ghosh, P
Zhang, HL
Zeid, R
Ren, XJ
Cibulskis, K
Sivachenko, AY
Wagle, N
Sucker, A
Sougnez, C
Onofrio, R
Ambrogio, L
Auclair, D
Fennell, T
Carter, SL
Drier, Y
Stojanov, P
Singer, MA
Voet, D
Jing, R
Saksena, G
Barretina, J
Ramos, AH
Pugh, TJ
Stransky, N
Parkin, M
Winckler, W
Mahan, S
Ardlie, K
Baldwin, J
Wargo, J
Schadendorf, D
Meyerson, M
Gabriel, SB
Golub, TR
Wagner, SN
Lander, ES
Getz, G
Chin, L
Garraway, LA
AF Berger, Michael F.
Hodis, Eran
Heffernan, Timothy P.
Deribe, Yonathan Lissanu
Lawrence, Michael S.
Protopopov, Alexei
Ivanova, Elena
Watson, Ian R.
Nickerson, Elizabeth
Ghosh, Papia
Zhang, Hailei
Zeid, Rhamy
Ren, Xiaojia
Cibulskis, Kristian
Sivachenko, Andrey Y.
Wagle, Nikhil
Sucker, Antje
Sougnez, Carrie
Onofrio, Robert
Ambrogio, Lauren
Auclair, Daniel
Fennell, Timothy
Carter, Scott L.
Drier, Yotam
Stojanov, Petar
Singer, Meredith A.
Voet, Douglas
Jing, Rui
Saksena, Gordon
Barretina, Jordi
Ramos, Alex H.
Pugh, Trevor J.
Stransky, Nicolas
Parkin, Melissa
Winckler, Wendy
Mahan, Scott
Ardlie, Kristin
Baldwin, Jennifer
Wargo, Jennifer
Schadendorf, Dirk
Meyerson, Matthew
Gabriel, Stacey B.
Golub, Todd R.
Wagner, Stephan N.
Lander, Eric S.
Getz, Gad
Chin, Lynda
Garraway, Levi A.
TI Melanoma genome sequencing reveals frequent PREX2 mutations
SO NATURE
LA English
DT Article
ID HUMAN CANCER; MALIGNANT-MELANOMA; SOMATIC MUTATIONS; INHIBITION;
PATTERNS; BRAF; REARRANGEMENTS; SPECIFICITY; ACTIVATION; SURVIVAL
AB Melanoma is notable for its metastatic propensity, lethality in the advanced setting and association with ultraviolet exposure early in life(1). To obtain a comprehensive genomic view of melanoma in humans, we sequenced the genomes of 25 metastatic melanomas and matched germline DNA. A wide range of point mutation rates was observed: lowest in melanomas whose primaries arose on non-ultraviolet-exposed hairless skin of the extremities (3 and 14 per megabase (Mb) of genome), intermediate in those originating from hair-bearing skin of the trunk (5-55 per Mb), and highest in a patient with a documented history of chronic sun exposure (111 per Mb). Analysis of whole-genome sequence data identified PREX2 (phosphatidylinositol-3,4,5-trisphosphate-dependent Rac exchange factor 2)-a PTEN-interacting protein and negative regulator of PTEN in breast cancer(2)-as a significantly mutated gene with a mutation frequency of approximately 14% in an independent extension cohort of 107 human melanomas. PREX2 mutations are biologically relevant, as ectopic expression of mutant PREX2 accelerated tumour formation of immortalized human melanocytes in vivo. Thus, whole-genome sequencing of human melanoma tumours revealed genomic evidence of ultraviolet pathogenesis and discovered a new recurrently mutated gene in melanoma.
C1 [Berger, Michael F.; Hodis, Eran; Lawrence, Michael S.; Nickerson, Elizabeth; Cibulskis, Kristian; Sivachenko, Andrey Y.; Sougnez, Carrie; Onofrio, Robert; Ambrogio, Lauren; Auclair, Daniel; Fennell, Timothy; Carter, Scott L.; Stojanov, Petar; Voet, Douglas; Jing, Rui; Saksena, Gordon; Barretina, Jordi; Ramos, Alex H.; Pugh, Trevor J.; Stransky, Nicolas; Parkin, Melissa; Winckler, Wendy; Mahan, Scott; Ardlie, Kristin; Baldwin, Jennifer; Meyerson, Matthew; Gabriel, Stacey B.; Golub, Todd R.; Lander, Eric S.; Getz, Gad; Chin, Lynda; Garraway, Levi A.] Broad Inst Harvard & MIT, Cambridge, MA 02142 USA.
[Heffernan, Timothy P.; Deribe, Yonathan Lissanu; Protopopov, Alexei; Ivanova, Elena; Watson, Ian R.; Ghosh, Papia; Zhang, Hailei; Zeid, Rhamy; Ren, Xiaojia; Wagle, Nikhil; Singer, Meredith A.; Pugh, Trevor J.; Meyerson, Matthew; Chin, Lynda; Garraway, Levi A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Wagle, Nikhil; Ramos, Alex H.; Pugh, Trevor J.; Meyerson, Matthew; Chin, Lynda; Garraway, Levi A.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Sucker, Antje; Schadendorf, Dirk] Univ Hosp Essen, Dept Dermatol, D-45122 Essen, Germany.
[Drier, Yotam] Weizmann Inst Sci, Dept Phys Complex Syst, IL-76100 Rehovot, Israel.
[Wargo, Jennifer] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Meyerson, Matthew; Golub, Todd R.; Garraway, Levi A.] Dana Farber Canc Inst, Ctr Canc Genome Discovery, Boston, MA 02115 USA.
[Golub, Todd R.] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Golub, Todd R.] Howard Hughes Med Inst, Chevy Chase, MD 20815 USA.
[Wagner, Stephan N.] Med Univ Vienna, Dept Dermatol, Div Immunol Allergy & Infect Dis, A-1090 Vienna, Austria.
[Wagner, Stephan N.] Austrian Acad Sci, CeMM Res Ctr Mol Med, A-1090 Vienna, Austria.
[Lander, Eric S.] Whitehead Inst Biomed Res, Cambridge, MA 02142 USA.
RP Chin, L (reprint author), Univ Texas MD Anderson Canc Ctr, Inst Appl Canc Sci, Dept Genom Med, Houston, TX 77030 USA.
EM LChin@mdanderson.org; levi_garraway@dfci.harvard.edu
RI Meyerson, Matthew/E-7123-2012; Drier, Yotam/K-5208-2012;
OI Drier, Yotam/0000-0003-1725-2995; Wagner, Stephan/0000-0003-4941-7029
FU National Human Genome Research Institute; National Cancer Institute;
FWF-Austrian Science Fund; NIH; Melanoma Research Alliance; Starr Cancer
Consortium; Burroughs-Wellcome Fund
FX Illumina sequencing was performed at the Broad Institute and array-based
genomic characterization and functional studies were performed at the
Belfer Institute of DFCI. We are grateful to the Broad Institute Genome
Sequencing Platform, Genome Analysis Platform and Biological Samples
Platform. This work was supported by the National Human Genome Research
Institute (S. B. G., E. S. L.), National Cancer Institute (M. M., L.
C.), FWF-Austrian Science Fund (S.N.W.), NIH Director's New Innovator
Award (L. A. G.), Melanoma Research Alliance (L. A. G., L. C.), Starr
Cancer Consortium (L.A.G.) and the Burroughs-Wellcome Fund (L.A.G.).
NR 29
TC 323
Z9 331
U1 5
U2 56
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD MAY 24
PY 2012
VL 485
IS 7399
BP 502
EP 506
DI 10.1038/nature11071
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 946IH
UT WOS:000304344500043
PM 22622578
ER
PT J
AU Baselga, J
Smith, BL
Rafferty, EA
Bombonati, A
AF Baselga, Jose
Smith, Barbara Lynn
Rafferty, Elizabeth A.
Bombonati, Alessandro
TI Case 16-2012: A 32-Year-Old Woman with HER2-Positive Breast Cancer
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID HER2/NEU-OVEREXPRESSING METASTATIC BREAST; NERVOUS-SYSTEM METASTASES;
MONOCLONAL-ANTIBODY; PHASE-II; PRIMARY TUMOR; 1ST-LINE TREATMENT; BRAIN
METASTASES; TRASTUZUMAB; SURVIVAL; CHEMOTHERAPY
C1 [Baselga, Jose] Massachusetts Gen Hosp, Div Hematol Oncol, Boston, MA 02114 USA.
[Smith, Barbara Lynn] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Rafferty, Elizabeth A.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Bombonati, Alessandro] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Baselga, Jose] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Smith, Barbara Lynn] Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA.
[Rafferty, Elizabeth A.] Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02115 USA.
[Bombonati, Alessandro] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
RP Baselga, J (reprint author), Massachusetts Gen Hosp, Div Hematol Oncol, Boston, MA 02114 USA.
NR 31
TC 6
Z9 6
U1 1
U2 5
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD MAY 24
PY 2012
VL 366
IS 21
BP 2018
EP 2026
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 946LL
UT WOS:000304353000013
PM 22621630
ER
PT J
AU Patel, SR
Sheth, SA
Mian, MK
Gale, JT
Greenberg, BD
Dougherty, DD
Eskandar, EN
AF Patel, Shaun R.
Sheth, Sameer A.
Mian, Matthew K.
Gale, John T.
Greenberg, Benjamin D.
Dougherty, Darin D.
Eskandar, Emad N.
TI Single-Neuron Responses in the Human Nucleus Accumbens during a
Financial Decision-Making Task
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID BEHAVIORAL-CONTROL; REWARD-SEEKING; DOPAMINE; PREDICTION; STRIATUM;
ERRORS; ROLES; BRAIN
AB Linking values to actions and evaluating expectations relative to outcomes are both central to reinforcement learningandarethoughtto underlie financial decision-making. However, neurophysiology studies of these processes in humans remain limited. Here, we recorded the activity of single human nucleus accumbens neurons while subjects performed a gambling task. We show that the nucleus accumbens encodes two signals related to subject behavior. First, we find that under relatively predictable conditions, single neuronal activity predicts future financial decisions on a trial-by-trial basis. Interestingly, we show that this activity continues to predict decisions even under conditions of uncertainty (e. g., when the probability of winning or losing is 50/50 and no particular financial choice predicts a rewarding outcome). Furthermore, we find that this activity occurs, on average, 2 s before the subjects physically manifest their decision. Second, we find that the nucleus accumbens encodes the difference between expectedandrealized outcomes, consistent with a prediction error signal. We show this activity occurs immediately after the subject has realized the outcome of the trial and is present on both the individual and population neuron levels. These results provide human single neuronal evidence that the nucleus accumbens is integral in making financial decisions.
C1 [Patel, Shaun R.; Sheth, Sameer A.; Mian, Matthew K.; Gale, John T.; Eskandar, Emad N.] Harvard Univ, Massachusetts Gen Hosp, Nayef Al Rodhan Labs, Sch Med,Dept Neurosurg, Boston, MA 02114 USA.
[Dougherty, Darin D.] Harvard Univ, Massachusetts Gen Hosp, Dept Psychiat, Sch Med, Boston, MA 02114 USA.
[Patel, Shaun R.] Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA.
[Greenberg, Benjamin D.] Butler Hosp, Dept Psychiat & Human Behav, Providence, RI 02906 USA.
[Greenberg, Benjamin D.] Brown Med Sch, Providence, RI 02906 USA.
RP Eskandar, EN (reprint author), Harvard Univ, Massachusetts Gen Hosp, Nayef Al Rodhan Labs, Sch Med,Dept Neurosurg, 55 Fruit St,White 502, Boston, MA 02114 USA.
EM eeskandar@partners.org
FU National Science Foundation [IOB 0645886]; National Institutes of Health
[NEI 1R01EY017658-01A1, NIDA 1R01NS063249]; NIMH [MH086400,
R25NS065743]; Klingenstein Foundation; Howard Hughes Medical Institute
FX This work was supported by grants from the National Science Foundation
(IOB 0645886), the National Institutes of Health (NEI 1R01EY017658-01A1,
NIDA 1R01NS063249, NIMH Conte Award MH086400, R25NS065743), the
Klingenstein Foundation, and the Howard Hughes Medical Institute. We
thank W.F. Asaad and L.J. Toth for their helpful comments and
discussion.
NR 24
TC 17
Z9 18
U1 0
U2 5
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD MAY 23
PY 2012
VL 32
IS 21
BP 7311
EP 7315
DI 10.1523/JNEUROSCI.0027-12.2012
PG 5
WC Neurosciences
SC Neurosciences & Neurology
GA 947HR
UT WOS:000304421000023
PM 22623676
ER
PT J
AU Ahmed, OJ
Mehta, MR
AF Ahmed, Omar J.
Mehta, Mayank R.
TI Running Speed Alters the Frequency of Hippocampal Gamma Oscillations
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID FREELY-MOVING RATS; HEAD-DIRECTION; PATH-INTEGRATION; PLACE CELLS; BAND
SYNCHRONIZATION; ENTORHINAL CORTEX; PYRAMIDAL CELLS; VISUAL-CORTEX;
UNIT-ACTIVITY; BEHAVING RAT
AB Successful spatial navigation is thought to employ a combination of at least two strategies: the following of landmark cues and path integration. Path integration requires that the brain use the speed and direction of movement in a meaningful way to continuously compute the position of the animal. Indeed, the running speed of rats modulates both the firing rate of neurons and the spectral properties of low frequency, theta oscillations seen in the local field potential (LFP) of the hippocampus, a region important for spatial memory formation. Higher frequency, gamma-band LFP oscillations are usually associated with decision-making, increased attention, and improved reaction times. Here, we show that increased running speed is accompanied by large, systematic increases in the frequency of hippocampal CA1 network oscillations spanning the entire gamma range (30-120 Hz) and beyond. These speed-dependent changes in frequency are seen on both linear tracks and two-dimensional platforms, and are thus independent of the behavioral task. Synchrony between anatomically distant CA1 regions also shifts to higher gamma frequencies as running speed increases. The changes in frequency are strongly correlated with changes in the firing rates of individual interneurons, consistent with models of gamma generation. Our results suggest that as a rat runs faster, there are faster gamma frequency transitions between sequential place cell-assemblies. This may help to preserve the spatial specificity of place cells and spatial memories at vastly different running speeds.
C1 [Ahmed, Omar J.] Brown Univ, Dept Neurosci, Providence, RI 02912 USA.
[Mehta, Mayank R.] Univ Calif Los Angeles, Integrat Ctr Learning & Memory, Keck Ctr Neurophys, Dept Phys & Astron,Dept Neurol,Dept Neurobiol, Los Angeles, CA 90095 USA.
RP Ahmed, OJ (reprint author), Massachusetts Gen Hosp, Dept Neurol, 55 Fruit St,Thier 423, Boston, MA 02114 USA.
EM omar.j.ahmed@gmail.com
FU NIMH [MH081477]; W.M. Keck foundation; Whitehall foundation; NSF
[0969034]; NIH/CRCNS [1-R01-MH-092925-01]; NARSAD
FX This work was supported by an NIMH Predoctoral Grant (MH081477) awarded
to O.J.A. and grants from the W.M. Keck foundation, the Whitehall
foundation, a NARSAD Young Investigator Award, NSF Career Award
#0969034, and NIH/CRCNS #1-R01-MH-092925-01 to M.R.M. We wish to thank
Dr. James Knierim for his helpful comments on a previous version of this
manuscript, and also Lucas Santos, James McFarland, Ammar Shaikhouni,
Luk Chong Yeung, Arvind Kumar, Annie van Beuningen, Alison Boyd, Ethan
Brown, Vivek Buch, Vivek Chellappa, Joshua Lai, Lyle Muller, Samuel
Reiter, Hank Schilling, and Valerie Yanofsky.
NR 68
TC 33
Z9 33
U1 0
U2 5
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD MAY 23
PY 2012
VL 32
IS 21
BP 7373
EP 7383
DI 10.1523/JNEUROSCI.5110-11.2012
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 947HR
UT WOS:000304421000030
PM 22623683
ER
PT J
AU Loewenstein, G
Asch, DA
Friedman, JY
Melichar, LA
Volpp, KG
AF Loewenstein, George
Asch, David A.
Friedman, Joelle Y.
Melichar, Lori A.
Volpp, Kevin G.
TI Can behavioural economics make us healthier?
SO BRITISH MEDICAL JOURNAL
LA English
DT Editorial Material
ID FINANCIAL INCENTIVES; ASYMMETRIC PATERNALISM; MEDICATION ADHERENCE;
RANDOMIZED-TRIAL; COPAYMENTS; VETERANS; INCREASE; SMOKING; IMPACT
AB Behavioural economics is becoming increasingly popular as a way to improve public health. George Loewenstein and colleagues point out some of the pitfalls and warn that it cannot be used as a substitute for conventional policies to tackle fundamental problems
C1 [Loewenstein, George] Carnegie Mellon Univ, Dept Social & Decis Sci, Pittsburgh, PA 15213 USA.
[Loewenstein, George; Asch, David A.; Friedman, Joelle Y.; Volpp, Kevin G.] Univ Penn, Ctr Hlth Incent & Behav Econ, Philadelphia, PA 19104 USA.
[Asch, David A.; Volpp, Kevin G.] Univ Penn, Dept Med, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Asch, David A.; Volpp, Kevin G.] Univ Penn, Wharton Sch, Dept Hlth Care Management, Philadelphia, PA 19104 USA.
[Asch, David A.; Volpp, Kevin G.] Philadelphia VA Med Ctr, Ctr Hlth Equ Res & Promot, Philadelphia, PA USA.
[Melichar, Lori A.] Robert Wood Johnson Fdn, Princeton, NJ 08540 USA.
RP Loewenstein, G (reprint author), Carnegie Mellon Univ, Dept Social & Decis Sci, 208 Porter Hall,5000 Forbes Ave, Pittsburgh, PA 15213 USA.
EM GL20@andrew.cmu.edu
OI Asch, David/0000-0002-7970-286X
NR 31
TC 17
Z9 17
U1 2
U2 27
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1756-1833
J9 BRIT MED J
JI Br. Med. J.
PD MAY 23
PY 2012
VL 344
AR e3482
DI 10.1136/bmj.e3482
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA 949QT
UT WOS:000304591500011
PM 22623635
ER
PT J
AU Volpp, KG
Loewenstein, G
Asch, DA
AF Volpp, Kevin G.
Loewenstein, George
Asch, David A.
TI Assessing Value in Health Care Programs
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
ID DISEASE
C1 [Volpp, Kevin G.; Asch, David A.] Univ Penn Sch, Philadelphia VA Med Ctr, Ctr Hlth Equity Res & Promot, Philadelphia, PA 19104 USA.
[Volpp, Kevin G.; Loewenstein, George; Asch, David A.] Univ Penn, Penn CMU Roybal Ctr Behav Econ & Hlth P30, Philadelphia, PA 19104 USA.
[Volpp, Kevin G.; Loewenstein, George; Asch, David A.] Univ Penn, Leonard Davis Inst Ctr Hlth Incent & Behav Econ, Philadelphia, PA 19104 USA.
[Volpp, Kevin G.; Asch, David A.] Univ Penn, Dept Med, Sch Med, Philadelphia, PA 19104 USA.
[Volpp, Kevin G.; Asch, David A.] Univ Penn, Dept Hlth Care Management, Wharton Sch Decis Sci, Philadelphia, PA 19104 USA.
[Loewenstein, George] Carnegie Mellon Univ, Dept Social & Decis Sci, Pittsburgh, PA 15213 USA.
RP Volpp, KG (reprint author), Univ Penn Sch, Philadelphia VA Med Ctr, Ctr Hlth Equity Res & Promot, 1120 Blockley Hall,423 Guardian Dr, Philadelphia, PA 19104 USA.
EM volpp70@wharton.upenn.edu
OI Asch, David/0000-0002-7970-286X
FU NIA NIH HHS [P30 AG034546]
NR 9
TC 7
Z9 7
U1 0
U2 6
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD MAY 23
PY 2012
VL 307
IS 20
BP 2153
EP 2154
DI 10.1001/jama.2012.3619
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 945YX
UT WOS:000304315200021
PM 22618919
ER
PT J
AU Hung, WW
Egol, KA
Zuckerman, JD
Siu, AL
AF Hung, William W.
Egol, Kenneth A.
Zuckerman, Joseph D.
Siu, Albert L.
TI Hip Fracture Management Tailoring Care for the Older Patient
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID RANDOMIZED-CONTROLLED-TRIAL; QUALITY-OF-LIFE; FEMORAL-NECK;
ELDERLY-PATIENTS; RISK-FACTORS; BIPOLAR HEMIARTHROPLASTY; FUNCTIONAL
RECOVERY; HOSPITAL DISCHARGE; HOME EXERCISE; VITAMIN-D
AB Hip fracture is a potentially devastating condition for older adults. Hip fracture leads to pain and immobilization with complications ranging from delirium to functional loss and death. Although a mainstay of treatment is orthopedic repair, a multidisciplinary comanagement approach, including medical specialists and rehabilitation, may maximize patient recovery. Using the case of Mr W, an older man who sustained a fall and hip fracture, we present evidence-based components of care both in the hospital and outpatient settings. Preoperatively, clinicians should correct medical abnormalities and consider the appropriateness, timing, and type of surgical repair in the context of the patient's life expectancy and goals of care. Perioperative care should include prophylaxis with antibiotics, chemoprophylaxis for venous thromboembolism, and correction of major clinical abnormalities prior to surgery. Pain control, delirium, and pressure ulcer prevention are important inpatient care elements. Multidisciplinary models incorporating these care elements can decrease complications during inpatient stay. Rehabilitation strategies should be tailored to patient needs; early mobilization followed by rehabilitation exercises in institutional, home, and group settings should be considered to maximize restoration of locomotive abilities. Attention to care transitions is necessary and treatment for osteoporosis should be considered. The road to recovery for hip fracture patients is long and most patients may not regain their prefracture functional status. Understanding and anticipating issues that may arise in the older patient with hip fracture, while delivering evidence-based care components, is necessary to maximize patient recovery.
C1 [Hung, William W.; Siu, Albert L.] Mt Sinai Sch Med, Dept Geriatr & Palliat Med, New York, NY 10029 USA.
[Hung, William W.; Siu, Albert L.] James J Peters Vet Affairs Med Ctr, Geriatr Res Educ & Clin Ctr, Bronx, NY USA.
[Hung, William W.; Siu, Albert L.] James J Peters Vet Affairs Med Ctr, Dev Res Enhancement Award Program, Bronx, NY USA.
[Hung, William W.; Siu, Albert L.] James J Peters Vet Affairs Med Ctr, Hlth Serv Res, Bronx, NY USA.
[Egol, Kenneth A.; Zuckerman, Joseph D.] NYU, Hosp Joint Dis, Dept Orthopaed Surg, New York, NY USA.
RP Hung, WW (reprint author), Mt Sinai Sch Med, Dept Geriatr & Palliat Med, 1 Gustave L Levy Pl,Box 1070, New York, NY 10029 USA.
EM william.hung@mssm.edu
FU Exactech; Orthopaedic Research & Education Foundation; Orthopaedic
Trauma Association; New York Academy of Medicine; Claude D. Pepper Older
Americans Independence Center at Mount Sinai School of Medicine
[P30-AG028741]; SCAN Foundation
FX All authors have completed and submitted the ICMJE Form for Disclosure
of Potential Conflicts of Interest. Dr Egol reports receipt of
consultancy fees and royalties from Exactech; grants or pending grants
from the Orthopaedic Research & Education Foundation and the Orthopaedic
Trauma Association; and holding stock/stock options with Johnson &
Johnson. The other authors report no disclosures.; Dr Hung is currently
supported by the New York Academy of Medicine Hoar Fellowship. This
article was supported in part by the Claude D. Pepper Older Americans
Independence Center at Mount Sinai School of Medicine (P30-AG028741).
The Care of the Aging Patient series is made possible by funding from
The SCAN Foundation.
NR 86
TC 53
Z9 58
U1 4
U2 22
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD MAY 23
PY 2012
VL 307
IS 20
BP 2185
EP 2194
DI 10.1001/jama.2012.4842
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 945YX
UT WOS:000304315200028
PM 22618926
ER
PT J
AU Henrickson, SE
Altshuler, D
AF Henrickson, Sarah E.
Altshuler, David
TI Risk and Return for the Clinician-Investigator
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Article
AB In this case study, an early-career clinician-investigator discusses impending and future career issues in an interview with an established translational scientist, who then shares ideas about pursuing clinically informed research questions.
C1 [Henrickson, Sarah E.] Childrens Hosp, Boston Combined Residency Program Pediat, Boston, MA 02115 USA.
[Henrickson, Sarah E.] Boston Med Ctr, Boston, MA 02115 USA.
[Henrickson, Sarah E.] Harvard Univ, Sch Med, Dept Microbiol & Immunobiol, Boston, MA 02115 USA.
[Altshuler, David] Cambridge Ctr, Program Med & Populat Genet, Broad Inst Harvard & MIT, Cambridge, MA 02142 USA.
[Altshuler, David] Harvard Univ, Dept Genet, Sch Med, Boston, MA 02116 USA.
[Altshuler, David] Harvard Univ, Dept Med, Sch Med, Boston, MA 02116 USA.
[Altshuler, David] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
[Altshuler, David] Massachusetts Gen Hosp, Diabet Unit, Boston, MA 02114 USA.
RP Henrickson, SE (reprint author), Childrens Hosp, Boston Combined Residency Program Pediat, 300 Longwood Ave, Boston, MA 02115 USA.
EM sarah.henrickson@childrens.harvard.edu
RI Altshuler, David/A-4476-2009
OI Altshuler, David/0000-0002-7250-4107
NR 2
TC 3
Z9 3
U1 0
U2 0
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1946-6234
J9 SCI TRANSL MED
JI Sci. Transl. Med.
PD MAY 23
PY 2012
VL 4
IS 135
AR 135cm6
DI 10.1126/scitranslmed.3004110
PG 4
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 946PS
UT WOS:000304365700007
PM 22623733
ER
PT J
AU Vogelstein, B
Roberts, NJ
Vogelstein, JT
Parmigiani, G
Kinzler, KW
Velculescu, VE
AF Vogelstein, Bert
Roberts, Nicholas J.
Vogelstein, Joshua T.
Parmigiani, Giovanni
Kinzler, Kenneth W.
Velculescu, Victor E.
TI Response to Comments on "The Predictive Capacity of Personal Genome
Sequencing"
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Letter
AB The power of personal genome sequencing to elucidate disease pathogenesis will ensure that it will become an essential tool in medical practice, but recognizing its limitations for improving public health will minimize false expectations and foster the most fruitful investigations.
C1 [Vogelstein, Bert; Roberts, Nicholas J.; Kinzler, Kenneth W.; Velculescu, Victor E.] Johns Hopkins Kimmel Canc Ctr, Ludwig Ctr Canc Genet & Therapeut, Baltimore, MD 21231 USA.
[Vogelstein, Bert; Roberts, Nicholas J.; Kinzler, Kenneth W.; Velculescu, Victor E.] Johns Hopkins Kimmel Canc Ctr, Howard Hughes Med Inst, Baltimore, MD 21231 USA.
[Vogelstein, Joshua T.] Johns Hopkins Univ, Dept Appl Math & Stat, Baltimore, MD 21287 USA.
[Parmigiani, Giovanni] Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Parmigiani, Giovanni] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
RP Vogelstein, B (reprint author), Johns Hopkins Kimmel Canc Ctr, Ludwig Ctr Canc Genet & Therapeut, Baltimore, MD 21231 USA.
EM vogelbe@jhmi.edu
NR 8
TC 1
Z9 1
U1 0
U2 6
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1946-6234
J9 SCI TRANSL MED
JI Sci. Transl. Med.
PD MAY 23
PY 2012
VL 4
IS 135
AR 135lr3
DI 10.1126/scitranslmed.3004246
PG 2
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 946PS
UT WOS:000304365700006
ER
PT J
AU MacArthur, DG
AF MacArthur, Daniel G.
TI Challenges in clinical genomics
SO GENOME MEDICINE
LA English
DT Editorial Material
AB A report on the Genomic Disorders 2012: Genomics of Rare Diseases meeting, Hinxton, UK, 21-23 March 2012.
C1 [MacArthur, Daniel G.] Massachusetts Gen Hosp, Analyt & Translat Genet Unit, Boston, MA 02114 USA.
[MacArthur, Daniel G.] Broad Inst Harvard & MIT, Program Med & Populat Genet, Cambridge, MA 02142 USA.
RP MacArthur, DG (reprint author), Broad Inst Harvard & MIT, Program Med & Populat Genet, Cambridge, MA 02142 USA.
EM macarthur@atgu.mgh.harvard.edu
NR 0
TC 2
Z9 2
U1 0
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1756-994X
J9 GENOME MED
JI Genome Med.
PD MAY 22
PY 2012
VL 4
AR 43
DI 10.1186/gm342
PG 3
WC Genetics & Heredity
SC Genetics & Heredity
GA 084WO
UT WOS:000314571000001
PM 22621759
ER
PT J
AU Zhang, C
Montgomery, TA
Fischer, SEJ
Garcia, SMDA
Riedel, CG
Fahlgren, N
Sullivan, CM
Carrington, JC
Ruvkun, G
AF Zhang, Chi
Montgomery, Taiowa A.
