FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Dossett, ML
Kohatsu, W
Nunley, W
Mehta, D
Davis, RB
Phillips, RS
Yeh, G
AF Dossett, Michelle L.
Kohatsu, Wendy
Nunley, William
Mehta, Darshan
Davis, Roger B.
Phillips, Russell S.
Yeh, Gloria
TI PROFESSIONALISM AND FACTORS ASSOCIATED WITH BURNOUT, EMPATHY, AND
RESILIENCE AMONG EARLY CAREER PHYSICIANS: RESULTS OF THE HEART ALUMNI
SURVEY
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Dossett, Michelle L.; Davis, Roger B.; Phillips, Russell S.; Yeh, Gloria] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Kohatsu, Wendy] Santa Rosa Family Med Residency Program, Santa Rosa, CA USA.
[Nunley, William] Yamhill Cty Mental Hlth, Mcminnville, OR USA.
[Mehta, Darshan] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 1
Z9 1
U1 3
U2 9
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S271
EP S271
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701270
ER
PT J
AU El-Jawahri, A
Baggett, M
AF El-Jawahri, Areej
Baggett, Meridale
TI MYCOPLASMA MYOCARDITIS: AN UNCOMMON COMPLICATION OF A COMMON INFECTION
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [El-Jawahri, Areej; Baggett, Meridale] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S410
EP S411
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812702243
ER
PT J
AU Englander, H
Davis, M
Kansagara, D
AF Englander, Honora
Davis, Melinda
Kansagara, Devan
TI UNDERSTANDING PROVIDER PERSPECTIVES ON CARE TRANSITIONS FROM HOSPITAL TO
HOME: FINDINGS FROM A 360 DEGREE QUALITATIVE EVALUATION
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Englander, Honora; Davis, Melinda] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Kansagara, Devan] Portland VA Med Ctr, Portland, OR USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S199
EP S199
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701134
ER
PT J
AU Feibelmann, S
Atlas, SJ
Sepucha, KR
AF Feibelmann, Sandra
Atlas, Steven J.
Sepucha, Karen R.
TI ASSESSING PROVIDER KNOWLEDGE OF A HERNIATED LUMBAR DISC: ARE SPECIALISTS
BETTER INFORMED THAN PRIMARY CARE PHYSICIANS?
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Feibelmann, Sandra; Atlas, Steven J.; Sepucha, Karen R.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S120
EP S120
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812700216
ER
PT J
AU Fox, M
O'Brien, JL
Hinchcliff, EM
Berman, R
AF Fox, Michelle
O'Brien, Jessica L.
Hinchcliff, Emily M.
Berman, Rebecca
TI THE CRIMSON CARE COLLABORATIVE: A MODEL FOR PRIMARY CARE MEDICAL
EDUCATION
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Fox, Michelle] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[O'Brien, Jessica L.; Hinchcliff, Emily M.] Harvard Univ, Sch Med, Boston, MA USA.
[Berman, Rebecca] Harvard Univ, Massachusetts Gen Hosp, Sch Med, John D Stoeckle Ctr, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S604
EP S605
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812703330
ER
PT J
AU Gellad, WF
Mor, MK
Zhao, XH
Donohue, JM
Good, CB
Fine, MJ
AF Gellad, Walid F.
Mor, Maria K.
Zhao, Xinhua
Donohue, Julie M.
Good, Chester B.
Fine, Michael J.
TI VARIATION IN PRESCRIPTION USE AMONG PATIENTS WITH DIABETES IN THE VA
HEALTHCARE SYSTEM
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Gellad, Walid F.] Univ Pittsburgh, VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Mor, Maria K.; Zhao, Xinhua; Good, Chester B.; Fine, Michael J.] VA Pittsburgh, Pittsburgh, PA USA.
[Donohue, Julie M.] Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S256
EP S256
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701241
ER
PT J
AU Gellad, WF
Wang, XQ
Handler, SM
Aspinall, SL
Stone, RA
Castle, N
Semla, TP
Good, CB
Fine, MJ
Dysken, M
Hanlon, JT
AF Gellad, Walid F.
Wang, Xiaoqiang
Handler, Steven M.
Aspinall, Sherrie L.
Stone, Roslyn A.
Castle, Nicholas
Semla, Todd P.
Good, Chester B.
Fine, Michael J.
Dysken, Maurice
Hanlon, Joseph T.
TI ANTIPSYCHOTIC PRESCRIBING IN OLDER VETERANS ADMINISTRATION NURSING HOME
PATIENTS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Gellad, Walid F.] Univ Pittsburgh, VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Wang, Xiaoqiang; Aspinall, Sherrie L.; Stone, Roslyn A.; Good, Chester B.; Fine, Michael J.; Hanlon, Joseph T.] VA Pittsburgh, Pittsburgh, PA USA.
[Handler, Steven M.; Castle, Nicholas] Univ Pittsburgh, Pittsburgh, PA USA.
[Semla, Todd P.] Dept Vet Affairs, Washington, DC USA.
[Dysken, Maurice] VA Minneapolis, Minneapolis, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S173
EP S173
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701083
ER
PT J
AU Gellad, WF
Donohue, JM
Zhao, XH
Banthin, JS
AF Gellad, Walid F.
Donohue, Julie M.
Zhao, Xinhua
Banthin, Jessica S.
TI TRENDS IN THE FINANCIAL BURDEN OF PRESCRIPTION DRUGS AMONG THE
NON-ELDERLY, 1999-2007
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Gellad, Walid F.; Zhao, Xinhua] Univ Pittsburgh, VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Donohue, Julie M.] Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA USA.
[Banthin, Jessica S.] AHRQ, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S96
EP S96
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812700170
ER
PT J
AU Gopal, RK
Yamashita, TE
Prochazka, AV
AF Gopal, Ravi K.
Yamashita, Traci E.
Prochazka, Allan V.
TI RESEARCH WITHOUT RESULTS: INADEQUATE PUBLIC REPORTING OF CLINICAL TRIAL
RESULTS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Gopal, Ravi K.; Prochazka, Allan V.] Denver VAMC, Denver, CO USA.
[Yamashita, Traci E.] Univ Colorado, Denver Hlth Sci Ctr, Aurora, CO USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S169
EP S170
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701076
ER
PT J
AU Gordon, HS
Street, R
Deswal, A
AF Gordon, Howard S.
Street, Richard
Deswal, Anita
TI FACTORS ASSOCIATED WITH ADHERENCE TO PHYSICIANS RECOMMENDATIONS IN A
PROSPECTIVE COHORT AFTER HOSPITALIZATION WITH HEART FAILURE
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Gordon, Howard S.] VAMC, Chicago, IL USA.
[Gordon, Howard S.] Univ Illinois, Chicago, IL USA.
[Street, Richard] Texas A&M Univ, College Stn, TX USA.
[Deswal, Anita] Houston VAMC, Houston, TX USA.
[Deswal, Anita] Baylor Coll Med, Houston, TX 77030 USA.
RI Gordon, Howard/E-4420-2010
OI Gordon, Howard/0000-0002-6712-5954
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S351
EP S351
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812702118
ER
PT J
AU Grant, R
Pajolek, H
Pelletier, A
Kvedar, J
AF Grant, Richard
Pajolek, Hannah
Pelletier, Alexandra
Kvedar, Joseph
TI THE MEDICATION SELF-TITRATION EVALUATION PROGRAM (MED-STEP): A
PATIENT-DIRECTED, IT-SUPPORTED HYPERTENSION TREATMENT PROGRAM
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Grant, Richard] Massachusetts Gneral Hosp, Boston, MA USA.
[Pajolek, Hannah] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Pelletier, Alexandra; Kvedar, Joseph] Partners Ctr Connected Hlth, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S563
EP S563
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812703250
ER
PT J
AU Hagler, BD
Chandan, P
Estrada, C
Roy, B
Huff, NG
Castiglioni, A
Centor, R
AF Hagler, Beau Daniel
Chandan, Priya
Estrada, Carlos
Roy, Brita
Huff, Nidhi Gupta
Castiglioni, Analia
Centor, Robert
TI PRIORITIES DURING WARD ATTENDING ROUNDS DIFFER BY TRAINING LEVEL OF TEAM
MEMBERS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Hagler, Beau Daniel] Univ Alabama Birmingham, SOM, Birmingham, AL USA.
[Chandan, Priya; Roy, Brita; Castiglioni, Analia; Centor, Robert] Univ Alabama Birmingham, Birmingham, AL USA.
[Estrada, Carlos] Univ Alabama Birmingham, Birmingham VAMC, Birmingham, AL USA.
[Huff, Nidhi Gupta] Univ Alabama Birmingham, Fultondale, AL USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S284
EP S284
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701295
ER
PT J
AU Han, M
Cooper, CM
AF Han, Maria
Cooper, Cynthia Margaret
TI METRONIDAZOLE-INDUCED ENCEPHALOPATHY
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Han, Maria; Cooper, Cynthia Margaret] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S463
EP S464
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812703031
ER
PT J
AU Hanchate, AD
Schwamm, L
Hylek, E
AF Hanchate, Amresh D.
Schwamm, Lee
Hylek, Elaine
TI USING INPATIENT MORTALITY DIFFERENTIAL FROM WEEKEND ADMISSION TO
IDENTIFY THE ROLE OF HOSPITAL STRUCTURES: THE CASE OF ISCHEMIC STROKE
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Hanchate, Amresh D.; Hylek, Elaine] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Schwamm, Lee] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S215
EP S216
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701165
ER
PT J
AU Hausmann, LRM
Kwoh, CK
Hannon, MJ
Ibrahim, SA
AF Hausmann, Leslie R. M.
Kwoh, C. Kent
Hannon, Michael J.
Ibrahim, Said A.
TI PATIENT RACE, PERCEPTIONS OF RACISM IN HEALTHCARE SETTINGS, AND
PHYSICIAN TRUST
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Hausmann, Leslie R. M.; Kwoh, C. Kent; Hannon, Michael J.] Univ Pittsburgh, VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Ibrahim, Said A.] Univ Penn, Sch Med, Philadelphia VA Med Ctr, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S74
EP S74
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812700131
ER
PT J
AU Heyworth, L
Kleinman, K
Oddleifson, S
Bernstein, L
Frampton, J
Salvato, K
Weiss, TW
Simon, S
Connelly, M
AF Heyworth, Leonie
Kleinman, Ken
Oddleifson, Stephanie
Bernstein, Lydia
Frampton, Judith
Salvato, Karen
Weiss, Thomas W.
Simon, Steven
Connelly, Maureen
TI SCREENING FOR OSTEOPOROSIS IN HIGH RISK, MENOPAUSAL WOMEN: A RANDOMIZED
TRIAL OF INTERACTIVE VOICE RESPONSE
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Heyworth, Leonie] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Kleinman, Ken; Oddleifson, Stephanie; Bernstein, Lydia; Frampton, Judith; Salvato, Karen] Harvard Pilgrim Hlth Care, Boston, MA USA.
[Weiss, Thomas W.] Merck Co Inc, West Point, PA USA.
[Simon, Steven] Brigham & Womens Hosp, VA Boston Healthcare, Boston, MA 02115 USA.
[Connelly, Maureen] Harvard Univ, Sch Med, Dept Populat Med, Boston, MA USA.
[Connelly, Maureen] Harvard Pilgrim Hlth Care, Boston, MA USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S207
EP S207
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701148
ER
PT J
AU Hong, C
Rodriguez, F
Chang, YC
Oertel, L
Singer, D
Lopez, L
AF Hong, Clemens
Rodriguez, Fatima
Chang, Yuchiao
Oertel, Lynn
Singer, Daniel
Lopez, Lenny
TI LIMITED ENGLISH PROFICIENT PATIENTS AND TIME SPENT IN THERAPEUTIC RANGE
IN A WARFARIN ANTICOAGULATION CLINIC
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Hong, Clemens; Chang, Yuchiao; Oertel, Lynn; Singer, Daniel; Lopez, Lenny] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Rodriguez, Fatima] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S348
EP S349
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812702113
ER
PT J
AU Hong, C
Atlas, SJ
Liu, LL
Wei, H
Stratton, L
Lopez, L
Grant, R
AF Hong, Clemens
Atlas, Steven J.
Liu, Lulu
Wei, He
Stratton, Lawrence
Lopez, Lenny
Grant, Richard
TI MAPPING QUALITY IN HEALTH CARE SYSTEMS -A NOVEL TOOL FOR POPULATION
MANAGEMENT
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Hong, Clemens; Atlas, Steven J.; Liu, Lulu; Wei, He; Stratton, Lawrence; Lopez, Lenny; Grant, Richard] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S340
EP S341
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812702100
ER
PT J
AU Hong, C
Grant, R
Wei, H
Liu, LL
Ward, C
Atlas, SJ
AF Hong, Clemens
Grant, Richard
Wei, He
Liu, Lulu
Ward, Charlotte
Atlas, Steven J.
TI IDENTIFYING TOP DOCTORS IN HEALTH SYSTEMS USING CLINICAL PERFORMANCE,
PRODUCTIVITY, AND PATIENT EXPERIENCE DATA
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Hong, Clemens; Grant, Richard; Wei, He; Liu, Lulu; Ward, Charlotte; Atlas, Steven J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S333
EP S334
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812702086
ER
PT J
AU Huff, NG
Roy, B
Estrada, C
Centor, R
Castiglioni, A
Willett, L
Cohen, S
AF Huff, Nidhi Gupta
Roy, Brita
Estrada, Carlos
Centor, Robert
Castiglioni, Analia
Willett, Lisa
Cohen, Stuart
TI NOMINAL GROUP TECHNIQUE TO IDENTIFY ATTRIBUTES OF TOP ATTENDING
PHYSICIANS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Huff, Nidhi Gupta] Univ Alabama Birmingham, Fultondale, AL USA.
[Roy, Brita; Castiglioni, Analia; Willett, Lisa; Cohen, Stuart] Univ Alabama Birmingham, Birmingham, AL USA.
[Estrada, Carlos; Centor, Robert] Univ Alabama Birmingham, Birmingham VAMC, Birmingham, AL USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S176
EP S176
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701089
ER
PT J
AU Hunt, SC
Burgo-Black, L
AF Hunt, Stephen C.
Burgo-Black, Lucille
TI HEALTH IMPACTS OF WAR: AN EDUCATIONAL CAMPAIGN FOR VA PROVIDERS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Hunt, Stephen C.] VA Puget Sound, Seattle, WA USA.
[Burgo-Black, Lucille] VA Connecticut Healthcare Syst, West Haven, CT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S589
EP S589
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812703303
ER
PT J
AU Ignacio, RAB
Finn, KM
AF Ignacio, Rachel Ann Bender
Finn, Kathleen M.
TI IMPROVING UPWARD FEEDBACK IN MEDICAL EDUCATION
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Ignacio, Rachel Ann Bender] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cambridge, MA 02138 USA.
[Finn, Kathleen M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S578
EP S579
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812703283
ER
PT J
AU Inagami, S
Gao, SS
Shendge, M
Probst, J
Karimi, H
Stone, R
Sevick, MA
Fine, M
AF Inagami, Sanae
Gao, Shasha
Shendge, Martine
Probst, Janice
Karimi, Hassan
Stone, Roslyn
Sevick, Mary Ann
Fine, Michael
TI USING THE INDEX OF RELATIVE RURALITY (IRR) TO ESTIMATE DEGREE OF
RURALITY AT THE SMALL-AREA LEVEL IN HEALTH SERVICES RESEARCH
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Inagami, Sanae; Gao, Shasha; Shendge, Martine; Fine, Michael] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Probst, Janice] Univ S Carolina, Charleston, SC USA.
[Karimi, Hassan; Stone, Roslyn] Univ Pittsburgh, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S155
EP S155
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701048
ER
PT J
AU Kansagara, D
Englander, H
Salanitro, A
Kagen, D
Theobald, C
Kripalani, S
AF Kansagara, Devan
Englander, Honora
Salanitro, Amanda
Kagen, David
Theobald, Cecelia
Kripalani, Sunil
TI READMISSION RISK MODELING: A SYSTEMATIC REVIEW
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Kansagara, Devan] Oregon Hlth & Sci Univ, Portland VA Med Ctr, Portland, OR 97201 USA.
[Englander, Honora] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Salanitro, Amanda; Theobald, Cecelia; Kripalani, Sunil] Vanderbilt Univ, Nashville, TN 37235 USA.
[Kagen, David] Portland VA Med Ctr, Portland, OR USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S125
EP S125
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812700226
ER
PT J
AU Kertesz, S
Pollio, D
Johnson-Roe, K
Steward, J
Borden, A
Kim, T
Stringfellow, E
Young, JA
Holt, C
AF Kertesz, Stefan
Pollio, David
Johnson-Roe, Kay
Steward, Jocelyn
Borden, Allison
Kim, Theresa
Stringfellow, Erin
Young, John Andrew
Holt, Cheryl
TI CROSSING QUALITY CHASM: PRIMARY CARE FROM THE PERSPECTIVE OF HOMELESS
PATIENTS AND THEIR CAREGIVERS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Kertesz, Stefan] Birmingham VA Med Ctr, Birmingham, AL USA.
[Pollio, David] Univ Alabama, Tuscaloosa, MD USA.
[Johnson-Roe, Kay; Steward, Jocelyn; Borden, Allison; Young, John Andrew] Birmingham VAMC, Birmingham, AL USA.
[Kim, Theresa] Boston Med Ctr, Boston, AL USA.
[Stringfellow, Erin] Boston Hlth Care Homeless, Boston, AL USA.
[Holt, Cheryl] Univ Maryland, Baltimore, AL USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S122
EP S123
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812700221
ER
PT J
AU Kullgren, JT
Volpp, KG
Polsky, DE
AF Kullgren, Jeffrey T.
Volpp, Kevin G.
Polsky, Daniel E.
TI UNDERSTANDING BEHAVIORAL RISK FACTORS IN HIGH-DEDUCTIBLE HEALTH PLANS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Kullgren, Jeffrey T.; Volpp, Kevin G.] Philadelphia VA Med Ctr, Philadelphia, PA USA.
[Kullgren, Jeffrey T.] Univ Penn, Philadelphia, PA 19104 USA.
[Kullgren, Jeffrey T.; Volpp, Kevin G.; Polsky, Daniel E.] Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA.
[Volpp, Kevin G.; Polsky, Daniel E.] Univ Penn, Sch Med, Div Gen Internal Med, Philadelphia, PA 19104 USA.
[Volpp, Kevin G.; Polsky, Daniel E.] Univ Penn, Wharton Sch, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S277
EP S277
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701281
ER
PT J
AU Kullgren, JT
McLaughlin, CG
Mitra, N
Armstrong, K
AF Kullgren, Jeffrey T.
McLaughlin, Catherine G.
Mitra, Nandita
Armstrong, Katrina
TI NON-AFFORDABILITY BARRIERS AND ACCESS TO CARE FOR US ADULTS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Kullgren, Jeffrey T.] Philadelphia VA Med Ctr, Philadelphia, PA USA.
[Kullgren, Jeffrey T.] Univ Penn, Philadelphia, PA 19104 USA.
[Kullgren, Jeffrey T.; Armstrong, Katrina] Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA.
[McLaughlin, Catherine G.] Math Policy Res Inc, Ann Arbor, MI USA.
[McLaughlin, Catherine G.] Univ Michigan, Sch Publ Hlth, Dept Hlth Management & Policy, Ann Arbor, MI 48109 USA.
[Mitra, Nandita] Univ Penn, Sch Med, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA.
[Armstrong, Katrina] Univ Penn, Abramson Canc Ctr, Sch Med, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S276
EP S277
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701280
ER
PT J
AU Laponis, R
O'Sullivan, P
Hollander, H
Cornett, P
Julian, K
AF Laponis, Ryan
O'Sullivan, Patricia
Hollander, Harry
Cornett, Patricia
Julian, Katherine
TI GENERATING GENERALISTS: FACTORS OF RESIDENT CONTINUITY CLINIC ASSOCIATED
WITH PERCEIVED IMPACT ON CHOOSING A GENERALIST CAREER
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Laponis, Ryan; O'Sullivan, Patricia; Hollander, Harry; Julian, Katherine] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Cornett, Patricia] San Francisco Vet Adm Med Ctr, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S281
EP S281
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701290
ER
PT J
AU LaRue, NM
Paasche-Orlow, MK
Volandes, AE
AF LaRue, Nicole M.
Paasche-Orlow, Michael K.
Volandes, Angelo E.
TI THE APPROPRIATE USE OF MEDICAL FUTILITY IN TREATMENT DECISIONS AT THE
END OF LIFE
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [LaRue, Nicole M.; Paasche-Orlow, Michael K.] Boston Univ, Med Ctr, Boston, MA USA.
[Volandes, Angelo E.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S507
EP S507
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812703126
ER
PT J
AU LaRue, NM
Paasche-Orlow, MK
Volandes, AE
AF LaRue, Nicole M.
Paasche-Orlow, Michael K.
Volandes, Angelo E.
TI USE OF A VIDEO DECISION SUPPORT TOOL TO SUPPLEMENT GOALS-OF-CARE
DISCUSSIONS WITH PATIENTS SEEN BY AN INPATIENT PALLIATIVE CARE SERVICE
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [LaRue, Nicole M.; Paasche-Orlow, Michael K.] Boston Univ, Med Ctr, Boston, MA USA.
[Volandes, Angelo E.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 3
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S98
EP S99
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812700174
ER
PT J
AU Laxmisan, A
Sittig, DF
Espadas, D
Pietz, K
Singh, H
AF Laxmisan, Archana
Sittig, Dean Forrest
Espadas, Donna
Pietz, Kenneth
Singh, Hardeep
TI IMPROVING FOLLOW-UP OF ABNORMAL TEST RESULTS: EVALUATING THE IMPACT OF A
MANDATORY NOTIFICATION
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Laxmisan, Archana; Singh, Hardeep] Baylor Coll Med, Houston VA HSR&D Ctr Excellence, Michael E DeBakey Vet Affairs Med Ctr, Houston, TX 77030 USA.
[Sittig, Dean Forrest] Univ Texas Hlth Sci Ctr Houston, Houston, TX 77030 USA.
[Espadas, Donna; Pietz, Kenneth] Michael E DeBakey VA Med Ctr, Houston VA HSR&D Ctr Excellence, Houston, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S154
EP S155
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701047
ER
PT J
AU Leung, AA
Wright, A
Pazo, V
Karson, A
Bates, DW
AF Leung, Alexander A.
Wright, Adam
Pazo, Valeria
Karson, Andrew
Bates, David W.
TI RISK OF THIAZIDE-INDUCED HYPONATREMIA IN PATIENTS WITH HYPERTENSION
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Leung, Alexander A.; Wright, Adam; Pazo, Valeria; Bates, David W.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Karson, Andrew] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S26
EP S26
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812700041
ER
PT J
AU Linsky, A
Hermos, JA
Shwartz, M
Rudolph, JL
AF Linsky, Amy
Hermos, John A.
Shwartz, Michael
Rudolph, James L.
TI ASSESSING VARIATION IN PPI DISCONTINUATION IN VA LONG-TERM CARE
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Linsky, Amy] Boston Med Ctr, Boston, MA USA.
[Linsky, Amy] VA Boston Healthcare Syst, Ctr Org Leadership & Management Res, Boston, MA USA.
[Hermos, John A.] VA Boston Healthcare Syst, VA Cooperat Studies Program, Massachusetts Vet Epidemiol Res & Informat Ctr, Boston, MA USA.
[Shwartz, Michael] VA Boston Healthcare Syst, Ctr Org Leadership & Management Res, Boston, MA USA.
[Rudolph, James L.] VA Boston Healthcare Syst, Geriatr Res Educ & Clin Ctr, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S82
EP S83
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812700144
ER
PT J
AU Liu, CF
Manning, WG
Burgess, JF
Hebert, PL
Bryson, CL
Fortney, J
Perkins, M
Sharp, ND
Maciejewski, ML
AF Liu, Chuan-Fen
Manning, Willard G.
Burgess, James F.
Hebert, Paul L.
Bryson, Christopher L.
Fortney, John
Perkins, Mark
Sharp, Nancy D.
Maciejewski, Matthew L.
TI RELIANCE ON VA OUTPATIENT SERVICES BY MEDICARE-ELIGIBLE VETERANS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Liu, Chuan-Fen] Dept Vet Affairs, Seattle, WA USA.
[Manning, Willard G.] Univ Chicago, Dept Hlth Studies, Chicago, IL 60637 USA.
[Burgess, James F.] VA BostonHealthcare Syst, Boston, MA USA.
[Burgess, James F.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Hebert, Paul L.] VA Puget Sound Hlth Care Syst, Washington, DC USA.
[Hebert, Paul L.] Univ Washington, Dept Hlth Serv, Seattle, WA 98195 USA.
[Bryson, Christopher L.; Perkins, Mark; Sharp, Nancy D.] VA Puget Sound Hlth Care Syst, Seattle, WA USA.
[Fortney, John] Cent Arkansas Vet Healthcare Syst, North Little Rock, AR USA.
[Fortney, John] Univ Arkansas Med Sci, North Little Rock, AR USA.
[Maciejewski, Matthew L.] Durham VA Med Ctr, Durham, NC USA.
[Maciejewski, Matthew L.] Duke Univ, Med Ctr, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S158
EP S159
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701055
ER
PT J
AU Long, JA
Jahnle, E
Richardson, D
Volpp, K
AF Long, Judith A.
Jahnle, Erica
Richardson, Diane
Volpp, Kevin
TI A RANDOMIZED CONTROLLED TRIAL OF PEER MENTORING AND FINANCIAL INCENTIVE
TO IMPROVE GLUCOSE CONTROL IN AFRICAN AMERICAN VETERANS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Long, Judith A.; Richardson, Diane; Volpp, Kevin] Philadelphia VA Ctr Hlth Equ Res & Promot, Philadelphia, PA USA.
[Jahnle, Erica] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S165
EP S165
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701067
ER
PT J
AU Lopez, L
Cook, N
Grant, R
Pabon-Nau, L
Hicks, L
AF Lopez, Lenny
Cook, Nakela
Grant, Richard
Pabon-Nau, Lina
Hicks, Leroi
TI HIGHER CARDIOLOGY CONSULTATION RATES FOR CARDIOVASCULAR DISEASE FOR
HISPANICS SEEN IN HIGH PROPORTION HISPANIC VS. LOW PROPORTION HISPANIC
CLINICS IN A LARGE INTEGRATED ACADEMIC HEALTHCARE SYSTEM
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Lopez, Lenny; Grant, Richard; Pabon-Nau, Lina] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Cook, Nakela] NHLBI, Bethesda, MD 20892 USA.
[Hicks, Leroi] Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S305
EP S305
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812702033
ER
PT J
AU Lopez, L
DesRoches, C
Vogeli, C
Grant, R
Iezzoni, L
Campbell, E
AF Lopez, Lenny
DesRoches, Catherine
Vogeli, Christine
Grant, Richard
Iezzoni, Lisa
Campbell, Eric
TI CHARACTERISTICS OF PRIMARY CARE SAFETY-NET PROVIDERS AND THEIR QUALITY
IMPROVEMENT ATTITUDES AND ACTIVITIES: RESULTS OF A NATIONAL SURVEY OF
PHYSICIAN PROFESSIONALISM
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Lopez, Lenny; DesRoches, Catherine; Vogeli, Christine; Grant, Richard; Iezzoni, Lisa; Campbell, Eric] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S302
EP S302
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812702027
ER
PT J
AU Lopez, L
Rodroguez, F
Peralta, C
Green, A
AF Lopez, Lenny
Rodroguez, Fatima
Peralta, Carmen
Green, Alexander
TI THE EFFECT OF ACCULTURATION ON C-REACTIVE PROTEIN LEVELS AMONG HISPANIC
ADULTS IN THE US
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Lopez, Lenny] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Rodroguez, Fatima] Harvard Univ, Sch Med, Boston, MA USA.
[Peralta, Carmen] Univ San Francisco, San Francisco, CA 94117 USA.
[Green, Alexander] Massachusetts Gen Hosp, Cambridge, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S295
EP S295
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812702012
ER
PT J
AU Mielke, B
Perkins, M
Wong, E
Liu, CF
Au, D
Bryson, C
AF Mielke, Beverly
Perkins, Mark
Wong, Edwin
Liu, Chuan-Fen
Au, David
Bryson, Christopher
TI PHARMACY SUPPORT IN VA PRIMARY CARE CLINICS AND MEDICATION ADHERENCE
AMONG PATIENTS WITH DIABETES
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Mielke, Beverly] VA Puget Sound Healthcare Syst, UW Med, Seattle, WA USA.
[Perkins, Mark; Wong, Edwin; Bryson, Christopher] VA Puget Sound Hlth Care Syst, Seattle, WA USA.
[Liu, Chuan-Fen] Dept Vet Affairs, Seattle, WA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S165
EP S165
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701066
ER
PT J
AU Miloslavsky, EM
Hayden, EM
Currier, PF
Gordon, JA
AF Miloslavsky, Eli M.
Hayden, Emily M.
Currier, Paul F.
Gordon, James A.
TI MEDICAL SIMULATION FOR CLINICAL DECISION MAKING TRAINING FOR INTERNAL
MEDICINE RESIDENTS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Miloslavsky, Eli M.] Massachusetts Gen Hosp, Brookline, MA USA.
[Hayden, Emily M.; Gordon, James A.] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
[Hayden, Emily M.; Currier, Paul F.; Gordon, James A.] MGH Learning Lab, Boston, MA USA.
[Currier, Paul F.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S571
EP S572
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812703270
ER
PT J
AU Moore, LD
Stone, VE
Olabisi, O
Knox, C
Wright, D
AF Moore, Lauren D.
Stone, Valerie E.
Olabisi, Opeyemi
Knox, Clayton
Wright, Douglas
TI WHEN A WHEEZING WOMAN HAS MORE THAN ASTHMA
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Moore, Lauren D.; Stone, Valerie E.; Olabisi, Opeyemi; Knox, Clayton; Wright, Douglas] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S487
EP S488
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812703083
ER
PT J
AU Morrill, JA
Carr, C
AF Morrill, James A.
Carr, Christina
TI A TALE OF TWO EPIDEMICS: UNIQUE CHARACTERISTICS OF YOUNG ADULT PATIENTS
WITH HEPATITIS C INFECTION FOLLOWED AT AN URBAN COMMUNITY HEALTH CENTER
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Morrill, James A.] Massachusetts Gen Hosp, Charlestown, MA USA.
[Carr, Christina] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S249
EP S249
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701226
ER
PT J
AU Moy, N
Pierluissi, E
AF Moy, Nicholas
Pierluissi, Edgar
TI TRANSITION OF CARE FROM ACUTE HOSPITALIZATION TO THE PATIENT CENTERED
MEDICAL HOME: A ELECTRONIC HANDOFF INTERVENTION
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Moy, Nicholas] San Francisco VA Med Ctr, San Francisco, CA USA.
[Pierluissi, Edgar] Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S559
EP S560
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812703242
ER
PT J
AU Nall, RW
Nall, RW
AF Nall, Ryan Wesley
Nall, Ryan Wesley
TI LOWER EXTREMITY NUMBNESS IN A PATIENT WITH ACUTE ARTERIAL THROMBOSIS
SECONDARY TO HEPARIN INDUCED THROMBOCYTOPENIA
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Nall, Ryan Wesley; Nall, Ryan Wesley] Beth Israel Deaconess Med Ctr Internal Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S529
EP S530
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812703175
ER
PT J
AU Peltan, ID
Lee, H
Wright, DE
AF Peltan, Ithan D.
Lee, Hang
Wright, Douglas E.
TI CONTRARY TO RESIDENT AND ATTENDING PERCEPTIONS, BEDSIDE CASE
PRESENTATIONS DO NOT PROLONG ROUNDS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Peltan, Ithan D.; Lee, Hang; Wright, Douglas E.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S33
EP S33
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812700054
ER
PT J
AU Pevnick, J
Asch, S
Li, N
Bell, DS
AF Pevnick, Joshua
Asch, Steven
Li, Ning
Bell, Douglas S.
TI ELECTRONIC PRESCRIBING WITH FORMULARY DECISION SUPPORT REDUCES PATIENT
COPAY AMOUNTS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Pevnick, Joshua] Cedars Sinai Hlth Syst, Los Angeles, CA USA.
[Asch, Steven] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Li, Ning] Cedars Sinai Hlth Syst, Biostat Core, Samuel Oschin Comprehens Canc Inst, Los Angeles, CA USA.
[Bell, Douglas S.] RAND Corp, Santa Monica, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S85
EP S86
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812700150
ER
PT J
AU Preisner, R
Jenkins, L
Khurana, A
AF Preisner, Ruth
Jenkins, Leonard
Khurana, Ajay
TI PROCEDURE CLINIC DOUBLES MEDICAL RESIDENTS' EXPERIENCE DOING KNEE AND
SHOULDER INJECTIONS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Preisner, Ruth] Univ Pittsburgh, Sch Med, VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Jenkins, Leonard; Khurana, Ajay] Vet Adm Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S601
EP S601
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812703323
ER
PT J
AU Rigotti, NA
Bitton, A
Kelley, JK
Hoeppner, BB
Levy, DE
Mort, E
AF Rigotti, Nancy A.
Bitton, Asaf
Kelley, Jennifer K.
Hoeppner, Bettina B.
Levy, Douglas E.
Mort, Elizabeth
TI SUPPLEMENTING OFFICE-BASED CARE WITH A POPULATION-BASED DIRECT-TO-SMOKER
OUTREACH INTERVENTION OFFERING FREE TREATMENT TO SMOKERS IN A COMMUNITY
HEALTH CENTER: A RANDOMIZED CONTROLLED TRIAL
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Rigotti, Nancy A.; Hoeppner, Bettina B.; Levy, Douglas E.; Mort, Elizabeth] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Bitton, Asaf] Brigham & Womens Hosp, Brookline, MA USA.
[Kelley, Jennifer K.] Partners Hlth Care, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S33
EP S34
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812700055
ER
PT J
AU Roy, B
Huff, N
Castiglioni, A
Willett, L
Estrada, C
Centor, R
AF Roy, Brita
Huff, Nidhi
Castiglioni, Analia
Willett, Lisa
Estrada, Carlos
Centor, Robert
TI FACTORS AFFECTING LEARNERS' DAILY PRIORITIES DURING WARD ATTENDING
ROUNDS AND ATTENDING PHYSICIANS' ADAPTABILITY
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Roy, Brita; Huff, Nidhi; Castiglioni, Analia; Willett, Lisa; Centor, Robert] Univ Alabama Birmingham, Birmingham, AL USA.
[Estrada, Carlos] Univ Alabama Birmingham, Birmingham VAMC, Birmingham, AL USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S170
EP S171
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701078
ER
PT J
AU Saadi, A
Bond, B
Percac-Lima, S
AF Saadi, Altaf
Bond, Barbara
Percac-Lima, Sanja
TI PERSPECTIVES ON PREVENTIVE HEALTH CARE AND BARRIERS TO BREAST CANCER
SCREENING AMONG IRAQI WOMEN REFUGEES
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Saadi, Altaf] Harvard Univ, Sch Med, Boston, MA USA.
[Bond, Barbara; Percac-Lima, Sanja] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S38
EP S39
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812700063
ER
PT J
AU Schnipper, JL
Liang, CL
Hamann, C
Karson, AS
Lee, J
Burdick, E
Bates, DW
AF Schnipper, Jeffrey L.
Liang, Catherine L.
Hamann, Claus
Karson, Andrew S.
Lee, Jennifer
Burdick, Elisabeth
Bates, David W.
TI EFFECTS OF AN ELECTRONIC POST-DISCHARGE MEDICATION RECONCILIATION TOOL
ON THE ACCURACY OF AMBULATORY MEDICATION DOCUMENTATION
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Schnipper, Jeffrey L.; Liang, Catherine L.; Lee, Jennifer; Burdick, Elisabeth; Bates, David W.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Hamann, Claus] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S324
EP S324
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812702068
ER
PT J
AU Seal, KH
Cohen, G
Bertenthal, D
Cohen, B
Maguen, S
Daley, A
AF Seal, Karen Hope
Cohen, Greg
Bertenthal, Daniel
Cohen, Beth
Maguen, Shira
Daley, Aaron
TI REDUCING BARRIERS TO MENTAL HEALTH AND SOCIAL SERVICES FOR IRAQ AND
AFGHANISTAN VETERANS: OUTCOMES OF A NEW INTEGRATED PRIMARY CARE CLINIC
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Seal, Karen Hope; Cohen, Beth] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Cohen, Greg; Bertenthal, Daniel; Cohen, Beth; Daley, Aaron] San Francisco VA Med Ctr, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S210
EP S210
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701154
ER
PT J
AU Simmons, L
Sepucha, K
Leavitt, L
Greipp, C
AF Simmons, Leigh
Sepucha, Karen
Leavitt, Lauren
Greipp, Christine
TI FROM SKEPTICS TO USERS: EDUCATING PHYSICIANS IN SHARED DECISION MAKING
AND INCREASING USE OF DECISION AIDS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Simmons, Leigh; Sepucha, Karen; Leavitt, Lauren; Greipp, Christine] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S291
EP S291
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812702006
ER
PT J
AU Snyder, C
Frick, K
Herbert, R
Blackford, A
Neville, B
Carducci, M
Wolff, A
Earle, C
AF Snyder, Claire
Frick, Kevin
Herbert, Robert
Blackford, Amanda
Neville, Bridget
Carducci, Michael
Wolff, Antonio
Earle, Craig
TI AVOIDING THE AVOIDABLE: QUALITY CARE FOR COMORBID CONDITIONS IN CANCER
SURVIVORS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Snyder, Claire; Blackford, Amanda; Carducci, Michael; Wolff, Antonio] Johns Hopkins Sch Med, Baltimore, MD USA.
[Frick, Kevin; Herbert, Robert] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Neville, Bridget] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Earle, Craig] Inst Clin Evaluat Sci, Toronto, ON, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S67
EP S68
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812700118
ER
PT J
AU Staton, L
Panda, M
Estrada, C
Roddy, D
Ortiz, D
AF Staton, Lisa
Panda, Mukta
Estrada, Carlos
Roddy, Donna
Ortiz, David
TI "I HAVE AWEALTH OF RESOURCES IN MY COMMUNITY" : A MULTI-METHOD APPROACH
FOR CROSS CULTURAL TRAINING FOR INTERNAL MEDICINE RESIDENTS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Staton, Lisa; Panda, Mukta] Univ Tennessee, Coll Med, Chattanooga, TN USA.
[Estrada, Carlos] Univ Alabama Birmingham, Birmingham VAMC, Birmingham, AL USA.
[Roddy, Donna] Blue Cross BlueShield Tennessee, Chattanooga, TN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S617
EP S618
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812703355
ER
PT J
AU Steinman, M
Peterson, C
Harlow, J
AF Steinman, Michael
Peterson, Carolyn
Harlow, John
TI PATIENT AGE, COMORBID BURDEN, AND THE USEFULNESS OF HEART FAILURE
GUIDELINES
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Steinman, Michael; Peterson, Carolyn; Harlow, John] San Francisco VA Med Ctr, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S72
EP S72
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812700126
ER
PT J
AU Stickrath, C
Shimek, D
Prochazka, A
AF Stickrath, Chad
Shimek, Danielle
Prochazka, Allan
TI INTERVENTIONS TO IMPROVE ATTENDING ROUNDS IN MEDICINE: A SYSTEMATIC
REVIEW
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Stickrath, Chad; Prochazka, Allan] Denver VA Med Ctr, Denver, CO USA.
[Shimek, Danielle] Univ Colorado Denver, Aurora, CO USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S298
EP S298
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812702019
ER
PT J
AU Stickrath, C
Anderson, M
Prochazka, A
Griffiths, M
Deloughry, M
Aagaard, E
AF Stickrath, Chad
Anderson, Melver
Prochazka, Allan
Griffiths, Megan
Deloughry, Melissa
Aagaard, Eva
TI ATTENDING ROUNDS: WHAT IS NOT HAPPENING?
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Stickrath, Chad; Anderson, Melver; Prochazka, Allan] Denver VA Med Ctr, Denver, CO USA.
[Griffiths, Megan] Univ Colorado Denver, Aurora, CO USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S268
EP S269
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701265
ER
PT J
AU Sun, VK
Cenzer, IS
Williams, BA
AF Sun, Vivien K.
Cenzer, Irena Stijacic
Williams, Brie A.
TI HOW SAFE IS YOUR NEIGHBORHOOD? PERCEIVED NEIGHBORHOOD SAFETY AND
FUNCTIONAL DECLINE IN OLDER ADULTS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Sun, Vivien K.] Univ Calif San Francisco, Sch Med, San Francisco, CA USA.