Fischer, Sylvia E. J.
Garcia, Susana M. D. A.
Riedel, Christian G.
Fahlgren, Noah
Sullivan, Christopher M.
Carrington, James C.
Ruvkun, Gary
TI The Caenorhabditis elegans RDE-10/RDE-11 Complex Regulates RNAi by
Promoting Secondary siRNA Amplification
SO CURRENT BIOLOGY
LA English
DT Article
ID GERM-LINE DEVELOPMENT; C-ELEGANS; INTERFERENCE; GENES; DCR-1; PATHWAYS;
HELICASE; HOMOLOG; REVEALS; RDE-1
AB Background: In nematodes, plants, and fungi, RNAi is remarkably potent and persistent due to the amplification of initial silencing signals by RNA-dependent RNA polymerases (RdRPs). In Caenorhabditis elegans (C. elegans), the interaction between the RNA-induced silencing complex (RISC) loaded with primary small interfering RNAs (siRNAs) and the target messenger RNA (mRNA) leads to the recruitment of RdRPs and synthesis of secondary siRNAs using the target mRNA as the template. The mechanism and genetic requirements for secondary siRNA accumulation are not well understood.
Results: From a forward genetic screen for C. elegans genes required for RNAi, we identified rde-10, and through proteomic analysis of RDE-10-interacting proteins, we identified a protein complex containing the new RNAi factor RDE-11, the known RNAi factors RSD-2 and ERGO-1, and other candidate RNAi factors. The RNAi defective genes rde-10 and rde-11 encode a novel protein and a RING-type zinc finger domain protein, respectively. Mutations in rde-10 and rde-11 genes cause dosage-sensitive RNAi deficiencies: these mutants are resistant to low dosage but sensitive to high dosage of double-stranded RNAs. We assessed the roles of rde-10, rde-11, and other dosage-sensitive RNAi-defective genes rsd-2, rsd-6, and haf-6 in both exogenous and endogenous small RNA pathways using high-throughput sequencing and qRT-PCR. These genes are required for the accumulation of secondary siRNAs in both exogenous and endogenous RNAi pathways.
Conclusions: The RDE-10/RDE-11 complex is essential for the amplification of RNAi in C. elegans by promoting secondary siRNA accumulation.
C1 [Zhang, Chi; Montgomery, Taiowa A.; Fischer, Sylvia E. J.; Garcia, Susana M. D. A.; Riedel, Christian G.; Ruvkun, Gary] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
[Zhang, Chi; Montgomery, Taiowa A.; Fischer, Sylvia E. J.; Garcia, Susana M. D. A.; Riedel, Christian G.; Ruvkun, Gary] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02114 USA.
[Fahlgren, Noah; Carrington, James C.] Donald Danforth Plant Sci Ctr, St Louis, MO 63132 USA.
[Sullivan, Christopher M.] Oregon State Univ, Ctr Genome Res & Biocomp, Corvallis, OR 97331 USA.
RP Ruvkun, G (reprint author), Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
EM ruykun@molbio.mgh.harvard.edu
RI Carrington, James/A-4656-2012; Fahlgren, Noah/D-4404-2011;
OI Carrington, James/0000-0003-3572-129X; Fahlgren,
Noah/0000-0002-5597-4537; Riedel, Christian/0000-0002-3689-8022;
Montgomery, Taiowa/0000-0001-7857-3253
FU National Institutes of Health (NIH) [GM44619, AI43288]; National Science
Foundation [MCB-1231726]; MGH ECOR; Damon Runyon Cancer Research
Foundation [DRG-2029-09]; American Heart Association [0825938D];
European Molecular Biology Organization; Human Frontier Science Program
FX We are very grateful to Huan Yang and Ho Yi Mak for rde-10 and rde-11
mutant and transgenic strains, as well as communicating unpublished
data. We thank Darryl Conte, Weifeng Gu, Pedro Batista, and Daniel
Chaves for providing protocols for immunoprecipitation and generation of
small RNA cDNA libraries for deep sequencing; Xiaoyun Wu for protocols
for large-scale immunoprecipitation; John Asara for mass spectrometry
analysis; Christian Daly, Jiangwen Zhang, Mark Borowsky, Tammy Gillis,
and Kaleena Shirley for Illumina deep sequencing and computational
assistance; and the Caenorhabditis Genetics Center and Shohei Mitani for
strains. This work was supported by a grant to G.R. from National
Institutes of Health (NIH) (GM44619), grants to J.C.C. from the National
Science Foundation (MCB-1231726) and NIH (AI43288), fellowships to C.Z.
and S.E.J.F. from the MGH ECOR Fund for Medical Discovery, fellowship to
T.A.M. from the Damon Runyon Cancer Research Foundation (DRG-2029-09),
fellowship to S.M.D.A.G. from the American Heart Association (0825938D),
and fellowships to C.G.R. from the European Molecular Biology
Organization and the Human Frontier Science Program.
NR 37
TC 18
Z9 28
U1 2
U2 19
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0960-9822
J9 CURR BIOL
JI Curr. Biol.
PD MAY 22
PY 2012
VL 22
IS 10
BP 881
EP 890
DI 10.1016/j.cub.2012.04.011
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 947LY
UT WOS:000304432700021
PM 22542102
ER
PT J
AU Tseng, ZH
Secemsky, EA
Dowdy, D
Vittinghoff, E
Moyers, B
Wong, JK
Havlir, DV
Hsue, PY
AF Tseng, Zian H.
Secemsky, Eric A.
Dowdy, David
Vittinghoff, Eric
Moyers, Brian
Wong, Joseph K.
Havlir, Diane V.
Hsue, Priscilla Y.
TI Sudden Cardiac Death in Patients With Human Immunodeficiency Virus
Infection
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Article
DE AIDS; arrhythmia; death; sudden
ID LEFT-VENTRICULAR DYSFUNCTION; CONGESTIVE-HEART-FAILURE;
MYOCARDIAL-INFARCTION; ANTIRETROVIRAL THERAPY; HIV; MORTALITY;
POPULATION; COMMUNITY; DISEASE; COHORT
AB Objectives The aim of this study was to determine the incidence and clinical characteristics of sudden cardiac death (SCD) in patients with human immunodeficiency virus (HIV) infection.
Background As the HIV-infected population ages, cardiovascular disease prevalence and mortality are increasing, but the incidence and features of SCD have not yet been described.
Methods The records of 2,860 consecutive patients in a public HIV clinic in San Francisco between April 2000 and August 2009 were examined. Identification of deaths, causes of death, and clinical characteristics were obtained by search of the National Death Index and/or clinic records. SCDs were determined using published retrospective criteria: 1) the International Classification of Diseases-10th Revision, code for all cardiac causes of death; and (2) circumstances of death meeting World Health Organization criteria.
Results Of 230 deaths over a median of 3.7 years of follow-up, 30 (13%) met SCD criteria, 131 (57%) were due to acquired immune deficiency syndrome (AIDS), 25 (11%) were due to other (natural) diseases, and 44 (19%) were due to overdoses, suicides, or unknown causes. SCDs accounted for 86% of all cardiac deaths (30 of 35). The mean SCD rate was 2.6 per 1,000 person-years (95% confidence interval: 1.8 to 3.8), 4.5-fold higher than expected. SCDs occurred in older patients than did AIDS deaths (mean 49.0 vs. 44.9 years, p = 0.02). Compared with AIDS and natural deaths combined, SCDs had a higher prevalence of prior myocardial infarction (17% vs. 1%, p < 0.0005), cardiomyopathy (23% vs. 3%, p < 0.0005), heart failure (30% vs. 9%, p = 0.004), and arrhythmias (20% vs. 3%, p = 0.003).
Conclusions SCDs account for most cardiac and many non-AIDS natural deaths in HIV-infected patients. Further investigation is needed to ascertain underlying mechanisms, which may include inflammation, antiretroviral therapy interruption, and concomitant medications. (J Am Coll Cardiol 2012;59:1891-6) (C) 2012 by the American College of Cardiology Foundation
C1 [Tseng, Zian H.; Moyers, Brian] Univ Calif San Francisco, Cardiac Electrophysiol Sect, Div Cardiol, San Francisco, CA 94143 USA.
[Secemsky, Eric A.] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA.
[Dowdy, David] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Vittinghoff, Eric] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Wong, Joseph K.] San Francisco VA Med Ctr, Dept Med, San Francisco, CA USA.
[Havlir, Diane V.] Univ Calif San Francisco, San Francisco Gen Hosp, Div HIV AIDS, San Francisco, CA 94143 USA.
[Hsue, Priscilla Y.] Univ Calif San Francisco, San Francisco Gen Hosp, Div Cardiol, San Francisco, CA 94143 USA.
RP Tseng, ZH (reprint author), Univ Calif San Francisco, Cardiac Electrophysiol Sect, Div Cardiol, 500 Parnassus Ave,MU-433,Box 1354, San Francisco, CA 94143 USA.
EM zhtseng@medicine.ucsf.edu
FU National Heart, Lung, and Blood Institute [5R01 HL102090, 5R01 HL095130,
5R01 HL091526]; Veterans Affairs Merit Review grant [R01 NS501132];
National Institutes of Health [K24 AI51982]
FX This work was supported by grants 5R01 HL102090 (Dr. Tseng), 5R01
HL095130 (Dr. Hsue), and 5R01 HL091526 (Dr. Hsue) from the National
Heart, Lung, and Blood Institute; Veterans Affairs Merit Review grant
R01 NS501132 (Dr. Wong); and grant K24 AI51982 (Dr. Havlir) from the
National Institutes of Health. Dr. Tseng has also received minor
honorarium from Biotronik. All other authors have reported that they
have no relationships relevant to the contents of this paper to
disclose.
NR 27
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Z9 71
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD MAY 22
PY 2012
VL 59
IS 21
BP 1891
EP 1896
DI 10.1016/j.jacc.2012.02.024
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 942PF
UT WOS:000304057200008
PM 22595409
ER
PT J
AU Wein, MN
Jones, DC
Shim, JH
Aliprantis, AO
Sulyanto, R
Lazarevic, V
Poliachik, SL
Gross, TS
Glimcher, LH
AF Wein, Marc N.
Jones, Dallas C.
Shim, Jae-Hyuck
Aliprantis, Antonios O.
Sulyanto, Rosalyn
Lazarevic, Vanja
Poliachik, Sandra L.
Gross, Ted S.
Glimcher, Laurie H.
TI Control of bone resorption in mice by Schnurri-3
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE cAMP response element binding protein; receptor activator of nuclear
factor-kappa B ligand; secondary hyperparathyroidism
ID DISTANT TRANSCRIPTIONAL ENHANCER; LIGAND GENE-EXPRESSION; RECEPTOR
ACTIVATOR; 1,25-DIHYDROXYVITAMIN D-3; OSTEOCLAST FORMATION; TARGETED
DELETION; RANKL; CELLS; MASS; OSTEOPOROSIS
AB Mice lacking the large zinc finger protein Schnurri-3 (Shn3) display increased bone mass, in part, attributable to augmented osteoblastic bone formation. Here, we show that in addition to regulating bone formation, Shn3 indirectly controls bone resorption by osteoclasts in vivo. Although Shn3 plays no cell-intrinsic role in osteoclasts, Shn3-deficient animals show decreased serum markers of bone turnover. Mesenchymal cells lacking Shn3 are defective in promoting osteoclastogenesis in response to selective stimuli, likely attributable to reduced expression of the key osteoclastogenic factor receptor activator of nuclear factor-kappa B ligand. The bone phenotype of Shn3-deficient mice becomes more pronounced with age, and mice lacking Shn3 are completely resistant to disuse osteopenia, a process that requires functional osteoclasts. Finally, selective deletion of Shn3 in the mesenchymal lineage recapitulates the high bone mass phenotype of global Shn3 KO mice, including reduced osteoclastic bone catabolism in vivo, indicating that Shn3 expression in mesenchymal cells directly controls osteoblastic bone formation and indirectly regulates osteoclastic bone resorption.
C1 [Wein, Marc N.; Jones, Dallas C.; Shim, Jae-Hyuck; Aliprantis, Antonios O.; Sulyanto, Rosalyn; Lazarevic, Vanja; Glimcher, Laurie H.] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
[Poliachik, Sandra L.; Gross, Ted S.] Univ Washington, Dept Orthoped & Sports Med, Seattle, WA 98104 USA.
[Wein, Marc N.] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
[Aliprantis, Antonios O.; Glimcher, Laurie H.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Rheumatol Allergy & Immunol,Dept Med, Boston, MA 02115 USA.
[Glimcher, Laurie H.] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[Glimcher, Laurie H.] Massachusetts Gen Hosp, MIT, Ragon Inst, Charlestown, MA 02129 USA.
[Glimcher, Laurie H.] Harvard Univ, Charlestown, MA 02129 USA.
RP Glimcher, LH (reprint author), Weill Cornell Med Coll, Deans Off, New York, NY 10021 USA.
EM lglimche@med.cornell.edu
RI Lazarevic, Vanja/B-1160-2009
FU National Institutes of Health [HD055601, K99AR055668]; National
Institute of Arthritis and Musculoskeletal and Skin Diseases
[K08AR054859, R01AR060363]
FX We thank Dorothy Zhang for histological preparations, Nicholas Brady and
Mary Bouxsein for mu CT analyses, David Burr for histomorphometric
analysis, Merck pharmaceuticals for assistance in generating the
Shn3f/f mice, and Charles O'Brien for the RANKL reporter
reagents. This work was supported by National Institutes of Health
Grants HD055601 (to L.H.G.) and K99AR055668 (to D.C.J.). A.O.A. holds a
Career Award for Medical Scientists from the Burroughs Wellcome Fund and
was supported by Grants K08AR054859 and R01AR060363 from the National
Institute of Arthritis and Musculoskeletal and Skin Diseases.
NR 38
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U1 0
U2 0
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD MAY 22
PY 2012
VL 109
IS 21
BP 8173
EP 8178
DI 10.1073/pnas.1205848109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 947QY
UT WOS:000304445800054
PM 22573816
ER
PT J
AU Meng, M
Cherian, T
Singal, G
Sinha, P
AF Meng, Ming
Cherian, Tharian
Singal, Gaurav
Sinha, Pawan
TI Lateralization of face processing in the human brain
SO PROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES
LA English
DT Article
DE face perception; pattern recognition; fusiform; lateralization;
functional magnetic resonance imaging
ID HUMAN FUSIFORM GYRUS; HUMAN VISUAL-CORTEX; OBJECT; RECOGNITION;
ASYMMETRIES; HEMISPHERE; PERCEPTION; SYSTEM; AREA; PART
AB Are visual face processing mechanisms the same in the left and right cerebral hemispheres? The possibility of such 'duplicated processing' seems puzzling in terms of neural resource usage, and we currently lack a precise characterization of the lateral differences in face processing. To address this need, we have undertaken a three-pronged approach. Using functional magnetic resonance imaging, we assessed cortical sensitivity to facial semblance, the modulatory effects of context and temporal response dynamics. Results on all three fronts revealed systematic hemispheric differences. We found that: (i) activation patterns in the left fusiform gyrus correlate with image-level face-semblance, while those in the right correlate with categorical face/non-face judgements. (ii) Context exerts significant excitatory/inhibitory influence in the left, but has limited effect on the right. (iii) Face-selectivity persists in the right even after activity on the left has returned to baseline. These results provide important clues regarding the functional architecture of face processing, suggesting that the left hemisphere is involved in processing 'low-level' face semblance, and perhaps is a precursor to categorical 'deep' analyses on the right.
C1 [Meng, Ming] Dartmouth Coll, Dept Psychol & Brain Sci, Hanover, NH 03755 USA.
[Cherian, Tharian] Univ Chicago, Pritzker Sch Med, Div Biol Sci, Sch Med, Chicago, IL 60637 USA.
[Singal, Gaurav] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Sinha, Pawan] MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA.
RP Meng, M (reprint author), Dartmouth Coll, Dept Psychol & Brain Sci, Hanover, NH 03755 USA.
EM ming.meng@dartmouth.edu
FU John Merck Foundation; Simons Foundation; James McDonnell Foundation;
NEI (NIH) [R21-EY015521]
FX The study was approved by the MIT Committee on the Use of Humans as
Experimental Subjects (COUHES). The authors wish to thank Profs Richard
Held, Sheng He, Nancy Kanwisher, Jim DiCarlo and Tomaso Poggio for their
helpful feedback regarding this work. Support for this work was provided
by the John Merck Foundation, the Simons Foundation, the James McDonnell
Foundation and a grant from the NEI (NIH, grant number R21-EY015521).
NR 34
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U1 2
U2 20
PU ROYAL SOC
PI LONDON
PA 6-9 CARLTON HOUSE TERRACE, LONDON SW1Y 5AG, ENGLAND
SN 0962-8452
J9 P ROY SOC B-BIOL SCI
JI Proc. R. Soc. B-Biol. Sci.
PD MAY 22
PY 2012
VL 279
IS 1735
BP 2052
EP 2061
DI 10.1098/rspb.2011.1784
PG 10
WC Biology; Ecology; Evolutionary Biology
SC Life Sciences & Biomedicine - Other Topics; Environmental Sciences &
Ecology; Evolutionary Biology
GA 925RT
UT WOS:000302779600023
PM 22217726
ER
PT J
AU Musunuru, K
Romaine, SPR
Lettre, G
Wilson, JG
Volcik, KA
Tsai, MY
Taylor, HA
Schreiner, PJ
Rotter, JI
Rich, SS
Redline, S
Psaty, BM
Papanicolaou, GJ
Ordovas, JM
Liu, K
Krauss, RM
Glazer, NL
Gabriel, SB
Fornage, M
Cupples, LA
Buxbaum, SG
Boerwinkle, E
Ballantyne, CM
Kathiresan, S
Rader, DJ
AF Musunuru, Kiran
Romaine, Simon P. R.
Lettre, Guillaume
Wilson, James G.
Volcik, Kelly A.
Tsai, Michael Y.
Taylor, Herman A., Jr.
Schreiner, Pamela J.
Rotter, Jerome I.
Rich, Stephen S.
Redline, Susan
Psaty, Bruce M.
Papanicolaou, George J.
Ordovas, Jose M.
Liu, Kiang
Krauss, Ronald M.
Glazer, Nicole L.
Gabriel, Stacey B.
Fornage, Myriam
Cupples, L. Adrienne
Buxbaum, Sarah G.
Boerwinkle, Eric
Ballantyne, Christie M.
Kathiresan, Sekar
Rader, Daniel J.
TI Multi-Ethnic Analysis of Lipid-Associated Loci: The NHLBI CARe Project
SO PLOS ONE
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; DENSITY-LIPOPROTEIN CHOLESTEROL;
CORONARY-HEART-DISEASE; TRIGLYCERIDES; DESIGN; GENES; RISK
AB Background: Whereas it is well established that plasma lipid levels have substantial heritability within populations, it remains unclear how many of the genetic determinants reported in previous studies (largely performed in European American cohorts) are relevant in different ethnicities.
Methodology/Principal Findings: We tested a set of similar to 50,000 polymorphisms from similar to 2,000 candidate genes and genetic loci from genome-wide association studies (GWAS) for association with low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) in 25,000 European Americans and 9,000 African Americans in the National Heart, Lung, and Blood Institute (NHLBI) Candidate Gene Association Resource (CARe). We replicated associations for a number of genes in one or both ethnicities and identified a novel lipid-associated variant in a locus harboring ICAM1. We compared the architecture of genetic loci associated with lipids in both African Americans and European Americans and found that the same genes were relevant across ethnic groups but the specific associated variants at each gene often differed.
Conclusions/Significance: We identify or provide further evidence for a number of genetic determinants of plasma lipid levels through population association studies. In many loci the determinants appear to differ substantially between African Americans and European Americans.
C1 [Musunuru, Kiran; Gabriel, Stacey B.] Broad Inst, Cambridge, MA USA.
[Musunuru, Kiran; Kathiresan, Sekar] Harvard Univ, Sch Med, Boston, MA USA.
[Musunuru, Kiran; Kathiresan, Sekar] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Romaine, Simon P. R.] Univ Leeds, Leeds, W Yorkshire, England.
[Lettre, Guillaume] Univ Montreal, Montreal Heart Inst, Montreal, PQ, Canada.
[Wilson, James G.; Taylor, Herman A., Jr.] Univ Mississippi, Med Ctr, Jackson, MS 39216 USA.
[Volcik, Kelly A.; Fornage, Myriam; Boerwinkle, Eric] Univ Texas Hlth Sci Ctr Houston, Houston, TX USA.
[Schreiner, Pamela J.] Univ Minnesota, Sch Publ Hlth, Minneapolis, MN USA.
[Taylor, Herman A., Jr.; Buxbaum, Sarah G.] Jackson State Univ, Jackson, MS USA.
[Rotter, Jerome I.] Cedars Sinai Med Ctr, Inst Med Genet, Los Angeles, CA 90048 USA.
[Rich, Stephen S.] Univ Virginia, Sch Med, Charlottesville, VA 22908 USA.
[Redline, Susan] Univ Hosp, Case Med Ctr, Cleveland, OH USA.
[Redline, Susan] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Psaty, Bruce M.] Univ Washington, Seattle, WA 98195 USA.
[Psaty, Bruce M.] Grp Hlth Cooperat Puget Sound, Grp Hlth Res Inst, Seattle, WA USA.
[Papanicolaou, George J.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Ordovas, Jose M.] Tufts Univ, Human Nutr Res Ctr Aging, JM United States Dept Agr, Boston, MA 02111 USA.
[Krauss, Ronald M.] Childrens Hosp Oakland, Res Inst, Oakland, CA 94609 USA.
[Glazer, Nicole L.; Cupples, L. Adrienne] Boston Univ, Boston, MA 02215 USA.
[Liu, Kiang] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Cupples, L. Adrienne] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Ballantyne, Christie M.] Baylor Coll Med, Houston, TX 77030 USA.
[Rader, Daniel J.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
RP Musunuru, K (reprint author), Broad Inst, Cambridge, MA USA.
EM cmb@bcm.edu; sekar@broadinstitute.org; rader@mail.med.upenn.edu
RI Buxbaum, Sarah/E-1970-2013;
OI Buxbaum, Sarah/0000-0002-4886-3564; Cupples, L.
Adrienne/0000-0003-0273-7965
FU T32 grant in Cell and Molecular Training for Cardiovascular Biology from
the National Heart, Lung, and Blood Institute [K99-HL098364]; University
of Virginia [R01-HL-071205]
FX The following nine parent studies have contributed parent study data,
ancillary study data, and DNA samples through the Broad Institute of
Massachusetts Institute of Technology and Harvard (N01-HC-65226):
Atherosclerosis Risk in Communities: University of North Carolina at
Chapel Hill (N01-HC-55015, N01-HC-55018), Baylor Medical College
(N01-HC-55016), University of Mississippi Medical Center (N01-HC-55021),
University of Minnesota (N01-HC-55019), Johns Hopkins University
(N01-HC-55020), University of Texas, Houston (N01-HC-55022);
Cardiovascular Health Study: University of Washington (N01-HC-85079,
N01-HC-55222, U01-HL-080295), Wake Forest University (N01-HC-85080),
Johns Hopkins University (N01-HC-85081, N01-HC-15103), University of
Pittsburgh (N01-HC-85082), University of California, Davis
(N01-HC-85083), University of California, Irvine (N01-HC-85084), New
England Medical Center (N01-HC-85085), University of Vermont
(N01-HC-85086), Georgetown University (N01-HC-35129), University of
Wisconsin (N01-HC-75150); Cleveland Family Study: Case Western Reserve
University (R01-HL-46380, M01-RR-00080); Cooperative Study of Sickle
Cell Disease: University of Illinois (N01-HB-72982, N01-HB-97062),
Howard University (N01-HB-72991, N01-HB-97061), University of Miami
(N01-HB-72992, N01-HB-97064), Duke University (N01-HB-72993), George
Washington University (N01-HB-72994), University of Tennessee
(N01-HB-72995, N01-HB-97070), Yale University (N01-HB-72996,
N01-HB-97072), Children's Hospital-Philadelphia (N01-HB-72997,
N01-HB-97056), University of Chicago (N01-HB-72998, N01-HB-97053),
Medical College of Georgia (N01-HB-73000, N01-HB-97060), Washington
University (N01-HB-73001, N01-HB-97071), Jewish Hospital and Medical
Center of Brooklyn (N01-HB-73002), Trustees of Health and Hospitals of
the City of Boston, Inc., (N01-HB-73003), Children's Hospital-Oakland
(N01-HB-73004, N01-HB-97054), University of Mississippi (N01-HB-73005),
St. Luke's Hospital-New York (N01-HB-73006), Alta Bates-Herrick Hospital
(N01-HB-97051), Columbia University (N01-HB-97058), St.; Jude's
Children's Research Hospital (N01-HB-97066), Research Foundation, State
University of New York-Albany (N01-HB-97068, N01-HB-97069), New England
Research Institute (N01-HB-97073), Interfaith Medical Center-Brooklyn
(N01-HB-97085); Coronary Artery Risk in Young Adults: University of
Alabama at Birmingham (N01-HC-48047, N01-HC-95095), University of
Minnesota (N01-HC-48048), Northwestern University (N01-HC-48049), Kaiser
Foundation Research Institute (N01-HC-48050), Tufts-New England Medical
Center (N01-HC-45204), Wake Forest University (N01-HC-45205),
Harbor-University of California Los Angeles Research and Education
Institute (N01-HC-05187), University of California, Irvine
(N01-HC-45134, N01-HC-95100) ;Framingham Heart Study: Boston University
(N01-HC-25195, R01-HL-092577, R01-HL-076784, R01-AG-028321); Jackson
Heart Study: Jackson State University (N01-HC-95170), University of
Mississippi (N01-HC-95171), Tougaloo College (N01-HC-95172);
Multi-Ethnic Study of Atherosclerosis: University of Washington
(N01-HC-95159), University of California, Los Angeles (N01-HC-95160),
Columbia University (N01-HC-95161), Johns Hopkins University
(N01-HC-95162, N01-HC-95168), University of Minnesota (N01-HC-95163),
Northwestern University (N01-HC-95164), Wake Forest University
(N01-HC-95165), University of Vermont (N01-HC-95166), New England
Medical Center (N01-HC-95167), Harbor-University of California Los
Angeles Research and Education Institute (N01-HC-95169), Cedars-Sinai
Medical Center (R01-HL-071205), University of Virginia (subcontract to
R01-HL-071205); Sleep Heart Health Study: Johns Hopkins University
(U01-HL-064360), Case Western University (U01-HL-063463), University of
California, Davis (U01-HL-053916), University of Arizona (U01-HL-053938,
U01-HL-053934), University of Pittsburgh (U01-HL-077813), Boston
University (U01-HL-053941), MedStar Research Institute (U01-HL-063429),
Johns Hopkins University (U01-HL-053937). This work was also supported
in part by a T32 grant in Cell and Molecular Training for Cardiovascular
Biology and K99-HL098364 from the National Heart, Lung, and Blood
Institute (KM). The funders had no role in study design, data collection
and analysis, decision to publish, or preparation of the manuscript.
NR 19
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U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAY 21
PY 2012
VL 7
IS 5
AR e36473
DI 10.1371/journal.pone.0036473
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 959VD
UT WOS:000305343100005
PM 22629316
ER
PT J
AU Song, YH
Tai, JHY
Bartsch, SM
Zimmerman, RK
Muder, RR
Lee, BY
AF Song, Yeohan
Tai, Julie H. Y.
Bartsch, Sarah M.
Zimmerman, Richard K.
Muder, Robert R.
Lee, Bruce Y.
TI The potential economic value of a Staphylococcus aureus vaccine among
hemodialysis patients
SO VACCINE
LA English
DT Article
DE Staphylococcus aureus; Vaccine; Economics; Hemodialysis;
Cost-effectiveness
ID COST-EFFECTIVENESS ANALYSIS; LONG-TERM HEMODIALYSIS;
METHICILLIN-RESISTANT; CLINICAL-OUTCOMES; CONJUGATE VACCINE;
RISK-FACTORS; BACTEREMIA; MANAGEMENT; INFECTION; DIALYSIS
AB Staphylococcus aureus infections are a substantial problem for hemodialysis patients. Several vaccine candidates are currently under development, with hemodialysis patients being one possible target population. To determine the potential economic value of an S. aureus vaccine among hemodialysis patients, we developed a Markov decision analytic computer simulation model. When S. aureus colonization prevalence was 1%, the incremental cost-effectiveness ratio (ICER) of vaccination was <=$25,217/quality-adjusted life year (QALY). Vaccination became more cost-effective as colonization prevalence, vaccine efficacy, or vaccine protection duration increased or vaccine cost decreased. Even at 10% colonization prevalence, a 25% efficacious vaccine costing $100 prevented 29 infections, 21 infection-related hospitalizations, and 9 inpatient deaths per 1000 vaccinated HD patients. Our results suggest that an S. aureus vaccine would be cost-effective (i.e., ICERs <= $50,000/QALY) among hemodialysis patients over a wide range of S. aureus prevalence, vaccine costs and efficacies, and vaccine protection durations and delineate potential target parameters for such a vaccine. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Lee, Bruce Y.] Univ Pittsburgh, Publ Hlth Computat & Operat Res Grp, Publ Hlth Computat & Operat Res PHICOR, Pittsburgh, PA 15213 USA.