[Cenzer, Irena Stijacic; Williams, Brie A.] Univ Calif San Francisco, Div Geriatr, San Francisco, CA 94143 USA.
[Cenzer, Irena Stijacic; Williams, Brie A.] San Francisco VA Med Ctr, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S95
EP S95
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812700168
ER
PT J
AU Thompson, R
Weil, E
Ferris, TG
AF Thompson, Ryan
Weil, Eric
Ferris, Timothy G.
TI A PILOT INITIATIVE FOR DIRECT ADMISSION TO SKILLED NURSING FACILITIES
FOR HIGH-COST MEDICARE BENEFICIARIES
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Thompson, Ryan] Massachusetts Gen Phys Org, Boston, MA USA.
[Weil, Eric; Ferris, Timothy G.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S330
EP S331
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812702080
ER
PT J
AU Thompson, R
Ferris, T
AF Thompson, Ryan
Ferris, Timothy
TI A NOVEL APPROACH TO MEASURING CONTINUITY OF HOSPITAL CARE
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Thompson, Ryan; Ferris, Timothy] Massachusetts Gen Phys Org, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S219
EP S220
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701172
ER
PT J
AU Tonks, S
Makwana, S
Salanitro, A
Foster, P
Safford, M
Houston, T
Allison, J
Curry, W
Estrada, C
AF Tonks, Stephen
Makwana, Sohil
Salanitro, Amanda
Foster, Pamela
Safford, Monika
Houston, Thomas
Allison, Jeroan
Curry, William
Estrada, Carlos
TI THE RELATIONSHIP BETWEEN RURALITY AND DIABETES CONTROL
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Tonks, Stephen; Makwana, Sohil; Safford, Monika; Curry, William] Univ Alabama Birmingham, Birmingham, AL USA.
[Salanitro, Amanda] Vanderbilt Univ, Nashville, TN 37235 USA.
[Foster, Pamela] Univ Alabama, Tuscaloosa, AL USA.
[Houston, Thomas; Allison, Jeroan] Univ Massachusetts, Sch Med, Boston, MA 02125 USA.
[Estrada, Carlos] Univ Alabama Birmingham, Birmingham VAMC, Birmingham, AL USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S252
EP S253
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812701233
ER
PT J
AU Volpp, K
Shea, JA
Borman, KR
Jones, AT
Weissman, A
McKinney, S
Biester, TW
Itani, KMF
AF Volpp, Kevin
Shea, Judy A.
Borman, Karen R.
Jones, Andrew T.
Weissman, Arlene
McKinney, Sean
Biester, Thomas W.
Itani, Kamal M. F.
TI INTERNAL MEDICINE AND SURGERY RESIDENTS' VIEWS OF DUTY HOUR RESTRICTIONS
AND CAUSES OF MEDICAL ERRORS
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Volpp, Kevin] Philadelphia VA, Philadelphia, PA USA.
[Volpp, Kevin] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Volpp, Kevin] Univ Penn, Wharton Sch, Philadelphia, PA 19104 USA.
[Shea, Judy A.] Univ Penn, Philadelphia, PA 19104 USA.
[Borman, Karen R.] Abington Mem Hosp, Philadelphia, PA USA.
[Jones, Andrew T.; Biester, Thomas W.] Amer Board Surg, Philadelphia, PA USA.
[Weissman, Arlene; McKinney, Sean] Amer Coll Physicians, Philadelphia, PA USA.
[Itani, Kamal M. F.] Boston Univ, VA Boston Hlth Care Syst, Boston, MA 02215 USA.
[Itani, Kamal M. F.] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S296
EP S296
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812702014
ER
PT J
AU Walling, A
Lorenz, K
Asch, S
Wenger, N
AF Walling, Anne
Lorenz, Karl
Asch, Steven
Wenger, Neil
TI PATIENT AND SERVICE LEVEL ASSOCIATIONS WITH THE QUALITY OF END OF LIFE
CARE AT AN ACADEMIC MEDICAL CENTER
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Walling, Anne; Wenger, Neil] Univ Calif Los Angeles, Los Angeles, CA USA.
[Lorenz, Karl; Asch, Steven] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S81
EP S82
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812700142
ER
PT J
AU Wenger, NS
Tarn, M
Diamant, A
Lorenz, K
Citko, J
O'Malley, K
AF Wenger, Neil S.
Tarn, Mimi
Diamant, Allison
Lorenz, Karl
Citko, Judy
O'Malley, Kate
TI POLST USE IN CALIFORNIA NURSING HOMES
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Meeting Abstract
C1 [Wenger, Neil S.; Diamant, Allison] Univ Calif Los Angeles, GIM & HSR, Los Angeles, CA USA.
[Tarn, Mimi] Univ Calif Los Angeles, Dept Family Med, Los Angeles, CA USA.
[Lorenz, Karl] Greater Los Angeles VA Med Ctr, Los Angeles, CA USA.
[Citko, Judy] Coalit Compassionate Care Calif, Sacramento, CA USA.
[O'Malley, Kate] Calif HealthCare Fdn, Oakland, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD MAY
PY 2011
VL 26
SU 1
BP S101
EP S101
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA V30JQ
UT WOS:000208812700179
ER
PT J
AU Durst, R
Avelar, E
McCarty, D
Poh, KK
Friera, LF
Llano, MF
Chu, J
Anumandla, AKR
Rodriguez, LL
Mack, MJ
Hanzel, G
Kodali, SK
Hung, J
Picard, MH
AF Durst, Ronen
Avelar, Erick
McCarty, David
Poh, Kian-Keong
Friera, Leticia Fernandez
Llano, Miguel F.
Chu, John
Anumandla, Anil Kumar Reddy
Rodriguez, Leonardo L.
Mack, Michael J.
Hanzel, George
Kodali, Susheel K.
Hung, Judy
Picard, Michael H.
TI Outcome and Improvement Predictors of Mitral Regurgitation After
Transcatheter Aortic Valve Implantation
SO JOURNAL OF HEART VALVE DISEASE
LA English
DT Article
ID DOPPLER-ECHOCARDIOGRAPHY; REPLACEMENT; STENOSIS; HEART; RECOMMENDATIONS;
SEVERITY; QUANTIFICATION; PROSTHESIS; EXPERIENCE; SYSTEM
AB Background and aim of the study: Mitral regurgitation (MR) is frequently present in patients with calcific aortic stenosis (AS). Yet, the issue of whether to surgically correct the MR during aortic valve replacement (AVR) remains uncertain. The study aim was to define the outcome of MR after transcatheter aortic valve implantation (TAVI) in the TRanscatheter EndoVascular Implantation of VALves (REVIVAL) II trial.
Methods: Echocardiography was performed before and at 24 h, and three and six months after valve implantation. The degree of MR was evaluated by expert readers and by the vena contracta (VC) method. Significant MR was defined as at least mild to moderate MR. Those patients with a 30% reduction in VC were classified as good responders (GR group), and the remainder as poor responders (PR group).
Results: The study comprised 35 subjects with at least mild to moderate MR before TAVI. The mean VC of the whole group declined from 0.5 +/- 0.2 cm initially to 0.32 +/- 0.2 cm and 0.38 +/- 0.2 cm at 24 h and three months, respectively (p<0.05). At three months, 12 patients had >30% VC reduction; these constituted the GR group, while the remainder constituted the PR group. The percentage of patients with mitral annular calcification with restriction (MACr), defined as calcification encroaching onto the leaflets and restricting leaflet motion, was significantly lower in the GR group compared to the PR group (17% versus 61%, respectively; p<0.05). The remaining pre-specified parameters did not differ significantly between the GR and PR groups, including age, gender, mitral valve tethering height and area (6 2 mm versus 5 +/- 3 mm and 10 +/- 4 mm2 versus 13 +/- 9 and 10 4 mm2, respectively), change in the aortic valve area (336 +/- 130% versus 285 +/- 180%), change in mean systolic aortic valve pressure (-20 +/- 8% versus -23 +/- 10%), and left ventricular ejection fraction (47 +/- 15% versus 45 +/- 18%).
Conclusion: MR is improved significantly after TAVI for AS. MACr was the only variable associated with a reduction in MR improvement. These results suggest that a careful echocardiographic evaluation of the mitral valve prior to TAVI may help to predict which patients should experience an improvement in their MR.
C1 [Durst, Ronen; Avelar, Erick; McCarty, David; Poh, Kian-Keong; Friera, Leticia Fernandez; Llano, Miguel F.; Chu, John; Anumandla, Anil Kumar Reddy; Hung, Judy; Picard, Michael H.] Massachusetts Gen Hosp, Cardiac Ultrasound Lab, Boston, MA 02114 USA.
[Durst, Ronen; Avelar, Erick; McCarty, David; Poh, Kian-Keong; Friera, Leticia Fernandez; Llano, Miguel F.; Chu, John; Anumandla, Anil Kumar Reddy; Hung, Judy; Picard, Michael H.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Rodriguez, Leonardo L.] Cleveland Clin Fdn, Div Cardiovasc Med, Cleveland, OH 44195 USA.
[Mack, Michael J.] Med City Dallas Hosp, Dallas, TX USA.
[Mack, Michael J.] Cardiopulm Res Sci & Technol Inst, Dallas, TX USA.
[Hanzel, George] William Beaumont Hosp, Dept Cardiol, Royal Oak, MI 48072 USA.
[Kodali, Susheel K.] Columbia Univ, New York Presbyterian Med Ctr, Div Cardiol, New York, NY USA.
RP Picard, MH (reprint author), Massachusetts Gen Hosp, Cardiac Ultrasound Lab, 55 Fruit St,Yawkey 5E, Boston, MA 02114 USA.
EM mhpicard@partners.org
RI Fernandez Friera, Leticia /E-9931-2015;
OI Fernandez Friera, Leticia /0000-0002-4237-2166; Picard,
Michael/0000-0002-9264-3243
FU American Physician Fellowship award; MSD training fellowship award
FX Dr. Durst was supported by the American Physician Fellowship award and
the MSD training fellowship award.
NR 34
TC 24
Z9 24
U1 0
U2 0
PU I C R PUBLISHERS
PI NORTHWOOD
PA CRISPIN HOUSE, 12/A SOUTH APPROACH, MOOR PARK, NORTHWOOD HA6 2ET,
ENGLAND
SN 0966-8519
J9 J HEART VALVE DIS
JI J. Heart Valve Dis.
PD MAY
PY 2011
VL 20
IS 3
BP 272
EP 281
PG 10
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 783YR
UT WOS:000292121300005
PM 21714416
ER
PT J
AU Hand, SC
Menze, MA
Borcar, A
Patil, Y
Covi, JA
Reynolds, JA
Toner, M
AF Hand, Steven C.
Menze, Michael A.
Borcar, Apu
Patil, Yuvraj
Covi, Joseph A.
Reynolds, Julie A.
Toner, Mehmet
TI Metabolic restructuring during energy-limited states: Insights from
Artemia franciscana embryos and other animals
SO JOURNAL OF INSECT PHYSIOLOGY
LA English
DT Review
DE Metabolic depression; Diapause; Anoxia; Vacuolar-ATPase; Intracellular
pH; Metabolic preconditioning; Glycolysis; Oxidative phosphorylation;
Hypoxia inducible factor-1
ID NEMATODE CAENORHABDITIS-ELEGANS; PYRUVATE-DEHYDROGENASE COMPLEX;
ACTIVATED PROTEIN-KINASE; KILLIFISH AUSTROFUNDULUS-LIMNAEUS; FATTY-ACID
OXIDATION; VACUOLAR H+-ATPASE; V-ATPASE; C-ELEGANS; OXYGEN-CONSUMPTION;
INTRACELLULAR PH
AB Many life history stages of animals that experience environmental insults enter developmental arrested states that are characterized by reduced cellular proliferation, with or without a concurrent reduction in overall metabolism. In the case of the most profound metabolic arrest reported in invertebrates, i.e., anaerobic quiescence in Artemia franciscana embryos, acidification of the intracellular milieu is a major factor governing catabolic and anabolic downregulation. Release of ions from intracellular compartments is the source for approximately 50% of the proton equivalents needed for the 1.5 unit acidification that is observed. Recovery from the metabolic arrest requires re-sequestration of the protons with a vacuolar-type ATPase (V-ATPase). The remarkable facet of this mechanism is the ability of embryonic cells to survive the dissipation of intracellular ion gradients. Across many diapause-like states, the metabolic reduction and subsequent matching of energy demand is accomplished by shifting energy metabolism from oxidative phosphorylation to aerobic glycolysis. Molecular pathways that are activated to induce these resilient hypometabolic states include stimulation of the AMP-activated protein kinase (AMPK) and insulin signaling via suite of daf (dauer formation) genes for diapause-like states in nematodes and insects. Contributing factors for other metabolically depressed states involve hypoxia-inducible factor-1 and downregulation of the pyruvate dehydrogenase complex. Metabolic similarities between natural states of stasis and some cancer phenotypes are noteworthy. Reduction of flux through oxidative phosphorylation helps prevent cell death in certain cancer types, similar to the way it increases viability of dauer stages in Caenorhabditis elegans. Mechanisms that underlie natural stasis are being used to pre-condition mammalian cells prior to cell biostabilization and storage. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Hand, Steven C.; Borcar, Apu; Patil, Yuvraj] Louisiana State Univ, Div Cellular Dev & Integrat Biol, Dept Biol, Baton Rouge, LA 70803 USA.
[Menze, Michael A.] Eastern Illinois Univ, Dept Biol Sci, Charleston, IL 61920 USA.
[Covi, Joseph A.] Univ Wisconsin, Dept Biol, Stevens Point, WI 54481 USA.
[Reynolds, Julie A.] Ohio State Univ, Dept Entomol, Columbus, OH 43210 USA.
[Toner, Mehmet] Harvard Univ, Sch Med, Ctr Engn Med & Surg Serv, Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Toner, Mehmet] Shriners Hosp Children, Boston, MA 02114 USA.
RP Hand, SC (reprint author), Louisiana State Univ, Div Cellular Dev & Integrat Biol, Dept Biol, Baton Rouge, LA 70803 USA.
EM shand@LSU.edu
OI Patil, Yuvraj/0000-0002-2255-9863; Covi, Joseph/0000-0001-5668-4577;
Menze, Michael/0000-0003-1072-5462
FU National Science Foundation [IOS-0920254]; National Institutes of Health
[1-RO1-GM071345-01, 2RO1DK046270-14A1]; Defense Advanced Research
Projects Agency [N00173-01-1-G011]; William Wright Family Foundation
FX We thank the National Science Foundation (grant IOS-0920254 to S.C.H.
and M.A.M.), the National Institutes of Health (grants 1-RO1-GM071345-01
and 2RO1DK046270-14A1 to M.T. and S.C.H.), Defense Advanced Research
Projects Agency (grant N00173-01-1-G011 to M.T. and S.C.H.) and the
William Wright Family Foundation (donation to S.C.H.) for generous
support. JAR. received GIARs from Sigma Xi and the Orthoptera Society.
NR 133
TC 26
Z9 27
U1 3
U2 110
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0022-1910
J9 J INSECT PHYSIOL
JI J. Insect Physiol.
PD MAY
PY 2011
VL 57
IS 5
SI SI
BP 584
EP 594
DI 10.1016/j.jinsphys.2011.02.010
PG 11
WC Entomology; Physiology; Zoology
SC Entomology; Physiology; Zoology
GA 781DX
UT WOS:000291911900006
PM 21335009
ER
PT J
AU Patti, JA
AF Patti, John A.
TI Health Care Reform and Radiology Education
SO JOURNAL OF THE AMERICAN COLLEGE OF RADIOLOGY
LA English
DT Editorial Material
C1 Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
RP Patti, JA (reprint author), Massachusetts Gen Hosp, Dept Radiol, 55 Fruit St,FND 202, Boston, MA 02114 USA.
EM jpatti@partners.org
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1546-1440
J9 J AM COLL RADIOL
JI J. Am. Coll. Radiol.
PD MAY
PY 2011
VL 8
IS 5
BP 293
EP 293
DI 10.1016/j.jacr.2011.04.002
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 971JX
UT WOS:000306201300001
PM 21531300
ER
PT J
AU Singh, S
Kalra, MK
Thrall, JH
Mahesh, M
AF Singh, Sarabjeet
Kalra, Mannudeep K.
Thrall, James H.
Mahesh, Mahadevappa
TI CT Radiation Dose Reduction by Modifying Primary Factors
SO JOURNAL OF THE AMERICAN COLLEGE OF RADIOLOGY
LA English
DT Editorial Material
ID IMAGE-QUALITY; STRATEGIES; PROTOCOLS; SIZE
C1 [Mahesh, Mahadevappa] Johns Hopkins Univ, Russell H Morgan Dept Radiol & Radiol Sci, Baltimore, MD 21287 USA.
[Singh, Sarabjeet; Kalra, Mannudeep K.; Thrall, James H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Mahesh, M (reprint author), Johns Hopkins Univ, Russell H Morgan Dept Radiol & Radiol Sci, 600 N Caroline St, Baltimore, MD 21287 USA.
EM mmahesh@jhmi.edu
NR 14
TC 14
Z9 14
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1546-1440
J9 J AM COLL RADIOL
JI J. Am. Coll. Radiol.
PD MAY
PY 2011
VL 8
IS 5
BP 369
EP 372
DI 10.1016/j.jacr.2011.02.001
PG 4
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 971JX
UT WOS:000306201300018
PM 21531317
ER
PT J
AU Arbelaez, C
Ganguli, I
AF Arbelaez, Christian
Ganguli, Ishani
TI The Personal Statement for Residency Application: Review and Guidance
SO JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION
LA English
DT Article
DE education
ID SELECTION; PLAGIARISM
AB All applicants to US residency programs are required to write a personal statement. Recent reports of plagiarism and homogeneity in these freeform essays suggest the need for better guidance in this process. The authors review the historical and current role of the personal statement and provide a practical framework for writing a unique and effective personal statement, which will help both applicants and residency directors to maximize their chances of a successful match.
C1 [Arbelaez, Christian] Brigham & Womens Hosp, Off Multicultural Careers, Boston, MA 02115 USA.
[Arbelaez, Christian] Harvard Univ, Harvard Affiliated Emergency Med Residency Progra, Cambridge, MA 02138 USA.
[Arbelaez, Christian] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Ganguli, Ishani] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
RP Arbelaez, C (reprint author), Brigham & Womens Hosp, Off Multicultural Careers, 75 Francis St, Boston, MA 02115 USA.
EM carbelaez@partners.org
NR 15
TC 2
Z9 2
U1 1
U2 5
PU NATL MED ASSOC
PI WASHINGON
PA 1012 10TH ST, N W, WASHINGON, DC 20001 USA
SN 0027-9684
J9 J NATL MED ASSOC
JI J. Natl. Med. Assoc.
PD MAY
PY 2011
VL 103
IS 5
BP 439
EP 442
PG 4
WC Medicine, General & Internal
SC General & Internal Medicine
GA 784QS
UT WOS:000292173900008
PM 21809794
ER
PT J
AU DaSilva, AF
Volz, MS
Bikson, M
Fregni, F
AF DaSilva, Alexandre F.
Volz, Magdalena Sarah
Bikson, Marom
Fregni, Felipe
TI Electrode Positioning and Montage in Transcranial Direct Current
Stimulation
SO JOVE-JOURNAL OF VISUALIZED EXPERIMENTS
LA English
DT Article
DE Neuroscience; Issue 51; Transcranial direct current stimulation; pain;
chronic pain; noninvasive brain stimulation; neuromodulation
AB Transcranial direct current stimulation (tDCS) is a technique that has been intensively investigated in the past decade as this method offers a non-invasive and safe alternative to change cortical excitability(2). The effects of one session of tDCS can last for several minutes, and its effects depend on polarity of stimulation, such as that cathodal stimulation induces a decrease in cortical excitability, and anodal stimulation induces an increase in cortical excitability that may last beyond the duration of stimulation(6). These effects have been explored in cognitive neuroscience and also clinically in a variety of neuropsychiatric disorders - especially when applied over several consecutive sessions(4). One area that has been attracting attention of neuroscientists and clinicians is the use of tDCS for modulation of pain-related neural networks(3,5). Modulation of two main cortical areas in pain research has been explored: primary motor cortex and dorsolateral prefrontal cortex(7). Due to the critical role of electrode montage, in this article, we show different alternatives for electrode placement for tDCS clinical trials on pain; discussing advantages and disadvantages of each method of stimulation.
C1 [DaSilva, Alexandre F.] Univ Michigan, Sch Dent, Ann Arbor, MI 48109 USA.
[Volz, Magdalena Sarah; Fregni, Felipe] Harvard Univ, Sch Med, Lab Neuromodulat, Dept Phys Med & Rehabil,Spaulding Rehabil Hosp, Cambridge, MA 02138 USA.
[Volz, Magdalena Sarah; Fregni, Felipe] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cambridge, MA 02138 USA.
[Volz, Magdalena Sarah] Univ Med Berlin, Charite, Berlin, Germany.
[Bikson, Marom] CUNY City Coll, Dept Biomed Engn, New York, NY 10031 USA.
RP DaSilva, AF (reprint author), Univ Michigan, Sch Dent, Ann Arbor, MI 48109 USA.
EM adasilva@umich.edu; fregni.felipe@mgh.harvard.edu
FU Stiftung Charite; CTSA high-tech funding grant, University of Michigan
FX DaSilva AF received funding support from CTSA high-tech funding grant,
University of Michigan to complete this review. Volz MS is funded by a
grant scholarship from Stiftung Charite.
NR 33
TC 15
Z9 15
U1 2
U2 7
PU JOURNAL OF VISUALIZED EXPERIMENTS
PI CAMBRIDGE
PA 1 ALEWIFE CENTER, STE 200, CAMBRIDGE, MA 02140 USA
SN 1940-087X
J9 JOVE-J VIS EXP
JI J. Vis. Exp.
PD MAY
PY 2011
IS 51
AR e2744
DI 10.3791/2744
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA V36MA
UT WOS:000209214800040
ER
PT J
AU Diep, CQ
Davidson, AJ
AF Diep, Cuong Q.
Davidson, Alan J.
TI Transplantation of Cells Directly into the Kidney of Adult Zebrafish
SO JOVE-JOURNAL OF VISUALIZED EXPERIMENTS
LA English
DT Article
DE Cellular Biology; Issue 51; zebrafish; kidney; regeneration;
transplantation
AB Regenerative medicine based on the transplantation of stem or progenitor cells into damaged tissues has the potential to treat a wide range of chronic diseases(1). However, most organs are not easily accessible, necessitating the need to develop surgical methods to gain access to these structures. In this video article, we describe a method for transplanting cells directly into the kidney of adult zebrafish, a popular model to study regeneration and disease(2). Recipient fish are pre-conditioned by irradiation to suppress the immune rejection of the injected cells(3). We demonstrate how the head kidney can be exposed by a lateral incision in the flank of the fish, followed by the injection of cells directly in to the organ. Using fluorescently labeled whole kidney marrow cells comprising a mixed population of renal and hematopoietic precursors, we show that nephron progenitors can engraft and differentiate into new renal tissue - the gold standard of any cell-based regenerative therapy. This technique can be adapted to deliver purified stem or progenitor cells and/or small molecules to the kidney as well as other internal organs and further enhances the zebrafish as a versatile model to study regenerative medicine.
C1 [Diep, Cuong Q.; Davidson, Alan J.] Massachusetts Gen Hosp, Ctr Regenerat Med, Boston, MA 02114 USA.
RP Davidson, AJ (reprint author), Massachusetts Gen Hosp, Ctr Regenerat Med, Boston, MA 02114 USA.
EM a.davidson@auckland.ac.nz
FU Harvard Stem Cell Institute; American Society of Nephrology; NIH/NIDDK
[P50DK074030]; Massachusetts General Hospital-Fund for Medical Discovery
FX We thank E.C. Liao for help with suturing, and R. Ethier and L. Gyr for
zebrafish care. A.J.D. was supported by the Harvard Stem Cell Institute,
the American Society of Nephrology, and NIH/NIDDK (P50DK074030). C.Q.D.
was supported by the Massachusetts General Hospital-Fund for Medical
Discovery.
NR 3
TC 0
Z9 0
U1 0
U2 0
PU JOURNAL OF VISUALIZED EXPERIMENTS
PI CAMBRIDGE
PA 1 ALEWIFE CENTER, STE 200, CAMBRIDGE, MA 02140 USA
SN 1940-087X
J9 JOVE-J VIS EXP
JI J. Vis. Exp.
PD MAY
PY 2011
IS 51
AR UNSP e2725
DI 10.3791/2725
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA V36MA
UT WOS:000209214800036
ER
PT J
AU Fotheringham, S
Levanon, K
Drapkin, R
AF Fotheringham, Susan
Levanon, Keren
Drapkin, Ronny
TI Ex Vivo Culture of Primary Human Fallopian Tube Epithelial Cells
SO JOVE-JOURNAL OF VISUALIZED EXPERIMENTS
LA English
DT Article
DE Cellular Biology; Issue 51; Primary human epithelial cells; ovarian
cancer; serous; ex-vivo; cell biology; fallopian tube; fimbria
AB Epithelial ovarian cancer is a leading cause of female cancer mortality in the United States. In contrast to other women-specific cancers, like breast and uterine carcinomas, where death rates have fallen in recent years, ovarian cancer cure rates have remained relatively unchanged over the past two decades (1). This is largely due to the lack of appropriate screening tools for detection of early stage disease where surgery and chemotherapy are most effective (2,) (3). As a result, most patients present with advanced stage disease and diffuse abdominal involvement. This is further complicated by the fact that ovarian cancer is a heterogeneous disease with multiple histologic subtypes (4, 5). Serous ovarian carcinoma (SOC) is the most common and aggressive subtype and the form most often associated with mutations in the BRCA genes. Current experimental models in this field involve the use of cancer cell lines and mouse models to better understand the initiating genetic events and pathogenesis of disease (6, 7). Recently, the fallopian tube has emerged as a novel site for the origin of SOC, with the fallopian tube (FT) secretory epithelial cell (FTSEC) as the proposed cell of origin (8, 9). There are currently no cell lines or culture systems available to study the FT epithelium or the FTSEC. Here we describe a novel ex vivo culture system where primary human FT epithelial cells are cultured in a manner that preserves their architecture, polarity, immunophenotype, and response to physiologic and genotoxic stressors. This ex vivo model provides a useful tool for the study of SOC, allowing a better understanding of how tumors can arise from this tissue, and the mechanisms involved in tumor initiation and progression.
C1 [Fotheringham, Susan; Levanon, Keren; Drapkin, Ronny] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA USA.
[Fotheringham, Susan; Levanon, Keren; Drapkin, Ronny] Harvard Univ, Sch Med, Boston, MA USA.
[Levanon, Keren] Chaim Sheba Med Ctr, Sheba Canc Res Ctr, Ramat Gan, Israel.
[Drapkin, Ronny] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
RP Drapkin, R (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Boston, MA USA.
EM ronny_drapkin@dfci.harvard.edu
RI Drapkin, Ronny/E-9944-2016
OI Drapkin, Ronny/0000-0002-6912-6977
FU NIH/National Cancer Institute [P50 CA105009, K08 CA108748, U01
CA152990]; Ovarian Cancer Research Fund; May Kay Foundation; Novartis
Pharmaceuticals; Robert and Deborah First Fund; Randi and Joel Cutler
Ovarian Cancer Research Fund; Marsha Rivkin Foundation - Scientific
Scholar Award; AACR - George and Patricia Sehl Fellowship for Cancer
Genetics Research; American Physician Fellowship for Medicine in Israel
- Claire and Emmanuel G. Rosenblatt Foundation
FX We thank the faculty, fellows, residents, and physician assistants of
the Brigham and Women's Hospital, Department of Pathology for making
tissue available for these studies. This work was supported by research
grants from the NIH/National Cancer Institute (P50 CA105009, K08
CA108748, U01 CA152990), Ovarian Cancer Research Fund, The May Kay
Foundation, Novartis Pharmaceuticals, Robert and Deborah First Fund,
Randi and Joel Cutler Ovarian Cancer Research Fund, Marsha Rivkin
Foundation - Scientific Scholar Award, AACR - George and Patricia Sehl
Fellowship for Cancer Genetics Research, and the American Physician
Fellowship for Medicine in Israel - Claire and Emmanuel G. Rosenblatt
Foundation Grant.
NR 11
TC 3
Z9 3
U1 0
U2 1
PU JOURNAL OF VISUALIZED EXPERIMENTS
PI CAMBRIDGE
PA 1 ALEWIFE CENTER, STE 200, CAMBRIDGE, MA 02140 USA
SN 1940-087X
J9 JOVE-J VIS EXP
JI J. Vis. Exp.
PD MAY
PY 2011
IS 51
AR UNSP e2728
DI 10.3791/2728
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA V36MA
UT WOS:000209214800037
ER
PT J
AU Maschmeyer, P
Flach, M
Winau, F
AF Maschmeyer, Patrick
Flach, Melanie
Winau, Florian
TI Seven Steps to Stellate Cells
SO JOVE-JOURNAL OF VISUALIZED EXPERIMENTS
LA English
DT Article
DE Immunology; Issue 51; Hepatic Stellate Cell; Ito Cell; Liver Immunology;
Retinoic Acid; Cell Isolation
AB Hepatic stellate cells are liver-resident cells of star-like morphology and are located in the space of Disse between liver sinusoidal endothelial cells and hepatocytes(1,2). Stellate cells are derived from bone marrow precursors and store up to 80% of the total body vitamin A(1,2). Upon activation, stellate cells differentiate into myofibroblasts to produce extracellular matrix, thus contributing to liver fibrosis(3). Based on their ability to contract, myofibroblastic stellate cells can regulate the vascular tone associated with portal hypertension(4). Recently, we demonstrated that hepatic stellate cells are potent antigen presenting cells and can activate NKT cells as well as conventional T lymphocytes(5).
Here we present a method for the efficient preparation of hepatic stellate cells from mouse liver. Due to their perisinusoidal localization, the isolation of hepatic stellate cells is a multi-step process. In order to render stellate cells accessible to isolation from the space of Disse, mouse livers are perfused in situ with the digestive enzymes Pronase E and Collagenase P. Following perfusion, the liver tissue is subjected to additional enzymatic treatment with Pronase E and Collagenase P in vitro. Subsequently, the method takes advantage of the massive amount of vitamin A-storing lipid droplets in hepatic stellate cells. This feature allows the separation of stellate cells from other hepatic cell types by centrifugation on an 8% Nycodenz gradient. The protocol described here yields a highly pure and homogenous population of stellate cells. Purity of preparations can be assessed by staining for the marker molecule glial fibrillary acidic protein (GFAP), prior to analysis by fluorescence microscopy or flow cytometry. Further, light microscopy reveals the unique appearance of star-shaped hepatic stellate cells that harbor high amounts of lipid droplets.
Taken together, we present a detailed protocol for the efficient isolation of hepatic stellate cells, including representative images of their morphological appearance and GFAP expression that help to define the stellate cell entity.
C1 [Maschmeyer, Patrick; Flach, Melanie; Winau, Florian] Harvard Univ, Sch Med, Dept Pathol, Immune Dis Inst,Program Cellular & Mol Med,Childr, Cambridge, MA 02138 USA.
RP Winau, F (reprint author), Harvard Univ, Sch Med, Dept Pathol, Immune Dis Inst,Program Cellular & Mol Med,Childr, Cambridge, MA 02138 USA.
EM Winau@idi.harvard.edu
FU Smith Family Award for Excellence in Biomedical Research; NIH [RO1
AI083426-01]; Boehringer Ingelheim Foundation
FX This work was funded by the Smith Family Award for Excellence in
Biomedical Research and NIH RO1 AI083426-01 (F.W.). Patrick Maschmeyer
and Melanie Flach are supported by PhD fellowships from the Boehringer
Ingelheim Foundation.
NR 7
TC 5
Z9 5
U1 3
U2 3
PU JOURNAL OF VISUALIZED EXPERIMENTS
PI CAMBRIDGE
PA 1 ALEWIFE CENTER, STE 200, CAMBRIDGE, MA 02140 USA
SN 1940-087X
J9 JOVE-J VIS EXP
JI J. Vis. Exp.
PD MAY
PY 2011
IS 51
AR UNSP e2710
DI 10.3791/2710
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA V36MA
UT WOS:000209214800031
ER
PT J
AU Sakadzic, S
Roussakis, E
Yaseen, MA
Mandeville, ET
Srinivasan, VJ
Arai, K
Ruvinskaya, S
Wu, WC
Devor, A
Lo, EH
Vinogradov, SA
Boas, DA
AF Sakadzic, Sava
Roussakis, Emmanuel
Yaseen, Mohammad A.
Mandeville, Emiri T.
Srinivasan, Vivek J.
Arai, Ken
Ruvinskaya, Svetlana
Wu, Weicheng
Devor, Anna
Lo, Eng H.
Vinogradov, Sergei A.
Boas, David A.
TI Cerebral Blood Oxygenation Measurement Based on Oxygen-dependent
Quenching of Phosphorescence
SO JOVE-JOURNAL OF VISUALIZED EXPERIMENTS
LA English
DT Article
DE Neuroscience; Issue 51; brain; blood; oxygenation; phosphorescence;
imaging
AB Monitoring of the spatiotemporal characteristics of cerebral blood and tissue oxygenation is crucial for better understanding of the neurometabolic- vascular relationship. Development of new pO2 measurement modalities with simultaneous monitoring of pO2 in larger fields of view with higher spatial and/or temporal resolution will enable greater insight into the functioning of the normal brain and will also have significant impact on diagnosis and treatment of neurovascular diseases such as stroke, Alzheimer's disease, and head injury.
Optical imaging modalities have shown a great potential to provide high spatiotemporal resolution and quantitative imaging of pO2 based on hemoglobin absorption in visible and near infrared range of optical spectrum. However, multispectral measurement of cerebral blood oxygenation relies on photon migration through the highly scattering brain tissue. Estimation and modeling of tissue optical parameters, which may undergo dynamic changes during the experiment, is typically required for accurate estimation of blood oxygenation. On the other hand, estimation of the partial pressure of oxygen (pO2) based on oxygen-dependent quenching of phosphorescence should not be significantly affected by the changes in the optical parameters of the tissue and provides an absolute measure of pO2. Experimental systems that utilize oxygen-sensitive dyes have been demonstrated in in vivo studies of the perfused tissue as well as for monitoring the oxygen content in tissue cultures, showing that phosphorescence quenching is a potent technology capable of accurate oxygen imaging in the physiological pO2 range.
Here we demonstrate with two different imaging modalities how to perform measurement of pO2 in cortical vasculature based on phosphorescence lifetime imaging. In first demonstration we present wide field of view imaging of pO2 at the cortical surface of a rat. This imaging modality has relatively simple experimental setup based on a CCD camera and a pulsed green laser. An example of monitoring the cortical spreading depression based on phosphorescence lifetime of Oxyphor R3 dye was presented. In second demonstration we present a high resolution two-photon pO2 imaging in cortical micro vasculature of a mouse. The experimental setup includes a custom built 2-photon microscope with femtosecond laser, electro-optic modulator, and photon-counting photo multiplier tube. We present an example of imaging the pO2 heterogeneity in the cortical microvasculature including capillaries, using a novel PtP-C343 dye with enhanced 2-photon excitation cross section.
C1 [Sakadzic, Sava; Yaseen, Mohammad A.; Srinivasan, Vivek J.; Ruvinskaya, Svetlana; Wu, Weicheng; Devor, Anna; Boas, David A.] Massachusetts Gen Hosp, Opt Div, Athinoula A Martinos Ctr Biomed Imaging, Dept Radiol, Boston, MA 02114 USA.
[Sakadzic, Sava; Yaseen, Mohammad A.; Mandeville, Emiri T.; Srinivasan, Vivek J.; Arai, Ken; Ruvinskaya, Svetlana; Wu, Weicheng; Devor, Anna; Lo, Eng H.; Boas, David A.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Roussakis, Emmanuel; Vinogradov, Sergei A.] Univ Penn, Dept Biochem & Biophys, Philadelphia, PA 19104 USA.
[Mandeville, Emiri T.; Arai, Ken; Lo, Eng H.] Massachusetts Gen Hosp, Neuroprotect Res Lab, Dept Radiol, Boston, MA 02114 USA.
[Mandeville, Emiri T.; Arai, Ken; Lo, Eng H.] Massachusetts Gen Hosp, Neuroprotect Res Lab, Dept Neurol, Boston, MA 02114 USA.
RP Sakadzic, S (reprint author), Massachusetts Gen Hosp, Opt Div, Athinoula A Martinos Ctr Biomed Imaging, Dept Radiol, Boston, MA 02114 USA.
FU US National Institutes of Health [R01NS057476, P50NS010828, P01NS055104,
R01EB000790, K99NS067050, R01HL081273, R01EB007279]; American Heart
Association [0855772D]
FX We would like to acknowledge support from US National Institutes of
Health grants R01NS057476, P50NS010828, P01NS055104, R01EB000790,
K99NS067050, R01HL081273 and R01EB007279 and American Heart Association
grant 0855772D.
NR 7
TC 0
Z9 0
U1 1
U2 2
PU JOURNAL OF VISUALIZED EXPERIMENTS
PI CAMBRIDGE
PA 1 ALEWIFE CENTER, STE 200, CAMBRIDGE, MA 02140 USA
SN 1940-087X
J9 JOVE-J VIS EXP
JI J. Vis. Exp.
PD MAY
PY 2011
IS 51
AR UNSP e1694
DI 10.3791/1694
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA V36MA
UT WOS:000209214800001
ER
PT J
AU Meyer, JD
Stegner, AJ
Natelson, BH
Cook, DB
AF Meyer, Jacob D.
Stegner, Aaron J.
Natelson, Benjamin H.
Cook, Dane B.
TI Psychobiological Response To Exercise Differs Between Chronic Fatigue
Syndrome (CFS) And CFS With Comorbid Fibromyalgia
SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
LA English
DT Meeting Abstract
C1 [Meyer, Jacob D.; Stegner, Aaron J.] Univ Wisconsin, Madison, WI USA.
[Natelson, Benjamin H.] Beth Israel Deaconess Med Ctr, New York, NY 10003 USA.
[Cook, Dane B.] William S Middleton Mem Vet Adm Med Ctr, Madison, WI USA.
EM jdmeyer3@wisc.edu
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 0195-9131
EI 1530-0315
J9 MED SCI SPORT EXER
JI Med. Sci. Sports Exerc.
PD MAY
PY 2011
VL 43
IS 5
SU 1
MA 1496
BP 325
EP 326
PG 3
WC Sport Sciences
SC Sport Sciences
GA V34IG
UT WOS:000209079501253
ER
PT J
AU Allsup, K
Lecker, S
Zavin, A
Joseph, J
Lazzari, A
Vokonas, P
Forman, DE
AF Allsup, Kelly
Lecker, Stewart
Zavin, Alexandra
Joseph, Jacob
Lazzari, Antonio
Vokonas, Pantel
Forman, Daniel E.
TI Comparing Physical And Funcational Measures In Heart Failure Patients
And Healthy Controls
SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
LA English
DT Meeting Abstract
C1 [Allsup, Kelly; Zavin, Alexandra; Joseph, Jacob; Lazzari, Antonio; Vokonas, Pantel; Forman, Daniel E.] VA Boston Healthcare Syst, Boston, MA USA.
[Lecker, Stewart] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
EM Kelly.Allsup@VA.gov
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 0195-9131
EI 1530-0315
J9 MED SCI SPORT EXER
JI Med. Sci. Sports Exerc.
PD MAY
PY 2011
VL 43
IS 5
SU 1
MA 2430
BP 658
EP 658
PG 1
WC Sport Sciences
SC Sport Sciences
GA V34IG
UT WOS:000209079502532
ER
PT J
AU Figoni, SF
Kunkel, CF
Phillips, AC
Scremin, AME
AF Figoni, Stephen F.
Kunkel, Charles F.
Phillips, Amanda C.
Scremin, A. M. Erika
TI Cardiovascular Reponses during Treadmill Exercise in Men with Peripheral
Arterial Disease and Intermittent Calf Claudication
SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
LA English
DT Meeting Abstract
C1 [Figoni, Stephen F.; Kunkel, Charles F.; Phillips, Amanda C.; Scremin, A. M. Erika] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
EM sfigoni@gmail.com
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 0195-9131
EI 1530-0315
J9 MED SCI SPORT EXER
JI Med. Sci. Sports Exerc.
PD MAY
PY 2011
VL 43
IS 5
SU 1
MA 2725
BP 761
EP 762
PG 2
WC Sport Sciences
SC Sport Sciences
GA V34IG
UT WOS:000209079503194
ER
PT J
AU Schaefer, PW
AF Schaefer, Pamela W.