[Song, Yeohan; Tai, Julie H. Y.; Bartsch, Sarah M.; Lee, Bruce Y.] Univ Pittsburgh, Sch Med, Dept Biomed Informat, Pittsburgh, PA 15260 USA.
[Song, Yeohan; Tai, Julie H. Y.; Bartsch, Sarah M.; Lee, Bruce Y.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15261 USA.
[Zimmerman, Richard K.] Univ Pittsburgh, Sch Med, Dept Family Med, Pittsburgh, PA 15261 USA.
[Muder, Robert R.] VA Pittsburgh Healthcare Syst, Div Infect Dis, Pittsburgh, PA 15240 USA.
RP Lee, BY (reprint author), Univ Pittsburgh, Publ Hlth Computat & Operat Res Grp, Publ Hlth Computat & Operat Res PHICOR, 200 Meyran Ave,Suite 200, Pittsburgh, PA 15213 USA.
EM ysongmd@umich.edu; juliehy@pitt.edu; smm168@pitt.edu; zimmrk@upmc.edu;
robert.muder@va.gov; BYL1@pitt.edu
OI Zimmerman, Richard/0000-0001-5941-6092
FU National Institute of General Medical Sciences Models of Infectious
Disease Agent Study (MIDAS) [5U54GM088491-02]; Pennsylvania Department
of Health (DOH) [4100047864]
FX This work was supported by the National Institute of General Medical
Sciences Models of Infectious Disease Agent Study (MIDAS) grant
5U54GM088491-02 and the Pennsylvania Department of Health (DOH) grant
4100047864. The funders had no role in the design and conduct of the
study; collection, management, analysis, and interpretation of the data;
and preparation, review, or approval of the manuscript.
NR 78
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U1 0
U2 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
J9 VACCINE
JI Vaccine
PD MAY 21
PY 2012
VL 30
IS 24
BP 3675
EP 3682
DI 10.1016/j.vaccine.2012.03.031
PG 8
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 951SY
UT WOS:000304741500024
PM 22464963
ER
PT J
AU Dowdell, SJ
Clasie, B
Depauw, N
Metcalfe, P
Rosenfeld, AB
Kooy, HM
Flanz, JB
Paganetti, H
AF Dowdell, Stephen J.
Clasie, Benjamin
Depauw, Nicolas
Metcalfe, Peter
Rosenfeld, Anatoly B.
Kooy, Hanne M.
Flanz, Jacob B.
Paganetti, Harald
TI Monte Carlo study of the potential reduction in out-of-field dose using
a patient-specific aperture in pencil beam scanning proton therapy
SO PHYSICS IN MEDICINE AND BIOLOGY
LA English
DT Article
ID DISTRIBUTIONS; DOSIMETRY; DELIVERY; TOOLKIT
AB This study is aimed at identifying the potential benefits of using a patient-specific aperture in proton beam scanning. For this purpose, an accurate Monte Carlo model of the pencil beam scanning (PBS) proton therapy (PT) treatment head at Massachusetts General Hospital (MGH) was developed based on an existing model of the passive double-scattering (DS) system. The Monte Carlo code specifies the treatment head at MGH with sub-millimeter accuracy. The code was configured based on the results of experimental measurements performed at MGH. This model was then used to compare out-of-field doses in simulated DS treatments and PBS treatments. For the conditions explored, the penumbra in PBS is wider than in DS, leading to higher absorbed doses and equivalent doses adjacent to the primary field edge. For lateral distances greater than 10 cm from the field edge, the doses in PBS appear to be lower than those observed for DS. We found that placing a patient-specific aperture at nozzle exit during PBS treatments can potentially reduce doses lateral to the primary radiation field by over an order of magnitude. In conclusion, using a patient-specific aperture has the potential to further improve the normal tissue sparing capabilities of PBS.
C1 [Dowdell, Stephen J.; Depauw, Nicolas; Metcalfe, Peter; Rosenfeld, Anatoly B.] Univ Wollongong, Ctr Med Radiat Phys, Wollongong, NSW 2522, Australia.
[Dowdell, Stephen J.; Clasie, Benjamin; Depauw, Nicolas; Kooy, Hanne M.; Flanz, Jacob B.; Paganetti, Harald] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
[Dowdell, Stephen J.; Clasie, Benjamin; Depauw, Nicolas; Kooy, Hanne M.; Flanz, Jacob B.; Paganetti, Harald] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Dowdell, SJ (reprint author), Univ Wollongong, Ctr Med Radiat Phys, Wollongong, NSW 2522, Australia.
EM sdowdell@partners.org
RI Rosenfeld, Anatoly/D-1989-2014; Metcalfe, Peter/D-4040-2014
OI Metcalfe, Peter/0000-0002-6820-0055
FU Australian Rotary Health and the Rotary Clubs of Riverside; Cancer
Institute of NSW; NIH/NCI [R01 CA140735]
FX One of the authors (SJD) acknowledges financial support from Australian
Rotary Health and the Rotary Clubs of Riverside. One of the authors (PM)
acknowledges support from the Cancer Institute of NSW Clinical Leaders
Program. One of the authors (HP) was in part funded by NIH/NCI R01
CA140735.
NR 23
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U1 0
U2 1
PU IOP PUBLISHING LTD
PI BRISTOL
PA TEMPLE CIRCUS, TEMPLE WAY, BRISTOL BS1 6BE, ENGLAND
SN 0031-9155
J9 PHYS MED BIOL
JI Phys. Med. Biol.
PD MAY 21
PY 2012
VL 57
IS 10
BP 2829
EP 2842
DI 10.1088/0031-9155/57/10/2829
PG 14
WC Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging
SC Engineering; Radiology, Nuclear Medicine & Medical Imaging
GA 937SD
UT WOS:000303677900003
PM 22513726
ER
PT J
AU Jia, ZK
Wang, JX
Yang, JJ
Xue, R
Zhang, D
Wang, GN
Ma, SL
Duan, ZF
AF Jia Zhan-kui
Wang Jia-xiang
Yang Jin-jian
Xue Rui
Zhang Da
Wang Guan-nan
Ma Sheng-li
Duan Zhen-feng
TI Discovery and identification of serum biomarkers of Wilms' tumor in mice
using proteomics technology
SO CHINESE MEDICAL JOURNAL
LA English
DT Article
DE proteomics; Wilms' tumor; biomarker
ID HUMAN APOLIPOPROTEIN(A); CANCER; SURVIVAL; PLASMINOGEN; EXPRESSION;
CARCINOMA; PATHWAY; APOE
AB Background Wilms' tumor (nephroblastoma) is a cancer of the kidneys that occurs typically in children and rarely in adults. Early diagnosis is very important for the treatment and prognosis of the disease. The aim of our study was to discover and identify potential non-invasive and convenient biomarkers for the diagnosis of Wilms' tumor.
Methods Nude mice were used to construct a Wilms' tumor model by injecting nephroblastoma cells into their bilateral abdomen. We collected 94 serum samples from mice consisting of 45 samples with Wilms' tumor and 49 controls. The serum proteomic profiles of the samples were analyzed via surface-enhanced laser desorption/ionization time-of-flight mass spectrometry. The candidate biomarkers were purified by high-performance liquid chromatography, identified by liquid chromatography mass spectrometry, and validated using ProteinChip immunoassays.
Results We finally retrieved two differential proteins (m/z 4509.2; 6207.9), which were identified as apolipoprotein A-II and polyubiquitin, respectively. The expression of apolipoprotein A-II was higher in the Wilms' tumor group than in the control group (P <0.01). By contrast, the expression of polyubiquitin was lower in the Wilms' tumor group than in the control group.
Conclusion Apolipoprotein A-II and polyubiquitin may be used as potential biomarkers for nephroblastoma in children, and the analysis of apolipoprotein A-II may help diagnose and treat Wilms' tumor.
C1 [Wang Jia-xiang; Zhang Da] Zhengzhou Univ, Affiliated Hosp 1, Dept Pediat Surg, Zhengzhou 450052, Henan, Peoples R China.
[Jia Zhan-kui; Yang Jin-jian; Xue Rui] Zhengzhou Univ, Affiliated Hosp 1, Dept Urol Surg, Zhengzhou 450052, Henan, Peoples R China.
[Wang Guan-nan] Zhengzhou Univ, Affiliated Hosp 1, Dept Pathol, Zhengzhou 450052, Henan, Peoples R China.
[Ma Sheng-li] Second Hosp Kaifeng City, Dept Orthoped Surg, Kaifeng 475002, Henan, Peoples R China.
[Duan Zhen-feng] Massachusetts Gen Hosp, Dept Hematol Oncol, Boston, MA 02138 USA.
RP Wang, JX (reprint author), Zhengzhou Univ, Affiliated Hosp 1, Dept Pediat Surg, Zhengzhou 450052, Henan, Peoples R China.
EM wangjiaxiang@126.com
FU National Natural Science Foundation of China [81071782]; Institution of
Higher Education [200804590004]
FX This work was supported by grants from the National Natural Science
Foundation of China (No. 81071782) and the Institution of Higher
Education Specialized Research Fund for Doctor (No. 200804590004).
NR 31
TC 1
Z9 1
U1 2
U2 2
PU MEDKNOW PUBLICATIONS & MEDIA PVT LTD
PI MUMBAI
PA B-9, KANARA BUSINESS CENTRE, OFF LINK RD, GHAKTOPAR-E, MUMBAI, 400075,
INDIA
SN 0366-6999
J9 CHINESE MED J-PEKING
JI Chin. Med. J.
PD MAY 20
PY 2012
VL 125
IS 10
BP 1727
EP 1732
DI 10.3760/cma.j.issn.0366-6999.2012.10.009
PG 6
WC Medicine, General & Internal
SC General & Internal Medicine
GA 958RX
UT WOS:000305259500009
PM 22800891
ER
PT J
AU Strother, DR
London, WB
Schmidt, ML
Brodeur, GM
Shimada, H
Thorner, P
Collins, MH
Tagge, E
Adkins, S
Reynolds, CP
Murray, K
Lavey, RS
Matthay, KK
Castleberry, R
Maris, JM
Cohn, SL
AF Strother, Douglas R.
London, Wendy B.
Schmidt, Mary Lou
Brodeur, Garrett M.
Shimada, Hiroyuki
Thorner, Paul
Collins, Margaret H.
Tagge, Edward
Adkins, Stanton
Reynolds, C. Patrick
Murray, Kevin
Lavey, Robert S.
Matthay, Katherine K.
Castleberry, Robert
Maris, John M.
Cohn, Susan L.
TI Outcome After Surgery Alone or With Restricted Use of Chemotherapy for
Patients With Low-Risk Neuroblastoma: Results of Children's Oncology
Group Study P9641
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID EXPRESSION-BASED CLASSIFICATION; NEURO-BLASTOMA; INFANTS; STAGE;
THERAPY; STRATIFICATION; CRITERIA; BIOLOGY
AB Purpose
The primary objective of Children's Oncology Group study P9641 was to demonstrate that surgery alone would achieve 3-year overall survival (OS) >= 95% for patients with asymptomatic International Neuroblastoma Staging System stages 2a and 2b neuroblastoma (NBL). Secondary objectives focused on other low-risk patients with NBL and on those who required chemotherapy according to protocol-defined criteria.
Patients and Methods
Patients underwent maximally safe resection of tumor. Chemotherapy was reserved for patients with, or at risk for, symptomatic disease, with less than 50% tumor resection at diagnosis, or with unresectable progressive disease after surgery alone.
Results
For all 915 eligible patients, 5-year event-free survival (EFS) and OS were 89% +/- 1% and 97% +/- 1%, respectively. For patients with asymptomatic stage 2a or 2b disease, 5-year EFS and OS were 87% +/- 2% and 96% +/- 1%, respectively. Among patients with stage 2b disease, EFS and OS were significantly lower for those with unfavorable histology or diploid tumors, and OS was significantly lower for those >= 18 months old. For patients with stage 1 and 4s NBL, 5-year OS rates were 99% +/- 1% and 91% +/- 1%, respectively. Patients who required chemotherapy at diagnosis achieved 5-year OS of 98% +/- 1%. Of all patients observed after surgery, 11.1% experienced recurrence or progression of disease.
Conclusion
Excellent survival rates can be achieved in asymptomatic low-risk patients with stages 2a and 2b NBL after surgery alone. Immediate use of chemotherapy may be restricted to a minority of patients with low-risk NBL. Patients with stage 2b disease who are older or have diploid or unfavorable histology tumors fare less well. Future studies will seek to refine risk classification. J Clin Oncol 30:1842-1848. (c) 2012 by American Society of Clinical Oncology
C1 [Strother, Douglas R.] Alberta Childrens Prov Gen Hosp, Calgary, AB T3B 6A8, Canada.
[Strother, Douglas R.] Univ Calgary, Calgary, AB, Canada.
[Thorner, Paul] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Thorner, Paul] Univ Toronto, Toronto, ON, Canada.
[London, Wendy B.] Childrens Hosp, Childrens Oncol Grp Stat, Boston, MA 02115 USA.
[London, Wendy B.] Childrens Hosp, Ctr Data, Boston, MA 02115 USA.
[London, Wendy B.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Schmidt, Mary Lou] Univ Illinois, Chicago Coll Med, Chicago, IL 60680 USA.
[Cohn, Susan L.] Univ Chicago, Chicago, IL 60637 USA.
[Brodeur, Garrett M.; Maris, John M.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Shimada, Hiroyuki] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Matthay, Katherine K.] Univ Calif San Francisco, Med Ctr, San Francisco, CA USA.
[Collins, Margaret H.] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH USA.
[Tagge, Edward] Univ S Carolina, Charleston, SC USA.
[Adkins, Stanton] S Carolina Canc Ctr, Columbia, SC USA.
[Reynolds, C. Patrick] Texas Tech Univ, Hlth Sci Ctr Amarillo, Lubbock, TX 79409 USA.
[Murray, Kevin] Hall Radiat Ctr, Cedar Rapids, IA USA.
[Lavey, Robert S.] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Castleberry, Robert] Univ Alabama Birmingham, Birmingham, AL USA.
RP Strother, DR (reprint author), Alberta Childrens Prov Gen Hosp, 2888 Shaganappi Trail NW, Calgary, AB T3B 6A8, Canada.
EM doug.strother@albertahealthservices.ca
OI Reynolds, C. Patrick/0000-0002-2827-8536; Cohn,
Susan/0000-0001-5749-7650
FU National Institutes of Health [U10-CA98543, U10-CA29139, U10 CA98413]
FX Supported by National Institutes of Health Grants No. U10-CA98543,
U10-CA29139, and U10 CA98413 to the Children's Oncology Group.
NR 23
TC 28
Z9 35
U1 2
U2 6
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
BP 1842
EP 1848
DI 10.1200/JCO.2011.37.9990
PG 7
WC Oncology
SC Oncology
GA 947JZ
UT WOS:000304427600020
PM 22529259
ER
PT J
AU Tap, WD
Demetri, G
Barnette, P
Desai, J
Kavan, P
Tozer, R
Benedetto, PW
Friberg, G
Deng, HJ
McCaffery, I
Leitch, I
Badola, S
Chang, S
Zhu, M
Tolcher, A
AF Tap, William D.
Demetri, George
Barnette, Phillip
Desai, Jayesh
Kavan, Petr
Tozer, Richard
Benedetto, Pasquale W.
Friberg, Gregory
Deng, Hongjie
McCaffery, Ian
Leitch, Ian
Badola, Sunita
Chang, Sung
Zhu, Min
Tolcher, Anthony
TI Phase II Study of Ganitumab, a Fully Human Anti-Type-1 Insulin-Like
Growth Factor Receptor Antibody, in Patients With Metastatic Ewing
Family Tumors or Desmoplastic Small Round Cell Tumors
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID MONOCLONAL-ANTIBODY; SARCOMA FAMILY; GENE-EXPRESSION; FUSION PROTEIN;
CANCER; RECURRENT; SURVIVAL; R1507; CT
AB Purpose
Ganitumab is a fully human monoclonal antibody against type-1 insulin-like growth factor receptor (IGF1R). An open-label phase II study was conducted to evaluate the efficacy and safety of ganitumab monotherapy in patients with metastatic Ewing family tumors (EFT) or desmoplastic small round cell tumors (DSRCT).
Patients and Methods
Patients >= 16 years of age with relapsed or refractory EFT or DSRCT received 12 mg/kg of ganitumab every 2 weeks. Objective response rate (ORR) was the primary end point. Secondary end points included clinical benefit rate (CBR = complete + partial responses + stable disease [SD] >= 24 weeks) and safety and pharmacokinetic profiles of ganitumab. The relationship between tumor response and EWS gene translocation status and IGF-1 levels was evaluated.
Results
Thirty-eight patients (22 with EFT; 16 with DSRCT) received one or more doses of ganitumab. Twenty-four patients (63%) experienced ganitumab-related adverse events. Grade 3 related events included hyperglycemia (n = 2), thrombocytopenia (n = 5), neutropenia (n = 2), leukopenia (n = 1), and transient ischemic attack (n = 1). There were no grade 4 or 5 treatment-related events. Of 35 patients assessed for response, two had partial responses (ORR, 6%) and 17 (49%) had SD. Four patients had SD >= 24 weeks, contributing to a CBR of 17%. The pharmacokinetic profile of ganitumab was similar to that observed in the first-in-human trial. Elevation of IGF-1 levels was observed postdose. EWS-Fli1 translocations were analyzed by RNA sequencing and fluorescent in situ hybridization, and novel translocations were observed in EFT and DSCRT. No apparent relationship between tumor response and IGF-1 levels or EWS gene translocations was observed.
Conclusion
Ganitumab was well tolerated and demonstrated antitumor activity in patients with advanced recurrent EFT or DSRCT. J Clin Oncol 30:1849-1856. (c) 2012 by American Society of Clinical Oncology
C1 [Tap, William D.] Univ Calif Los Angeles, Los Angeles Med Ctr, Los Angeles, CA USA.
[Friberg, Gregory; Deng, Hongjie; McCaffery, Ian; Leitch, Ian; Badola, Sunita; Zhu, Min] Amgen Inc, Thousand Oaks, CA USA.
[Demetri, George] Dana Farber Harvard Canc Ctr, Boston, MA USA.
[Barnette, Phillip] Primary Childrens Med Ctr, Salt Lake City, UT 84103 USA.
[Desai, Jayesh] Royal Melbourne Hosp, Parkville, Vic 3050, Australia.
[Kavan, Petr] McGill Univ, Jewish Gen Hosp, Montreal, PQ H3T 1E2, Canada.
[Tozer, Richard] McMaster Univ, Juravinski Canc Ctr, Hamilton, ON, Canada.
[Benedetto, Pasquale W.] Univ Miami Sylvester, Ctr Comprehens Canc, Miami, FL USA.
[Badola, Sunita] Amgen Inc, Cambridge, MA USA.
[Tolcher, Anthony] START, San Antonio, TX USA.
RP Tap, WD (reprint author), Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10065 USA.
EM tapw@mskcc.org
FU Amgen; Pfizer; Ariad; Johnson Johnson; PharmaMar; Infinity
Pharmaceuticals; Daiichi-Sankyo; Bristol-Myers Squibb; Genentech;
OrthoBiotech; Schering-Plough Research Institute; Biogen Idec; ArQule;
Bayer; Merck; Novartis; Array BioPharma
FX Supported by Amgen.; Employment or Leadership Position: Gregory Friberg,
Amgen (C); Hongjie Deng, Amgen (C); Ian McCaffery, Amgen (C); Ian
Leitch, Amgen (C); Sunita Badola, Amgen (C); Sung Chang, Amgen (C); Min
Zhu, Amgen (C) Consultant or Advisory Role: George Demetri, Amgen (C),
Novartis (C), Pfizer (C), Ariad (C), Johnson & Johnson (C), PharmaMar
(C), Genentech (C), Infinity Pharmaceuticals (C), EMD-Serono (C),
GlaxoSmithKline (C), Daiichi-Sankyo (C), ArQule (C); Anthony Tolcher,
Abraxis (C), Amgen (C), Exelixis (C), Genentech (C), GlaxoSmithKline
(C), Merck (C), Pfizer (C), Biogen Idec (C), Novartis (C), Regeneron
Pharmaceuticals (C), Ariad Pharmaceuticals (C), OrthoBiotec (C) Stock
Ownership: Pasquale W. Benedetto, Amgen; Gregory Friberg, Amgen; Hongjie
Deng, Amgen; Ian McCaffery, Amgen; Ian Leitch, Amgen; Sunita Badola,
Amgen; Sung Chang, Amgen; Min Zhu, Amgen Honoraria: George Demetri,
Novartis, Pfizer Research Funding: George Demetri, Pfizer, Ariad,
Johnson & Johnson, PharmaMar, Infinity Pharmaceuticals, Amgen,
Daiichi-Sankyo; Pasquale W. Benedetto, Amgen; Anthony Tolcher, Amgen,
Bristol-Myers Squibb, Genentech, Pfizer, OrthoBiotech, Schering-Plough
Research Institute, Biogen Idec, ArQule, Bayer, Merck, Novartis, Array
BioPharma Expert Testimony: George Demetri, Ariad (U), Johnson & Johnson
(U), PharmaMar (U) Other Remuneration: None
NR 21
TC 72
Z9 73
U1 0
U2 7
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
BP 1849
EP 1856
DI 10.1200/JCO.2011.37.2359
PG 8
WC Oncology
SC Oncology
GA 947JZ
UT WOS:000304427600021
PM 22508822
ER
PT J
AU Metzger, O
Tutt, A
de Azambuja, E
Saini, KS
Viale, G
Loi, S
Bradbury, I
Bliss, JM
Azim, HA
Ellis, P
Di Leo, A
Baselga, J
Sotiriou, C
Piccart-Gebhart, M
AF Metzger-Filho, Otto
Tutt, Andrew
de Azambuja, Evandro
Saini, Kamal S.
Viale, Giuseppe
Loi, Sherene
Bradbury, Ian
Bliss, Judith M.
Azim, Hatem A., Jr.
Ellis, Paul
Di Leo, Angelo
Baselga, Jose
Sotiriou, Christos
Piccart-Gebhart, Martine
TI Dissecting the Heterogeneity of Triple-Negative Breast Cancer
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Review
ID INVASIVE DUCTAL CARCINOMA; BASAL-LIKE PHENOTYPE; LONG-TERM SURVIVAL;
ESTROGEN-RECEPTOR; POLY(ADP-RIBOSE) POLYMERASE; MOLECULAR SUBTYPES;
SPORADIC BREAST; NEOADJUVANT CHEMOTHERAPY; CYTOKERATIN EXPRESSION;
EPITHELIAL PHENOTYPE
AB Triple-negative breast cancer (TNBC) accounts for 15% to 20% of breast cancers. It is a heterogeneous disease, not only on the molecular level, but also on the pathologic and clinical levels. TNBC is associated with a significantly higher probability of relapse and poorer overall survival in the first few years after diagnosis when compared with other breast cancer subtypes. This is observed despite its usual high sensitivity to chemotherapy. In the advanced setting, responses observed with chemotherapy lack durability. Early-stage clinical studies suggested impressive potential when a poly (ADP-ribose) polymerase (PARP) inhibitor is given for the treatment of advanced TNBC with BRCA gene dysfunction. The molecular complexity of TNBC has led to proposed subclassifications, which will be of great value for the development of targeted therapies. In this review, we discuss the biology of TNBC at the pathologic and the molecular levels. We also elaborate on the role of systemic therapies and the results of the first phase III clinical trial evaluating the addition of iniparib, a novel investigational anticancer agent that does not possess characteristics typical of the PARP inhibitor class, in combination with chemotherapy in advanced TNBC. J Clin Oncol 30:1879-1887. (c) 2012 by American Society of Clinical Oncology
C1 [Metzger-Filho, Otto; de Azambuja, Evandro; Saini, Kamal S.; Loi, Sherene; Azim, Hatem A., Jr.; Sotiriou, Christos; Piccart-Gebhart, Martine] Univ Libre Brussels, Inst Jules Bordet, B-1000 Brussels, Belgium.
[Tutt, Andrew; Ellis, Paul] Kings Coll London, London, England.
[Bliss, Judith M.] Inst Canc Res, Sutton, Surrey, England.
[Bradbury, Ian] Frontier Sci, Kincraig, Scotland.
[Viale, Giuseppe] Univ Milan, European Inst Oncol, Milan, Italy.
[Di Leo, Angelo] Hosp Prato, Prato, Italy.
[Baselga, Jose] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
RP Piccart-Gebhart, M (reprint author), Univ Libre Brussels, Inst Jules Bordet, Blvd Waterloo 121, B-1000 Brussels, Belgium.
EM martine.piccart@bordet.be
RI Loi, Sherene/H-1979-2016;
OI Loi, Sherene/0000-0001-6137-9171
FU sanofi-aventis; AstraZeneca
FX Employment or Leadership Position: None Consultant or Advisory Role:
Andrew Tutt, sanofi-aventis (U), AstraZeneca (U), Eisai (C), Clovis (C);
Judith M. Bliss, sanofi-aventis (U); Hatem A. Azim Jr, Celgene (C); Paul
Ellis, Roche (C), GlaxoSmithKline (C), sanofi-aventis (C), Esai (C);
Angelo Di Leo, AstraZeneca (C), Pfizer (C), sanofi-aventis (C); Jose
Baselga, sanofi-aventis (C); Martine Piccart-Gebhart, sanofi-aventis
(C), Amgen (C), Roche (C), GlaxoSmithKline (C), PharmaMar (C) Stock
Ownership: None Honoraria: Andrew Tutt, AstraZeneca, sanofi-aventis;
Paul Ellis, Roche, Esai, sanofi-aventis; Angelo Di Leo, AstraZeneca,
Pfizer, sanofi-aventis; Martine Piccart-Gebhart, sanofi-aventis, Amgen,
Roche, GlaxoSmithKline, PharmaMar Research Funding: Andrew Tutt,
sanofi-aventis; Judith M. Bliss, sanofi-aventis; Angelo Di Leo,
AstraZeneca Expert Testimony: None Other Remuneration: Andrew Tutt,
AstraZeneca, sanofi-aventis; Judith M. Bliss, sanofi-aventis
NR 126
TC 158
Z9 169
U1 14
U2 51
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
BP 1879
EP 1887
DI 10.1200/JCO.2011.38.2010
PG 9
WC Oncology
SC Oncology
GA 947JZ
UT WOS:000304427600025
PM 22454417
ER
PT J
AU Mayer, EL
Gropper, AB
Neville, BA
Partridge, AH
Cameron, DB
Winer, EP
Earle, CC
AF Mayer, Erica L.
Gropper, Adrienne B.
Neville, Bridget A.
Partridge, Ann H.
Cameron, Danielle B.
Winer, Eric P.
Earle, Craig C.
TI Follow-Up of Breast Cancer Survivors Reply
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Letter
ID PRIMARY-CARE; RANDOMIZED-TRIAL; SPECIALIST CARE; PATIENT
C1 [Mayer, Erica L.; Neville, Bridget A.; Partridge, Ann H.; Winer, Eric P.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Gropper, Adrienne B.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Cameron, Danielle B.] Univ Miami, Miller Sch Med, Boca Raton, FL USA.
[Earle, Craig C.] Inst Clin Evaluat Sci, Toronto, ON, Canada.
RP Mayer, EL (reprint author), Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 8
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
BP 1893
EP 1894
DI 10.1200/JCO.2012.42.1339
PG 3
WC Oncology
SC Oncology
GA 947JZ
UT WOS:000304427600029
ER
PT J
AU Abbas, KS
Li, A
Rivero, G
Mitsiades, N
Yellapragada, S
AF Abbas, Kanza S.
Li, Ang
Rivero, Gustavo
Mitsiades, Nicholas
Yellapragada, Sarvari
TI Survival outcome of veterans with myelodysplastic syndrome (MDS) treated
with statins.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Baylor Coll Med, Houston, TX 77030 USA.
Baylor Coll Med, Dan L Duncan Canc Ctr, Michael E DeBakey Vet Affairs Med Ctr, Houston, TX 77030 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA e17018
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801859
ER
PT J
AU Abel, GA
Lee, S
Stone, RM
Steensma, DP
Young, N
Houk, A
Hastings, BT
Martins, Y
Klaassen, R
AF Abel, Gregory Alan
Lee, Stephanie
Stone, Richard M.
Steensma, David P.
Young, Nancy
Houk, Alice
Hastings, B. Taylor
Martins, Yolanda
Klaassen, Robert
TI Development of a disease-specific measure of quality of life in
myelodysplastic syndromes (MDS): The "QUALMS-1".
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
Laurentian Univ, Sudbury, ON P3E 2C6, Canada.
Aplast Anemia & MDS Int Fdn, Rockville, MD USA.
Univ Ottawa, Ottawa, ON, Canada.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 6103
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804010
ER
PT J
AU Abrams, TA
Meyer, G
Moloney, J
Meyerhardt, JA
Schrag, D
Fuchs, CS
AF Abrams, Thomas Adam
Meyer, Gary
Moloney, Julie
Meyerhardt, Jeffrey A.
Schrag, Deborah
Fuchs, Charles S.
TI Patterns of chemotherapy (CT) use in a US-wide population-based cohort
of patients (pts) with metastatic colorectal cancer (mCRC)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
IntrinsiQ LLC, Burlington, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 3537
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804812
ER
PT J
AU Ackerman, A
McDermott, DF
Lawrence, DP
Gunturi, A
Flaherty, KT
Giobbie-Hurder, A
Hodi, FS
Ibrahim, N
Atkins, MB
Cho, DC
Sullivan, RJ
AF Ackerman, Allison
McDermott, David F.
Lawrence, Donald P.
Gunturi, Anasuya
Flaherty, Keith T.
Giobbie-Hurder, Anita
Hodi, F. Stephen
Ibrahim, Nageatte
Atkins, Michael B.
Cho, Daniel C.
Sullivan, Ryan J.
TI Outcomes of patients with malignant melanoma treated with immunotherapy
prior to or after vemurafenib.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 12
Z9 12
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 8569
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801678
ER
PT J
AU Alexander, BM
Wen, PY
Lee, EQ
Batchelor, T
Cloughesy, TF
Parmigiani, G
Trippa, L
AF Alexander, Brian Michael
Wen, Patrick Y.
Lee, Eudocia Quant
Batchelor, Tracy
Cloughesy, Timothy Francis
Parmigiani, Giovanni
Trippa, Lorenzo
TI Bayesian adaptive randomized trial design for patients with recurrent
glioblastoma
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Brigham & Womens Canc Ctr, Dana Farber Canc Inst, Boston, MA USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 2005
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801469
ER
PT J
AU Ali, SM
Zubritsky, L
Jacobus, SJ
Leitzel, K
Regan, MM
Nakabayashi, M
Knight, RD
Laadem, A
Sherman, ML
Lipton, A
Kantoff, P
AF Ali, Suhail M.
Zubritsky, Lindsey
Jacobus, Susanna J.
Leitzel, Kim
Regan, Meredith M.
Nakabayashi, Mari
Knight, Robert D.
Laadem, Abderrahmane
Sherman, Matthew L.
Lipton, Allan
Kantoff, Philip
TI Elevated serum activin A and survival in CRPC.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Penn State Hershey Med Ctr, Hershey, PA USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Celgene Corp, Summit, NJ USA.
Acceleron Pharma, Cambridge, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA e15170
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803136
ER
PT J
AU Alsina, M
Tabernero, J
Shapiro, G
Burris, H
Infante, JR
Weiss, GJ
Cervantes-Ruiperez, A
Gounder, MM
Paz-Ares, L
Falzone, R
Hill, J
Cehelsky, J
Vaishnaw, A
Gollob, J
LoRusso, P
AF Alsina, Maria
Tabernero, Josep
Shapiro, Geoffrey
Burris, Howard
Infante, Jeffrey R.
Weiss, Glen J.
Cervantes-Ruiperez, Andres
Gounder, Mrinal M.
Paz-Ares, Luis
Falzone, Rick
Hill, Jamie
Cehelsky, Jeffrey
Vaishnaw, Akshay
Gollob, Jared
LoRusso, Patricia
TI Open-label extension study of the RNAi therapeutic ALN-VSP02 in cancer
patients responding to therapy.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Vall dHebron Univ Hosp, Mol Therapeut Res Unit, Barcelona, Spain.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Sarah Cannon Res Inst, Nashville, TN USA.
Scottsdale Healthcare, Virginia G Piper Canc Ctr, Scottsdale, AZ USA.
Univ Valencia, INCLIVA, Dept Hematol & Med Oncol, Valencia, Spain.
Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Univ Hosp Virgen del Rocio, Seville, Spain.
Alnylam Pharmaceut, Cambridge, MA USA.
Karmanos Canc Inst, Detroit, MI USA.
RI IBIS, NUEVAS TERAPIA/P-3415-2015
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 3062
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802301
ER
PT J
AU Alsina, M
Schlossman, RL
Weber, DM
Coutre, SE
Lonial, S
Gasparetto, C
Warsi, G
Ondovik, MS
Mukhopadhyay, S
Paley, CS
Richardson, PGG
AF Alsina, Melissa
Schlossman, Robert L.
Weber, Donna M.
Coutre, Steven E.
Lonial, Sagar
Gasparetto, Cristina
Warsi, Ghulam
Ondovik, Michael S.
Mukhopadhyay, Sutapa
Paley, Carole S.
Richardson, Paul Gerard Guy
TI PANORAMA 2: A phase II study of panobinostat in combination with
bortezomib and dexamethasone in patients with relapsed and
bortezomib-refractory multiple myeloma.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Stanford Univ, Sch Med, Stanford, CA 94305 USA.
Emory Univ, Winship Canc Ctr, Atlanta, GA 30322 USA.
Duke Univ, Med Ctr, Durham, NC USA.
Novartis Pharmaceut, E Hanover, NJ USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 8012
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803836
ER
PT J
AU Altwairgi, AK
Parulekar, W
Chapman, JAW
Shepherd, LE
Pritchard, KI
Han, L
Goss, PE
Whelan, TJ
AF Altwairgi, Abdullah Khalaf
Parulekar, Wendy
Chapman, Judy-Anne W.
Shepherd, Lois E.
Pritchard, Kathleen I.
Han, Lei
Goss, Paul Edward
Whelan, Timothy Joseph
CA NCIC Clinical Trials Grp
TI Impact of concurrent (CON) and sequential (SEQ) radiotherapy (RT) with
adjuvant aromatase inhibitors (AI) in early-stage breast cancer (EBC):
NCIC CTG MA.27.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Queens Univ, NCIC Clin Trials Grp, Kingston, ON, Canada.
Univ Toronto, Sunnybrook Odette Canc Ctr, Toronto, ON, Canada.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Hamilton Hlth Sci, Juravinski Canc Ctr, Hamilton, ON, Canada.
RI Whelan, Timothy/D-3185-2017
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 500
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800176
ER
PT J
AU Amrein, PC
Attar, EC
Fathi, AT
McAfee, SL
Wadleigh, M
DeAngelo, DJ
Steensma, DP
Foster, J
Stone, RM
Neuberg, DS
Ballen, KK
AF Amrein, Philip C.
Attar, Eyal C.
Fathi, Amir Tahmasb
McAfee, Steven L.
Wadleigh, Martha
DeAngelo, Daniel J.
Steensma, David P.
Foster, Julia
Stone, Richard M.
Neuberg, Donna S.
Ballen, Karen K.
CA Massachusetts Gen Hosp
TI Phase I dose escalation study of bortezomib in combination with
lenalidomide in patients with myelodysplastic syndromes (MDS) and acute
myeloid leukemia (AML)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
Harvard Univ, Dana Farber Canc Inst, Boston, MA 02115 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 6621
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800701
ER
PT J
AU Apolo, AB
Philips, G
Ostrovnaya, I
Rosenberg, JE
Milowsky, MI
Small, EJ
Bajorin, DF
Halabi, S
AF Apolo, Andrea Borghese
Philips, George
Ostrovnaya, Irina
Rosenberg, Jonathan E.
Milowsky, Matthew I.
Small, Eric Jay
Bajorin, Dean F.
Halabi, Susan
TI External validation of prognostic models for overall survival (OS) in
patients (pts) with advanced cancer (UC) treated with cisplatin-based
chemotherapy.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
Georgetown Univ, Washington, DC USA.
Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Harvard Univ, Brigham & Womens Hosp, Dana Farber Canc Inst, Lank Ctr Genitourinary Oncol,Med Sch, Boston, MA 02115 USA.
Univ Calif San Francisco, San Francisco, CA 94143 USA.
Duke Univ, Med Ctr, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 4592
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803088
ER
PT J
AU Arteaga, CL
Mayer, IA
O'Neill, AM
Swaby, RF
Alpaugh, RK
Yang, XMJ
Wagner, LI
Meropol, NJ
Saphner, TJ
Jahanzeb, M
Perez, EA
Lin, NU
Sledge, GW
AF Arteaga, Carlos L.
Mayer, Ingrid A.
O'Neill, Anne M.
Swaby, Ramona F.
Alpaugh, R. Katherine
Yang, Ximing J.
Wagner, Lynne I.
Meropol, Neal J.
Saphner, Thomas James
Jahanzeb, Mohammad
Perez, Edith A.
Lin, Nancy U.
Sledge, George W.
TI A randomized phase III double-blinded placebo-controlled trial of
first-line chemotherapy and trastuzumab with or without bevacizumab for
patients with HER2/neu-overexpressing metastatic breast cancer
(HER2+MBC): A trial of the Eastern Cooperative Oncology Group (E1105)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Vanderbilt Univ, Nashville, TN USA.
Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
Northwestern Univ, Chicago, IL 60611 USA.
Case Western Reserve Univ, Cleveland, OH 44106 USA.
Green Bay Oncol, Green Bay, WI USA.
Univ Miami, Sylvester Comprehens Canc Ctr, Coral Gables, FL 33124 USA.
Mayo Clin, Jacksonville, FL 32224 USA.
Indiana Univ, Simon Canc Ctr, Indianapolis, IN 46204 USA.
NR 0
TC 2
Z9 2
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 605
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800386
ER
PT J
AU Attar, EC
Johnson, JL
Amrein, PC
Lozanski, G
Wadleigh, M
DeAngelo, DJ
Kolitz, JE
Powell, BL
Voorhees, PM
Wang, ES
Blum, WG
Marcucci, G
Bloomfield, CD
Moser, BK
Stone, RM
Larson, RA
AF Attar, Eyal C.
Johnson, Jeffrey L.
Amrein, Philip C.
Lozanski, Gerard
Wadleigh, Martha
DeAngelo, Daniel J.
Kolitz, Jonathan E.
Powell, Bayard L.
Voorhees, Peter Michael
Wang, Eunice S.
Blum, William G.
Marcucci, Guido
Bloomfield, Clara D.
Moser, Barry K.
Stone, Richard M.
Larson, Richard A.
CA CALGB
TI A phase II study of bortezomib added to standard daunorubicin and
cytarabine during induction therapy and to intermediate-dose cytarabine
(Int-DAC) for consolidation in patients with previously untreated acute
myeloid leukemia (AML) age 60-75 years: CALGB study 10502.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
Duke Canc Stat Ctr, Durham, NC USA.
Ohio State Univ, Columbus, OH 43210 USA.
Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Hofstra North Shore LIJ Sch Med, Lake Success, NY USA.
Wake Forest Univ, Winston Salem, NC 27109 USA.
Univ N Carolina, Chapel Hill, NC USA.
Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
Duke Univ, Med Ctr, Durham, NC USA.
Univ Chicago, Chicago, IL 60637 USA.
RI Blum, William/E-2769-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 6526
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800142
ER
PT J
AU Azaro, A
Baselga, J
Sepulveda, JM
Seoane, J
Ahnert, JR
Brana, I
Gueorguieva, I
Cleverly, A
Lahn, MMF
Pillay, S
Paz-Ares, L
Holdhoff, M
Blakeley, JO
Carducci, MA
AF Azaro, Analia
Baselga, Jose
Sepulveda, Juan Manuel
Seoane, Joan
Ahnert, Jordi Rodon
Brana, Irene
Gueorguieva, Ivelina
Cleverly, Ann
Lahn, Michael M. F.
Pillay, Sada
Paz-Ares, Luis
Holdhoff, Matthias
Blakeley, Jaishri O'Neill
Carducci, Michael Anthony
TI The oral transforming growth factor-beta (TGF-beta) receptor I kinase
inhibitor LY2157299 plus lomustine in patients with treatment-refractory
malignant glioma: The first human dose study.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
Hosp Univ 12 Octubre, Med Oncol Serv, Madrid, Spain.
Vall dHebron Univ Hosp, Inst Oncol, Barcelona, Spain.
Vall dHebron Univ Hosp, Mol Therapeut Res Unit, Barcelona, Spain.
Vall dHebron Univ Hosp, Barcelona, Spain.
Eli Lilly & Co, Indianapolis, IN 46285 USA.
Eli Lilly & Co, Div Early Phase Oncol Clin Invest, Indianapolis, IN 46285 USA.
Univ Hosp Virgen del Rocio, Seville, Spain.
Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
RI IBIS, NUEVAS TERAPIA/P-3415-2015
NR 0
TC 1
Z9 1
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 2042
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801506
ER
PT J
AU Badve, SS
Gray, RJ
Baehner, FL
Solin, LJ
Butler, SM
Yoshizawa, C
Shak, S
Hughes, LL
Page, DL
Sledge, GW
Davidson, NE
Perez, EA
Ingle, JN
Wood, WC
Sparano, JA
AF Badve, Sunil S.
Gray, Robert James
Baehner, Frederick L.
Solin, Lawrence J.
Butler, Steven M.
Yoshizawa, Carl
Shak, Steven
Hughes, Lorie L.
Page, David L.
Sledge, George W.
Davidson, Nancy E.
Perez, Edith A.
Ingle, James N.
Wood, William C.
Sparano, Joseph A.
TI Correlation between the DCIS score and traditional clinicopathologic
features in the prospectively designed E5194 clinical validation study
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Indiana Univ Sch Med, Indianapolis, IN USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Genom Hlth, Redwood City, CA USA.
Albert Einstein Med Ctr, Philadelphia, PA 19141 USA.
Hope Ctr, Cartersville, GA USA.
Vanderbilt Univ, Nashville, TN USA.
Indiana Univ, Simon Canc Ctr, Indianapolis, IN 46204 USA.
Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA.
Mayo Clin, Jacksonville, FL 32224 USA.
Mayo Clin, Rochester, MN USA.
Emory Univ, Dept Surg, Atlanta, GA 30322 USA.
Albert Einstein Coll Med, Bronx, NY 10467 USA.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 1005
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800722
ER
PT J
AU Balmana, J
Tung, NM
Isakoff, SJ
Grana, B
Ryan, PD
Rafi, R
Tracy, M
Winer, E
Baselga, J
Garber, JE
AF Balmana, Judith
Tung, Nadine M.
Isakoff, Steven J.
Grana, Begona
Ryan, Paula D.
Rafi, Rezvan
Tracy, Michael
Winer, Eric
Baselga, Jose
Garber, Judy Ellen
TI Phase I, open-label study of olaparib plus cisplatin in patients with
advanced solid tumors
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Vall dHebron Univ Hosp, Barcelona, Spain.
Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
AstraZeneca, Wilmington, DE USA.
AstraZeneca, Macclesfield, Cheshire, England.
Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 1009
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800723
ER
PT J
AU Bandman, O
Delcayre, A
Laus, R
Godfrey, WR
Kantoff, PW
Schlom, J
Gulley, JL
AF Bandman, Olga
Delcayre, Alain
Laus, Reiner
Godfrey, Wayne Russell
Kantoff, Philip W.
Schlom, Jeffrey
Gulley, James L.
TI Prospect: A randomized, double-blind, phase III efficacy trial of
PROSTVAC.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 BN ImmunoTherapeut, Mountain View, CA USA.
Bavarian Nord Immunotherapeut, Mountain View, CA USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
NCI, Bethesda, MD 20892 USA.
NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RI Gulley, James/K-4139-2016
OI Gulley, James/0000-0002-6569-2912
NR 0
TC 1
Z9 1
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA TPS4699
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803319
ER
PT J
AU Bao, T
Betts, K
Tarpinian, K
Cai, L
Gould, J
Jeter, S
Medeiros, M
Tait, N
Chumsri, S
Armstrong, DK
Bardia, A
Tan, MT
Stebbing, J
Kelleher, WP
Folkerd, E
Dowsett, M
Singh, H
Snyder, CF
Tkaczuk, KH
Stearns, V
AF Bao, Ting
Betts, Kelly
Tarpinian, Karineh
Cai, Ling
Gould, Jeff
Jeter, Stacie
Medeiros, Michelle
Tait, Nancy
Chumsri, Saranya
Armstrong, Deborah Kay
Bardia, Aditya
Tan, Ming Tony
Stebbing, Justin
Kelleher, William Peter
Folkerd, Elizabeth
Dowsett, Mitchell
Singh, Harvinder
Snyder, Claire Frances
Tkaczuk, Katherine Hanna
Stearns, Vered
TI Changes in patient-reported outcomes in women with breast cancer in a
multicenter double-blind randomized controlled trial assessing the
effect of acupuncture in reducing aromatase inhibitor-induced
musculoskeletal symptoms (AIMSS)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Univ Maryland, Baltimore, MD 21201 USA.
Greenebaum Canc Ctr, Baltimore, MD USA.
Johns Hopkins Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
Harvard Univ, Massachusetts Gen Hosp, Ctr Canc, Sch Med, Boston, MA 02114 USA.
Imperial Coll Healthcare NHS Trust, London, England.
Univ London Imperial Coll Sci Technol & Med, London, England.
Inst Canc Res, Sutton, Surrey, England.
Royal Marsden Hosp, London SW3 6JJ, England.
Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 2
U2 3
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 9103
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804534
ER
PT J
AU Barnholt, KE
Do, CB
Kiefer, AK
Nelson, M
Garber, JE
Robson, ME
Maki, RG
Demetri, GD
Wojcicki, A
AF Barnholt, Kimberly E.
Do, Chuong B.
Kiefer, Amy K.
Nelson, Marisa
Garber, Judy Ellen
Robson, Mark E.
Maki, Robert G.
Demetri, George D.
Wojcicki, Anne
TI Genome-wide analysis and characterization of an online sarcoma cohort
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 23andMe Inc, Mountain View, CA USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Mt Sinai Sch Med, New York, NY USA.
Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 10097
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801206
ER
PT J
AU Baselga, J
Cortes, J
Im, SA
Pivot, XB
Clark, E
Knott, A
Ross, G
Swain, SM
AF Baselga, Jose
Cortes, Javier
Im, Seock-Ah
Pivot, Xavier B.
Clark, Emma
Knott, Adam
Ross, Graham
Swain, Sandra M.
TI Adverse events with pertuzumab and trastuzumab: Evolution during
treatment with and without docetaxel in CLEOPATRA
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Harvard Univ, Sch Med, Boston, MA USA.
Vall dHebron Univ Hosp, Dept Oncol, Barcelona, Spain.
Seoul Natl Univ, Coll Med, Dept Internal Med, Div Hematol Med Oncol, Seoul, South Korea.
CHU Jean Minjoz, Besancon, France.
Roche Prod Ltd, Welwyn Garden City AL7 3AY, Herts, England.
MedStar Washington Hosp Ctr, Washington Canc Inst, Washington, DC USA.
NR 0
TC 3
Z9 3
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 597
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800010
ER
PT J
AU Beck, JT
Rugo, HS
Burris, HA
Baselga, J
Noguchi, S
Gnant, M
Pritchard, KI
Bennett, L
Ricci, JF
Hortobagyi, GN
AF Beck, J. Thaddeus
Rugo, Hope S.
Burris, Howard A.
Baselga, Jose
Noguchi, Shinzaburo
Gnant, Michael
Pritchard, Kathleen I.
Bennett, Lee
Ricci, Jean-Francois
Hortobagyi, Gabriel N.
TI BOLERO-2: Health-related quality-of-life in metastatic breast cancer
patients treated with everolimus and exemestane versus exemestane
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Highlands Oncol Grp, Fayetteville, AR USA.
Univ Calif San Francisco, San Francisco Helen Diller Family Comprehens Canc, San Francisco, CA 94143 USA.
Sarah Cannon Res Inst, Nashville, TN USA.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Harvard Univ, Sch Med, Boston, MA USA.
Osaka Univ, Dept Breast & Endocrine Surg, Osaka, Japan.
Med Univ Vienna, Dept Surg, Ctr Comprehens Canc, Vienna, Austria.
Univ Toronto, Sunnybrook Odette Canc Ctr, Toronto, ON, Canada.
RTI Hlth Solut, Res Triangle Pk, NC USA.
Wellmera AG, Basel, Switzerland.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 539
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800366
ER
PT J
AU Berry, DL
Hong, FX
Halpenny, B
Wang, Q
Partridge, AH
Fann, JR
Wolpin, S
Lober, WB
Bush, N
Bosco, JLF
Parvathaneni, U
Amtmann, D
Back, A
AF Berry, Donna Lynn
Hong, Fangxin
Halpenny, Barbara
Wang, Qian
Partridge, Ann H.
Fann, Jesse R.
Wolpin, Seth
Lober, William B.
Bush, Nigel
Bosco, Jaclyn Lee Fong
Parvathaneni, Upendra
Amtmann, Dagmar
Back, Anthony
TI Electronic self-report assessment for cancer: Results of a multisite
randomized trial.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Univ Washington, Seattle, WA 98195 USA.
Seattle Canc Care Alliance, Seattle, WA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 9008
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803173
ER
PT J
AU Blackwell, KL
Miles, D
Gianni, L
Krop, IE
Welslau, M
Baselga, J
Pegram, MD
Oh, DY
Dieras, V
Olsen, SR
Fang, L
Lu, MW
Guardino, E
Verma, S
AF Blackwell, Kimberly L.
Miles, David
Gianni, Luca
Krop, Ian E.
Welslau, Manfred
Baselga, Jose
Pegram, Mark D.
Do-Youn Oh
Dieras, Veronique
Olsen, Steven R.
Fang, Liang
Lu, Michael W.
Guardino, Ellie
Verma, Sunil
TI Primary results from EMILIA, a phase III study of trastuzumab emtansine
(T-DM1) versus capecitabine (X) and lapatinib (L) in HER2-positive
locally advanced or metastatic breast cancer (MBC) previously treated
with trastuzumab (T) and a taxane.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol
C1 Duke Univ, Med Ctr, Durham, NC USA.
Mt Vernon Canc Ctr, Middlesex, England.
Hosp San Raffaele, I-20132 Milan, Italy.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Harvard Univ, Sch Med, Boston, MA USA.
Univ Miami, Sylvester Comprehens Canc Ctr, Miami, FL USA.
Seoul Natl Univ Hosp, Dept Internal Med, Seoul 110744, South Korea.
Inst Curie, Dept Med Oncol, Paris, France.
Genentech Inc, San Francisco, CA 94080 USA.
Univ Toronto, Sunnybrook Odette Canc Ctr, Toronto, ON, Canada.
NR 0
TC 5
Z9 5
U1 1
U2 2
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 MAY 20
PY 2012
VL 30
IS 15
SU S
MA LBA1
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803703
ER
PT J
AU Blay, JY
Leahy, MG
Nguyen, BB
Patel, S
Santoro, A
Hohenberger, P
Demetri, GD
Lardelli, P
Perez, I
Chawla, SP
AF Blay, Jean-Yves
Leahy, Michael Gordon
Binh Bui Nguyen
Patel, Shreyaskumar
Santoro, Armando
Hohenberger, Peter
Demetri, George D.
Lardelli, Pilar
Perez, Iratxe
Chawla, Sant P.
TI Randomized multicenter phase III trial of trabectedin (T) versus
doxorubicin-based chemotherapy as first-line therapy in patients with
translocation-related sarcoma (TRS).
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Ctr Leon Berard, F-69373 Lyon, France.
Christie NHS Fdn Trust, Manchester, Lancs, England.
Inst Bergonie, Bordeaux, France.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Ist Clin Humanitas IRCCS, Humanitas Canc Ctr, Rozzano, Italy.
Univ Klinikum Mannheim, Mannheim, Germany.
Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
PharmaMar, Madrid, Spain.
Sarcoma Oncol Ctr, Santa Monica, CA USA.
RI Blay, Jean-Yves/N-3966-2016
OI Blay, Jean-Yves/0000-0001-7190-120X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA TPS10101
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801542
ER
PT J
AU Blay, JY
Chawla, SP
Ray-Coquard, I
Le Cesne, A
Staddon, AP
Milhem, MM
Penel, N
Riedel, RF
Nguyen, BB
Cranmer, LD
Reichardt, P
Bompas, E
Alcindor, T
Rushing, DA
Song, Y
Ebbinghaus, S
Haluska, FG
Dodion, PF
Demetri, GD
AF Blay, Jean-Yves
Chawla, Sant P.
Ray-Coquard, Isabelle
Le Cesne, Axel
Staddon, Arthur P.
Milhem, Mohammed M.
Penel, Nicolas
Riedel, Richard F.
Binh Bui Nguyen
Cranmer, Lee D.
Reichardt, Peter
Bompas, Emmanuelle
Alcindor, Thierry
Rushing, Daniel A.
Song, Yang
Ebbinghaus, Scot
Haluska, Frank G.
Dodion, Pierre F.
Demetri, George D.
TI Phase III, placebo-controlled trial (SUCCEED) evaluating ridaforolimus
as maintenance therapy in advanced sarcoma patients following clinical
benefit from prior standard cytotoxic chemotherapy: Long-term (>= 24
months) overall survival results.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Univ Lyon 1, Ctr Leon Berard, F-69365 Lyon, France.
Sarcoma Oncol Ctr, Santa Monica, CA USA.
Ctr Leon Berard, F-69373 Lyon, France.
Inst Gustave Roussy, Dept Med Oncol, Villejuif, France.
Univ Penn, Philadelphia, PA 19104 USA.
Univ Iowa Hosp & Clin, Iowa City, IA 52242 USA.
Ctr Oscar Lambret, F-59020 Lille, France.
Duke Univ, Med Ctr, Duke Canc Inst, Durham, NC USA.
Inst Bergonie, Bordeaux, France.
Univ Arizona, Ctr Canc, Tucson, AZ USA.
HELIOS Klinikum Bad Saarow, Bad Saarow Pieskow, Germany.
Ctr Rene Gauducheau, F-44035 Nantes, France.
McGill Univ, Ctr Hlth, Montreal, PQ, Canada.
Indiana Univ, Indianapolis, IN 46204 USA.
Merck & Co Inc, Whitehouse Stn, NJ USA.
Merck Res Labs, N Wales, PA USA.
ARIAD Pharmaceut Inc, Cambridge, MA 02139 USA.
Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
RI Blay, Jean-Yves/N-3966-2016
OI Blay, Jean-Yves/0000-0001-7190-120X
NR 0
TC 2
Z9 2
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 10010
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801327
ER
PT J
AU Bobiak, S
Choti, MA
Benson, AB
Strosberg, JR
Bloomston, M
Bergsland, EK
Zornosa, CC
Kulke, M
Nakakura, EK
Shah, MH
Yao, JC
AF Bobiak, Sarah
Choti, Michael A.
Benson, Al B.
Strosberg, Jonathan R.
Bloomston, Mark
Bergsland, Emily K.
Zornosa, Carrie C.
Kulke, Matthew
Nakakura, Eric K.
Shah, Manisha H.
Yao, James C.
TI Description of initial treatment for newly diagnosed metastatic
carcinoid (cNET) and pancreatic neuroendocrine (pNET) patients
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Natl Comprehens Canc Network, Ft Washington, PA USA.
Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
Ohio State Univ, Ctr Comprehens Canc, James Canc Hosp, Columbus, OH 43210 USA.
Solove Res Inst, Columbus, OH USA.
Univ Calif San Francisco, San Francisco Helen Diller Family Comprehens Canc, San Francisco, CA 94143 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
RI Bloomston, Mark/E-2767-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA e14542
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804889
ER
PT J
AU Boyer, MJ
Janne, PA
Mok, T
O'Byrne, KJ
Paz-Ares, LG
Ramalingam, SS
Liang, JQ
Taylor, I
Campbell, A
O'Connell, JP
Letrent, SP
Antic, V
AF Boyer, Michael J.
Janne, Pasi A.
Mok, Tony
O'Byrne, Kenneth John
Paz-Ares, Luis G.
Ramalingam, Suresh S.
Liang, Jane Q.
Taylor, Ian
Campbell, Alicyn
O'Connell, Joseph P.
Letrent, Stephen P.
Antic, Vladan
TI ARCHER: Dacomitinib (D; PF-00299804) versus erlotinib (E) for advanced
(adv) non-small cell lung cancer (NSCLC)-A randomized double-blind phase
III study.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Sydney Canc Ctr, Camperdown, NSW, Australia.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Chinese Univ Hong Kong, State Key Lab South China, Sha Tin, Hong Kong, Peoples R China.
St James Hosp, Dublin, Ireland.
Hosp Univ Virgen del Rocio, Seville, Spain.
Emory Univ, Winship Canc Inst, Atlanta, GA 30322 USA.
Pfizer Oncol, Groton, CT USA.
Pfizer Oncol, La Jolla, CA USA.
Pfizer AG, Zurich, Switzerland.
RI IBIS, NUEVAS TERAPIA/P-3415-2015
NR 0
TC 1
Z9 1
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA TPS7615
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804169
ER
PT J
AU Boyle, F
Smith, IE
O'Shaughnessy, J
Ejlertsen, B
Kaufmann, M
Buzdar, A
Fumoleau, P
Gradishar, WJ
Martin, M
Moy, B
Piccart-Gebhart, MJ
Pritchard, KI
Lindquist, D
Amonkar, M
Huang, YJ
Williams, LS
Wang, Q
Finkelstein, DM
Goss, PE
AF Boyle, Frances
Smith, Ian Edward
O'Shaughnessy, Joyce
Ejlertsen, Bent
Kaufmann, Manfred
Buzdar, Aman
Fumoleau, Pierre
Gradishar, William John
Martin, Miguel
Moy, Beverly
Piccart-Gebhart, Martine J.
Pritchard, Kathleen I.
Lindquist, Deborah
Amonkar, Mayur
Huang, Yingjie
Williams, Lisa Simone
Wang, Qing
Finkelstein, Dianne M.