TI Imaging Acute Stroke is Rapidly Evolving
SO NEUROIMAGING CLINICS OF NORTH AMERICA
LA English
DT Editorial Material
C1 Harvard Univ, Dept Radiol, Div Neuroradiol, Massachusetts Gen Hosp,Sch Med, Boston, MA 02114 USA.
RP Schaefer, PW (reprint author), Harvard Univ, Dept Radiol, Div Neuroradiol, Massachusetts Gen Hosp,Sch Med, 55 Fruit St, Boston, MA 02114 USA.
EM pschaefer@partners.org
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1052-5149
J9 NEUROIMAG CLIN N AM
JI Neuroimaging Clin. N. Am.
PD MAY
PY 2011
VL 21
IS 2
BP XV
EP XV
DI 10.1016/j.nic.2011.05.012
PG 1
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 782KP
UT WOS:000292007900002
PM 21640294
ER
PT J
AU Almandoz, JED
Romero, JM
AF Almandoz, Josser E. Delgado
Romero, Javier M.
TI Advanced CT Imaging in the Evaluation of Hemorrhagic Stroke
SO NEUROIMAGING CLINICS OF NORTH AMERICA
LA English
DT Article
DE Multidetector CT angiography; Hemorrhagic stroke; Secondary
intracerebral hemorrhage score; CT angiography spot sign
ID PRIMARY INTRACEREBRAL HEMORRHAGE; ANGIOGRAPHY SPOT SIGN;
COMPUTED-TOMOGRAPHY ANGIOGRAPHY; CONTRAST-INDUCED NEPHROPATHY; PREDICTS
HEMATOMA EXPANSION; ARTERIOVENOUS-MALFORMATIONS; HIGHEST RISK;
CEREBRAL-HEMORRHAGE; IDENTIFIES PATIENTS; NATURAL-HISTORY
AB Multidetector computed tomographic (CT) angiography is rapidly becoming a pivotal examination in the initial evaluation of patients with hemorrhagic stroke. This article provides an update of the literature on this dynamic topic, focusing on (1) the utility of CT angiography in the identification of hemorrhagic stroke patients who harbor an underlying vascular etiology and the role of the secondary intracerebral hemorrhage score, as well as (2) the clinical value of the CT angiography spot sign and spot sign score in patients with primary intracerebral hemorrhage.
C1 [Almandoz, Josser E. Delgado; Romero, Javier M.] Massachusetts Gen Hosp, Div Neuroradiol, Neurovasc Lab, Boston, MA 02114 USA.
[Almandoz, Josser E. Delgado] Washington Univ, Sch Med, Mallinckrodt Inst Radiol, Div Neuroradiol, St Louis, MO 63110 USA.
[Romero, Javier M.] Harvard Univ, Sch Med, Boston, MA USA.
[Romero, Javier M.] Ultrasound Imaging Serv, Boston, MA USA.
RP Almandoz, JED (reprint author), Massachusetts Gen Hosp, Div Neuroradiol, Neurovasc Lab, Gray 2,Room 273A,55 Fruit St, Boston, MA 02114 USA.
EM josser.delgado@gmail.com
NR 30
TC 11
Z9 11
U1 0
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1052-5149
EI 1557-9867
J9 NEUROIMAG CLIN N AM
JI Neuroimaging Clin. N. Am.
PD MAY
PY 2011
VL 21
IS 2
BP 197
EP +
DI 10.1016/j.nic.2011.01.001
PG 18
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 782KP
UT WOS:000292007900003
ER
PT J
AU Konstas, AA
Wintermark, M
Lev, MH
AF Konstas, Angelos A.
Wintermark, Max
Lev, Michael H.
TI CT Perfusion Imaging in Acute Stroke
SO NEUROIMAGING CLINICS OF NORTH AMERICA
LA English
DT Article
DE Acute stroke; CT perfusion; Cerebral blood volume; Cerebral blood flow;
Ischemic core; Ischemic penumbra; CBV/CBF mismatch
ID ACUTE ISCHEMIC-STROKE; CEREBRAL-BLOOD-FLOW;
TISSUE-PLASMINOGEN-ACTIVATOR; ANGIOGRAPHY SOURCE IMAGES; ACUTE
HEMISPHERIC STROKE; SINGULAR-VALUE DECOMPOSITION; SUSCEPTIBILITY
CONTRAST MRI; POSITRON-EMISSION-TOMOGRAPHY; INITIAL CLINICAL-EXPERIENCE;
3-DIMENSIONAL FUNCTIONAL CT
AB Computed tomographic perfusion (CTP) imaging is an advanced modality that provides important information about capillary-level hemodynamics of the brain parenchyma. CTP can aid in diagnosis, management, and prognosis of acute stroke patients by clarifying acute cerebral physiology and hemodynamic status, including distinguishing severely hypoperfused but potentially salvageable tissue from both tissue likely to be irreversibly infarcted ("core") and hypoperfused but metabolically stable tissue ("benign oligemia"). A qualitative estimate of the presence and degree of ischemia is typically required for guiding clinical management. Radiation dose issues with CTP imaging, a topic of much current concern, are also addressed in this review.
C1 [Konstas, Angelos A.; Lev, Michael H.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Wintermark, Max] Univ Virginia, Dept Radiol, Neuroradiol Div, Charlottesville, VA 22908 USA.
RP Konstas, AA (reprint author), Massachusetts Gen Hosp, Dept Radiol, 55 Fruit St, Boston, MA 02114 USA.
EM akonstas@partners.org
OI Wintermark, Max/0000-0002-6726-3951
NR 178
TC 37
Z9 38
U1 0
U2 5
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1052-5149
J9 NEUROIMAG CLIN N AM
JI Neuroimaging Clin. N. Am.
PD MAY
PY 2011
VL 21
IS 2
BP 215
EP +
DI 10.1016/j.nic.2011.01.008
PG 25
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 782KP
UT WOS:000292007900004
PM 21640296
ER
PT J
AU Copen, WA
Schaefer, PW
Wu, O
AF Copen, William A.
Schaefer, Pamela W.
Wu, Ona
TI MR Perfusion Imaging in Acute Ischemic Stroke
SO NEUROIMAGING CLINICS OF NORTH AMERICA
LA English
DT Article
DE Stroke; Brain ischemia; Magnetic resonance imaging; Cerebrovascular
circulation
ID CEREBRAL-BLOOD-FLOW; DIFFUSION-WEIGHTED MR;
POSITRON-EMISSION-TOMOGRAPHY; TISSUE-PLASMINOGEN ACTIVATOR; ARTERIAL
INPUT FUNCTIONS; SINGULAR-VALUE DECOMPOSITION; SUSCEPTIBILITY CONTRAST
MRI; HIGH-RESOLUTION MEASUREMENT; PLACEBO-CONTROLLED TRIAL; TRACER BOLUS
PASSAGES
AB Magnetic resonance (MR) perfusion imaging offers the potential for measuring brain perfusion in acute stroke patients, at a time when treatment decisions based on these measurements may affect outcomes dramatically. Rapid advancements in both acute stroke therapy and perfusion imaging techniques have resulted in continuing redefinition of the role that perfusion imaging should play in patient management. This review discusses the basic pathophysiology of acute stroke, the utility of different kinds of perfusion images, and research on the continually evolving role of MR perfusion imaging in acute stroke care.
C1 [Copen, William A.; Schaefer, Pamela W.] Harvard Univ, Dept Radiol, Div Neuroradiol, Massachusetts Gen Hosp,Sch Med, Boston, MA 02114 USA.
[Copen, William A.; Wu, Ona] MGH MIT HMS Athinoula Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
RP Copen, WA (reprint author), Harvard Univ, Dept Radiol, Div Neuroradiol, Massachusetts Gen Hosp,Sch Med, GRB 273A,55 Fruit St, Boston, MA 02114 USA.
EM wcopen@partners.org
FU National Institutes of Health [R01 NS059775]
FX This work was supported in part by grant R01 NS059775 from the National
Institutes of Health.
NR 159
TC 14
Z9 14
U1 0
U2 3
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1052-5149
J9 NEUROIMAG CLIN N AM
JI Neuroimaging Clin. N. Am.
PD MAY
PY 2011
VL 21
IS 2
BP 259
EP +
DI 10.1016/j.nic.2011.02.007
PG 26
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 782KP
UT WOS:000292007900007
PM 21640299
ER
PT J
AU Sorensen, AG
Ay, H
AF Sorensen, A. Gregory
Ay, Hakan
TI Transient Ischemic Attack: Definition, Diagnosis, and Risk
Stratification
SO NEUROIMAGING CLINICS OF NORTH AMERICA
LA English
DT Article
DE Transient ischemic attack; Definition; Diffusion-weighted imaging;
Imaging; Risk stratification; Risk scores
ID DIFFUSION-WEIGHTED MRI; CEREBRAL INFARCTION; MINOR STROKE; TIA PATIENTS;
POPULATION; SCORE; EMERGENCY; PERFUSION; PREDICT; ABNORMALITIES
AB Transient ischemic attack (TIA) can convey a high imminent risk for the development of a major stroke and is therefore considered to be a medical emergency. Recent evidence indicates that TIA with imaging proof of brain infarction represents an extremely unstable condition with early risk of stroke that is as much as 20 times higher than the risk after TIA without tissue damage. The use of neuroimaging in TIA is therefore critical not only for diagnosis but also for accurate risk stratification. In this article, recent advances in diagnostic imaging, categorizations, and risk stratification in TIA are discussed.
C1 [Ay, Hakan] Harvard Univ, Sch Med, AA Martinos Ctr Biomed Imaging, Massachusetts Gen Hosp,Stroke Serv, Boston, MA 02129 USA.
[Sorensen, A. Gregory] Harvard Univ, Sch Med, AA Martinos Ctr Biomed Imaging, Massachusetts Gen Hosp,Dept Radiol, Boston, MA 02129 USA.
RP Ay, H (reprint author), Harvard Univ, Sch Med, AA Martinos Ctr Biomed Imaging, Massachusetts Gen Hosp,Stroke Serv, 13th St,CNY149-2301, Boston, MA 02129 USA.
EM hay@partners.org
FU NINDS NIH HHS [R01 NS038477, R01 NS059710, R01 NS059710-02,
R01-NS038477, R01-NS059710]
NR 54
TC 14
Z9 15
U1 1
U2 5
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1052-5149
J9 NEUROIMAG CLIN N AM
JI Neuroimaging Clin. N. Am.
PD MAY
PY 2011
VL 21
IS 2
BP 303
EP +
DI 10.1016/j.nic.2011.01.013
PG 12
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 782KP
UT WOS:000292007900009
PM 21640301
ER
PT J
AU Fung, SH
Roccatagliata, L
Gonzalez, RG
Schaefer, PW
AF Fung, Steve H.
Roccatagliata, Luca
Gonzalez, R. Gilberto
Schaefer, Pamela W.
TI MR Diffusion Imaging in Ischemic Stroke
SO NEUROIMAGING CLINICS OF NORTH AMERICA
LA English
DT Article
DE MR imaging; Diffusion-weighted imaging; Diffusion tensor imaging;
Diffusion kurtosis imaging; Brain ischemia
ID TISSUE-PLASMINOGEN ACTIVATOR; FOCAL CEREBRAL-ISCHEMIA; WHITE-MATTER
INJURY; INTRACELLULAR APPARENT DIFFUSION; ANISOTROPIC WATER DIFFUSION;
BRAIN-STEM INFARCTION; TERM-EQUIVALENT AGE; HYPER-ACUTE STROKE;
OF-HEALTH STROKE; WEIGHTED MRI
AB Diffusion-weighted MRI provides image contrast that is dependent on the molecular motion of water. Diffusion-weighted imaging is the most reliable method for early detection of cerebral ischemia, for the definition of infarct core, and for the differentiation of acute ischemia from other disease processes that mimic stroke. Diffusion tensor imaging and diffusion kurtosis imaging may offer additional diagnostic information on the microstructural status of tissue. This review discusses the development and applications of diffusion-weighted imaging, diffusion tensor imaging, and diffusion kurtosis imaging in acute and chronic ischemia.
C1 [Fung, Steve H.] Methodist Hosp, Dept Radiol, Weill Cornell Med Coll, Neuroradiol Sect, Houston, TX 77030 USA.
[Roccatagliata, Luca] Univ Genoa, Dept Neurosci Ophthalmol & Genet, I-16132 Genoa, Italy.
[Gonzalez, R. Gilberto; Schaefer, Pamela W.] Harvard Univ, Massachusetts Gen Hosp, Dept Radiol, Sch Med,Neuroradiol Div, Boston, MA 02114 USA.
RP Fung, SH (reprint author), Methodist Hosp, Dept Radiol, Weill Cornell Med Coll, Neuroradiol Sect, 6565 Fannin St, Houston, TX 77030 USA.
EM steve_fung@post.harvard.edu
OI Fung, Steve/0000-0002-1177-682X
NR 198
TC 31
Z9 35
U1 2
U2 14
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1052-5149
J9 NEUROIMAG CLIN N AM
JI Neuroimaging Clin. N. Am.
PD MAY
PY 2011
VL 21
IS 2
BP 345
EP +
DI 10.1016/j.nic.2011.03.001
PG 34
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 782KP
UT WOS:000292007900012
PM 21640304
ER
PT J
AU Garshick, E
Stolzmann, KL
Gagnon, DR
Morse, LR
Brown, R
AF Garshick, Eric
Stolzmann, Kelly L.
Gagnon, David R.
Morse, Leslie R.
Brown, Robert
TI Systemic Inflammation and Reduced Pulmonary Function in Chronic Spinal
Cord Injury
SO PM&R
LA English
DT Article
ID C-REACTIVE PROTEIN; LUNG-FUNCTION; METABOLIC SYNDROME; CIRCULATING
LEVELS; PHYSICAL-ACTIVITY; DIURNAL-VARIATION; BODY-COMPOSITION;
YOUNG-ADULTS; POPULATION; DISEASE
AB Objective: To evaluate the relationship between systemic inflammation and pulmonary function in persons with chronic spinal cord injury (SCI).
Design: Cross-sectional study
Setting: Veterans Affairs Medical Center.
Participants: Fifty-nine men with chronic SCI participating in a prior epidemiologic study.
Methods: Standardized assessment of pulmonary function and measurement of plasma C-reactive protein (CRP) and interleukin-6 (IL-6).
Main Outcome Measurements: Forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC).
Results: Persons with the highest values of IL-6 had the lowest %-predicted FEV1 and FVC. There was a significant inverse linear trend between quartile of IL-6 and %-predicted FEV1 (P < .001) and FVC (P < .006), unadjusted and adjusted for SCI level and completeness of injury, obstructive lung disease history, smoking, and body mass index (P = .010-.039). Although not as strong as for IL-6, there also were similar trends for %-predicted FEV1 and FVC wit:a CRP.
Conclusions: In chronic SCI, higher levels of IL-6 and CRP were associated with a lower FEV, and FVC, independent of level and completeness of injury. These results suggest that the reduction of pulmonary function after SCI is related not only to neuromuscular impairment but also to factors that promote systemic inflammation. PM R 2011;3:433-439
C1 [Garshick, Eric] VA Boston Healthcare Syst, Med Serv, Pulm & Crit Care Med Sect, W Roxbury, MA 02132 USA.
[Garshick, Eric] Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA.
[Stolzmann, Kelly L.] Harvard Univ, Sch Med, Programs Res VA Boston, Boston, MA USA.
[Gagnon, David R.] VA Boston Healthcare Syst, VA Cooperat Studies Program, Boston, MA USA.
[Gagnon, David R.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Morse, Leslie R.] Spaulding Rehabil Hosp, Dept Phys Med & Rehabil, Boston, MA USA.
[Brown, Robert] Massachusetts Gen Hosp, Pulm & Crit Care Med Unit, Boston, MA 02114 USA.
[Brown, Robert] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
RP Garshick, E (reprint author), VA Boston Healthcare Syst, Med Serv, Pulm & Crit Care Med Sect, 1400 VFW Pkwy, W Roxbury, MA 02132 USA.
EM eric.garshick@va.gov
RI Morse, Leslie/C-9442-2015;
OI Morse, Leslie/0000-0002-7426-6341; Gagnon, David/0000-0002-6367-3179
FU NIH; Department of Veteran's Affairs [B6618R]; National Institute of
Child Health and Human Development [RO1 HD042141]; Merit Review grant
[B6618R]; Office of Research and Development, Rehabilitation Research
and Development [B6618R]; Massachusetts Veterans Epidemiology Research
and Information Center; Cooperative Studies Program; Department of
Veterans Affairs
FX 8B, investigator on VA and NIH grants used to collect and analyze data,
Merit Review grant B6618R, Department of Veteran's Affairs; National
Institute of Child Health and Human Development RO1 HD042141; 8B, salary
support via Merit Review grant B6618R; Office of Research and
Development, Rehabilitation Research and Development (Merit Review Grant
B6618R) and Massachusetts Veterans Epidemiology Research and Information
Center, Cooperative Studies Program, Department of Veterans Affairs;
National Institute of Child Health and Human Development (RO1 HD042141).
The content is solely the responsibility of the authors and does not
necessarily represent the official views of the National Institute of
Child Health and Human Development or the Department of Veterans
Affairs.
NR 44
TC 10
Z9 10
U1 1
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1934-1482
J9 PM&R
JI PM&R
PD MAY
PY 2011
VL 3
IS 5
BP 433
EP 439
DI 10.1016/j.pmrj.2011.02.003
PG 7
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA 961AZ
UT WOS:000305437600006
PM 21570031
ER
PT J
AU Hameed, F
McInnis, KC
AF Hameed, Farah
McInnis, Kelly C.
TI Sacral Stress Fracture Causing Radiculopathy in a Female Runner: A Case
Report
SO PM&R
LA English
DT Article
ID DAMAGE
C1 [Hameed, Farah] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Sports Med, Boston, MA 02115 USA.
[McInnis, Kelly C.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
RP Hameed, F (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Sports Med, 125 Nashua St, Boston, MA 02115 USA.
EM fhameed@partners.org
NR 10
TC 3
Z9 3
U1 1
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1934-1482
J9 PM&R
JI PM&R
PD MAY
PY 2011
VL 3
IS 5
BP 489
EP 491
DI 10.1016/j.pmrj.2010.10.009
PG 3
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA 961AZ
UT WOS:000305437600017
PM 21570039
ER
PT J
AU Ge, Y
Wang, TJ
AF Ge, Yin
Wang, Thomas J.
TI Circulating, Imaging, and Genetic Biomarkers in Cardiovascular Risk
Prediction
SO TRENDS IN CARDIOVASCULAR MEDICINE
LA English
DT Review
ID CORONARY-HEART-DISEASE; C-REACTIVE PROTEIN; INTIMA-MEDIA THICKNESS;
HIGHLY SENSITIVE ASSAY; CAROTID-ARTERY INTIMA; MYOCARDIAL-INFARCTION;
COMPUTED-TOMOGRAPHY; OLDER-ADULTS; TASK-FORCE; SUBCLINICAL
ATHEROSCLEROSIS
AB In the primary prevention of cardiovascular disease, the study of biomarkers to identify at-risk individuals is an expanding field. Several developments have fueled this trend, including improved understanding of the pathophysiological processes underlying atherosclerosis, advances in imaging technology to enable the quantification of subclinical disease burden, and the identification of new genetic susceptibility variants for cardiovascular disease. Furthermore, the advent of high-throughput platforms for molecular profiling has increased the pace of biomarker discovery. The rising interest in biomarkers has been balanced by the recognition that standardized and rigorous statistical approaches are needed to evaluate the clinical utility of candidate risk markers. This article reviews the issues surrounding the evaluation of biomarkers, evidence from studies of existing biomarkers, and recent applications of biomarker discovery platforms. (Trends Cardiovasc Med 2011;21:105-112) (C) 2011 Elsevier Inc. All rights reserved.
C1 [Ge, Yin; Wang, Thomas J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, Boston, MA 02114 USA.
RP Wang, TJ (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, GRB 800,55 Fruit St, Boston, MA 02114 USA.
EM tjwang@partners.org
FU Siemens; Brahms; Critical Diagnostics; Singulex; Diasorin; Pfizer;
Roche; LabCorp
FX Dr. Wang has participated on the scientific advisory board of Diasorin,
Inc., and has received assay support or research funding from Siemens,
Brahms, Critical Diagnostics, Singulex, Diasorin, Pfizer, Roche, and
LabCorp. Dr. Wang has received honoraria from Roche, Diasorin, and Quest
Diagnostics. Dr. Wang is named as a co-inventor on patent applications
relating to the use of metabolomic or neurohormonal biomarkers in risk
prediction.
NR 79
TC 6
Z9 6
U1 0
U2 4
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 1050-1738
J9 TRENDS CARDIOVAS MED
JI Trends Cardiovasc. Med.
PD MAY
PY 2011
VL 21
IS 4
BP 105
EP 112
AR PII S1050-1738(12)00061-8
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 961AM
UT WOS:000305435800002
PM 22681965
ER
PT J
AU Kaufman, JS
AF Kaufman, James S.
TI Relationship of Erythropoiesis-Stimulating Agent Dose and Responsiveness
and Adverse Outcomes in CKD
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Editorial Material
ID CHRONIC KIDNEY-DISEASE; RECOMBINANT-HUMAN-ERYTHROPOIETIN; STAGE
RENAL-DISEASE; HEMODIALYSIS-PATIENTS; EPOETIN-ALPHA; CLINICAL-TRIAL;
ANEMIA; MORTALITY; HEMOGLOBIN; SURVIVAL
C1 [Kaufman, James S.] VA Boston Healthcare Syst, Renal Sect, Boston, MA 02130 USA.
[Kaufman, James S.] Boston Univ, Sch Med, Boston, MA 02118 USA.
RP Kaufman, JS (reprint author), VA Boston Healthcare Syst, Renal Sect, 111-RE,150 S Huntington Ave, Boston, MA 02130 USA.
EM james.kaufman@va.gov
NR 21
TC 2
Z9 2
U1 0
U2 3
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0272-6386
EI 1523-6838
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD MAY
PY 2011
VL 57
IS 5
BP 661
EP 663
DI 10.1053/j.ajkd.2011.02.001
PG 3
WC Urology & Nephrology
SC Urology & Nephrology
GA 749ZW
UT WOS:000289513600007
PM 21411198
ER
PT J
AU Lobb, R
Opdyke, KM
McDonnell, CJ
Pagaduan, MG
Hurlbert, M
Gates-Ferris, K
Chi, B
Allen, JD
AF Lobb, Rebecca
Opdyke, Kelly Morrison
McDonnell, Cheryl J.
Pagaduan, Mary Grace
Hurlbert, Marc
Gates-Ferris, Kathryn
Chi, Banghee
Allen, Jennifer D.
TI Use of Evidence-Based Strategies to Promote Mammography Among Medically
Underserved Women
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID CLIENT-DIRECTED INTERVENTIONS; LATE-STAGE DIAGNOSIS; BREAST-CANCER;
CERVICAL-CANCER; UNITED-STATES; SOCIOECONOMIC-STATUS; SCREENING
MAMMOGRAPHY; PREVENTIVE CARE; HEALTH; DISPARITIES
AB Background: Several web-based resources recommend effective intervention strategies to promote use of mammography but there is limited information on whether the strategies are used, particularly by organizations that serve medically underserved women.
Purpose: In 2010, data collected by the Avon Breast Health Outreach Program (BHOP) were analyzed to examine the diffusion of evidence-based intervention strategies among funded organizations.
Methods: Data on intervention strategies were obtained from a 2009 survey of Avon BHOP organizations funded during 2006-2009. Self-reported use of mammography was reported from annual intake forms administered to medically underserved women aged >= 40 years, excluding those with a history of breast cancer or initial enrollees not exposed to the strategies. Strategies reflected interventions reviewed in the Guide to Community Preventive Services. Those recommended to increase demand and use of mammography included (1) client reminders; (2) small media; (3) one-to-one education; (4) removal of structural barriers to rescreening; and (5) group education-and one that lacked sufficient evidence to warrant a recommendation (6) client incentives.
Results: Among 86 organizations, 96% used three or more intervention strategies. The most common strategies were group education (91%) and client reminders (83%). The overall crude-percentage of recent mammography use was 84%. This percentage was similar for clinical sites and nonclinical sites, despite the disproportionate enrollment of medically underserved women in nonclinical sites.
Conclusions: The wide use of evidence-based strategies among Avon BHOP-funded organizations and high percentage of recent mammography use among women exposed to the strategies suggests that medically underserved women are benefiting from effective interventions to increase use of mammography. (Am J Prev Med 2011; 40(5): 561-565) (C) 2011 American Journal of Preventive Medicine
C1 [Lobb, Rebecca] St Michaels Hosp, Ctr Res Inner City Hlth, Toronto, ON M5B 1W8, Canada.
[Lobb, Rebecca; Allen, Jennifer D.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Allen, Jennifer D.] Harvard Univ, Sch Med, Boston, MA USA.
[Opdyke, Kelly Morrison; Pagaduan, Mary Grace; Gates-Ferris, Kathryn; Chi, Banghee] Cicatelli Associates Incorp, New York, NY USA.
[Hurlbert, Marc] Avon Fdn Women, New York, NY USA.
[McDonnell, Cheryl J.] James Bell Associates, Arlington, VA USA.
RP Lobb, R (reprint author), St Michaels Hosp, Ctr Res Inner City Hlth, 30 Bond St, Toronto, ON M5B 1W8, Canada.
EM lobbr@smh.ca
RI Allen, Jennifer/M-2113-2015;
OI Hurlbert, Marc/0000-0003-3301-3572; Lobb, Rebecca/0000-0003-3503-0675
FU Avon Foundation for Women (Avon); Canadian Institutes for Health
Research; Ontario Ministry of Health and Long-Term Care
FX Funding for this evaluation was provided by the Avon Foundation for
Women (Avon). Dr. Lobb gratefully acknowledges the support of the
Canadian Institutes for Health Research and the Ontario Ministry of
Health and Long-Term Care.
NR 37
TC 4
Z9 4
U1 3
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD MAY
PY 2011
VL 40
IS 5
BP 561
EP 565
DI 10.1016/j.amepre.2010.12.024
PG 5
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 749YC
UT WOS:000289506900012
PM 21496756
ER
PT J
AU Park, KJ
Kiyokawa, T
Soslow, RA
Lamb, CA
Oliva, E
Zivanovic, O
Juretzka, MM
Pirog, EC
AF Park, Kay J.
Kiyokawa, Takako
Soslow, Robert A.
Lamb, Colleen A.
Oliva, Esther
Zivanovic, Oliver
Juretzka, Margrit M.
Pirog, Edyta C.
TI Unusual Endocervical Adenocarcinomas: An Immunohistochemical Analysis
With Molecular Detection of Human Papillomavirus
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE cervical adenocarcinoma; unusual adenocarcinoma; HPV;
immunohistochemistry; HIK1083; p16; gastric-type; minimal deviation
ID MINIMAL DEVIATION ADENOCARCINOMA; PAPILLARY SEROUS CARCINOMA; CLEAR-CELL
ADENOCARCINOMAS; UTERINE CERVIX; GLANDULAR-HYPERPLASIA; ADENOMA
MALIGNUM; GASTRIC MORPHOLOGY; CANCER; EXPRESSION; INFECTION
AB Background: Endocervical adenocarcinomas of the usual type are etiologically related to infection with oncogenic human papillomaviruses (HPVs). These tumors are typically diffusely positive for p16 and carcinoembryonic antigen (CEA) immunostains. The goal of our study was to determine the HPV status and immunohistochemical profiles of unusual histologic subtypes of endocervical adenocarcinoma.
Methods: The study consisted of a total of 26 cases of unusual subtypes including clear cell carcinoma (CCC, n = 9), gastrictype adenocarcinoma (GAS, n = 11), minimal deviation adenocarcinoma (MDA, n = 3), mesonephric adenocarcinoma (MSN, n = 1), serous adenocarcinoma (SER, n = 1), and malignant mixed Mullerian tumor (n = 1). In addition, 5 cases of usualtype endocervical adenocarcinoma (UEA) were included in the study as a control group. The cases were tested for HPV using SPF-10 PCR and LiPA assays, and immunostained for p16, HIK1083, hepatocyte nuclear factor 1-b, p53, CEA, estrogen receptor (ER), and progesterone receptor (PR).
Results: HPV DNA was not detected in any of the unusual adenocarcinoma subtypes, with the exception of a single case of SER in which HPV16 was detected. p16 positivity did not correlate with HPV status, as 42% of HPV-negative tumors showed patchy/diffuse p16 overexpression; however, p16 positivity was uncommon in GAS/MDA. HIK1083 positivity was limited to GAS and MDA, indicating relative specificity for tumors with gastric mucin expression. Hepatocyte nuclear factor 1-b was positive in the majority of CCCs and also in other tumor variants and in some UEA as well, indicating a lack of specificity for clear cell differentiation. CEA was consistently negative in CCCs and in a single MSN, but positive in GAS, MDA, SER, and UEA, suggesting that it may serve as a negative marker of clear cell differentiation. p53 was diffusely positive in almost half of the GAS cases, whereas UEA showed mostly negative staining and other variants showed focal staining. PR was negative in all variant cases and in all UEA. ER expression, although mostly negative, showed focal staining in a few variant cases and UEA.
Conclusions: Unusual variants of endocervical adenocarcinoma are not related to HPV infection, with only rare exceptions, and p16 overexpression in non-UEA does not correlate with HPV status. Negative staining for PR and ER may serve as a general marker of endocervical neoplasia. GAS/MDA may be differentiated from all other adenocarcinomas with either positive HIK1083 stain or negative/focal p16 stain. Positive CEA stain differentiates GAS/MDA from CCC and negative PR and ER stains differentiate GAS/MDA from benign endocervical glands. CCC may be distinguished from all other adenocarcinomas, except MSN, with a negative CEA stain. Strong and diffuse p53 positivity in SER may be useful in differentiation from UEA. MSN may be identified with negative CEA, ER, and PR stains.
C1 [Park, Kay J.; Soslow, Robert A.] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10065 USA.
[Pirog, Edyta C.] New York Presbyterian Hosp, Weill Cornell Med Ctr, Dept Pathol & Lab Med, New York, NY USA.
[Kiyokawa, Takako] Chiba Univ, Grad Sch Med, Dept Mol Pathol, Chou Ku, Chiba, Japan.
[Kiyokawa, Takako] Chiba Univ, Sch Med, Chou Ku, Chiba 280, Japan.
[Lamb, Colleen A.; Oliva, Esther] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Zivanovic, Oliver] Univ Hosp Bonn, Dept Gynecol Oncol, Bonn, Germany.
[Juretzka, Margrit M.] Kaiser Permanente, Oakland, CO USA.
RP Soslow, RA (reprint author), Mem Sloan Kettering Canc Ctr, Dept Pathol, 1275 York Ave,Box 261, New York, NY 10065 USA.
EM gynbreast@mskcc.org
OI Park, Kay/0000-0001-8989-2938; Soslow, Robert/0000-0002-7269-5898
FU NCI NIH HHS [P30 CA008748]
NR 51
TC 61
Z9 64
U1 0
U2 8
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 MAY
PY 2011
VL 35
IS 5
BP 633
EP 646
DI 10.1097/PAS.0b013e31821534b9
PG 14
WC Pathology; Surgery
SC Pathology; Surgery
GA 749XZ
UT WOS:000289506600003
PM 21490443
ER
PT J
AU Farris, AB
Demicco, EG
Le, LP
Finberg, KE
Miller, J
Mandal, R
Fukuoka, J
Cohen, C
Gaissert, HA
Zukerberg, LR
Lauwers, GY
Iafrate, AJ
Mino-Kenudson, M
AF Farris, Alton B., III
Demicco, Elizabeth G.
Le, Long Phe
Finberg, Karin E.
Miller, Julie
Mandal, Rajni
Fukuoka, Junya
Cohen, Cynthia
Gaissert, Henning A.
Zukerberg, Lawrence R.
Lauwers, Gregory Y.
Iafrate, A. John
Mino-Kenudson, Mari
TI Clinicopathologic and Molecular Profiles of Microsatellite Unstable
Barrett Esophagus-associated Adenocarcinoma
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE Barrett esophagus; esophageal adenocarcinoma; microsatellite
instability; histology; medullary carcinoma; tumor-infiltrating
lymphocyte
ID NONPOLYPOSIS COLORECTAL-CANCER; LYMPHOEPITHELIOMA-LIKE CARCINOMA; ISLAND
METHYLATOR PHENOTYPE; GASTRIC-CARCINOMA; MISMATCH-REPAIR; COLON-CANCER;
ESOPHAGOGASTRIC JUNCTION; MEDULLARY CARCINOMA; LYMPHOID STROMA; BRAF
MUTATION
AB Microsatellite instability (MSI) has been reported in various tumors, with colon cancer as the prototype. However, little is known about MSI in Barrett esophagus (BE)-associated adenocarcinoma. Thus, the aim of this study was to compare the clinicopathologic and molecular features of BE-associated adenocarcinomas with and without MSI. The study cohort consisted of 76 patients with BE-associated adenocarcinomas (66 male, 10 female), with a mean age of 65.1 years. Immunohistochemistry (IHC) for MLH1, MSH2, MSH6, PMS2, and CD3 and in situ hybridization for Epstein-Barr virus-encoded RNA were performed. MLH1 and PMS2 expression was lost by IHC in 5 cases (6.6%); of these, 5 showed high-level MSI (MSI-H) by polymerase chain reaction assay, and 4 showed hMLH1 promoter methylation. Histologically, tumors with MSI-H were heterogenous and included conventional adenocarcinomas with tumor-infiltrating lymphocytes (n = 1), medullary carcinoma (n = 2), signet ring cells (n = 1), and signet ring cell and mucinous components (n = 1). Compared with tumors negative for MSI by IHC, BE-associated adenocarcinomas with MSI-H were associated with older patient age (P = 0.0060), lymphovascular invasion (P = 0.027), and significantly larger numbers of tumor-infiltrating lymphocytes (P < 0.0001). However, there was no statistical difference in overall survival between the 2 groups (P = 0.285). In conclusion, MSI-H is uncommon in BE-associated adenocarcinomas, but is associated with clinicopathologic features fairly similar to sporadic microsatellite unstable colorectal cancers. Given the growing evidence that indicates lack of benefits from adjuvant therapy with fluorouracil in the colonic counterpart, it may be important to identify MSI-H in BE-associated adenocarcinomas.
C1 [Farris, Alton B., III; Demicco, Elizabeth G.; Le, Long Phe; Finberg, Karin E.; Miller, Julie; Mandal, Rajni; Zukerberg, Lawrence R.; Lauwers, Gregory Y.; Iafrate, A. John; Mino-Kenudson, Mari] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Gaissert, Henning A.] Massachusetts Gen Hosp, Dept Thorac Surg, Boston, MA 02114 USA.
[Mino-Kenudson, Mari] Harvard Univ, Sch Med, Boston, MA USA.
[Farris, Alton B., III; Cohen, Cynthia] Emory Univ, Sch Med, Dept Pathol, Atlanta, GA 30322 USA.
[Finberg, Karin E.] Duke Univ, Med Ctr, Dept Pathol, Durham, NC 27710 USA.
[Fukuoka, Junya] Toyama Med Univ, Toyama, Japan.
RP Mino-Kenudson, M (reprint author), Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
EM mminokenudson@partners.org
NR 46
TC 9
Z9 10
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0147-5185
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD MAY
PY 2011
VL 35
IS 5
BP 647
EP 655
DI 10.1097/PAS.0b013e31820f18a2
PG 9
WC Pathology; Surgery
SC Pathology; Surgery
GA 749XZ
UT WOS:000289506600004
PM 21422910
ER
PT J
AU Phadke, PA
Rakheja, D
Le, LP
Selim, MA
Kapur, P
Davis, A
Mihm, MC
Hoang, MP
AF Phadke, Pushkar A.
Rakheja, Dinesh
Le, Long P.
Selim, Maria Angelica
Kapur, Payal
Davis, Amy
Mihm, Martin C., Jr.
Hoang, Mai P.
TI Proliferative Nodules Arising Within Congenital Melanocytic Nevi: A
Histologic, Immunohistochemical, and Molecular Analyses of 43 Cases
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE proliferative nodule; congenital nevi; immunohistochemistry; mutational
analyses
ID MALIGNANT-MELANOMA; MUTATIONAL ANALYSIS; SPITZ NEVI; BRAF GENE;
MONOCLONAL-ANTIBODY; KIT EXPRESSION; HIGH-FREQUENCY; C-KIT; N-RAS;
BENIGN
AB The histopathologic interpretation of proliferative nodules (PNs) in congenital melanocytic nevi can present significant challenges as some PNs may exhibit atypical features that make the distinction from melanoma difficult. We compared histologic features, Ki-67%, PHH3, and CD117% expression levels by immunohistochemistry in 18 benign and 25 atypical PNs (from 41 patients) with that of background congenital nevi (of these 43 cases), 10 congenital nevi, and 3 dermal melanomas arising in congenital melanocytic lesions. In addition, we evaluated the presence of BRAF, GNAQ, HRAS, KRAS, and NRAS mutations in all groups using the SNaPshot Multiplex System. Follow-up was available on 19 patients (9 benign and 10 atypical PNs) (range, 2 to 20 y; median, 8 y) and all were alive with no evidence of disease. The specific histologic features of atypical PNs, such as sharp demarcation (P < 0.001), expansile growth (P < 0.001), epidermal effacement (P < 0.001), nuclear pleomorphism (P < 0.001), and increased mitoses (P < 0.001), differed significantly from those of benign PNs. Immunohistochemical results showed that Ki-67% and PHH3 scores, but not CD117% expression, were significantly higher (P < 0.05) in atypical PNs. Molecular analyses showed that the PNs and background congenital melanocytic nevi of the giant congenital nevi possess more frequent NRAS mutations and infrequent BRAF mutations when compared with those of the remaining cases. These findings suggest that histologic features and Ki-67 and PHH3 expression levels are the strongest parameters to distinguish between benign versus atypical PNs. The immunohistochemical results suggest that atypical PNs are distinct borderline lesions residing between benign PNs and dermal melanomas. Although numerous mutations are detected in the samples, the diagnostic use of molecular analysis in this regard is limited.
C1 [Hoang, Mai P.] Massachusetts Gen Hosp, Dermatopathol Unit, Dept Pathol, Boston, MA 02114 USA.
[Phadke, Pushkar A.; Le, Long P.; Mihm, Martin C., Jr.; Hoang, Mai P.] Harvard Univ, Sch Med, Boston, MA USA.
[Rakheja, Dinesh; Kapur, Payal; Davis, Amy] Univ Texas SW Med Ctr Dallas, Dept Pathol, Dallas, TX 75390 USA.
[Selim, Maria Angelica] Duke Univ, Med Ctr, Dept Pathol & Dermatol, Durham, NC USA.
RP Hoang, MP (reprint author), Massachusetts Gen Hosp, Dermatopathol Unit, Dept Pathol, 55 Fruit St,Warren 820, Boston, MA 02114 USA.
EM mhoang@partners.org
NR 48
TC 33
Z9 34
U1 0
U2 7
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 MAY
PY 2011
VL 35
IS 5
BP 656
EP 669
DI 10.1097/PAS.0b013e31821375ea
PG 14
WC Pathology; Surgery
SC Pathology; Surgery
GA 749XZ
UT WOS:000289506600005
PM 21436676
ER
PT J
AU Gonzalez-Obeso, E
Fujita, H
Deshpande, V
Ogawa, F
Lisovsky, M
Genevay, M
Grzyb, K
Brugge, W
Lennerz, JK
Shimizu, M
Srivastava, A
Lauwers, GY
AF Gonzalez-Obeso, Elvira
Fujita, Hiroshi
Deshpande, Vikram
Ogawa, Fumihiro
Lisovsky, Mikhail
Genevay, Muriel
Grzyb, Krzysztof
Brugge, William
Lennerz, Jochen K.
Shimizu, Michio
Srivastava, Amitabh
Lauwers, Gregory Y.
TI Gastric Hyperplastic Polyps: A Heterogeneous Clinicopathologic Group
Including a Distinct Subset Best Categorized as Mucosal Prolapse Polyp
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE hyperplastic polyp; stomach; foveolar hyperplasia; prolapse; gastritis
cystica polyposa
ID CYSTICA-POLYPOSA; UNOPERATED STOMACH; GASTROENTEROSTOMY SITE; HISTOLOGIC
PATTERNS; ASSOCIATIONS; MANAGEMENT; PROFUNDA; ATROPHY
AB Background: Gastric hyperplastic polyps are the second most common subtype of gastric polyps. There has been an ongoing debate about their precise diagnostic criteria and etiological associations.