Goss, Paul Edward
TI Lapatinib in HER2+early breast cancer: Quality of life analysis
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Mater Hosp, Sydney, NSW, Australia.
Royal Marsden Hosp, London SW3 6JJ, England.
Baylor Sammons Canc Ctr, Dallas, TX USA.
US Oncol, Dallas, TX USA.
Rigshosp, DK-2100 Copenhagen, Denmark.
Goethe Univ Frankfurt, D-60054 Frankfurt, Germany.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Ctr Georges Francois Leclerc, Dijon, France.
Northwestern Univ, Chicago, IL 60611 USA.
Hosp Univ Gregorio Maranon, Madrid, Spain.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
Inst Jules Bordet, B-1000 Brussels, Belgium.
Sunnybrook Odette Canc Ctr, Toronto, ON, Canada.
Arizona Oncol, Sedona, AZ USA.
US Oncol, Sedona, AZ USA.
GlaxoSmithKline, Collegeville, PA USA.
GlaxoSmithKline, Uxbridge, Middx, England.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 604
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800016
ER
PT J
AU Bradbury, AR
Moy, B
Peppercorn, JM
Egleston, B
Sands, CB
Sheikh-Salah, M
Storm, CD
Helft, PR
AF Bradbury, Angela R.
Moy, Beverly
Peppercorn, Jeffrey M.
Egleston, Brian
Sands, Colleen B.
Sheikh-Salah, Moktar
Storm, Courtney D.
Helft, Paul R.
TI Financial relationships with commercial interests (COI) among abstracts
at the ASCO Annual Meeting
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
Duke Univ, Med Ctr, Durham, NC USA.
ASCO, Alexandria, VA USA.
Indiana Univ, Indianapolis, IN 46204 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 6128
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800341
ER
PT J
AU Brahmer, JR
Horn, L
Antonia, S
Spigel, DR
Gandhi, L
Sequist, LV
Wigginton, J
McDonald, D
Kollia, G
Gupta, AK
Gettinger, SN
AF Brahmer, Julie R.
Horn, Leora
Antonia, Scott
Spigel, David R.
Gandhi, Leena
Sequist, Lecia V.
Wigginton, Jon
McDonald, Dan
Kollia, Georgia
Gupta, Ashok Kumar
Gettinger, Scott N.
TI Clinical activity and safety of anti-PD1 (BMS-936558, MDX-1106) in
patients with advanced non-small-cell lung cancer (NSCLC).
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
SCRI Tennessee Oncol PLLC, Nashville, TN USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Bristol Myers Squibb Co, Princeton, NJ USA.
Yale Univ, Sch Med, New Haven, CT USA.
NR 0
TC 8
Z9 9
U1 0
U2 4
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 7509
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804176
ER
PT J
AU Brastianos, PK
Horowitz, P
Santagata, S
Jones, RT
McKenna, A
Ligon, K
Palescandolo, E
Van Hummelen, P
Getz, G
Hahn, WC
Dunn, IF
Beroukhim, R
AF Brastianos, Priscilla Kaliopi
Horowitz, Peleg
Santagata, Sandro
Jones, Robert T.
McKenna, Aaron
Ligon, Keith
Palescandolo, Emanuele
Van Hummelen, Paul
Getz, Gad
Hahn, William C.
Dunn, Ian F.
Beroukhim, Rameen
TI Genomic characterization of meningiomas
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Brigham & Womens Hosp, Boston, MA 02115 USA.
Broad Inst MIT & Harvard, Cambridge, MA USA.
Dana Farber Canc Inst, Ctr Canc Genome Discovery, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 2020
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801373
ER
PT J
AU Brooks, G
Li, L
Sharma, DB
Schrag, D
AF Brooks, Gabriel
Li, Ling
Sharma, Dhruv B.
Schrag, Deborah
TI Regional variation in Medicare spending and survival among older adults
with advanced cancer.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 [Brooks, Gabriel; Li, Ling; Sharma, Dhruv B.; Schrag, Deborah] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 6003
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802842
ER
PT J
AU Brown, JR
Sharman, JP
Harb, WA
Kelly, KR
Schreeder, MT
Sweetenham, JW
Barr, PM
Foran, JM
Gabrilove, JL
Kipps, TJ
Ma, S
O'Brien, SM
Evans, E
Lounsbury, H
Silver, BA
Singh, J
Stiede, K
Westlin, W
Witowski, S
Mahadevan, D
AF Brown, Jennifer R.
Sharman, Jeff Porter
Harb, Wael A.
Kelly, Kevin R.
Schreeder, Marshall T.
Sweetenham, John W.
Barr, Paul M.
Foran, James M.
Gabrilove, Janice Lynn
Kipps, Thomas J.
Ma, Shuo
O'Brien, Susan Mary
Evans, Erica
Lounsbury, Heather
Silver, Bruce A.
Singh, Juswinder
Stiede, Kathryn
Westlin, William
Witowski, Steven
Mahadevan, Daruka
TI Phase Ib trial of AVL-292, a covalent inhibitor of Bruton's tyrosine
kinase (Btk), in chronic lymphocytic leukemia (CLL) and B-non-Hodgkin
lymphoma (B-NHL).
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
US Oncol, Willamette Valley Canc Inst, Springfield, OR USA.
Horizon Oncol Ctr, Lafayette, IN USA.
Univ Texas Hlth Sci Ctr San Antonio, Canc Therapy & Res Ctr, Inst Drug Dev, San Antonio, TX 78229 USA.
Clearview Canc Inst, Huntsville, AL USA.
Cleveland Clin Fdn, Cleveland, OH 44195 USA.
Univ Rochester, Med Ctr, Rochester, NY 14642 USA.
Mayo Clin, Ctr Canc, Jacksonville, FL 32224 USA.
Mt Sinai Sch Med, New York, NY USA.
Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA.
Northwestern Univ, Sch Med, Chicago, IL USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Avila Therapeut, Bedford, MA USA.
Univ Arizona, Ctr Canc, Tucson, AZ USA.
NR 0
TC 4
Z9 4
U1 1
U2 3
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 8032
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803716
ER
PT J
AU Bunnell, CA
Gross, A
Kalfin, M
Partridge, AH
Lane, S
Burstein, HJ
Fine, B
Hilton, N
Sullivan, C
Colicchio, L
Hagemeister, E
Kelly, A
Szabatura, A
Winer, E
Mann, S
Weingart, S
AF Bunnell, Craig A.
Gross, Anne
Kalfin, Michael
Partridge, Ann H.
Lane, Sharon
Burstein, Harold J.
Fine, Barbara
Hilton, Nancy
Sullivan, Clare
Colicchio, Lynn
Hagemeister, Erin
Kelly, Anne
Szabatura, Audrea
Winer, Eric
Mann, Susan
Weingart, Saul
TI Implementation of a team training program in the treatment of breast
cancer patients
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA e16515
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801124
ER
PT J
AU Butaney, M
Porter, J
Lindeman, NI
Janne, PA
Rabin, MS
Marcoux, JP
Johnson, BE
Jackman, DM
AF Butaney, Mohit
Porter, Jennifer
Lindeman, Neal Ian
Janne, Pasi A.
Rabin, Michael S.
Marcoux, J. Paul
Johnson, Bruce E.
Jackman, David Michael
TI Clinical characteristics of KRAS mutations in NSCLC and their impact on
outcomes to first-line chemotherapy
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 7588
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804386
ER
PT J
AU Cahill, DP
Beiko, J
Suki, D
Prabhu, SS
Weinberg, J
Lang, FF
Gilbert, MR
Rao, G
McCutcheon, IE
Aldape, KD
Sawaya, R
AF Cahill, Daniel P.
Beiko, Jason
Suki, Dima
Prabhu, Sujit S.
Weinberg, Jeffrey
Lang, Frederick F.
Gilbert, Mark R.
Rao, Ganesh
McCutcheon, Ian E.
Aldape, Kenneth D.
Sawaya, Raymond
TI IDH1 status and survival benefit from surgical resection of enhancing
and nonenhancing tumor in malignant astrocytomas
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
Univ Manitoba, Winnipeg, MB, Canada.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
RI Gilbert, Mark/J-7494-2016
OI Gilbert, Mark/0000-0003-2556-9722
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 2019
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801566
ER
PT J
AU Capelletti, M
Lipson, D
Otto, G
Yelensky, R
Ercan, D
Kim, J
Sasaki, H
Kim, HR
Park, SI
Ross, JS
Stephens, P
Cronin, MT
Janne, PA
AF Capelletti, Marzia
Lipson, Doron
Otto, Geoff
Yelensky, Roman
Ercan, Dalia
Kim, Jhingook
Sasaki, Hidefumi
Kim, Hyeong Ryul
Park, Seung-Il
Ross, Jeffrey S.
Stephens, Philip
Cronin, Maureen T.
Janne, Pasi Antero
TI Discovery of recurrent KIF5B-RET fusions and other targetable
alterations from clinical NSCLC specimens
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Fdn Med, Cambridge, MA USA.
Fdn Med Inc, Cambridge, MA USA.
Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Seoul, South Korea.
Nagoya City Univ, Grad Sch Med, Nagoya, Aichi, Japan.
Univ Ulsan, Coll Med, Asan Med Ctr, Seoul, South Korea.
Univ Ulsan, Coll Med, Asan Med Ctr, Dept Thorac Surg, Seoul, South Korea.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 7510
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804329
ER
PT J
AU Carvajal, RD
Chugh, R
Milhem, MM
Ryan, CW
George, S
Chmielowski, B
Agulnik, M
Rodler, ET
Elias, AD
Budd, GT
Tawbi, H
Movva, S
Van Tine, BA
Dickson, MA
Hensley, ML
Keohan, ML
Tap, WD
Bennett, CM
Maki, RG
Schwartz, GK
AF Carvajal, Richard D.
Chugh, Rashmi
Milhem, Mohammed M.
Ryan, Christopher W.
George, Suzanne
Chmielowski, Bartosz
Agulnik, Mark
Rodler, Eve T.
Elias, Anthony D.
Budd, G. Thomas
Tawbi, Hussein
Movva, Sujana
Van Tine, Brian Andrew
Dickson, Mark Andrew
Hensley, Martee Leigh
Keohan, Mary Louise
Tap, William D.
Bennett, Cathryn M.
Maki, Robert G.
Schwartz, Gary K.
TI Randomized multicenter double-blind phase II trial: The immunological
adjuvant OPT-821 with or without a trivalent ganglioside vaccine in
metastatic sarcoma patients following metastasectomy.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Univ Michigan, Ann Arbor, MI 48109 USA.
Univ Iowa Hosp & Clin, Iowa City, IA 52242 USA.
Oregon Hlth & Sci Univ, Knight Canc Inst, Portland, OR 97201 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Univ Calif Los Angeles, Translat Oncol Res Lab, Los Angeles, CA USA.
Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
Seattle Canc Care Alliance, Seattle, WA USA.
Univ Colorado, Ctr Canc, Aurora, CO USA.
Cleveland Clin, Cleveland, OH 44106 USA.
Univ Pittsburgh, Med Ctr Canc Pavil, Pittsburgh, PA USA.
Wihship Canc Inst Emory Midtown, Atlanta, GA USA.
Washington Univ, St Louis, MO USA.
MabVax Therapeut Inc, San Diego, CA USA.
Mt Sinai Sch Med, New York, NY USA.
RI Movva, Sujana/I-3513-2016
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA TPS10103
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801583
ER
PT J
AU Cervantes-Ruiperez, A
Juric, D
Hidalgo, M
Messersmith, WA
Blumenschein, GR
Baselga, J
Perez, DR
Dienstmann, R
Calles, A
Jimeno, A
Sanabria, S
Littman, C
Amler, LC
Pirzkall, A
Tabernero, J
AF Cervantes-Ruiperez, Andres
Juric, Dejan
Hidalgo, Manuel
Messersmith, Wells A.
Blumenschein, George R.
Baselga, Jose
Perez, Desamparados Roda
Dienstmann, Rodrigo
Calles, Antonio
Jimeno, Antonio
Sanabria, Sandra
Littman, Catherine
Amler, Lukas C.
Pirzkall, Andrea
Tabernero, Josep
TI A phase I study of MEHD7945A (MEHD), a first-in-class HER3/EGFR
dual-action antibody, in patients (pts) with refractory/recurrent
epithelial tumors: Expansion cohorts.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Univ Valencia, INCLIVA, Dept Hematol & Med Oncol, Valencia, Spain.
Massachusetts Gen Hosp, Dana Farber Canc Inst, Boston, MA 02114 USA.
START Madrid, Ctr Integral Oncol Clara Campal, Madrid, Spain.
Univ Colorado, Aurora, CO USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
Hosp Clin, Dept Med Oncol, Colorectal Unit, Dept Surg, Valencia, Spain.
Vall dHebron Univ Hosp, Mol Therapeut Res Unit, Barcelona, Spain.
Univ Colorado Denver, Div Med Oncol, Aurora, CO USA.
Genentech Inc, San Francisco, CA 94080 USA.
Vall dHebron Univ Hosp, Vall dHebron Inst Oncol, Barcelona, Spain.
NR 0
TC 2
Z9 2
U1 1
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 2568
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801689
ER
PT J
AU Chapman, PB
Hauschild, A
Robert, C
Larkin, JMG
Haanen, JBAG
Ribas, A
Hogg, D
Hamid, O
Ascierto, PA
Testori, A
Lorigan, P
Dummer, R
Sosman, JA
Garbe, C
Maio, M
Nolop, KB
Nelson, BJ
Joe, AK
Flaherty, KT
McArthur, GA
AF Chapman, Paul B.
Hauschild, Axel
Robert, Caroline
Larkin, James M. G.
Haanen, John B. A. G.
Ribas, Antoni
Hogg, David
Hamid, Omid
Ascierto, Paolo Antonio
Testori, Alessandro
Lorigan, Paul
Dummer, Reinhard
Sosman, Jeffrey Alan
Garbe, Claus
Maio, Michele
Nolop, Keith B.
Nelson, Betty J.
Joe, Andrew K.
Flaherty, Keith T.
McArthur, Grant A.
TI Updated overall survival (OS) results for BRIM-3, a phase III
randomized, open-label, multicenter trial comparing BRAF inhibitor
vemurafenib (vem) with dacarbazine (DTIC) in previously untreated
patients with BRAF(V600E)-mutated melanoma.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Univ Klinikum Schleswig Holstein, Kiel Schleswig Holstein, Germany.
Canc Inst Gustave Roussy, Villejuif, France.
Royal Marsden Hosp, London SW3 6JJ, England.
Antoni van Leeuwenhoek Hosp, Netherlands Canc Inst, Amsterdam, Netherlands.
Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90024 USA.
Princess Margaret Hosp, Dept Med Oncol, Toronto, ON M4X 1K9, Canada.
Univ Toronto, Toronto, ON, Canada.
Angeles Clin & Res Inst, Santa Monica, CA USA.
Ist Nazl Tumori Fdn Pascale, Unit Med Oncol & Innovat Therapy, Naples, Italy.
European Inst Oncol, Milan, Italy.
Univ Manchester, Manchester, Lancs, England.
Univ Zurich Hosp, Dept Dermatol, CH-8091 Zurich, Switzerland.
Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
Univ Tubingen, Tubingen, Germany.
Univ Hosp Siena, Siena, Italy.
Plexxikon Inc, Berkeley, CA USA.
Genentech Inc, San Francisco, CA 94080 USA.
Hoffmann La Roche Inc, Nutley, NJ 07110 USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
Peter MacCallum Canc Ctr, Dept Med Oncol, Melbourne, Vic, Australia.
RI Lorigan, Paul/J-6898-2015
OI Lorigan, Paul/0000-0002-8875-2164
NR 0
TC 38
Z9 38
U1 1
U2 9
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 8502
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800505
ER
PT J
AU Chodak, G
Schellhammer, PF
Whitmore, JB
Sims, RB
Kantoff, PW
AF Chodak, Gerald
Schellhammer, Paul F.
Whitmore, James Boyd
Sims, Robert Brownell
Kantoff, Philip W.
TI Overall survival (OS) benefit with sipuleucel-T by baseline PSA: An
exploratory analysis from the phase III IMPACT trial
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Weiss Mem Hosp, Chicago, IL USA.
Eastern Virginia Med Sch Urol Virginia, Norfolk, VA USA.
Dendreon Corp, Seattle, WA USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 4648
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802609
ER
PT J
AU Choti, MA
Bobiak, S
Strosberg, JR
Benson, A
Bloomston, M
Yao, JC
Zornosa, CC
Bergsland, EK
Kulke, M
Nakakura, EK
Shah, MH
AF Choti, Michael A.
Bobiak, Sarah
Strosberg, Jonathan R.
Benson, Al Bowen
Bloomston, Mark
Yao, James C.
Zornosa, Carrie C.
Bergsland, Emily K.
Kulke, Matthew
Nakakura, Eric K.
Shah, Manisha H.
TI Prevalence of functional tumors in neuroendocrine carcinoma: An analysis
from the NCCN NET database.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
Natl Comprehens Canc Network, Ft Washington, PA USA.
Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
Ohio State Univ, Ctr Comprehens Canc, James Canc Hosp, Columbus, OH 43210 USA.
Solove Res Inst, Columbus, OH USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
RI Bloomston, Mark/E-2767-2011
NR 0
TC 2
Z9 2
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 4126
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800598
ER
PT J
AU Choueiri, TK
Pal, SK
McDermott, DF
Ramies, DA
Morrissey, S
Lee, Y
Miles, D
Holland, J
Dutcher, JP
AF Choueiri, Toni K.
Pal, Sumanta Kumar
McDermott, David F.
Ramies, David A.
Morrissey, Stephanie
Lee, Yihua
Miles, Dale
Holland, Jaymes
Dutcher, Janice P.
TI Efficacy of cabozantinib (XL184) in patients (pts) with metastatic,
refractory renal cell carcinoma (RCC)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Harvard Univ, Brigham & Womens Hosp, Sch Med, Lank Ctr Genitourinary Oncol,Dana Farber Canc Ins, Boston, MA 02115 USA.
City Hope Natl Med Ctr, Duarte, CA USA.
Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
Exelixis, San Francisco, CA USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
St Lukes Roosevelt Hosp, New York, NY USA.
NR 0
TC 11
Z9 11
U1 0
U2 3
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 4504
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802872
ER
PT J
AU Clark, RM
Growdon, WB
Wiechert, A
del Carmen, MG
Goodman, A
Boruta, DM
Bradford, L
Garrett, LA
Schorge, JO
AF Clark, Rachel Marie
Growdon, Whitfield Board
Wiechert, Andrew
del Carmen, Marcela G.
Goodman, Annekathryn
Boruta, David M.
Bradford, Leslie
Garrett, Leslie A.
Schorge, John O.
TI Hospital readmission after surgical cytoreduction for epithelial ovarian
carcinoma: An assessment of risk
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 [Clark, Rachel Marie; Growdon, Whitfield Board; Wiechert, Andrew; del Carmen, Marcela G.; Goodman, Annekathryn; Boruta, David M.; Bradford, Leslie; Garrett, Leslie A.; Schorge, John O.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA e15545
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803471
ER
PT J
AU Cohen, SJ
Feng, Y
Landry, JC
Staley, CA
Whittington, R
Sigurdson, ER
Nimeiri, HS
Verma, UN
Benson, A
AF Cohen, Steven J.
Feng, Yang
Landry, Jerome Carl
Staley, Charles A.
Whittington, Richard
Sigurdson, Elin R.
Nimeiri, Halla Sayed
Verma, Udit N.
Benson, Al Bowen
TI Phase II study of preoperative radiation with concurrent capecitabine,
oxaliplatin, and bevacizumab followed by surgery and postoperative 5-FU,
leucovorin, oxaliplatin (FOLFOX), and bevacizumab in patients with
locally advanced rectal cancer: A trial of the Eastern Cooperative
Oncology Group (E3204)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Emory Univ, Dept Radiat Oncol, Winship Canc Inst, Atlanta, GA 30322 USA.
Emory Univ, Winship Canc Inst, Atlanta, GA 30322 USA.
VA Med Ctr, Philadelphia, PA USA.
Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 3605
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804673
ER
PT J
AU Corcoran, RB
Falchook, GS
Infante, JR
Hamid, O
Messersmith, WA
Kwak, EL
Ryan, DP
Kurzrock, R
Brenner, AA
Luan, J
Sun, P
Allred, AJ
Little, SM
Patel, K
Kopetz, S
Venook, AP
AF Corcoran, Ryan Bruce
Falchook, Gerald Steven
Infante, Jeffrey R.
Hamid, Omid
Messersmith, Wells A.
Kwak, Eunice Lee
Ryan, David P.
Kurzrock, Razelle
Brenner, Adrienne A.
Luan, Jennifer
Sun, Peng
Allred, Alicia J.
Little, Shonda M.
Patel, Kiran
Kopetz, Scott
Venook, Alan Paul
TI BRAF V600 mutant colorectal cancer (CRC) expansion cohort from the phase
I/II clinical trial of BRAF inhibitor dabrafenib (GSK2118436) plus MEK
inhibitor trametinib (GSK1120212)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapeut, Houston, TX 77030 USA.
Tennessee Oncol PLLC, Sarah Cannon Res Inst, Nashville, TN USA.
Angeles Clin & Res Inst, Dept Med Oncol, Los Angeles, CA USA.
Univ Colorado, Dept Med Oncol, Aurora, CO USA.
Univ Calif San Francisco, San Francisco, CA 94143 USA.
GlaxoSmithKline, Collegeville, PA USA.
Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 3528
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804562
ER
PT J
AU Corcoran, RB
Falchook, GS
Infante, JR
Hamid, O
Messersmith, WA
Kwak, EL
Ryan, DP
Kurzrock, R
Brenner, AA
Luan, J
Sun, P
Allred, AJ
Little, SM
Patel, K
Kopetz, S
Venook, AP
AF Corcoran, Ryan Bruce
Falchook, Gerald Steven
Infante, Jeffrey R.
Hamid, Omid
Messersmith, Wells A.
Kwak, Eunice Lee
Ryan, David P.
Kurzrock, Razelle
Brenner, Adrienne A.
Luan, Jennifer
Sun, Peng
Allred, Alicia J.
Little, Shonda M.
Patel, Kiran
Kopetz, Scott
Venook, Alan Paul
TI BRAF V600 mutant colorectal cancer (CRC) expansion cohort from the phase
I/II clinical trial of BRAF inhibitor dabrafenib (GSK2118436) plus MEK
inhibitor trametinib (GSK1120212).
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapeut, Houston, TX 77030 USA.
Tennessee Oncol PLLC, Sarah Cannon Res Inst, Nashville, TN USA.
Angeles Clin & Res Inst, Dept Med Oncol, Los Angeles, CA USA.
Univ Colorado, Dept Med Oncol, Aurora, CO USA.
Univ Calif San Francisco, San Francisco, CA 94143 USA.
GlaxoSmithKline, Collegeville, PA USA.
Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 3528
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802046
ER
PT J
AU Corless, CL
Neff, T
Heinrich, MC
Beadling, C
AF Corless, Christopher L.
Neff, Tanaya
Heinrich, Michael C.
Beadling, Carol
TI Combining semiconductor-based sequencing with amplicon-based cancer gene
panels: A rapid next-gen approach to clinical cancer genotyping.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Oregon Hlth & Sci Univ, Knight Diagnost Labs, Portland, OR 97201 USA.
Portland VA Med Ctr, Portland, OR USA.
Oregon Hlth & Sci Univ, Knight Canc Inst, Portland, OR 97201 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 10591
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803550
ER
PT J
AU Cortes, J
Baselga, J
Im, YH
Ross, G
Clark, E
Knott, A
Swain, SM
AF Cortes, Javier
Baselga, Jose
Im, Young-Hyuck
Ross, Graham
Clark, Emma
Knott, Adam
Swain, Sandra M.
TI Quality of life assessment in CLEOPATRA, a phase III study combining
pertuzumab with trastuzumab and docetaxel in metastatic breast cancer.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Vall dHebron Univ Hosp, Dept Oncol, Barcelona, Spain.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Harvard Univ, Sch Med, Boston, MA USA.
Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Med,Div Hematol Oncol, Seoul, South Korea.
Roche Prod Ltd, Welwyn Garden City AL7 3AY, Herts, England.
MedStar Washington Hosp Ctr, Washington Canc Inst, Washington, DC USA.
NR 0
TC 2
Z9 2
U1 0
U2 3
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 598
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800205
ER
PT J
AU Cortes, JE
Kim, DW
Pinilla-Ibarz, J
Paquette, R
le Coutre, PD
Chuah, C
Nicolini, FE
Apperley, J
Khoury, HJ
Talpaz, M
DiPersio, JF
DeAngelo, DJ
Rea, D
Abruzzese, E
Muller, MC
Baccarani, M
Gambacorti-Passerini, C
Turner, CD
Haluska, FG
Kantarjian, H
AF Cortes, Jorge E.
Kim, Dong-Wook
Pinilla-Ibarz, Javier
Paquette, Ronald
le Coutre, Philipp D.
Chuah, Charles
Nicolini, Franck E.
Apperley, Jane
Khoury, Hanna Jean
Talpaz, Moshe
DiPersio, John F.
DeAngelo, Daniel J.
Rea, Delphine
Abruzzese, Elisabetta
Mueller, Martin C.
Baccarani, Michele
Gambacorti-Passerini, Carlo
Turner, Christopher D.
Haluska, Frank G.
Kantarjian, Hagop
TI PACE: A pivotal phase II trial of ponatinib in patients with CML and Ph
plus ALL resistant or intolerant to dasatinib or nilotinib, or with the
T315I mutation.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Catholic Univ Korea, Seoul, South Korea.
Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
Ronald Reagan UCLA Med Ctr, Los Angeles, CA USA.
Charite, D-13353 Berlin, Germany.
Singapore Gen Hosp, Singapore, Singapore.
Ctr Hosp Lyon Sud, Pierre Benite, France.
Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, London, England.
Emory Winship Canc Inst, Atlanta, GA USA.
Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
Washington Univ, Sch Med, St Louis, MO USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Hop St Louis, Serv Malad Sang, Paris, France.
Osped S Eugenio, Rome, Italy.
Heidelberg Univ, Med Fak Mannheim, Med Klin 3, Mannheim, Germany.
Univ Hosp Bologna, Bologna, Italy.
Univ Milano Bicocca, Azienda Osped San Gerardo, Unita Ric Clin Ematol, Monza, Italy.
ARIAD Pharmaceut, Cambridge, MA USA.
NR 0
TC 1
Z9 1
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 6503
PG 2
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801016
ER
PT J
AU D'Ambrosio, L
Brusa, F
D'Ascenzo, F
Cavallero, E
Biondi-Zoccai, G
Boccone, P
Bironzo, P
Levin, GN
Eckel, RH
Milani, RV
Sagalowsky, AI
Gasparini, M
Grignani, G
Gaita, F
Ciuffreda, L
Aglietta, M
AF D'Ambrosio, Lorenzo
Brusa, Federica
D'Ascenzo, Fabrizio
Cavallero, Erica
Biondi-Zoccai, Giuseppe
Boccone, Paola
Bironzo, Paolo
Levin, Glenn N.
Eckel, Robert H.
Milani, Richard V.
Sagalowsky, Arthur I.
Gasparini, Mauro
Grignani, Giovanni
Gaita, Fiorenzo
Ciuffreda, Libero
Aglietta, Massimo
TI Risk of adverse cardiovascular events (CVE) and incident diabetes
mellitus (DM) in patients (pts) with prostate cancer (PC) treated with
androgen deprivation therapy (ADT): A meta-analysis of adjusted
observational results
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Inst Canc Res & Treatment, Candiolo, Italy.
Ctr Oncol & Ematol Subalpino, Turin, Italy.
Univ Turin, Div Cardiol, Turin, Italy.
Univ Modena & Reggio Emilia, Div Cardiol, Modena, Italy.
Baylor Coll Med, Cardiac Care Unit, Houston, TX 77030 USA.
Michael E DeBakey Med Ctr, Houston, TX USA.
Univ Colorado, Aurora, CO USA.
Ochsner Med Ctr, Div Cardiol, New Orleans, LA USA.
Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
Politecn Torino, Dept Math, I-10128 Turin, Italy.
Univ Turin, Div Cardiol, Corso Dogliotti, Italy.
AOU S Giovanni Battista Molinette, Div Oncol, Turin, Italy.
RI Milani, Richard/A-6045-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA e15192
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802859
ER
PT J
AU Luu, DCN
Mamet, R
Zornosa, CC
Niland, JC
D'Amico, TA
Kalemkerian, GP
Koczywas, M
Pisters, K
Rabin, MS
Otterson, GA
AF Dai Chu Nguyen Luu
Mamet, Rizvan
Zornosa, Carrie C.
Niland, Joyce C.
D'Amico, Thomas A.
Kalemkerian, Gregory Peter
Koczywas, Marianna
Pisters, Katherine
Rabin, Michael S.
Otterson, Gregory Alan
TI Retrospective analysis of the impact of age on overall survival in
patients with non-small cell lung cancer.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Ohio State Univ, Med Ctr, Columbus, OH 43210 USA.
City Hope Natl Med Ctr, Duarte, CA USA.
Natl Comprehens Canc Network, Ft Washington, PA USA.
Duke Univ, Med Ctr, Durham, NC USA.
Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Ohio State Univ, Dept Internal Med, Ctr Comprehens Canc, Columbus, OH 43210 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA e18018
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804097
ER
PT J
AU Dang, CT
Gianni, L
Romieu, G
Dirix, L
Campone, M
Citron, ML
Zamagni, C
Krop, IE
Xu, N
Smitt, M
Suter, T
AF Dang, Chau T.
Gianni, Luca
Romieu, Gilles
Dirix, Luc
Campone, Mario
Citron, Marc L.
Zamagni, Claudio
Krop, Ian E.
Xu, Na
Smitt, Melanie
Suter, Thomas
TI Cardiac safety in a phase II study of trastuzumab emtansine (T-DM1)
following anthracycline-based chemotherapy as adjuvant or neoadjuvant
therapy for early-stage HER2-positive breast cancer.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Hosp San Raffaele, I-20132 Milan, Italy.
CRLC Val dAurelle, Montpellier, France.
Sint Augustinus Hosp, Brussels, Belgium.
Inst Cancerol Ouest Rene Gauducheau, Nantes, France.
Albert Einstein Coll Med, Lake Success, NY USA.
St Orsola Marcello Malpighi Hosp, Addarii Med Oncol Unit, Bologna, Italy.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Genentech Inc, San Francisco, CA 94080 USA.
Univ Hosp Bern, CH-3010 Bern, Switzerland.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 532
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800125
ER
PT J
AU De Bono, JS
Fizazi, K
Saad, F
Taplin, ME
Sternberg, CN
Miller, K
Mulders, P
Chi, KN
Armstrong, AJ
Hirmand, M
Selby, B
Scher, HI
AF De Bono, Johann Sebastian
Fizazi, Karim
Saad, Fred
Taplin, Mary-Ellen
Sternberg, Cora N.
Miller, Kurt
Mulders, Peter
Chi, Kim N.
Armstrong, Andrew J.
Hirmand, Mohammad
Selby, Brian
Scher, Howard I.
CA AFFIRM Investigators
TI Primary, secondary, and quality-of-life endpoint results from the phase
III AFFIRM study of MDV3100, an androgen receptor signaling inhibitor
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Inst Canc Res, London SW3 6JB, England.
Univ Paris 11, Orsay, France.
Univ Montreal Hosp Ctr, Montreal, PQ, Canada.
Dana Farber Canc Inst, Boston, MA 02115 USA.
San Camillo & Forlanini Hosp, Rome, Italy.
Charite, D-13353 Berlin, Germany.
Radboud Univ Nijmegen, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
British Columbia Canc Agcy, Vancouver Canc Ctr, Vancouver, BC V5Z 4E6, Canada.
Duke Univ, Med Ctr, Duke Canc Inst, Durham, NC USA.
Medivation Inc, San Francisco, CA USA.
Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
RI Mulders, Peter/H-8076-2014
NR 0
TC 9
Z9 9
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 4519
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802767
ER
PT J
AU Demetri, GD
Reichardt, P
Kang, YK
Blay, JY
Joensuu, H
Maki, RG
Rutkowski, P
Hohenberger, P
Gelderblom, H
Leahy, MG
von Mehren, M
Schoffski, P
Blackstein, ME
Le Cesne, A
Badalamenti, G
Xu, JM
Nishida, T
Laurent, D
Kuss, I
Casali, PG
AF Demetri, George D.
Reichardt, Peter
Kang, Yoon-Koo
Blay, Jean-Yves
Joensuu, Heikki
Maki, Robert G.
Rutkowski, Piotr
Hohenberger, Peter
Gelderblom, Hans
Leahy, Michael Gordon
von Mehren, Margaret
Schoffski, Patrick
Blackstein, Martin E.
Le Cesne, Axel
Badalamenti, Giuseppe
Xu, Jian-Ming
Nishida, Toshirou
Laurent, Dirk
Kuss, Iris
Casali, Paolo Giovanni
CA GRID Invest
TI Randomized phase III trial of regorafenib in patients (pts) with
metastatic and/or unresectable gastrointestinal stromal tumor (GIST)
progressing despite prior treatment with at least imatinib (IM) and
sunitinib (SU): GRID trial.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
HELIOS Klinikum Bad Saarow, Bad Saarow Pieskow, Germany.
Univ Ulsan, Coll Med, Asan Med Ctr, Seoul, South Korea.
Univ Lyon 1, Ctr Leon Berard, F-69365 Lyon, France.
Univ Helsinki, Cent Hosp, Dept Oncol, Helsinki, Finland.
Mt Sinai Sch Med, New York, NY USA.
Maria Sklodowska Curie Mem Canc Ctr, Warsaw, Poland.
Inst Oncol, Warsaw, Poland.
Univ Mannheim, Med Ctr, Dept Surg, D-68131 Mannheim, Germany.
Leiden Univ, Med Ctr, Dept Clin Oncol, Leiden, Netherlands.
Christie NHS Fdn Trust, Manchester, Lancs, England.
Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
Univ Ziekenhuis Gasthuisberg, Louvain, Belgium.
Mt Sinai Hosp, Toronto, ON M5G 1X5, Canada.
Inst Gustave Roussy, Villejuif, France.
Univ Palermo, Dept Oncol, Div Med Oncol, Palermo, Italy.
Acad Mil Med Sci, Affiliated Hosp, Beijing, Peoples R China.
Osaka Police Hosp, Dept Surg, Osaka, Japan.
Bayer HealthCare Pharmaceut, Berlin, Germany.
Fdn IRCCS Ist Nazl Tumori, Milan, Italy.
RI Blay, Jean-Yves/N-3966-2016
OI Blay, Jean-Yves/0000-0001-7190-120X
NR 0
TC 2
Z9 2
U1 0
U2 0
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 MAY 20
PY 2012
VL 30
IS 15
SU S
MA LBA10008
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801304
ER
PT J
AU Desai, P
Braun, E
Dehghan-Paz, I
Gattuso, P
Canar, J
Cobleigh, MA
AF Desai, Palak
Braun, Eduardo
Dehghan-Paz, Irene
Gattuso, Paolo
Canar, Jeff
Cobleigh, Melody A.
TI Synchronous bilateral breast cancer (SBBC): Concordance of receptor
status between right and left breast
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Rush Univ, Med Ctr, Chicago, IL 60612 USA.
US Dept Vet Affairs, Vet Affairs Edward Hines Jr Hosp, Hines, IL 60141 USA.
Rush Univ, Natl Surg Adjuvant Breast & Bowel Project, Med Ctr, Chicago, IL 60612 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 572
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800078
ER
PT J
AU Dimopoulos, MA
Facon, T
Richardson, PGG
Orlowski, RZ
San-Miguel, JF
Lonial, S
Anderson, KC
Moreau, P
Reece, DE
Singhal, A
Shazer, RL
Kopit, J
Palumbo, AP
AF Dimopoulos, Meletios A.
Facon, Thierry
Richardson, Paul Gerard Guy
Orlowski, Robert Z.
San-Miguel, Jesus F.
Lonial, Sagar
Anderson, Kenneth Carl
Moreau, Philippe
Reece, Donna Ellen
Singhal, Anil
Shazer, Ronald L.
Kopit, Justin
Palumbo, Antonio Pierangelo
TI ELOQUENT-1: A phase III, randomized, open-label trial of
lenalidomide/dexamethasone with or without elotuzumab in subjects with
previously untreated multiple myeloma (CA204-006).
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Hellen Cooperat Oncol Grp, Athens, Greece.
Hop Claude Huriez, Lille, France.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Hosp Univ Salamanca, Salamanca, Spain.
Multiple Myeloma Res Consortium, Norwalk, CT USA.
Emory Univ, Winship Canc Inst, Atlanta, GA 30322 USA.
Univ Hosp, Nantes, France.
Princess Margaret Hosp, Program Multiple Myeloma, Toronto, ON M4X 1K9, Canada.
Abbott Biotherapeut, Redwood City, CA USA.
Bristol Myers Squibb Co, Wallingford, CT 06492 USA.
Bristol Myers Squibb Co, Princeton, NJ USA.
Univ Turin, Turin, Italy.
RI FACON, THIERRY/M-9736-2014; richard, chrystelle/K-8595-2015
OI FACON, THIERRY/0000-0001-7705-8460;
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA TPS8113
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804080
ER
PT J
AU Drake, CG
Fishman, MN
Curti, BD
Kim, JJ
Stadler, WM
McNeel, DG
Choueiri, TK
Redman, B
Hudes, GR
Jure-Kunkel, M
McDonald, D
Gupta, AK
Pathak, AK
Wigginton, J
Sznol, M
AF Drake, Charles G.
Fishman, Mayer N.
Curti, Brendan D.
Kim, Jenny J.
Stadler, Walter Michael
McNeel, Douglas G.
Choueiri, Toni K.
Redman, Bruce
Hudes, Gary R.
Jure-Kunkel, Maria
McDonald, Dan
Gupta, Ashok Kumar
Pathak, Ashutosh Kumar
Wigginton, Jon
Sznol, Mario
TI An exploratory study to investigate the immunomodulatory activity of
BMS-936558 in patients with metastatic clear-cell renal cell carcinoma.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
H Lee Moffitt Canc Canter & Res Inst, Tampa, FL USA.
Providence Onc & Hem Clin, Portland, OR USA.
Univ Chicago, Chicago, IL 60637 USA.
Univ Wisconsin, Carbone Canc Ctr, Madison, WI USA.
Harvard Univ, Brigham & Womens Hosp, Sch Med, Dana Farber Canc Inst,Lank Ctr Genitourinary Onco, Boston, MA 02115 USA.
Univ Michigan, Ann Arbor, MI 48109 USA.
Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
Bristol Myers Squibb Co, Princeton, NJ USA.
Yale Canc Ctr, New Haven, CT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA TPS2613
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802123
ER
PT J
AU Drapkin, BJ
Sadrzadeh, H
Brunner, AM
Werner, L
Babirak, L
Attar, EC
Ballen, KK
McAfee, SL
Amrein, PC
Chen, YBA
Stone, RM
Fathi, AT
AF Drapkin, Benjamin Jacob
Sadrzadeh, Hossein
Brunner, Andrew Mark
Werner, Lillian
Babirak, Loren
Attar, Eyal C.
Ballen, Karen K.
McAfee, Steven L.
Amrein, Philip C.
Chen, Yi-Bin Albert
Stone, Richard M.
Fathi, Amir Tahmasb
TI A seasonal pattern of presentation in younger patients with de novo
acute myeloid leukemia (AML).
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 6617
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802366
ER
PT J
AU DuBois, SG
Krailo, MD
Gebhardt, MC
Donaldson, SS
Marcus, KC
Dormans, JP
Shamberger, RC
Sailer, SL
Nicholas, RW
Healey, JH
Tarbell, N
Devidas, M
Meyer, JS
Granowetter, L
Womer, R
Bernstein, ML
Marina, N
Grier, HE
AF DuBois, Steven G.
Krailo, Mark D.
Gebhardt, Mark C.
Donaldson, Sarah S.
Marcus, Karen Chayt
Dormans, John P.
Shamberger, Robert C.
Sailer, Scott Lee
Nicholas, Richard W.
Healey, John H.
Tarbell, Nancy
Devidas, Meenakshi
Meyer, James S.
Granowetter, Linda
Womer, Richard
Bernstein, Mark L.
Marina, Neyssa
Grier, Holcombe E.
TI Evaluation of local control strategies in patients with localized Ewing
sarcoma of bone: A report from the Children's Oncology Group.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Univ Calif San Francisco, San Francisco, CA 94143 USA.
Childrens Oncol Grp, Arcadia, CA USA.
Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
Stanford Canc Ctr, Stanford, CA USA.
Childrens Hosp, Boston, MA 02115 USA.
Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
Canc Ctr N Carolina, Cary, NC USA.
Univ Arkansas Med Sci, Little Rock, AR 72205 USA.
Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Harvard Univ, Sch Med, Boston, MA USA.
Childrens Oncol Grp, Gainesville, FL USA.
NYU, New York, NY USA.
IWK Hlth Ctr, Halifax, NS, Canada.
Stanford Univ, Sch Med, Palo Alto, CA 94304 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 9537
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802115
ER
PT J
AU Dueck, AC
Mendoza, TR
Mitchell, SA
Reeve, BB
Castro, KM
Denicoff, A
O'Mara, AM
Rogak, LJ
Clauser, SB
Bryant, DM
Gillis, TA
Bearden, JD
Siegel, RD
Harness, JK
Paul, DB
Cleeland, CS
Sloan, JA
Schrag, D
Minasian, LM
Basch, EM
AF Dueck, Amylou C.
Mendoza, Tito R.
Mitchell, Sandra A.
Reeve, Bryce B.
Castro, Kathleen M.
Denicoff, Andrea
O'Mara, Ann M.
Rogak, Lauren J.
Clauser, Steven B.
Bryant, Donna M.
Gillis, Theresa A.
Bearden, James D.
Siegel, Robert D.
Harness, Jay K.
Paul, Diane B.
Cleeland, Charles S.
Sloan, Jeff A.
Schrag, Deborah
Minasian, Lori M.
Basch, Ethan M.
TI Validity and reliability of the patient-reported outcomes version of the
common terminology criteria for adverse events (PRO-CTCAE)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Mayo Clin, Scottsdale, AZ USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
NCI, Bethesda, MD 20892 USA.
Univ N Carolina, Chapel Hill, NC USA.
NCI, Rockville, MD USA.
Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Canc Program Our Lady Lake & Mary Bird Perkins, Baton Rouge, LA USA.
Christiana Care Hlth Syst, Helen F Graham Canc Ctr, Newark, DE USA.
Gibbs Canc Ctr, Spartanburg, SC USA.
Hartford Hosp, Helen & Harry Gray Canc Ctr, Hartford, CT 06115 USA.
St Joseph Hosp Orange, Ctr Canc Prevent & Treatment, Orange, CA USA.
Mayo Clin, Rochester, MN USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 1
Z9 1
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 9047
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804389
ER
PT J
AU Durie, BG
Moreau, P
Sonneveld, P
Morgan, GJ
Lahuerta, JJ
Beksac, M
Terpos, E
Hajek, R
Hungria, VTD
Maiolino, A
Chng, W
Lee, JH
Jian, H
Richardson, PGG
Chen, WM
Knop, S
Hoerring, A
Leleu, X
San-Miguel, JF
Kumar, S
AF Durie, Brian G.
Moreau, Philippe
Sonneveld, Pieter
Morgan, Gareth J.
Lahuerta, Juan Jose
Beksac, Meral
Terpos, Evangelos
Hajek, Roman
de Moraes Hungria, Vania Tietsche
Maiolino, Angelo
Chng, WeeJoo
Lee, Jae Hoon
Jian, Hou
Richardson, Paul Gerard Guy
Chen, Wenming
Knop, Stefan
Hoerring, Antje
Leleu, Xavier
San-Miguel, Jesus F.
Kumar, Shaji
CA Int Myeloma Working Grp
TI Regional differences in the treatment approaches for relapsed multiple
myeloma: An IMF study.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Cedars Sinai Comprehens Canc Ctr, Los Angeles, CA USA.
Univ Hosp Nantes, Nantes, France.
Erasmus Univ, Med Ctr, Rotterdam, Netherlands.
Royal Marsden Hosp, Inst Canc Res, London SW3 6JJ, England.
Univ Hosp, Serv Hematol, Madrid, Spain.
Ankara Univ, Sch Med, TR-06100 Ankara, Turkey.
Univ Athens, Athens, Greece.
Univ Hosp Brno, Brno, Czech Republic.
Irmandade Santa Casa de Misericordia Sao Paulo, Sao Paulo, Brazil.
Univ Fed Rio de Janeiro, Hosp Univ Clementino Fraga Filho, Rio De Janeiro, Brazil.
Natl Univ Hlth Syst, Queenstown, Singapore.
Gachon Univ Gil Hosp, Dept Internal Med, Inchon, South Korea.
Shanghai Changzheng Hosp, Shanghai, Peoples R China.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Beijing Chaoyang Hosp, Beijing, Peoples R China.
Univ Wurzburg, D-97070 Wurzburg, Germany.
Canc Res & Biostat, Seattle, WA USA.
Hop Claude Huriez, Serv Malad Sang, Lille, France.
Hosp Univ Salamanca, Salamanca, Spain.
Mayo Clin, Rochester, MN USA.
RI Kumar, Shaji/A-9853-2008; richard, chrystelle/K-8595-2015
OI Kumar, Shaji/0000-0001-5392-9284;
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 8095
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804019
ER
PT J
AU Edelman, MJ
Tan, MT
Fidler, MJ
Sanborn, RE
Otterson, GA
Sequist, LV
Evans, TL
Schneider, BJ
Keresztes, R
Rogers, JS
de Mayolo, JA
Medeiros, M
Zaknoen, SL
AF Edelman, Martin J.
Tan, Ming Tony
Fidler, Mary J.
Sanborn, Rachel E.
Otterson, Gregory Alan
Sequist, Lecia V.
Evans, Tracey L.
Schneider, Bryan J.
Keresztes, Roger
Rogers, John S.
de Mayolo, Jorge Antunez
Medeiros, Michelle
Zaknoen, Sara L.
TI A randomized, double-blind, placebo-controlled multicenter phase II
study of the COX-2 inhibitor apricoxib (A) in combination with either
docetaxel (doc) or pemetrexed (pem) in advanced non-small cell lung
cancer (NSCLC) patients (pts) selected by urinary PGE-m suppression.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Univ Maryland, Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
Rush Univ, Med Ctr, Chicago, IL 60612 USA.
Providence Portland Med Ctr, Portland, OR USA.
Ohio State Univ, Dept Internal Med, Ctr Comprehens Canc, Columbus, OH 43210 USA.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
Weill Cornell Med Coll, New York, NY USA.
SUNY Stony Brook, Stony Brook, NY 11794 USA.
W Virginia Univ, Sch Med, Mary Babb Randolph Canc Ctr, Morgantown, WV 26506 USA.
Mercy Res Inst, Miami, FL USA.
Univ Maryland, Sch Med, Marlene & Stewart Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
Tragara Pharmaceut, San Diego, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 7546
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804123
ER
PT J
AU Eisenberger, MA
Kattan, MW
Sternberg, CN
De Wit, R
Epstein, JI
Ecstein-Fraisse, EB
Kibel, AS
AF Eisenberger, Mario A.
Kattan, Michael W.
Sternberg, Cora N.
De Wit, Ronald
Epstein, Jonathan I.
Ecstein-Fraisse, Evelyne B.
Kibel, Adam Stuart
TI A multinational phase III adjuvant study of immediate (I) versus
deferred (D) chemotherapy (C)/hormone therapy (HT) after radical
prostatectomy (RP): TAX-3501
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
Cleveland Clin, Dept Quantitat Hlth Sci, Cleveland, OH 44106 USA.
San Camillo Hosp, Rome, Italy.
Forlanini Hosp, Rome, Italy.
Erasmus Univ, Med Ctr, Rotterdam, Netherlands.
Johns Hopkins Sch Med, Baltimore, MD USA.
Sanofi, Paris, France.
Brigham & Womens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 4570
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803347
ER
PT J
AU El-Jawahri, A
Traeger, L
Park, ER
Greer, JA
Pirl, WF
Lennes, IT
Jackson, VA
Gallagher, ER
Temel, JS
AF El-Jawahri, Areej
Traeger, Lara
Park, Elyse R.
Greer, Joseph A.
Pirl, William F.
Lennes, Inga Tolin
Jackson, Vicki A.
Gallagher, Emily R.
Temel, Jennifer S.
TI Advanced gastrointestinal cancer patients' perceptions of prognosis and
goals of treatment.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 6106
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802572
ER
PT J
AU Emadi, A
Sadrzadeh, H
Patal, P
Burns, KH
Duffield, A
Ballen, KK
Amrein, PC
Attar, EC
Smith, BD
Fathi, AT
AF Emadi, Ashkan
Sadrzadeh, Hossein
Patal, Payal
Burns, Kathleen H.
Duffield, Amy
Ballen, Karen K.
Amrein, Philip C.
Attar, Eyal C.
Smith, B. Douglas
Fathi, Amir Tahmasb
TI History of autoimmunity to predict clinical response to DNA
methyltransferase inhibitors (DNMTI) in myelodysplastic syndromes (MDS),
and MDS-derived acute myeloid leukemias (AML).
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Johns Hopkins Univ, Baltimore, MD USA.
Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 6629
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801325
ER
PT J
AU Enzinger, PC
Kwak, EL
Szymonifka, J
Abrams, TA
Regan, E
Malinowski, P
Shih, KC
Allen, JN
Jackson, N
Chan, JA
Fidias, P
Ryan, DP
Fuchs, CS
Bendell, JC
AF Enzinger, Peter C.
Kwak, Eunice Lee
Szymonifka, Jackie
Abrams, Thomas Adam
Regan, Eileen
Malinowski, Paige
Shih, Kent C.
Allen, Jill N.
Jackson, Nadine
Chan, Jennifer A.
Fidias, Panos
Ryan, David P.
Fuchs, Charles S.
Bendell, Johanna C.
TI Multicenter randomized phase II trial of cisplatin, irinotecan plus
bevacizumab (PCA) versus docetaxel, cisplatin, irinotecan plus
bevacizumab (TPCA) in patients (pts) with metastatic esophagogastric
cancer (MEGCA).
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
Tennessee Oncol PLLC, Sarah Cannon Res Inst, Nashville, TN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 4027
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804121
ER
PT J
AU Epstein, AS
Volandes, AE
Gary, K
Chen, LY
Li, YL
Agre, P
Levin, T
Reidy, DL
Meng, RD
Segal, NH
Yu, KH
Janjigian, YY
Abou-Alfa, GK
Kelsen, DP
O'Reilly, EM
AF Epstein, Andrew S.
Volandes, Angelo E.
Gary, Kristen
Chen, Ling Y.
Li, Yuelin
Agre, Pat
Levin, Tomer
Reidy, Diane Lauren
Meng, Raymond D.
Segal, Neil Howard
Yu, Kenneth H.
Janjigian, Yelena Yuriy
Abou-Alfa, Ghassan K.
Kelsen, David Paul
O'Reilly, Eileen Mary
TI A randomized trial of a cardiopulmonary resuscitation (CPR) video (V) in
advance care planning (ACP) for progressive hepatopancreaticobiliary
cancer patients
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Mt Sinai, New York, NY USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Genentech Inc, San Francisco, CA 94080 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 9105
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800365
ER
PT J
AU Epstein-Peterson, Z
Sullivan, A
Phelps, AC
Balboni, MJ
Vanderweele, TJ
Balboni, TA
AF Epstein-Peterson, Zachary
Sullivan, Adam
Phelps, Andrea C.
Balboni, Michael J.
Vanderweele, Tyler J.
Balboni, Tracy A.
TI Spiritual care provided by oncology physicians and nurses to advanced
cancer patients
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Harvard Univ, Sch Med, Boston, MA USA.
Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
Dana Farber Canc Inst, Ctr Psychooncol & Palliat Care Res, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 9116
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804298
ER
PT J
AU Epstein-Peterson, Z
Sullivan, A
Phelps, AC
Balboni, MJ
Vanderweele, TJ
Balboni, TA
AF Epstein-Peterson, Zachary
Sullivan, Adam
Phelps, Andrea C.
Balboni, Michael J.
Vanderweele, Tyler J.
Balboni, Tracy A.
TI Spiritual care provided by oncology physicians and nurses to advanced
cancer patients.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Harvard Univ, Sch Med, Boston, MA USA.
Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
Dana Farber Canc Inst, Ctr Psychooncol & Palliat Care Res, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 9116
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804099
ER
PT J
AU Etchin, J
Kentsis, A
Sanda, T
Kung, AL
Stone, RM
McCauley, D
Kauffman, M
Shacham, S
Look, AT
AF Etchin, Julia
Kentsis, Alex
Sanda, Takaomi
Kung, Andrew L.
Stone, Richard M.
McCauley, Dilara
Kauffman, Michael
Shacham, Sharon
Look, A. Thomas
TI Evaluation of KPT-SINE (Selective Inhibitors of CRM1-Mediated Nuclear
Export) in AML and T-ALL.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Childrens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
Karyopharm Therapeut, Boston, MA USA.
Karyopharm Therapeut, Newton, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA e13586
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802569
ER
PT J
AU Ewer, M
Baselga, J
Clark, E
Benyunes, M
Ross, G
Swain, SM
AF Ewer, Michael
Baselga, Jose
Clark, Emma
Benyunes, Mark
Ross, Graham
Swain, Sandra M.
TI Cardiac tolerability of pertuzumab plus trastuzumab plus docetaxel in
patients with HER2-positive metastatic breast cancer in the CLEOPATRA
study
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Harvard Univ, Sch Med, Boston, MA USA.
Roche Prod Ltd, Welwyn Garden City AL7 3AY, Herts, England.
Genentech Inc, San Francisco, CA 94080 USA.
MedStar Washington Hosp Ctr, Washington Canc Inst, Washington, DC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 533
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800327
ER
PT J
AU Fakhro, SA
Jennings, D
Pinho, MC
Lin, NU
Sorensen, AG
Batchelor, T
Gerstner, ER
AF Fakhro, Summer A.
Jennings, Dominique
Pinho, Marco C.
Lin, Nancy U.
Sorensen, A. Gregory
Batchelor, Tracy
Gerstner, Elizabeth Robins
TI Response of nonenhancing regions in glioblastoma to VEGF-signaling
inhibitor cediranib correlates with tumor infiltration
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hop, Martinos Ctr Biomed Imaging, Charlestown, MA USA.
Massachusetts Gen Hop, Martinos Ctr Biomed Imaging, Boston, MA USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Simemens Healthcare USA, Malvern, PA USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 3036
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802550
ER
PT J
AU Faris, JE
Hong, TS
McDermott, S
Borger, DR
Guimaraes, AR
Wo, JYL
Sahani, D
Dias, LE
Allen, JN
Zhu, AX
Murphy, JE
Kwak, EL
Ryan, DP
Clark, JW
Blaszkowsky, LS
AF Faris, Jason Edward
Hong, Theodore S.
McDermott, Shaunagh
Borger, Darrell R.
Guimaraes, Alexander R.
Wo, Jennifer Yon-Li
Sahani, Dushyant
Dias, Lauren Elizabeth
Allen, Jill N.
Zhu, Andrew X.
Murphy, Janet E.
Kwak, Eunice Lee
Ryan, David P.
Clark, Jeffrey W.
Blaszkowsky, Lawrence Scott
TI FOLFIRINOX in locally advanced and metastatic pancreatic cancer.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
North Shore Canc Ctr, Danvers, MA USA.
Massachusetts Gen Hosp, Div Hematol & Oncol, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA e14615
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801437
ER
PT J
AU Fathi, AT
Abdel-Wahab, OI
Sadrzadeh, H
Foster, J
Burke, M
Borger, DR
Iafrate, AJ
Adamia, S
Liu, SY
Ballen, KK
Amrein, PC
Attar, EC
Straley, K
Yen, K
Schenkein, DP
Neuberg, DS
Levine, RL
Chen, YBA
Stone, RM
AF Fathi, Amir Tahmasb
Abdel-Wahab, Omar Ibrahim
Sadrzadeh, Hossein
Foster, Julia
Burke, Meghan
Borger, Darrell R.
Iafrate, A. John
Adamia, Sophia
Liu, Suiyang
Ballen, Karen K.
Amrein, Philip C.
Attar, Eyal C.
Straley, Kimberly
Yen, Katharine
Schenkein, David P.
Neuberg, Donna S.
Levine, Ross L.
Chen, Yi-Bin Albert
Stone, Richard M.
TI Prospective evaluation of serial 2-hydroxyglutarate in acute myeloid
leukemia (AML) to determine response to therapy and predict relapse
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
Mem Sloan Kettering Canc Ctr, Leukemia Serv, New York, NY 10021 USA.
Mem Sloan Kettering Canc Ctr, Human Oncol & Pathogenesis Program, New York, NY 10021 USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Agios Pharmaceut, Cambridge, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 6606
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802662
ER
PT J
AU Fiore, M
Coppola, S
Colombo, C
Bertagnolli, MM
George, S
Le Cesne, A
Casali, PG
Gronchi, A
Bonvalot, S
Raut, CP
AF Fiore, Marco
Coppola, Sara
Colombo, Chiara
Bertagnolli, Monica M.
George, Suzanne
Le Cesne, Axel
Casali, Paolo Giovanni
Gronchi, Alessandro
Bonvalot, Sylvie
Raut, Chandrajit P.
TI Desmoid fibromatosis and pregnancy: A multi-institutional analysis of
recurrence and obstetric risk
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Fdn IRCCS Ist Nazl Tumori, Milan, Italy.
Inst Gustave Roussy, Villejuif, France.
Fdn IRCCS Ist Nazl Tumori, Milan, Italy.
Harvard Univ, Sch Med, Dana Farber Canc Inst, Brigham & Womens Hosp, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol,Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 10017
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800372
ER
PT J
AU Fisch, M
Zhao, FM
O'Mara, AM
Wang, XS
Cella, D
Cleeland, CS
AF Fisch, Michael
Zhao, Fengmin
O'Mara, Ann M.
Wang, Xin Shelley
Cella, David
Cleeland, Charles S.
CA Eastern Cooperative Oncology Grp
TI Determinants of fatigue improvement in outpatient oncology according to
baseline categories of fatigue severity
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
NCI, Bethesda, MD 20892 USA.
Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 9112
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804287
ER
PT J
AU Fisch, M
Zhao, FM
O'Mara, AM
Wang, XS
Cella, D
Cleeland, CS
AF Fisch, Michael
Zhao, Fengmin
O'Mara, Ann M.
Wang, Xin Shelley
Cella, David
Cleeland, Charles S.
CA Eastern Cooperative Oncology Grp
TI Determinants of fatigue improvement in outpatient oncology according to
baseline categories of fatigue severity.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
NCI, Bethesda, MD 20892 USA.
Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 9112
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804085
ER
PT J
AU Fizazi, K
Massard, C
Smith, MR
Rader, ME
Brown, JE
Milecki, P
Shore, ND
Oudard, S
Karsh, LI
Carducci, MA
Damiao, R
Wang, H
Goessl, CD
AF Fizazi, Karim
Massard, Christophe
Smith, Matthew Raymond
Rader, Michael E.
Brown, Janet Elizabeth
Milecki, Piotr
Shore, Neal D.
Oudard, Stephane
Karsh, Lawrence Ivan
Carducci, Michael Anthony
Damiao, Ronaldo
Wang, Huei
Goessl, Carsten Dietrich
TI Baseline covariates impacting overall survival (OS) in a phase III study
of men with bone metastases from castration-resistant prostate cancer.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Inst Gustave Roussy, Villejuif, France.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Nyack Hosp, Nyack, NY USA.
Canc Res UK Expt Canc Med Ctr, Leeds, W Yorkshire, England.
Canc Res UK Expt Canc Med Ctr, Sheffield, S Yorkshire, England.
Greater Poland Canc Ctr, Poznan, Poland.
Med Univ, Poznan, Poland.
Carolina Urol Res Ctr, Myrtle Beach, SC USA.
Georges Pompidou European Hosp, Paris, France.
Urol Ctr Colorado, Denver, CO USA.
Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
Hosp Univ Pedro Ernesto, Rio De Janeiro, Brazil.
Amgen Inc, Thousand Oaks, CA 91320 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 4642
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803097
ER
PT J
AU Fletcher, KM
Prigerson, HG
Maciejewski, PK
AF Fletcher, Kalen M.
Prigerson, Holly Gwen
Maciejewski, Paul K.
TI Women know, and men wish they knew, prognostic information in advanced
cancer.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 9037
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800148
ER
PT J
AU Fougeray, R
Choueiri, TK
Pons, F
Schutz, FAB
Salhi, Y
Rosenberg, JE
Bellmunt, J
AF Fougeray, Ronan
Choueiri, Toni K.
Pons, Francesc
Schutz, Fabio Augusto Barros
Salhi, Yacine
Rosenberg, Jonathan E.
Bellmunt, Joaquim
TI Impact of first-line platinum therapy on survival in patients with
platinum-refractory advanced transitional cell carcinoma of the
urothelium (TCCU) treated with vinflunine
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Inst Rech Pierre Fabre, Boulogne, France.
Harvard Univ, Sch Med, Dana Farber Canc Inst, Lank Ctr Genitourinary Oncol,Brigham & Womens Hos, Boston, MA 02115 USA.
Univ Hosp del Mar IMIM, Dept Med Oncol, Barcelona, Spain.
Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA e15007
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803188
ER
PT J
AU Freedman, RA
Virgo, KS
Labadie, J
Partridge, AH
Keating, NL
AF Freedman, Rachel A.
Virgo, Katherine S.
Labadie, Julia
Partridge, Ann H.
Keating, Nancy Lynn
TI Receipt of locoregional therapy among young women with breast cancer
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Amer Canc Soc, Intramural Res Dept, Hlth Serv Res Program, Atlanta, GA 30329 USA.
Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 1100
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801032
ER
PT J
AU Galanina, N
Sprecher, E
Bossuyt, V
Sarkar, S
Krop, IE
Winer, E
Tuck, DP
Bruce, C
Harris, L
AF Galanina, Natalie
Sprecher, Emmet
Bossuyt, Veerle
Sarkar, Sudipa
Krop, Ian E.
Winer, Eric
Tuck, David P.
Bruce, Can
Harris, Lyndsay
TI Evaluation of gene expression by RNA-seq after single dose of
trastuzumab (T) reveals predictors of pathologic complete response (pCR)
in HER2-positive early breast cancer.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Yale Univ Sch Med, Yale Comprehens Canc Ctr, New Haven, CT USA.
Yale Univ Sch Med, New Haven, CT USA.
Yale Comprehens Canc Ctr, Dept Pathol, New Haven, CT USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Yale Univ Sch Med, Dept Pathol, New Haven, CT USA.
Keck Bioinformat Resource, New Haven, CT USA.
Case Western Seidman Canc Ctr, Cleveland, OH USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 10558
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804146
ER
PT J
AU Gandhi, L
Heist, RS
Lucca, JV
Temel, JS
Fidias, P
Morse, LK
Johnson, BE
AF Gandhi, Leena
Heist, Rebecca Suk
Lucca, Joan Vern
Temel, Jennifer S.
Fidias, Panos
Morse, Linda K.
Johnson, Bruce E.
TI A phase II trial of pazopanib in relapsed/refractory small cell lung
cancer (SCLC).
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 7099
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802825
ER
PT J
AU Garg, M
Lee, JY
Kachnic, LA
Catalano, PJ
Henry, DH
Cooley, TP
Ratner, L
Wachsman, W
Aboulafia, DM
Benson, AB
Palefsky, J
Whittington, R
Mitsuyasu, RT
Sparano, JA
AF Garg, Madhur
Lee, Jeanette Y.
Kachnic, Lisa A.
Catalano, Paul J.
Henry, David H.
Cooley, Timothy Patrick
Ratner, Lee
Wachsman, William
Aboulafia, David Michael
Benson, Al Bowen
Palefsky, Joel
Whittington, Richard
Mitsuyasu, Ronald T.
Sparano, Joseph A.
TI Phase II trials of cetuximab (CX) plus cisplatin (CDDP), 5-fluorouracil
(5-FU) and radiation (RT) in immunocompetent (ECOG 3205) and
HIV-positive (AMC045) patients with squamous cell carcinoma of the anal
canal (SCAC): Safety and preliminary efficacy results
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Yeshiva Univ Albert Einstein Coll Med, Montefiore Med Ctr, Bronx, NY 10461 USA.
Univ Arkansas Med Sci, Dept Biostat, Little Rock, AR 72205 USA.
Boston Med Ctr, Boston, MA USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Penn Hosp, Philadelphia, PA 19107 USA.
Washington Univ, St Louis, MO USA.
VASDHS, La Jolla, CA USA.
UCSD Sch Med, La Jolla, CA USA.
Virginia Mason Med Ctr, Seattle, WA 98101 USA.
Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
Univ Calif San Francisco, San Francisco, CA 94143 USA.
VA Med Ctr, Philadelphia, PA USA.
Univ Calif Los Angeles, Los Angeles Care Ctr, Los Angeles, CA USA.
Yeshiva Univ Albert Einstein Coll Med, Bronx, NY 10461 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 4030
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804686
ER
PT J
AU Garon, EB
Moran, T
Barlesi, F
Gandhi, L
Sequist, LV
Kim, SW
Groen, HJM
Besse, B
Smit, EF
Kim, DW
Akimov, M
Avsar, E
Bailey, S
Felip, E
AF Garon, Edward B.
Moran, Teresa
Barlesi, Fabrice
Gandhi, Leena
Sequist, Lecia V.
Kim, Sang-We
Groen, Harry J. M.
Besse, Benjamin
Smit, Egbert F.
Kim, Dong-Wan
Akimov, Mikhail
Avsar, Emin
Bailey, Stuart
Felip, Enriqueta
TI Phase II study of the HSP90 inhibitor AUY922 in patients with previously
treated, advanced non-small cell lung cancer (NSCLC).
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
Hosp Germans, Catalan Inst Oncol, Barcelona, Spain.
Aix Marseille Univ, Marseille, France.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Asan Med Ctr, Seoul, South Korea.
Univ Med Ctr Groningen, NL-9713 AV Groningen, Netherlands.
Inst Gustave Roussy, Villejuif, France.
Vrije Univ Amsterdam, Med Ctr, Dept Pulm Dis, Amsterdam, Netherlands.
Seoul Natl Univ Hosp, Seoul 110744, South Korea.
Novartis Pharma AG, Basel, Switzerland.
Novartis Pharmaceut, E Hanover, NJ USA.
Vall dHebron Univ Hosp, Barcelona, Spain.
NR 0
TC 5
Z9 5
U1 0
U2 3
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 7543
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804271
ER
PT J
AU Garrett, LA
Growdon, WB
Boruta, DM
del Carmen, MG
Priebe, AM
Goodman, A
Bradford, L
Clark, RM
Schorge, JO
AF Garrett, Leslie A.
Growdon, Whitfield Board
Boruta, David M.
del Carmen, Marcela G.
Priebe, Anna M.
Goodman, Annekathryn
Bradford, Leslie
Clark, Rachel Marie
Schorge, John O.
TI Primary debulking surgery (PDS) for stage IIIc ovarian cancer: Quo
vadis?
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 [Garrett, Leslie A.; Growdon, Whitfield Board; Boruta, David M.; del Carmen, Marcela G.; Priebe, Anna M.; Goodman, Annekathryn; Bradford, Leslie; Clark, Rachel Marie; Schorge, John O.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA e15568
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803597
ER
PT J
AU Gartrell, BA
Hahn, NM
Hutson, TE
Sonpavde, G
Hauke, RJ
Starodub, A
Small, AC
Tsao, CK
Galsky, MD
AF Gartrell, Benjamin Adam
Hahn, Noah M.
Hutson, Thomas E.
Sonpavde, Guru
Hauke, Ralph J.
Starodub, Alexander
Small, Alexander C.
Tsao, Che-Kai
Galsky, Matt D.
TI Phase II trial of gemcitabine and cisplatin plus ipilimumab as
first-line treatment for metastatic urothelial carcinoma
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Mt Sinai Sch Med, Tisch Canc Inst, Div Hematol & Med Oncol, New York, NY USA.
Indiana Univ, Melvin & Bren Simon Canc Ctr, Indianapolis, IN 46204 USA.
Texas Oncol Baylor Charles A Sammons Canc Ctr, Dallas, TX USA.
Texas Oncol, Houston, TX USA.
Baylor Coll Med, Michael E DeBakey Vet Affairs Med Ctr, Sect Med Oncol, Dept Med, Houston, TX 77030 USA.
Nebraska Canc Specialists, Omaha, NE USA.
Goshen Ctr Canc Care, Goshen, IN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA TPS4676
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803064
ER
PT J
AU Gaughan, EM
Cryer, SK
Yeap, BY
Jackman, DM
Costa, DB
AF Gaughan, Elizabeth Mary
Cryer, Sarah K.
Yeap, Beow Yong
Jackman, David Michael
Costa, Daniel Botelho
TI Family history of lung cancer in never smokers with non-small cell lung
cancer (NSCLC) and its association with tumors harboring epidermal
growth factor receptor (EGFR) mutations.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Boston, MA 02215 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 7579
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804222
ER
PT J
AU Geoerger, B
Aerts, I
Casanova, M
Chisholm, JC
Hargrave, DR
Leary, S
Ashley, DM
Bouffet, E
MacDonald, T
Hurh, E
Dey, J
Kalambakas, S
Amakye, DD
Kieran, MW
AF Geoerger, Birgit
Aerts, Isabelle
Casanova, Michela
Chisholm, Julia C.
Hargrave, Darren R.
Leary, Sarah
Ashley, David M.
Bouffet, Eric
MacDonald, Tobey
Hurh, Eunju
Dey, Jyotirmoy
Kalambakas, Stacey
Amakye, Dereck Dokyi
Kieran, Mark W.
TI A phase I/II study of LDE225, a smoothened (Smo) antagonist, in
pediatric patients with recurrent medulloblastoma (MB) or other solid
tumors.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Inst Gustave Roussy, Villejuif, France.
Inst Curie, Paris, France.
Natl Canc Inst, I-20133 Milan, Italy.
Royal Marsden Hosp, Sutton, Surrey, England.
Seattle Childrens Hosp, Seattle, WA USA.
Royal Childrens Hosp, Melbourne, Vic, Australia.
Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
Emory Univ, Atlanta, GA 30322 USA.
Novartis Pharmaceut, E Hanover, NJ USA.
Novartis Pharmaceut, Florham Pk, NJ USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 3
Z9 3
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 9519
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800268
ER
PT J
AU George, DJ
Corn, PG
Michaelson, MD
Hammers, HJ
Alumkal, JJ
Ryan, CJ
Bruce, JY
Moran, S
Lee, SY
Mortimer, P
Hussain, M
AF George, Daniel J.
Corn, Paul G.
Michaelson, M. Dror
Hammers, Hans J.
Alumkal, Joshi J.
Ryan, Charles J.
Bruce, Justine Yang
Moran, Susan
Lee, Shih-Yuan
Mortimer, Peter
Hussain, Maha
TI Safety and activity of the investigational agent orteronel (ortl)
without prednisone in men with nonmetastatic castration-resistant
prostate cancer (nmCRPC) and rising prostate-specific antigen (PSA):
Updated results of a phase II study
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Duke Univ, Med Ctr, Durham, NC USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
UCSF Helen Diller Family Comprehens Canc Ctr, San Francisco, CA USA.
Univ Wisconsin, Carbone Canc Ctr, Madison, WI USA.
Millennium Pharmaceut Inc, Cambridge, MA USA.
Takeda Global Res & Dev Ctr Europe Ltd, London, England.
Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 4549
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803344
ER
PT J
AU Gerstner, ER
Zhang, Z
Fink, JR
Sorensen, GA
L'Heureux, D
Heckel, ML
Dunning, B
Muzi, M
Mankoff, DA
Barboriak, D
AF Gerstner, Elizabeth Robins
Zhang, Zheng
Fink, James R.
Sorensen, Gregory A.
L'Heureux, Darryl
Heckel, Martha L.
Dunning, Bernadine
Muzi, Mark
Mankoff, David A.
Barboriak, Daniel
TI ACRIN 6684 assessment of tumor hypoxia in glioblastoma using
18F-fluoromisonidazole with PET and MRI.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
Brown Univ, Providence, RI 02912 USA.
Univ Washington, Seattle, WA 98195 USA.
Amer Coll Radiol, Philadelphia, PA USA.
Amer Coll Radiol Imaging Network, Philadelphia, PA USA.
Duke Univ, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA TPS10635
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801722
ER
PT J
AU Gerstner, ER
Emblem, KE
Chi, AS
Eichler, AF
Hochberg, F
Drappatz, J
Quant, EC
Norden, AD
Pinho, MC
Polaskova, P
Jennings, D
Ancukiewicz, M
Ivy, SP
Wen, PY
Jain, RK
Sorensen, AG
Batchelor, T
AF Gerstner, Elizabeth Robins
Emblem, Kyrre E.
Chi, Andrew S.
Eichler, April F.
Hochberg, Fred
Drappatz, Jan
Quant, Eudocia Carmen
Norden, Andrew David
Pinho, Marco C.
Polaskova, Pavlina
Jennings, Dominique
Ancukiewicz, Marek
Ivy, S. Percy
Wen, Patrick Y.
Jain, Rakesh K.
Sorensen, A. Gregory
Batchelor, Tracy
TI Effects of cediranib, a VEGF signaling inhibitor, in combination with
chemoradiation on tumor blood flow and survival in newly diagnosed
glioblastoma.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
AA Martinos Ctr Biomed Imaging, Boston, MA USA.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Univ Pittsburgh, Pittsburgh, PA USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, Charlestown, MA USA.
Massachusetts Gen Hop, Martinos Ctr Biomed Imaging, Boston, MA USA.
NCI, Bethesda, MD 20892 USA.
Massachusetts Gen Hosp, Charlestown, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 2009
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801527
ER
PT J
AU Gerstner, ER
Emblem, KE
Chi, AS
Eichler, AF
Hochberg, F
Drappatz, J
Quant, EC
Norden, AD
Pinho, MC
Polaskova, P
Jennings, D
Ancukiewicz, M
Ivy, SP
Wen, PY
Jain, RK
Sorensen, AG
Batchelor, T
AF Gerstner, Elizabeth Robins
Emblem, Kyrre E.
Chi, Andrew S.
Eichler, April F.
Hochberg, Fred
Drappatz, Jan
Quant, Eudocia Carmen
Norden, Andrew David
Pinho, Marco C.
Polaskova, Pavlina
Jennings, Dominique
Ancukiewicz, Marek
Ivy, S. Percy
Wen, Patrick Y.
Jain, Rakesh K.
Sorensen, A. Gregory
Batchelor, Tracy
TI Effects of cediranib, a VEGF signaling inhibitor, in combination with
chemoradiation on tumor blood flow and survival in newly diagnosed
glioblastoma.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
AA Martinos Ctr Biomed Imaging, Boston, MA USA.
Massachusetts Gen Hosp Canc Ctr, Boston, MA USA.
Univ Pittsburgh, Pittsburgh, PA USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, Charlestown, MA USA.
Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, Boston, MA 02114 USA.
NCI, Bethesda, MD 20892 USA.
Massachusetts Gen Hosp, Charlestown, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 2009
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801525
ER
PT J
AU Ghobrial, IM
Gertz, MA
LaPlant, B
Camoriano, JK
Hayman, SR
Lacy, M
Chuma, S
Harris, B
Boswell, E
Banwait, R
Sheehy, P
Ansell, SM
DeAngelo, DJ
Dispenzieri, A
Bergsagel, L
Reeder, CB
Anderson, KC
Richardson, PGG
Treon, SP
Witzig, TE
AF Ghobrial, Irene M.
Gertz, Morie A.
LaPlant, Betsy
Camoriano, John Kelly
Hayman, Suzanne R.
Lacy, Martha
Chuma, Stacey
Harris, Brianna
Boswell, Erica
Banwait, Ranjit
Sheehy, Patricia
Ansell, Stephen Maxted
DeAngelo, Daniel J.
Dispenzieri, Angela
Bergsagel, Leif
Reeder, Craig B.
Anderson, Kenneth Carl
Richardson, Paul Gerard Guy
Treon, Steven P.
Witzig, Thomas E.
TI Long-term results of the phase II trial of the oral mTOR inhibitor
everolimus (RAD001) in relapsed or refractory Waldenstrom
macroglobulinemia.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Mayo Clin, Rochester, MN USA.
Mayo Clin, Scottsdale, AZ USA.
Mayo Clin, Coll Med, Scottsdale, AZ USA.
Mayo Fdn, Scottsdale, AZ USA.
Mayo Clin, Div Hematol, Rochester, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 8043
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804009
ER
PT J
AU Gill, RR
Heon, S
Yeap, BY
Butaney, M
Lindeman, NI
Rabin, MS
Jackman, DM
Janne, PA
Johnson, BE
AF Gill, Ritu R.
Heon, Stephanie
Yeap, Beow Yong
Butaney, Mohit
Lindeman, Neal Ian
Rabin, Michael S.
Jackman, David Michael
Janne, Pasi Antero
Johnson, Bruce E.
CA Dana-Farber Canc Ctr
TI Genomic profiling of non-small cell lung cancer (NSCLC) for personalized
targeted therapy using CT-guided transthoracic needle biopsy (TTNB).
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 10592
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803566
ER
PT J
AU Gnant, M
Baselga, J
Rugo, HS
Noguchi, S
Pritchard, KI
Burris, HA
Piccart-Gebhart, MJ
Hart, LL
Eakle, JF
Mukai, H
Iwata, H
El-Hashimy, M
Rao, S
Taran, T
Sahmoud, T
Lebwohl, DE
Hortobagyi, GN
AF Gnant, Michael
Baselga, Jose
Rugo, Hope S.
Noguchi, Shinzaburo
Pritchard, Kathleen I.
Burris, Howard A.
Piccart-Gebhart, Martine J.
Hart, Lowell L.
Eakle, Janice F.
Mukai, Hirofumi
Iwata, Hiroji
El-Hashimy, Mona
Rao, Shantha
Taran, Tanya
Sahmoud, Tarek
Lebwohl, David Edward
Hortobagyi, Gabriel N.
TI Effects of everolimus (EVE) on disease progression in bone and bone
markers (BM) in patients (pts) with bone metastases (mets).
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Med Univ Vienna, Dept Surg, Ctr Comprehens Canc, Vienna, Austria.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Harvard Univ, Sch Med, Boston, MA USA.
Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.
Osaka Univ, Osaka, Japan.
Univ Toronto, Sunnybrook Odette Canc Ctr, Toronto, ON, Canada.
Sarah Cannon Res Inst, Nashville, TN USA.
Inst Jules Bordet, B-1000 Brussels, Belgium.
Florida Canc Specialists, Ft Myers, FL USA.
Natl Canc Ctr Hosp East, Kashiwa, Chiba, Japan.
Aichi Canc Ctr Hosp, Nagoya, Aichi 464, Japan.
Novartis Pharmaceut, E Hanover, NJ USA.
Novarits Pharmaceut, Florham Pk, NJ USA.
Univ Texas Houston, Houston, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 512
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800245
ER
PT J
AU Goldberg, SB
Oxnard, GR
Digumarthy, S
Muzikansky, A
Jackman, DM
Lennes, IT
Sequist, LV
AF Goldberg, Sarah B.
Oxnard, Geoffrey R.
Digumarthy, Subba
Muzikansky, Alona
Jackman, David Michael
Lennes, Inga Tolin
Sequist, Lecia V.
TI Chemotherapy with erlotinib or chemotherapy alone in advanced NSCLC with
acquired resistance to EGFR tyrosine kinase inhibitors (TKI)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 7524
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804377
ER
PT J
AU Goldkorn, A
Ely, B
Quinn, DI
Tangen, CM
Tai, YC
Twardowski, P
Van Veldhuizen, PJ
Agarwal, N
Anthony, M
Monk, CJP
Garzotto, M
Mack, PC
Lara, P
Higano, CS
Hussain, M
Vogelzang, NJ
Cote, RJ
Thompson, IM
AF Goldkorn, Amir
Ely, Benjamin
Quinn, David I.
Tangen, Catherine M.
Tai, Yu-Chong
Twardowski, Przemyslaw
Van Veldhuizen, Peter J.
Agarwal, Neeraj
Anthony, Michael
Monk, Carducci J. P.
Garzotto, Mark
Mack, Philip C.
Lara, Primo
Higano, Celestia S.
Hussain, Maha
Vogelzang, Nicholas J.
Cote, Richard J.
Thompson, Ian Murchie
CA Southwest Oncology Grp
TI Results of telomerase activity measurements from live circulating tumor
cells captured on a slot microfilter in a phase III SWOG-coordinated
prostate cancer trial (S0421)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Univ So Calif, Norris Comprehens Canc Ctr, Los Angeles, CA USA.
SWOG Stat Ctr, Seattle, WA USA.
CALTECH, Pasadena, CA 91125 USA.
City Hope Natl Med Ctr, Duarte, CA USA.
Univ Kansas, Ctr Canc, Westwood, KS USA.
Univ Utah, Huntsman Canc Inst, Salt Lake City, UT USA.
Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
Ohio State Univ, Columbus, OH 43210 USA.
Portland VA Med Ctr, Portland, OR USA.
Univ Calif Davis, Davis, CA 95616 USA.
Univ Washington, Seattle Canc Care Alliance, Puget Sound Oncol Consortium, Seattle, WA 98195 USA.
Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
Comprehens Canc Ctr Nevada, Las Vegas, NV USA.
Univ Miami, Miller Sch Med, Miami, FL 33136 USA.
Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 4663
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803108
ER
PT J
AU Gordon, MS
Kluger, HM
Shapiro, G
Kurzrock, R
Edelman, G
Samuel, TA
Moussa, AH
Ramies, DA
Laird, AD
Schimmoller, F
Shen, XD
Daud, A
AF Gordon, Michael S.
Kluger, Harriet M.
Shapiro, Geoffrey
Kurzrock, Razelle
Edelman, Gerald
Samuel, Thomas A.
Moussa, Ali H.
Ramies, David A.
Laird, A. Douglas
Schimmoller, Frauke
Shen, Xiaodong
Daud, Adil
TI Activity of cabozantinib (XL184) in metastatic melanoma: Results from a
phase II randomized discontinuation trial (RDT)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Pinnacle Oncol Hematol, Scottsdale, AZ USA.
Yale Canc Ctr, New Haven, CT USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Texas Oncol, Irving, TX USA.
Georgia Hlth Sci Univ, Augusta, GA USA.
Canc Care Associates, Tulsa, OK USA.
Exelixis, San Francisco, CA USA.
Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 8531
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800567
ER
PT J
AU Goss, PE
Barrios, CH
Bell, R
Finkelstein, DM
Iwata, H
Martin, M
Braun, AH
Ke, CL
Maniar, T
Coleman, RE
AF Goss, Paul Edward
Barrios, Carlos H.
Bell, Richard
Finkelstein, Dianne M.
Iwata, Hiroji
Martin, Miguel
Braun, Ada H.
Ke, Chunlei
Maniar, Tapan
Coleman, Robert Edward
TI Denosumab versus placebo as adjuvant treatment for women with
early-stage breast cancer who are at high risk of disease recurrence
(D-CARE): An international, randomized, double-blind, placebo-controlled
phase III clinical trial.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
PUCRS Sch Med, Porto Alegre, RS, Brazil.
Barwon Hlth, Geelong, Vic, Australia.
Aichi Canc Ctr Hosp, Nagoya, Aichi 464, Japan.
Hosp Gen Gregorio Maranon, Madrid, Spain.
Amgen Inc, Thousand Oaks, CA 91320 USA.
Univ Sheffield, Sheffield, S Yorkshire, England.
RI Barrios, Carlos/G-8525-2015
NR 0
TC 1
Z9 1
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA TPS670
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800240
ER
PT J
AU Govindan, R
Hammerman, PS
Hayes, DN
Wilkerson, MD
Baylin, S
Meyerson, M
AF Govindan, Ramaswamy
Hammerman, Peter S.
Hayes, David N.
Wilkerson, Matthew D.
Baylin, Stephen
Meyerson, Matthew
CA Canc Genome Atlas TCGA Grp
TI Comprehensive genomic characterization of squamous cell carcinoma of the
lung
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Washington Univ, Sch Med, St Louis, MO USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
UNC Lineberger Comprehens Canc Ctr, Chapel Hill, NC USA.
Univ N Carolina, Chapel Hill, NC USA.
Johns Hopkins Univ, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 7006
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800025
ER
PT J
AU Greenup, RA
Bardia, A
Buckley, JM
Niemierko, A
Camp, M
Coopey, S
Gadd, M
Schapira, L
Taghian, AG
Smith, BL
Specht, MC
AF Greenup, Rachel Adams
Bardia, Aditya
Buckley, Julliette M.
Niemierko, Andrzej
Camp, Melissa
Coopey, Suzanne
Gadd, Michele
Schapira, Lidia
Taghian, Alphonse G.
Smith, Barbara L.
Specht, Michelle Connolly
TI Association of pathologic complete response following neoadjuvant
chemotherapy with survival among young women with breast cancer
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
Harvard Univ, Massachusetts Gen Hosp, Ctr Canc, Sch Med, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 1122
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800856
ER
PT J
AU Greer, JA
McMahon, PM
Tramontano, A
Gallagher, ER
Pirl, WF
Jackson, VA
Temel, JS
AF Greer, Joseph A.
McMahon, Pamela M.
Tramontano, Angela
Gallagher, Emily R.
Pirl, William F.
Jackson, Vicki A.
Temel, Jennifer S.
TI Effect of early palliative care on health care costs in patients with
metastatic NSCLC.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 6004
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801235
ER
PT J
AU Gross, A
Mann, S
Kalfin, M
Lane, S
Weingart, S
Bunnell, CA
AF Gross, Anne
Mann, Susan
Kalfin, Michael
Lane, Sharon
Weingart, Saul
Bunnell, Craig A.
TI Performance teamwork training in ambulatory oncology
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA e16559
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800570
ER
PT J
AU Haas, NB
Manola, J
Ky, B
Flaherty, KT
Uzzo, RG
Wood, CG
Kane, CJ
Jewett, MAS
Atkins, MB
Dutcher, JP
DiPaola, RS
AF Haas, Naomi B.
Manola, Judith
Ky, Bonnie
Flaherty, Keith T.
Uzzo, Robert G.
Wood, Christopher G.
Kane, Christopher J.
Jewett, Michael A. S.
Atkins, Michael B.
Dutcher, Janice P.
DiPaola, Robert S.
CA Eastern Cooperative Oncology Grp
TI Cardiac safety analysis for a phase III trial of sunitinib (SU) or
sorafenib (SO) or placebo (PLC) in patients (pts) with resected renal
cell carcinoma (RCC)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Univ Penn, Philadelphia, PA 19104 USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA.
Princess Margaret Hosp, Dept Urol, Toronto, ON M4X 1K9, Canada.
Univ Toronto, Toronto, ON, Canada.
Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
St Lukes Roosevelt Hosp, New York, NY USA.
Canc Inst New Jersey, New Brunswick, NJ USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 4500
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803239
ER
PT J
AU Haddad, RI
Rabinowits, G
Tishler, RB
Adkins, D
Khuri, FR
Clark, J
Lorch, JH
Limaye, SA
Wirth, LJ
O'Neill, A
Riley, S
Posner, MR
AF Haddad, Robert I.