Materials and Methods: A total of 208 gastric polyps that were originally diagnosed as hyperplastic polyps in our department during an 8-year period were reviewed using recently emphasized diagnostic criteria, and their clinicopathologic associations were explored.
Results: Only 41 cases were confirmed as hyperplastic polyps, whereas 103 cases (49%) were reclassified as polypoid foveolar hyperplasia, and 64 cases (31%) were diagnosed as gastric mucosal prolapse polyps. Gastric mucosal prolapse polyps were distinguished by basal glandular elements, hypertrophic muscle fibers ascending perpendicularly from the muscularis mucosae, and by thick-walled blood vessels. This hitherto undescribed polyp is more commonly sessile than hyperplastic polyps (P = 0.0452) and is found more often in the antropyloric region (P: 0.0053). Only 20.6% of hyperplastic polyps were associated with Helicobacter pylori infection.
Conclusions: Our findings highlight that gastric polypoid lesions that have morphologic similarities may be related to various mechanisms, including inflammatory and prolapse processes. The predominantly antral location of gastric mucosal prolapse polyps, a zone of pronounced peristalsis, suggests that mucosal prolapse plays a role in the development of these common polyps. Evaluation of the prevalence and clinical associations of these distinctive polyps awaits further studies.
C1 [Lauwers, Gregory Y.] Massachusetts Gen Hosp, Dept Pathol, Gastrointestinal Pathol Serv, Boston, MA 02114 USA.
[Gonzalez-Obeso, Elvira; Ogawa, Fumihiro] Hosp Gen Ciudad Real, Ciudad Real, Spain.
[Fujita, Hiroshi] Kagoshima Univ, Grad Sch Med & Dent, Dept Digest & Life Style Related Dis, Kagoshima 890, Japan.
[Genevay, Muriel] Ctr Univ Hosp Geneve, Geneva, Switzerland.
[Grzyb, Krzysztof] Oslo Univ Hosp, Rikshosp, Dept Pathol, Oslo, Norway.
[Lisovsky, Mikhail; Srivastava, Amitabh] Dartmouth Med Sch, Lebanon, NH USA.
[Lisovsky, Mikhail; Srivastava, Amitabh] Dartmouth Hitchcock Med Ctr, Lebanon, NH 03766 USA.
[Shimizu, Michio] Saitama Med Univ, Saitama Int Med Ctr, Dept Pathol, Saitama, Japan.
Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Brugge, William] Massachusetts Gen Hosp, Dept Gastroenterol, Boston, MA 02114 USA.
RP Lauwers, GY (reprint author), Massachusetts Gen Hosp, Dept Pathol, Gastrointestinal Pathol Serv, 55 Fruit St,WRN 2, Boston, MA 02114 USA.
EM glauwers@partners.org
NR 22
TC 5
Z9 5
U1 1
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 MAY
PY 2011
VL 35
IS 5
BP 670
EP 677
DI 10.1097/PAS.0b013e3182127d2b
PG 8
WC Pathology; Surgery
SC Pathology; Surgery
GA 749XZ
UT WOS:000289506600006
PM 21451363
ER
PT J
AU Deshpande, V
Khosroshahi, A
Nielsen, GP
Hamilos, DL
Stone, JH
AF Deshpande, Vikram
Khosroshahi, Arezou
Nielsen, Gunnlaugur P.
Hamilos, Daniel L.
Stone, John H.
TI Eosinophilic Angiocentric Fibrosis Is a Form of IgG4-related Systemic
Disease
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE eosinophilic angiocentric fibrosis; IgG4; IgG4-related systemic disease
ID AUTOIMMUNE PANCREATITIS; GRANULOMA FACIALE; SCLEROSING DISEASE;
CLINICOPATHOLOGICAL FEATURES; MUCOSAL VARIANT; ENTITY; TRACT
AB Background: Eosinophilic angiocentric fibrosis (EAF) is an uncommon tumefactive lesion of the orbit and upper respiratory tract of unknown etiology. The condition is characterized histologically by concentric layers of fibrosis around small-caliber arteries and a mixed inflammatory infiltrate dominated by eosinophils. After the serendipitous observation of an elevated serum concentration of IgG4 in 1 patient with EAF, we investigated the hypothesis that EAF is an IgG4-related systemic disease.
Methods: We retrospectively identified 5 EAF cases from our files. Demographic, clinical, and serological data were reviewed, and the histologic features and tissue IgG4 staining patterns were examined on biopsies from each case.
Results: Patients (2 male, 3 female) ranged in age from 31 to 82 years (mean, 56 y). The extent of disease varied from isolated involvement of the nasal cavity or the lacrimal gland to multicentric disease affecting the sinuses, nasal tract, and lower respiratory tract. The duration of symptoms ranged from 6 months to > 20 years. The demographic features of the patients and disease extent were consistent with previously published reports of EAF, except for involvement of the lower respiratory tract in 1 case. Four of the 5 cases showed concentric perivascular fibrosis surrounding small-caliber vascular channels, embedded in an inflammatory infiltrate composed of lymphocytes, plasma cells, and eosinophils. One lacrimal gland biopsy showed a periductal inflammatory infiltrate, and 2 cases showed a storiform pattern of fibrosis. The index case had a serum IgG4 concentration of 1490 mg/dL (normal, 8 to 140 mg/dL). IgG4-positive plasma cells were identified in biopsies from 4 of the 5 cases. The numbers of IgG4-positive plasma cells ranged from 43 to 118 per high-power field, and the IgG4: IgG ratios ranged from 0.68 to 0.97. Neither IgG4-bearing nor IgG-bearing plasma cells were identified in 1 patient, whose longstanding disease was characterized principally by concentric perivascular fibrosis.
Conclusion: Our data suggest that EAF is part of the spectrum of IgG4-related systemic disease.
C1 [Deshpande, Vikram; Nielsen, Gunnlaugur P.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Khosroshahi, Arezou; Hamilos, Daniel L.; Stone, John H.] Massachusetts Gen Hosp, Dept Med, Div Rheumatol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
RP Deshpande, V (reprint author), Massachusetts Gen Hosp, Dept Pathol, 55 Fruit Street,Warren 2, Boston, MA 02114 USA.
EM vdeshpande@partners.org
NR 31
TC 41
Z9 43
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 MAY
PY 2011
VL 35
IS 5
BP 701
EP 706
DI 10.1097/PAS.0b013e318213889e
PG 6
WC Pathology; Surgery
SC Pathology; Surgery
GA 749XZ
UT WOS:000289506600010
PM 21502911
ER
PT J
AU Jutras-Aswad, D
Scimeca, MM
AF Jutras-Aswad, Didier
Scimeca, Michael M.
TI Buprenorphine Plasma Concentration in the Management of Opioid
Dependence
SO AMERICAN JOURNAL ON ADDICTIONS
LA English
DT Article
ID MAINTENANCE
C1 [Jutras-Aswad, Didier] Univ Montreal, Dept Psychiat, Montreal, PQ H3C 3J7, Canada.
[Jutras-Aswad, Didier; Scimeca, Michael M.] Mt Sinai Sch Med, Dept Psychiat, New York, NY USA.
[Jutras-Aswad, Didier] Univ Montreal, CRCHUM, Ctr Hosp, Montreal, PQ H3C 3J7, Canada.
RP Scimeca, MM (reprint author), James J Peters Vet Affairs Med Ctr, 130 W Kingsbridge Rd, Bronx, NY 10468 USA.
EM michael.scimeca@va.gov
NR 6
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1055-0496
J9 AM J ADDICTION
JI Am. J. Addict.
PD MAY-JUN
PY 2011
VL 20
IS 3
BP 304
EP 305
DI 10.1111/j.1521-0391.2011.00133.x
PG 2
WC Substance Abuse
SC Substance Abuse
GA 746NQ
UT WOS:000289254400017
PM 21477061
ER
PT J
AU Pai, S
Ledoux, WR
AF Pai, Shruti
Ledoux, William R.
TI The Quasi-Linear Viscoelastic Properties of Diabetic and Non-Diabetic
Plantar Soft Tissue
SO ANNALS OF BIOMEDICAL ENGINEERING
LA English
DT Article
DE Foot; Subcutaneous; Compressive; Stress relaxation; Quasi-linear;
Diabetes; Adipose; Ulcer; Viscoelastic; Heel pad
ID MEDIAL COLLATERAL LIGAMENT; AORTIC-VALVE TISSUE; MECHANICAL-PROPERTIES;
HEEL-PAD; STRESS-RELAXATION; FAT PAD; FOOT; MELLITUS; BEHAVIOR; SHEAR
AB The purpose of this study was to characterize the viscoelastic behavior of diabetic and non-diabetic plantar soft tissue at six ulcer-prone/load-bearing locations beneath the foot to determine any changes that may play a role in diabetic ulcer formation and subsequent amputation in this predisposed population. Four older diabetic and four control fresh frozen cadaveric feet were each dissected to isolate plantar tissue specimens from the hallux, first, third, and fifth metatarsals, lateral midfoot, and calcaneus. Stress relaxation experiments were used to quantify the viscoelastic tissue properties by fitting the data to the quasi-linear viscoelastic (QLV) theory using two methods, a traditional frequency-insensitive approach and an indirect frequency-sensitive approach, and by measuring several additional parameters from the raw data including the rate and amount of overall relaxation. The stress relaxation response of both diabetic and non-diabetic specimens was unexpectedly similar and accordingly few of the QLV parameters for either fit approach and none of raw data parameters differed. Likewise, no differences were found between plantar locations. The accuracy of both fit methods was comparable, however, neither approach predicted the ramp behavior. Further, fit coefficients varied considerably from one method to the other, making it hard to discern meaningful trends. Future testing using alternate loading modes and intact feet may provide more insight into the role that time-dependent properties play in diabetic foot ulceration.
C1 [Pai, Shruti; Ledoux, William R.] VA Puget Sound, VA RR&DCtr Excellence Limb Loss Prevent & Prosthe, Seattle, WA 98108 USA.
[Pai, Shruti; Ledoux, William R.] Univ Washington, Dept Mech Engn, Seattle, WA 98195 USA.
[Ledoux, William R.] Univ Washington, Dept Orthopaed & Sports Med, Seattle, WA 98195 USA.
RP Ledoux, WR (reprint author), VA Puget Sound, VA RR&DCtr Excellence Limb Loss Prevent & Prosthe, MS 151,1660 S Columbian Way, Seattle, WA 98108 USA.
EM wrledoux@u.washington.edu
RI Ledoux, William/K-6815-2015
OI Ledoux, William/0000-0003-4982-7714
FU National Institutes of Health [1R01 DK75633-03]; Department of Veterans
Affairs, RRD Service [A4843C]
FX This study was funded by the National Institutes of Health grant 1R01
DK75633-03 and the Department of Veterans Affairs, RR&D Service grant
A4843C. The authors would also like to thank Jane Shofer, M. S., for the
statistical analysis, Michael Fassbind, M. S., for equipment design, and
Paul Vawter for assisting with data analysis.
NR 46
TC 14
Z9 14
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0090-6964
EI 1573-9686
J9 ANN BIOMED ENG
JI Ann. Biomed. Eng.
PD MAY
PY 2011
VL 39
IS 5
BP 1517
EP 1527
DI 10.1007/s10439-011-0263-z
PG 11
WC Engineering, Biomedical
SC Engineering
GA 746JR
UT WOS:000289243100012
PM 21327701
ER
PT J
AU Chakraborty, N
Chang, A
Elmoazzen, H
Menze, MA
Hand, SC
Toner, M
AF Chakraborty, Nilay
Chang, Anthony
Elmoazzen, Heidi
Menze, Michael A.
Hand, Steven C.
Toner, Mehmet
TI A Spin-Drying Technique for Lyopreservation of Mammalian Cells
SO ANNALS OF BIOMEDICAL ENGINEERING
LA English
DT Article
DE Lyopreservation; Spin drying; Vitrification; Trehalose
ID DESICCATION TOLERANCE; INTRACELLULAR TREHALOSE; HYDROXYETHYL STARCH;
COATING PROCESS; STABILIZATION; VITRIFICATION; PRESERVATION; MODEL;
FILMS; REHYDRATION
AB Stabilization of cellular material in the presence of glass-forming sugars at ambient temperatures is a viable approach that has many potential advantages over current cryogenic strategies. Experimental evidence indicates the possibility to preserve biomolecules in glassy matrices of low-molecular mobility using "glass-forming" sugars like trehalose at ambient temperatures. However, when cells are desiccated in trehalose solution using passive drying techniques, a glassy skin is formed at the liquid/vapor interface of the sample. This glassy skin prevents desiccation of the sample beyond a certain level of dryness and induces non-uniformities in the final water content. Cells trapped underneath this glassy skin may degrade due to a relatively high molecular mobility in the sample. This undesirable result underscores the need for development of a uniform, fast drying technique. In the present study, we report a new technique based on the principles of "spin drying" that can effectively address these problems. Forced convective evaporation of water along with the loss of solution due to centrifugal force leads to rapid vitrification of a thin layer of trehalose containing medium that remains on top of cells attached to the spinning glass substrate. The glassy layer produced has a consistent thickness and a small "surface-area-to-volume" ratio that minimizes any non-homogeneity. Thus, the chance of entrapping cells in a high-mobility environment decreases substantially. We compared numerical predictions to experimental observations of the drying time of 0.2-0.6 M trehalose solutions at a variety of spinning speeds ranging from 1000 to 4000 rpm. The model developed here predicts the formation of sugar films with thicknesses of 200-1000 nm, which was in good agreement with experimental results. Preliminary data suggest that after spin drying cells to about 0.159 +/- A 0.09 gH(2)O/gdw (n = 11, +/- SE), more than 95% of cells were able to preserve their membrane integrity. Membrane integrity after spin drying is therefore considerably higher than what is achieved by conventional drying methods; where about 90% of cells lose membrane integrity at 0.4 gH(2)O/gdw (Acker et al. Cell Preserv. Technol. 1(2):129-140, 2002; Elliott et al. Biopreserv. Biobank. 6(4):253-260, 2009).
C1 [Chakraborty, Nilay; Chang, Anthony; Elmoazzen, Heidi; Toner, Mehmet] Harvard Univ, Sch Med, Massachusetts Gen Hosp,Shriners Burns Hosp Childr, BioMEMS Resource Ctr,Ctr Engn Med, Boston, MA 02114 USA.
[Hand, Steven C.] Louisiana State Univ, Dept Biol Sci, Div Cellular Dev & Integrat Biol, Baton Rouge, LA 70803 USA.
[Menze, Michael A.] Eastern Illinois Univ, Dept Biol Sci, Charleston, IL 61920 USA.
RP Chakraborty, N (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp,Shriners Burns Hosp Childr, BioMEMS Resource Ctr,Ctr Engn Med, 51 Blossom St, Boston, MA 02114 USA.
EM chakraborty.nilay@mgh.harvard.edu
RI Chakraborty, Nilay/C-3118-2009;
OI Menze, Michael/0000-0003-1072-5462
FU National Institutes of Health [2 RO1 DK046270-14A1]
FX We gratefully acknowledge Headway Research for partially donating the
spin drier system. This work was supported by National Institutes of
Health grant 2 RO1 DK046270-14A1.
NR 53
TC 10
Z9 10
U1 0
U2 21
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0090-6964
EI 1573-9686
J9 ANN BIOMED ENG
JI Ann. Biomed. Eng.
PD MAY
PY 2011
VL 39
IS 5
BP 1582
EP 1591
DI 10.1007/s10439-011-0253-1
PG 10
WC Engineering, Biomedical
SC Engineering
GA 746JR
UT WOS:000289243100019
PM 21293974
ER
PT J
AU Li, PY
Hu, XM
Gan, Y
Gao, YQ
Liang, WM
Chen, J
AF Li, Peiying
Hu, Xiaoming
Gan, Yu
Gao, Yanqin
Liang, Weimin
Chen, Jun
TI Mechanistic Insight into DNA Damage and Repair in Ischemic Stroke:
Exploiting the Base Excision Repair Pathway as a Model of
Neuroprotection
SO ANTIOXIDANTS & REDOX SIGNALING
LA English
DT Review
ID GLOBAL CEREBRAL-ISCHEMIA; NEURONAL CELL-DEATH; DEPENDENT PROTEIN-KINASE;
TRANSIENT FOCAL ISCHEMIA; DOUBLE-STRAND BREAKS; POLYMERASE-BETA;
OXIDATIVE STRESS; RAT-BRAIN; POLY(ADP-RIBOSE) POLYMERASE-1; GERBIL
HIPPOCAMPUS
AB Stroke is a common cause of death and serious long-term adult disability. Oxidative DNA damage is a severe consequence of oxidative stress associated with ischemic stroke. The accumulation of DNA lesions, including oxidative base modifications and strand breaks, triggers cell death in neurons and other vulnerable cell populations in the ischemic brain. DNA repair systems, particularly base excision repair, are endogenous defense mechanisms that combat oxidative DNA damage. The capacity for DNA repair may affect the susceptibility of neurons to ischemic stress and influence the pathological outcome of stroke. This article reviews the accumulated understanding of molecular pathways by which oxidative DNA damage is triggered and repaired in ischemic cells, and the potential impact of these pathways on ischemic neuronal cell death/survival. Genetic or pharmacological strategies that target the signaling molecules in DNA repair responses are promising for potential clinically effective treatment. Further understanding of mechanisms for oxidative DNA damage and its repair processes may lead to new avenues for stroke management. Antioxid. Redox Signal. 14, 1905-1918.
C1 [Li, Peiying; Hu, Xiaoming; Gan, Yu; Gao, Yanqin; Chen, Jun] Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15213 USA.
[Li, Peiying; Hu, Xiaoming; Gan, Yu; Gao, Yanqin; Chen, Jun] Univ Pittsburgh, Sch Med, Ctr Cerebrovasc Dis Res, Pittsburgh, PA 15213 USA.
[Li, Peiying; Gan, Yu; Gao, Yanqin; Liang, Weimin; Chen, Jun] Fudan Univ, Huashan Hosp, Dept Anesthesiol, State Key Lab Med Neurobiol, Shanghai 200433, Peoples R China.
[Li, Peiying; Gan, Yu; Gao, Yanqin; Liang, Weimin; Chen, Jun] Fudan Univ, Inst Brain Sci, Shanghai 200433, Peoples R China.
[Hu, Xiaoming; Chen, Jun] Vet Affairs Pittsburgh Hlth Care Syst, Ctr Geriatr Res Educ & Clin, Pittsburgh, PA USA.
RP Chen, J (reprint author), Univ Pittsburgh, Sch Med, Dept Neurol, S-507,Biomed Sci Tower, Pittsburgh, PA 15213 USA.
EM chenj2@upmc.edu
RI Gao, Yanqin/I-6790-2016
OI Gao, Yanqin/0000-0002-4915-9819
FU National Institutes of Health [NS36736, NS43802, NS45048]; Chinese
Natural Science Foundation [30772079, 30870794, 30670642]; Shanghai
Science and Technology Bureau [08410703000]; Chinese Ministry of Science
and Technology; American Heart Association [10POST4150028]
FX Jun Chen is supported by National Institutes of Health Grants NS36736,
NS43802, and NS45048. Weimin Liang is supported by the Chinese Natural
Science Foundation Grant 30772079. Yanqin Gao is supported by the
Chinese Natural Science Foundation Grants 30870794 and 30670642. Jun
Chen and Yanqin Gao are also supported by an International Collaboration
grant (08410703000) from Shanghai Science and Technology Bureau and
Special Research Funds from Chinese Ministry of Science and Technology
to State Key laboratories. Xiaoming Hu is supported by a fellowship
award (10POST4150028) from the American Heart Association. We thank
Carol Culver for editorial assistance.
NR 89
TC 14
Z9 15
U1 0
U2 5
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1523-0864
EI 1557-7716
J9 ANTIOXID REDOX SIGN
JI Antioxid. Redox Signal.
PD MAY
PY 2011
VL 14
IS 10
BP 1905
EP 1918
DI 10.1089/ars.2010.3451
PG 14
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 751NJ
UT WOS:000289624500012
PM 20677909
ER
PT J
AU Lin, J
Murrell, DF
Marinovic, B
Fivenson, D
Borradori, L
Hashimoto, T
Cianchini, G
Caux, F
Iranzo, P
Venugopal, S
Martin, L
Taylor, L
Werth, VP
AF Lin, J.