Rabinowits, Guilherme
Tishler, Roy B.
Adkins, Douglas
Khuri, Fadlo Raja
Clark, Joseph
Lorch, Jochen H.
Limaye, Sewanti Atul
Wirth, Lori J.
O'Neill, Anne
Riley, Sarah
Posner, Marshall R.
TI The PARADIGM trial: A phase III study comparing sequential therapy (ST)
to concurrent chemoradiotherapy (CRT) in locally advanced head and neck
cancer (LANHC)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA.
Washington Univ, Sch Med, St Louis, MO USA.
Emory Univ, Winship Canc Inst, Atlanta, GA 30322 USA.
Loyola Univ, Med Ctr, Maywood, IL 60153 USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Mt Sinai, New York, NY USA.
NR 0
TC 7
Z9 7
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 5501
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803185
ER
PT J
AU Hahn, NM
Daneshmand, S
Posadas, EM
Koch, MO
Bihrle, R
Foster, R
Masterson, TA
Cheng, L
Liu, ZY
Breen, T
Fleming, MT
Lance, R
Ryan, CW
Corless, CL
Galsky, MD
Alva, AS
Mitchell, C
Shen, SS
Lerner, SP
Sonpavde, G
AF Hahn, Noah M.
Daneshmand, Siamak
Posadas, Edwin M.
Koch, Michael O.
Bihrle, Richard
Foster, Richard
Masterson, Timothy A.
Cheng, Liang
Liu, Ziyue
Breen, Timothy
Fleming, Mark T.
Lance, Ray
Ryan, Christopher W.
Corless, Christopher L.
Galsky, Matt D.
Alva, Ajjai Shivaram
Mitchell, Carmen
Shen, Steven S.
Lerner, Seth P.
Sonpavde, Guru
TI A phase II trial of neoadjuvant dasatinib (Neo-D) in muscle-invasive
urothelial carcinoma of the bladder (miUCB): Hoosier Oncology Group
GU07-122 trial.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Indiana Univ, Melvin & Bren Simon Canc Ctr, Indianapolis, IN 46204 USA.
Univ So Calif, Kenneth Norris Jr Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
Cedars Sinai Med Ctr, Samuel Oschin Comprehens Canc Inst, Los Angeles, CA 90048 USA.
Indiana Univ, Med Ctr, Indianapolis, IN USA.
Indiana Univ, Indianapolis, IN 46204 USA.
Indiana Univ, Med Ctr, Dept Pathol & Lab Med, Indianapolis, IN USA.
Indiana Univ, Div Biostat, Indianapolis, IN 46204 USA.
Hoosier Oncol Grp, Indianapolis, IN USA.
US Oncol Res, The Woodlands, TX USA.
Virginia Oncol Associates, Hampton, VA USA.
Eastern Virginia Med Sch, Norfolk, VA 23501 USA.
Oregon Hlth & Sci Univ, Knight Canc Inst, Portland, OR 97201 USA.
Oregon Hlth & Sci Univ, Knight Diagnost Labs, Portland, OR 97201 USA.
Mt Sinai Sch Med, Tisch Canc Inst, New York, NY USA.
Univ Michigan, Ann Arbor, MI 48109 USA.
Baylor Coll Med, Houston, TX 77030 USA.
Methodist Hosp, Houston, TX 77030 USA.
Texas Oncol, Houston, TX USA.
Baylor Coll Med, Michael E DeBakey Vet Affairs Med Ctr, Dept Med, Sect Med Oncol, Houston, TX 77030 USA.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 4586
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802889
ER
PT J
AU Hale, J
Olson, TA
Nicholson, J
Dang, H
Krailo, MD
Billmire, D
Donachie, P
Thornton, C
Rodriguez-Galindo, C
Frazier, AL
AF Hale, Juliet
Olson, Thomas Arthur
Nicholson, James
Dang, Ha
Krailo, Mark D.
Billmire, Deborah
Donachie, Paul
Thornton, Claire
Rodriguez-Galindo, Carlos
Frazier, A. Lindsay
TI Carboplatin (CBP) versus cisplatin (CP) within prognostic groups in
pediatric extracranial malignant germ cell tumors (MGCTs).
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Newcastle Upon Tyne Hosp Trust, Newcastle Upon Tyne, Tyne & Wear, England.
Emory Univ, Atlanta, GA 30322 USA.
Addenbrookes NHS Trust, Cambridge CB2 2QQ, England.
Childrens Oncol Grp, Arcadia, CA USA.
Riley Hosp Children, Indianapolis, IN USA.
Childrens Canc & Leukaemia Grp, Leicester, Leics, England.
Royal Hosp, Belfast, Antrim, North Ireland.
Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 9539
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800588
ER
PT J
AU Haluska, P
Menefee, ME
Plimack, ER
Rosenberg, JE
Northfelt, DW
LaVallee, T
Huang, WM
Yu, XQ
Viner, J
LoRusso, P
AF Haluska, Paul
Menefee, Michael E.
Plimack, Elizabeth R.
Rosenberg, Jonathan E.
Northfelt, Donald W.
LaVallee, Theresa
Huang, Wenmei
Yu, Xiang-Qing
Viner, Jaye
LoRusso, Patricia
TI Safety, pharmacokinetics, and antitumor activity of MEDI-573, an
investigational monoclonal antibody that targets IGF-I and IGF-II, in
adult patients with advanced solid tumors.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Mayo Clin, Rochester, MN USA.
Mayo Clin, Jacksonville, FL 32224 USA.
Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
Harvard Univ, Brigham & Womens Hosp, Sch Med, Lank Ctr Genitourinary Oncol,Dana Farber Canc Ins, Boston, MA 02115 USA.
Mayo Clin, Scottsdale, AZ USA.
MedImmune, Gaithersburg, MD USA.
Karmanos Canc Inst, Detroit, MI USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA TPS2618
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802125
ER
PT J
AU Hamid, O
Hwu, WJ
Richards, JM
Weber, JS
Wolchok, JD
Sznol, M
Minor, DR
Pavlick, AC
Urba, WJ
Hodi, FS
Yang, A
Michener, T
Balogh, A
McDermott, DF
AF Hamid, Omid
Hwu, Wen-Jen
Richards, Jon M.
Weber, Jeffrey S.
Wolchok, Jedd D.
Sznol, Mario
Minor, David R.
Pavlick, Anna C.
Urba, Walter John
Hodi, F. Stephen
Yang, Arvin
Michener, Tracy
Balogh, Agnes
McDermott, David F.
TI Ipilimumab (Ipi) expanded access program (EAP) for patients (pts) with
stage III/IV melanoma: 10 mg/kg cohort interim results
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Angeles Clin & Res Inst, Santa Monica, CA USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Oncol Specialists SC, Park Ridge, IL USA.
Univ S Florida, H Lee Moffitt Canc Ctr, Comprehens Melanoma Res Ctr, Tampa, FL 33682 USA.
Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Yale Canc Ctr, New Haven, CT USA.
Calif Pacific Melanoma Ctr, San Francisco, CA USA.
NYU, Inst Canc, New York, NY USA.
Providence Portland Med Ctr, Portland, OR USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Bristol Myers Squibb Co, Plainsboro, NJ USA.
Bristol Myers Squibb Co, Braine Lalleud, Belgium.
Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 8508
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800027
ER
PT J
AU Hanna, NH
Dahlberg, SE
Kolesar, J
Hirsch, FR
Ramalingam, SS
Schiller, JH
AF Hanna, Nasser H.
Dahlberg, Suzanne Eleanor
Kolesar, Jill
Hirsch, Fred R.
Ramalingam, Suresh S.
Schiller, Joan H.
TI Three-arm randomized phase II study of carboplatin (C) and paclitaxel
(P) in combination with cetuximab (CET), IMC-A12, or both for advanced
non-small cell lung cancer (NSCLC) patients who will not receive
bevacizumab-based therapy: An Eastern Cooperative Oncology Group (ECOG)
study (E4508)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Indiana Univ, Indianapolis, IN 46204 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Univ Wisconsin, Carbone Canc Ctr, Madison, WI USA.
Univ Colorado, Ctr Canc, Aurora, CO USA.
Emory Univ, Winship Canc Inst, Atlanta, GA 30322 USA.
Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 7516
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804330
ER
PT J
AU Hawryluk, EB
O'Regan, KN
Sheehy, N
Guo, Y
Dorosario, A
Sakellis, C
Jacene, HA
Wang, LDC
AF Hawryluk, Elena B.
O'Regan, Kevin N.
Sheehy, Niall
Guo, Ye
Dorosario, Andrew
Sakellis, Chris
Jacene, Heather A.
Wang, Linda C.
TI Positron emission tomography/computed tomography to improve staging and
restaging in Merkel cell carcinoma.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Harvard Univ, Sch Med, Dept Dermatol, Boston, MA 02115 USA.
Cork Univ Hosp, Dept Radiol, Cork, Ireland.
St James Hosp, Dublin, Ireland.
Brigham & Womens Hosp, Dept Dermatol, Boston, MA 02115 USA.
Dana Farber Brigham & Womens Canc Ctr, Ctr Cutaneous Oncol, Boston, MA USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Dana Farber Canc Inst, Dept Radiol, Boston, MA 02115 USA.
Brigham & Womens Hosp, Boston, MA 02115 USA.
Mercy Med Ctr, Inst Canc Care, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 8552
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800166
ER
PT J
AU Heist, RS
Wang, XFF
Hodgson, L
Otterson, GA
Stinchcombe, T
Vokes, EE
Socinski, MA
AF Heist, Rebecca Suk
Wang, Xiaofei F.
Hodgson, Lydia
Otterson, Gregory Alan
Stinchcombe, Tom
Vokes, Everett E.
Socinski, Mark A.
TI CALGB 30704: A randomized phase II study to assess the efficacy of
pemetrexed or sunitinib or pemetrexed plus sunitinib in the second-line
treatment of advanced non-small cell lung cancer (NSCLC)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Canc & Leukemia Grp, Ctr Stat B, Durham, NC USA.
Duke Univ, Durham, NC USA.
Ohio State Univ, Ctr Comprehens Canc, Dept Internal Med, Columbus, OH 43210 USA.
Univ N Carolina, Chapel Hill, NC USA.
Univ Chicago, Med Ctr, Chicago, IL 60637 USA.
Univ Pittsburgh, Med Ctr, UPMC Canc Pavil, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 7513
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804312
ER
PT J
AU Heng, DYC
Choueiri, TK
Lee, JL
Harshman, LC
Bjarnason, GA
Knox, JJ
MacKenzie, MJ
Vaishampayan, UN
Yuasa, T
Tan, MH
Rha, SY
Donskov, F
Agarwal, N
Pal, SK
Kollmannsberger, CK
North, SA
Rini, BI
Wood, L
AF Heng, Daniel Yick Chin
Choueiri, Toni K.
Lee, Jae-Lyun
Harshman, Lauren Christine
Bjarnason, Georg A.
Knox, Jennifer J.
MacKenzie, Mary J.
Vaishampayan, Ulka N.
Yuasa, Takeshi
Tan, Min-Han
Rha, Sun Young
Donskov, Frede
Agarwal, Neeraj
Pal, Sumanta Kumar
Kollmannsberger, Christian K.
North, Scott A.
Rini, Brian I.
Wood, Lori
TI An in-depth multicentered population-based analysis of outcomes of
patients with metastatic renal cell carcinoma (mRCC) that do not meet
eligibility criteria for clinical trials.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Univ Calgary, Tom Baker Canc Ctr, Calgary, AB, Canada.
Harvard Univ, Brigham & Womens Hosp, Dana Farber Canc Inst, Lank Ctr Genitourinary Oncol,Med Sch, Boston, MA 02115 USA.
Univ Ulsan, Asan Med Ctr, Coll Med, Seoul, South Korea.
Stanford Univ, Sch Med, Stanford, CA 94305 USA.
Univ Toronto, Sunnybrook Odette Canc Ctr, Toronto, ON, Canada.
Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
London Reg Canc Program, London, ON, Canada.
Wayne State Univ, Karmanos Canc Inst, Detroit, MI USA.
Canc Inst Hosp JFCR, Tokyo, Japan.
Natl Canc Ctr, Singapore, Singapore.
Yonsei Univ, Coll Med, Yonsei Canc Ctr, Seoul, South Korea.
Aarhus Univ Hosp, DK-8000 Aarhus, Denmark.
Univ Utah, Huntsman Canc Inst, Salt Lake City, UT USA.
City Hope Natl Med Ctr, Duarte, CA USA.
British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada.
Cross Canc Inst, Edmonton, AB T6G 1Z2, Canada.
Cleveland Clin, Taussig Canc Inst, Cleveland, OH 44106 USA.
Queen Elizabeth 2 Hlth Sci Ctr, Halifax, NS, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 4536
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803080
ER
PT J
AU Heon, S
Nishino, M
Goldberg, SB
Porter, J
Sequist, LV
Jackman, DM
Johnson, BE
AF Heon, Stephanie
Nishino, Mizuki
Goldberg, Sarah B.
Porter, Jennifer
Sequist, Lecia V.
Jackman, David Michael
Johnson, Bruce E.
TI Response to EGFR tyrosine kinase inhibitor (TKI) retreatment after a
drug-free interval in EGFR-mutant advanced non-small cell lung cancer
(NSCLC) with acquired resistance.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 7525
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804267
ER
PT J
AU Hidalgo, M
Calles, A
Juric, D
Dienstmann, R
Perez, DR
Messersmith, WA
Blumenschein, GR
Baselga, J
Tabernero, J
Cervantes-Ruiperez, A
Jimeno, A
Jin, D
Bai, S
Gurevich, P
Nijem, I
Holden, SN
Davis, JD
Halpern, W
Pirzkall, A
Xin, Y
AF Hidalgo, Manuel
Calles, Antonio
Juric, Dejan
Dienstmann, Rodrigo
Perez, Desamparados Roda
Messersmith, Wells A.
Blumenschein, George R.
Baselga, Jose
Tabernero, Josep
Cervantes-Ruiperez, Andres
Jimeno, Antonio
Jin, Denise
Bai, Shuang
Gurevich, Pavel
Nijem, Ihsan
Holden, Scott N.
Davis, John D.
Halpern, Wendy
Pirzkall, Andrea
Xin, Yan
TI Human pharmacokinetic (PK) characterization of the novel dual-action
anti-HER3/EGFR antibody MEHD7945A (MEHD) in patients with
refractory/recurrent epithelial tumors
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 START Madrid, Ctr Integral Oncol Clara Campal, Madrid, Spain.
Massachusetts Gen Hosp, Dana Farber Canc Inst, Boston, MA 02114 USA.
Vall dHebron Univ Hosp, Mol Therapeut Res Unit, Barcelona, Spain.
Hosp Clin, Dept Med Oncol, Colorectal Unit, Dept Surg, Valencia, Spain.
Univ Colorado, Aurora, CO USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
Vall dHebron Univ Hosp, Barcelona, Spain.
Univ Valencia, Dept Hematol & Med Oncol, INCLIVA, Valencia, Spain.
Univ Colorado Denver, Div Med Oncol, Aurora, CO USA.
Genentech Inc, San Francisco, CA 94080 USA.
RI DAVIS, JOHN/I-7261-2012
OI DAVIS, JOHN/0000-0001-6282-1670
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 2567
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801620
ER
PT J
AU Hodi, FS
Sznol, M
McDermott, DF
Carvajal, RD
Lawrence, DP
Topalian, SL
Wigginton, J
McDonald, D
Kollia, G
Gupta, AK
Sosman, JA
AF Hodi, F. Stephen
Sznol, Mario
McDermott, David F.
Carvajal, Richard D.
Lawrence, Donald P.
Topalian, Suzanne Louise
Wigginton, Jon
McDonald, Dan
Kollia, Georgia
Gupta, Ashok Kumar
Sosman, Jeffrey Alan
TI Clinical activity and safety of anti-PD-1 (BMS-936558, MDX-1106) in
patients with advanced melanoma (MEL).
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Yale Canc Ctr, New Haven, CT USA.
Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
Bristol Myers Squibb Co, Princeton, NJ USA.
Vanderbilt Univ, Med Ctr, Nashville, TN USA.
NR 0
TC 3
Z9 3
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 8507
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802847
ER
PT J
AU Hong, NJL
Hornicek, FJ
Harmon, DC
Choy, E
Chen, YL
Yoon, SS
Nielsen, GP
Szymonifka, J
Yeap, BY
DeLaney, TF
Mullen, JT
AF Hong, Nicole Jannelle Look
Hornicek, Francis J.
Harmon, David C.
Choy, Edwin
Chen, Yen-Lin
Yoon, Sam S.
Nielsen, G. Petur
Szymonifka, Jackie
Yeap, Beow Yong
DeLaney, Thomas F.
Mullen, John Thomas
TI Neoadjuvant chemoradiotherapy for patients with high-risk extremity and
truncal sarcomas: A 10-year follow-up study.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 [Hong, Nicole Jannelle Look; Hornicek, Francis J.; Harmon, David C.; Choy, Edwin; Chen, Yen-Lin; Yoon, Sam S.; Nielsen, G. Petur; Szymonifka, Jackie; Yeap, Beow Yong; DeLaney, Thomas F.; Mullen, John Thomas] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 10058
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801385
ER
PT J
AU Hong, TS
Ryan, DP
Borger, DR
Blaszkowsky, LS
Yeap, BY
Deshpande, V
Wo, JYL
Wadlow, RC
Kwak, EL
Allen, JN
Clark, JW
Zhu, AX
Ferrone, C
Mamon, HJ
Adams, JA
Winrich, B
Grillo, T
DeLaney, TF
Fernandez-del Castillo, C
AF Hong, Theodore S.
Ryan, David P.
Borger, Darrell R.
Blaszkowsky, Lawrence Scott
Yeap, Beow Yong
Deshpande, Vikram
Wo, Jennifer Yon-Li
Wadlow, Raymond Couric
Kwak, Eunice Lee
Allen, Jill N.
Clark, Jeffrey W.
Zhu, Andrew X.
Ferrone, Cristina
Mamon, Harvey J.
Adams, Judith A.
Winrich, Barbara
Grillo, Tarin
DeLaney, Thomas F.
Fernandez-del Castillo, Carlos
TI Phase I/II study of preoperative (pre-op) short course chemoradiation
(CRT) with proton beam therapy (PBT) and capecitabine (cape) followed by
early surgery for resectable pancreatic ductal adenocarcinoma (PDAC) of
the head
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
Massachusetts Gen Hosp, Div Hematol & Oncol, Boston, MA 02114 USA.
Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
Brigham & Womens Hosp, Dept Radiat Oncol, Dana Farber Canc Inst, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 4021
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804685
ER
PT J
AU Hunter, ZR
Xu, L
Yang, G
Zhou, YS
Liu, X
Cao, Y
Tripsas, C
Manning, RJ
Patterson, CJ
Sheehy, PS
Treon, SP
AF Hunter, Zachary R.
Xu, Lian
Yang, Guang
Zhou, Yangsheng
Liu, Xia
Cao, Yang
Tripsas, Christina
Manning, Robert J.
Patterson, Christopher J.
Sheehy, Patricia S.
Treon, Steven P.
TI Use of whole genome sequencing to identify highly recurrent somatic
mutations in Waldenstrom's macroglobulinemia.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 [Hunter, Zachary R.; Xu, Lian; Yang, Guang; Zhou, Yangsheng; Liu, Xia; Cao, Yang; Tripsas, Christina; Manning, Robert J.; Patterson, Christopher J.; Sheehy, Patricia S.; Treon, Steven P.] Dana Farber Canc Inst, Boston, MA 02115 USA.
RI Hunter, Zachary/H-3018-2013
OI Hunter, Zachary/0000-0002-1689-1691
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 8107
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803727
ER
PT J
AU Hutson, TE
Dang, LH
Lauer, RC
Starodub, A
Hauke, RJ
Galsky, MD
Bylow, KA
Logan, T
Cowey, CL
Bibby, DC
Kremmidiotis, G
Doolin, EE
Lavranos, TC
Sonpavde, G
Hahn, NM
Sweeney, C
Sarantopoulos, J
AF Hutson, Thomas E.
Dang, Long H.
Lauer, Richard C.
Starodub, Alexander
Hauke, Ralph J.
Galsky, Matt D.
Bylow, Kathryn A.
Logan, Theodore
Cowey, Charles Lance
Bibby, David C.
Kremmidiotis, Gabriel
Doolin, Elizabeth E.
Lavranos, Tina C.
Sonpavde, Guru
Hahn, Noah M.
Sweeney, Christopher
Sarantopoulos, John
CA Hoosier Oncol Grp
TI Phase I results of a phase I/II trial of BNC105P with everolimus in
metastatic renal cell carcinoma (mRCC) patients previously treated with
VEGFR tyrosine kinase inhibitors
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 US Oncol Res LLC, McKesson Specialty Hlth, The Woodlands, TX USA.
Baylor Sammons Canc Ctr, Texas Oncol PA, Dallas, TX USA.
Univ Florida, Gainesville, FL USA.
Univ New Mexico, Ctr Canc, Albuquerque, NM 87131 USA.
Goshen Ctr Canc Care, Goshen, IN USA.
Nebraska Canc Specialists, Omaha, NE USA.
Mt Sinai Sch Med, Tisch Canc Inst, Div Hematol & Med Oncol, New York, NY USA.
Med Coll Wisconsin, Milwaukee, WI 53226 USA.
Indiana Univ, Melvin & Bren Simon Canc Ctr, Indianapolis, IN 46204 USA.
Baylor Sammons Canc Ctr, Dallas, TX USA.
Bionomics Ltd, Thebarton, Australia.
Texas Oncol, Houston, TX USA.
Baylor Coll Med, Michael E DeBakey Vet Affairs Med Ctr, Dept Med, Sect Med Oncol, Houston, TX 77030 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Univ Texas Hlth Sci Ctr San Antonio, Inst Drug Dev, Canc Therapy & Res Ctr, San Antonio, TX 78229 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 4603
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802786
ER
PT J
AU Hutson, TE
Rathmell, K
Hudes, GR
Kabbinavar, F
Vogelzang, NJ
Knox, JJ
Cowey, CL
Cho, DC
Choueiri, TK
AF Hutson, Thomas E.
Rathmell, Kimryn
Hudes, Gary R.
Kabbinavar, Fairooz
Vogelzang, Nicholas J.
Knox, Jennifer J.
Cowey, C. Lance
Cho, Daniel C.
Choueiri, Toni K.
TI A phase II biomarker assessment of tivozanib in oncology (BATON) trial
in patients (pts) with advanced renal cell carcinoma (RCC)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Texas Oncol Baylor A Charles Sammons Canc Ctr, Dallas, TX USA.
Univ N Carolina, Sch Med, Dept Genet, Chapel Hill, NC USA.
Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
Univ Calif Los Angeles, Inst Urol Oncol, Los Angeles, CA USA.
Comprehens Canc Ctr Nevada, Las Vegas, NV USA.
US Oncol Res, Las Vegas, NV USA.
Univ Hlth Network, Toronto, ON, Canada.
US Oncol Res, Dallas, TX USA.
Beth Israel Deaconess Med Ctr, Boston, MA USA.
Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA TPS4686
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802664
ER
PT J
AU Iasonos, A
Keung, E
Zivanovic, O
Mancari, R
Peiretti, M
Nucci, M
George, S
Colombo, N
Carinelli, S
Hensley, ML
Raut, CP
AF Iasonos, Alexia
Keung, Emily
Zivanovic, Oliver
Mancari, Rosanna
Peiretti, Michele
Nucci, Marisa
George, Suzanne
Colombo, Nicoletta
Carinelli, Silvestro
Hensley, Martee Leigh
Raut, Chandrajit P.
TI External validation of a nomogram predicting overall survival (OS) of
women with uterine leiomyosarcoma (ULMS).
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Harvard Univ, Brigham & Womens Hosp, Dana Farber Canc Inst, Sch Med, Boston, MA 02115 USA.
Univ Hosp Bonn, Bonn, Germany.
European Inst Oncol, Milan, Italy.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Univ Milano Bicocca, Milan, Italy.
Brigham & Womens Hosp, Div Surg Oncol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 5090
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009803583
ER
PT J
AU Infante, JR
Gandhi, L
Shapiro, G
Burris, HA
Bendell, JC
Baselga, J
Hsu, K
Faivre, T
Asatiani, E
Heist, RS
AF Infante, Jeffrey R.
Gandhi, Leena
Shapiro, Geoffrey
Burris, Howard A.
Bendell, Johanna C.
Baselga, Jose
Hsu, Karl
Faivre, Thea
Asatiani, Ekatherine
Heist, Rebecca Suk
TI Phase lb combination trial of a MEK inhibitor, pimasertib (MSC1936369B),
and a PI3K/mTOR inhibitor, SAR245409, in patients with locally advanced
or metastatic solid tumors
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Sarah Cannon Res Inst, Nashville, TN USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
Sanofi, Cambridge, MA USA.
Merck Serono SA, Geneva, Switzerland.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA TPS3118
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009802382
ER
PT J
AU Irwin, M
Gottlieb, L
Cartmel, B
Ercolano, E
Rothbard, M
Zhou, Y
Schwartz, PE
Ligibel, JA
Von Gruenigen, VE
Risch, H
AF Irwin, Melinda
Gottlieb, Linda
Cartmel, Brenda
Ercolano, Elizabeth
Rothbard, Marianna
Zhou, Yang
Schwartz, Peter E.
Ligibel, Jennifer A.
Von Gruenigen, Vivian E.
Risch, Harvey
TI Trial of exercise in ovarian cancer survivors.
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Yale Univ, New Haven, CT USA.
Yale Univ, Sch Publ Hlth, New Haven, CT USA.
Yale Univ, Sch Med, New Haven, CT USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Summa Akron City Hosp, Akron, OH USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA TPS1614
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009801175
ER
PT J
AU Irwin, M
Cartmel, B
Ercolano, E
Fiellin, M
Rothbard, M
Capozza, S
Zhou, Y
Schmitz, K
Ligibel, JA
Hershman, DL
Neogi, T
Gross, CP
AF Irwin, Melinda
Cartmel, Brenda
Ercolano, Elizabeth
Fiellin, Martha
Rothbard, Marianna
Capozza, Scott
Zhou, Yang
Schmitz, Kathryn
Ligibel, Jennifer A.
Hershman, Dawn L.
Neogi, Tuhina
Gross, Cary P.
TI Aromatase inhibitors, arthralgias, and exercise in breast cancer
survivors
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Yale Univ, New Haven, CT USA.
Yale Univ, Sch Publ Hlth, New Haven, CT USA.
Univ Penn, Philadelphia, PA 19104 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Columbia Univ, Med Ctr, New York, NY USA.
Boston Univ, Boston, MA 02215 USA.
Yale Univ, Sch Med, New Haven, CT USA.
NR 0
TC 0
Z9 0
U1 1
U2 7
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA TPS669
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800322
ER
PT J
AU Janne, PA
Shaw, AT
Pereira, JR
Jeannin, G
Vansteenkiste, J
Barrios, CH
Franke, FA
Grinsted, L
Smith, PD
Zazulina, V
Smith, IC
Crino, L
AF Janne, Pasi A.
Shaw, Alice Tsang
Pereira, Jose Rodrigues
Jeannin, Gaelle
Vansteenkiste, Johan
Barrios, Carlos H.
Franke, Fabio A.
Grinsted, Lynda
Smith, Paul D.
Zazulina, Victoria
Smith, Ian C.
Crino, Lucio
TI Phase II double-blind, randomized study of selumetinib (SEL) plus
docetaxel (DOC) versus DOC plus placebo as second-line treatment for
advanced KRAS mutant non-small cell lung cancer (NSCLC).
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
Inst Brasileiro Cancerol Torac, Sao Paulo, Brazil.
Serv Pneumol Oncol Thorac, Clermont Ferrand, France.
Univ Hosp Gasthuisberg, Resp Oncol Unit, B-3000 Louvain, Belgium.
PUCRS Sch Med, Porto Alegre, RS, Brazil.
Hosp Caridade Ijui, Ijui, Brazil.
AstraZeneca, Macclesfield, Cheshire, England.
Univ Perugia, I-06100 Perugia, Italy.
RI Vansteenkiste, Johan/B-8191-2014; Barrios, Carlos/G-8525-2015
OI Vansteenkiste, Johan/0000-0002-6721-2775;
NR 0
TC 11
Z9 12
U1 1
U2 6
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA 7503
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009804172
ER
PT J
AU Jeon, JY
Jeong, DH
Park, MK
Ligibel, JA
Meyerhardt, JA
Kim, NK
AF Jeon, Justin Y.
Jeong, Deok Hyun
Park, Min Keun
Ligibel, Jennifer A.
Meyerhardt, Jeffrey A.
Kim, Nam Kyu
TI Impact of diabetes on site-specific oncologic outcome in stage I-III
colorectal cancer
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)
CY JUN 01-06, 2012
CL Chicago, IL
SP Amer Soc Clin Oncol (ASCO)
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Yonsei Univ Coll Med, Dept Surg, Seoul, South Korea.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD MAY 20
PY 2012
VL 30
IS 15
SU S
MA e14114
PG 1
WC Oncology
SC Oncology
GA 131QQ
UT WOS:000318009800827
ER
EF