Murrell, D. F.
Marinovic, B.
Fivenson, D.
Borradori, L.
Hashimoto, T.
Cianchini, G.
Caux, F.
Iranzo, P.
Venugopal, S.
Martin, L.
Taylor, L.
Werth, V. P.
TI Photovalidation of two outcome measure instruments for pemphigus
SO AUSTRALASIAN JOURNAL OF DERMATOLOGY
LA English
DT Meeting Abstract
C1 [Lin, J.] Univ Vermont, Dept Med, Burlington, VT USA.
[Murrell, D. F.; Venugopal, S.; Martin, L.] Univ NSW, Dept Dermatol, St George Hosp, Sydney, NSW, Australia.
[Marinovic, B.] Univ Zagreb, Ctr Hosp, Univ Dept Dermatol & Venereol, Zagreb 41000, Croatia.
[Marinovic, B.] Univ Zagreb, Sch Med, Zagreb 41001, Croatia.
[Fivenson, D.] St Joseph Mercy Hosp, Div Dermatol, Dept Internal Med, Ann Arbor, MI 48104 USA.
[Borradori, L.] Univ Med Hosp Insel, Dept Dermatol, Bern, Switzerland.
[Hashimoto, T.] Kurume Univ, Sch Med, Dept Dermatol, Kurume, Fukuoka 830, Japan.
[Cianchini, G.] IRCCS, Dept Dermatol, Ist Dermopat Immacolata, Rome, Italy.
[Caux, F.] Hop Avicenne Bobigny, Serv Dermatol, Bobigny, France.
[Caux, F.] Hop Avicenne Bobigny, Ctr Reference Dermatoses Bulleuses Toxiques & Aut, Bobigny, France.
[Iranzo, P.] Univ Barcelona, Sch Med, Dept Dermatol, Hosp Clin, Barcelona, Spain.
[Taylor, L.] Univ Penn, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA.
[Werth, V. P.] Univ Penn, Dept Dermatol, Philadelphia, PA 19104 USA.
[Werth, V. P.] Philadelphia VA Med Ctr, Philadelphia, PA USA.
RI Cianchini, Giuseppe/I-8877-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0004-8380
J9 AUSTRALAS J DERMATOL
JI Australas. J. Dermatol.
PD MAY
PY 2011
VL 52
SU 1
BP 34
EP 35
PG 2
WC Dermatology
SC Dermatology
GA 749MC
UT WOS:000289470400099
ER
PT J
AU Maritz, MF
van der Watt, PJ
Holderness, N
Birrer, MJ
Leaner, VD
AF Maritz, Michelle F.
van der Watt, Pauline J.
Holderness, Nina
Birrer, Michael J.
Leaner, Virna D.
TI Inhibition of AP-1 suppresses cervical cancer cell proliferation and is
associated with p21 expression
SO BIOLOGICAL CHEMISTRY
LA English
DT Article
DE AP-1; cervical cancer; p21; Tam67
ID NEGATIVE C-JUN; NF-KAPPA-B; ANCHORAGE-INDEPENDENT GROWTH;
HUMAN-PAPILLOMAVIRUS TYPE-16; BREAST-CANCER; HUMAN KERATINOCYTES; CYCLE
PROGRESSION; EPITHELIAL-CELLS; BINDING-SITES; RAT1A CELLS
AB AP-1, a transcription factor comprised primarily of Jun and Fos family proteins, regulates genes involved in proliferation, differentiation and oncogenesis. Previous studies demonstrated that elevated expression of Jun and Fos family member proteins is associated with numerous human cancers and in cancer-relevant biological processes. In this study we used a dominant-negative mutant of c-Jun, Tam67, which interferes with the functional activity of all AP-1 complexes, to investigate the requirement of AP-1 in the proliferation and cell cycle progression of cervical cancer cells. Transient and stable expression of Tam67 in CaSki cervical cancer cells resulted in decreased AP-1 activity that correlated with a significant inhibition of cell proliferation and anchorage-independent colony formation. Inhibiting AP-1 activity resulted in a two-fold increase in cells located in the G(2)/M phase of the cell cycle and an accompanying increase in the expression of the cell cycle regulatory protein, p21. The increase in p21 was associated with a decrease in HPV E6 expression and an increase in p53. Importantly, blocking the induction of p21 in CaSki-Tam67-expressing cells accelerated their proliferation rate to that of CaSki, implicating p21 as a key player in the growth arrest induced by Tam67. Our results suggest a role for AP-1 in the proliferation, G(2)/M progression and inhibition of p21 expression in cervical cancer.
C1 [Maritz, Michelle F.; van der Watt, Pauline J.; Holderness, Nina; Leaner, Virna D.] Univ Cape Town, Inst Infect Dis & Mol Med, Fac Hlth Sci, Div Med Biochem, ZA-7700 Rondebosch, South Africa.
[Birrer, Michael J.] Harvard Univ, Massachusetts Gen Hosp, Gillette Ctr Gynecol Oncol, Sch Med,Gynecol Canc Res Program, Boston, MA 02114 USA.
RP Leaner, VD (reprint author), Univ Cape Town, Inst Infect Dis & Mol Med, Fac Hlth Sci, Div Med Biochem, ZA-7700 Rondebosch, South Africa.
EM Virna.Leaner@uct.ac.za
FU University of Cape Town; Carnegie Corporation of New York; Medical
Research Council of South Africa; CANSA
FX This work was supported by grants from the University of Cape Town, the
Carnegie Corporation of New York, the Medical Research Council of South
Africa and CANSA.
NR 51
TC 7
Z9 8
U1 1
U2 8
PU WALTER DE GRUYTER & CO
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1431-6730
J9 BIOL CHEM
JI Biol. Chem.
PD MAY
PY 2011
VL 392
IS 5
BP 439
EP 448
DI 10.1515/BC.2011.036
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 747TR
UT WOS:000289343100006
PM 21417953
ER
PT J
AU Seidman, LJ
Biederman, J
Liang, LC
Valera, EM
Monuteaux, MC
Brown, A
Kaiser, J
Spencer, T
Faraone, SV
Makris, N
AF Seidman, Larry J.
Biederman, Joseph
Liang, Lichen
Valera, Eve M.
Monuteaux, Michael C.
Brown, Ariel
Kaiser, Jonathan
Spencer, Thomas
Faraone, Stephen V.
Makris, Nikos
TI Gray Matter Alterations in Adults with Attention-Deficit/Hyperactivity
Disorder Identified by Voxel Based Morphometry
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Attention-deficit/hyperactivity disorder; caudate; cerebellum;
prefrontal cortex; structural MRI; voxel based morphometry
ID DEFICIT HYPERACTIVITY DISORDER; ANATOMICALLY SPECIFIED METHOD; ANTERIOR
CINGULATE CORTEX; AGE-DEPENDENT DECLINE; FUNCTIONAL NEUROANATOMY;
SUBTHRESHOLD DIAGNOSES; LEARNING-DISABILITIES; VALID DIAGNOSIS;
WORKING-MEMORY; BASAL GANGLIA
AB Background: Gray and white matter volume deficits have been reported in many structural magnetic resonance imaging (MRI) studies of children with attention-deficit/hyperactivity disorder (ADHD); however, there is a paucity of structural MRI studies of adults with ADHD. This study used voxel based morphometry and applied an a priori region of interest approach based on our previous work, as well as from well-developed neuroanatomical theories of ADHD.
Methods: Seventy-four adults with DSM-IV ADHD and 54 healthy control subjects comparable on age, sex, race, handedness, IQ, reading achievement, frequency of learning disabilities, and whole brain volume had an MRI on a 1.5T Siemens scanner. A priori region of interest hypotheses focused on reduced volumes in ADHD in dorsolateral prefrontal cortex, anterior cingulate cortex, caudate, putamen, inferior parietal lobule, and cerebellum. Analyses were carried out by FSL-VBM 1.1.
Results: Relative to control subjects, ADHD adults had significantly smaller gray matter volumes in parts of six of these regions at p <= .01, whereas parts of the dorsolateral prefrontal cortex and inferior parietal lobule were significantly larger in ADHD at this threshold. However, a number of other regions were smaller and larger in ADHD (especially fronto-orbital cortex) at this threshold. Only the caudate remained significantly smaller at the family-wise error rate.
Conclusions: Adults with ADHD have subtle volume reductions in the caudate and possibly other brain regions involved in attention and executive control supporting frontostriatal models of ADHD. Modest group brain volume differences are discussed in the context of the nature of the samples studied and voxel based morphometry methodology.
C1 [Seidman, Larry J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat,Clin & Res Program Pediat Psychopha, Boston, MA 02114 USA.
[Seidman, Larry J.] Beth Israel Deaconess Med Ctr, Massachusetts Mental Hlth Ctr, Publ Psychiat Div, Boston, MA 02215 USA.
[Seidman, Larry J.; Biederman, Joseph; Valera, Eve M.; Monuteaux, Michael C.; Brown, Ariel; Spencer, Thomas; Faraone, Stephen V.; Makris, Nikos] Massachusetts Gen Hosp, Neuroimaging Program, Clin Program Pediat Psychopharmacol & Adult Atten, Boston, MA 02114 USA.
[Seidman, Larry J.; Biederman, Joseph; Valera, Eve M.; Monuteaux, Michael C.; Brown, Ariel; Spencer, Thomas; Faraone, Stephen V.; Makris, Nikos] Massachusetts Gen Hosp, Res Program Pediat Psychopharmacol & Adult Attent, Boston, MA 02114 USA.
[Seidman, Larry J.; Valera, Eve M.; Makris, Nikos] Harvard Univ, Sch Med, Martinos Ctr Biomed Imaging, MIT, Charlestown, MA USA.
[Seidman, Larry J.; Valera, Eve M.; Makris, Nikos] Massachusetts Gen Hosp, Charlestown, MA USA.
[Liang, Lichen; Kaiser, Jonathan; Makris, Nikos] Harvard Univ, Dept Neurol, Sch Med, Ctr Morphometr Anal,Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Liang, Lichen; Kaiser, Jonathan; Makris, Nikos] Harvard Univ, Dept Radiol Serv, Sch Med, Ctr Morphometr Anal,Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Brown, Ariel] MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA.
[Faraone, Stephen V.] SUNY Upstate Med Univ, Dept Psychiat, Syracuse, NY USA.
[Faraone, Stephen V.] SUNY Upstate Med Univ, Dept Neurosci & Physiol, Syracuse, NY USA.
RP Seidman, LJ (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat,Clin & Res Program Pediat Psychopha, Fruit St,Warren 7, Boston, MA 02114 USA.
EM lseidman@bidmc.harvard.edu
OI Faraone, Stephen/0000-0002-9217-3982
FU National Institute of Mental Health (NIMH) [MH/HD 62152]; March of Dimes
Foundation; Mental Illness and Neuroscience Discovery Institute;
Common-wealth Research Center of the Massachusetts Department of Mental
Health; National Research Service [NIMH F32 MH065040-01A1]; Harvard
Medical School Department of Psychiatry; Clinical Research Training
Program [MH 16259, MH 071535]; National Alliance for Research on
Schizophrenia and Depression Distinguished Investigator Award; Johnson
and Johnson Center; National Center for Research Resources [P41RR14075];
Janssen Pharmaceuticals; Alza; AstraZeneca; Bristol-Myers Squibb; Eli
Lilly and Co.; Janssen Pharmaceuticals Inc.; McNeil; Merck; Organon;
Otsuka; Shire; National Institute of Child Health and Human Development;
Abbott; Celltech; Cephalon; Eisai; Forest; Glaxo; Gliatech; Janssen;
National Alliance for Research on Schizophrenia and Depression; National
Institute on Drug Abuse; New River; Novartis; Noven; Neurosearch;
Pfizer; Pharmacia; Prechter Foundation; Stanley Foundation; UCB Pharma
Inc.; Wyeth; National Institutes of Health
FX This work was supported in part by National Institute of Mental Health
(NIMH) MH/HD 62152, the March of Dimes Foundation, the Mental Illness
and Neuroscience Discovery Institute, and the Common-wealth Research
Center of the Massachusetts Department of Mental Health (to LJS);
National Research Service Award (NIMH F32 MH065040-01A1), Peter
Livingston Fellowship through the Harvard Medical School Department of
Psychiatry, and the Clinical Research Training Program Fellowship in
Biological and Social Psychiatry MH 16259 and MH 071535 (to EMV); NIMH
MH57934 (to SVF); the National Alliance for Research on Schizophrenia
and Depression Distinguished Investigator Award and the Johnson and
Johnson Center for the Study of Psychopathology (to JB); and The
National Center for Research Resources (P41RR14075). These 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.; Dr. Larry J. Seidman reports no financial
disclosures or conflicts of interest for the past 2 years. He has been a
speaker for Shire Pharmaceuticals and received an unrestricted
educational grant from Janssen Pharmaceuticals in the past 5 years. Dr.
Joseph Biederman is currently receiving research support from the
following sources: Alza, AstraZeneca, Bristol-Myers Squibb, Eli Lilly
and Co., Janssen Pharmaceuticals Inc., McNeil, Merck, Organon, Otsuka,
Shire, NIMH, and National Institute of Child Health and Human
Development. In 2009, Dr. Joseph Biederman received a speaker's fee from
the following sources: Fundacion Areces, Medice Pharmaceuticals, and the
Spanish Child Psychiatry Association. In previous years, Dr. Joseph
Biederman received research support, consultation fees, or speaker's
fees for/from the following additional sources: Abbott, AstraZeneca,
Celltech, Cephalon, Eli Lilly and Co., Eisai, Forest, Glaxo, Gliatech,
Janssen, McNeil, National Alliance for Research on Schizophrenia and
Depression, National Institute on Drug Abuse, New River, Novartis,
Noven, Neurosearch, Pfizer, Pharmacia, The Prechter Foundation, Shire,
The Stanley Foundation, UCB Pharma Inc., and Wyeth. Dr. Eve M. Valera
has received travel support and honoraria from Shire Pharmaceuticals and
the McNeil and Janssen divisions of Ortho-McNeil-Janssen
Pharmaceuticals. Dr. Thomas Spencer has received research support from,
has been a speaker on a speaker bureau, or has been on an advisory board
of the following sources: Shire Laboratories Inc., Eli Lilly and
Company, GlaxoSmith-Kline, Janssen Pharmaceutical, McNeil
Pharmaceutical, Novartis Pharmaceuticals, Cephalon, Pfizer, and the
National Institute of Mental Health. In the past year, Dr. Stephen
Faraone has received consulting fees and has been on advisory boards for
Eli Lilly, McNeil, and Shire and has received research support from Eli
Lilly, Pfizer, Shire, and the National Institutes of Health. In previous
years, Dr. Faraone has received consulting fees, has been on advisory
boards, or has been a speaker for the following sources: Shire, McNeil,
Janssen, Novartis, Pfizer, and Eli Lilly. In previous years, he has
received research support from Eli Lilly, Shire, Pfizer, and the
National Institutes of Health. All other authors report no biomedical
financial interests or potential conflicts of interest.
NR 85
TC 60
Z9 62
U1 2
U2 25
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 MAY 1
PY 2011
VL 69
IS 9
BP 857
EP 866
DI 10.1016/j.biopsych.2010.09.053
PG 10
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 750PI
UT WOS:000289560100011
PM 21183160
ER
PT J
AU Bush, D
Smith, B
Younger, J
Michaelson, JS
AF Bush, Devon
Smith, Barbara
Younger, Jerry
Michaelson, James S.
TI The non-breast-cancer death rate among breast cancer patients
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Breast cancer; Non-cancer death; Radiation oncology; Survival; Trends;
Cardiotoxicity; Side effects; Mortality
ID HEART-DISEASE; RANDOMIZED-TRIALS; RADIATION-THERAPY; HEALTH BEHAVIORS;
MORTALITY; RADIOTHERAPY; SURVIVORS; RISK; COHORT; DIAGNOSIS
AB Non-breast-cancer deaths currently account for almost half of deaths among breast carcinoma patients in the 15 years following diagnosis. Understanding the trends of non-breast-cancer death is vital for calibrating treatment and survival expectations, and for understanding the consequences of potentially toxic therapies. To observe trends over time in non-breast-cancer relative survival-the non-breast-cancer survival rates of breast cancer patients relative to the non-breast-cancer survival rates of the population as a whole, matched for gender, race, age, region, and year of diagnosis. Non-breast-cancer relative survival between breast carcinoma patients and the general population was measured using SEER public-use data of patients diagnosed with breast carcinoma between 1973 and 2007. Non-breast-cancer relative survival improved significantly from 1973 to the present. From 1986 onward, the non-breast-cancer survival rate among breast carcinoma patients is equal to, or slightly higher than, matched populations who did not have breast carcinoma. This improvement over time occurred across almost all patient stratifications, including race, age, tumor size, and nodal status. However, patients receiving full mastectomies, and patients not receiving radiotherapy experienced no increase in relative survival. The most dramatic relative survival improvements occurred in patients who received radiation and patients receiving partial mastectomies, and such improvements were seen even after controlling for changes in tumor size over time. Non-breast-cancer relative survival among breast carcinoma patients has improved significantly since 1973; breast cancer patients are currently no more likely to die of other causes than the general population.
C1 [Michaelson, James S.] Massachusetts Gen Hosp, Lab Quantitat Med, Cambridge, MA 02139 USA.
[Smith, Barbara; Younger, Jerry; Michaelson, James S.] Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA.
[Michaelson, James S.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Younger, Jerry] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[Bush, Devon; Smith, Barbara; Younger, Jerry; Michaelson, James S.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Michaelson, James S.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Younger, Jerry] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
RP Michaelson, JS (reprint author), Massachusetts Gen Hosp, Lab Quantitat Med, Partners Res Bldg,65 Landsdowne St,Suite 205 A, Cambridge, MA 02139 USA.
EM michaelj@helix.mgh.harvard.edu
FU Department of Surgical Oncology at Massachusetts General Hospital
FX Work in this paper was supported through funds from the Department of
Surgical Oncology at Massachusetts General Hospital.
NR 30
TC 6
Z9 6
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
EI 1573-7217
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD MAY
PY 2011
VL 127
IS 1
BP 243
EP 249
DI 10.1007/s10549-010-1186-3
PG 7
WC Oncology
SC Oncology
GA 747DL
UT WOS:000289300400028
PM 20927583
ER
PT J
AU Niles, J
AF Niles, J.
TI Rituximab in induction therapy for anti-neutrophil cytoplasmic antibody
(ANCA) vasculitis
SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY
LA English
DT Article; Proceedings Paper
CT 15th International Vasculitis/ANCA Workshop
CY MAY 15-18, 2011
CL Chapel Hill, NC
DE ANCA; ANCA-associated vasculitis; rituximab
ID RHEUMATOID-ARTHRITIS; ANTIMYELOPEROXIDASE ANTIBODIES;
WEGENERS-GRANULOMATOSIS; RENAL VASCULITIS; GLOMERULONEPHRITIS;
AUTOANTIBODIES; NEUTROPHILS; SAFETY; TRIAL; CYCLOPHOSPHAMIDE
AB Anti-neutrophil cytoplasmic antibodies (ANCA) have been associated with a spectrum of vasculitis that includes granulomatous polyangiitis (formerly known as Wegener's granulomatosis), microscopic polyangiitis, the Churg-Strauss syndrome, primary pauciimmune necrotizing and crescentic glomerulonephritis and related forms of vasculitis. In vitro, in vivo and clinical evidence support the conclusion that ANCA participate in the pathophysiology of this disease spectrum. Rituximab is a potent tool that can interrupt B cell-mediated immunity without major compromise of T cell-mediated immunity. Thus, it has great appeal as a tool to interrupt antibody-mediated autoimmune disease. The results of two prospective randomized trials confirm that rituximab can be effective as part of induction therapy for active ANCA-associated vasculitis. The safety profile for rituximab appears favourable relative to cyclophosphamide and steroids. However, there remain many patients who require individualized adjustments of ancillary therapy, as breakthrough disease, relapses and infectious complications do occur. Based on our current knowledge, rituximab should now be incorporated as part of induction therapy in many patients with ANCA-associated vasculitis. However, more work is needed to determine how rituximab may best be integrated into the overall immunosuppression of these patients.
C1 [Niles, J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Niles, J (reprint author), 149 13th St, Charlestown, MA 02129 USA.
EM jlniles@partners.org
NR 27
TC 7
Z9 9
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0009-9104
J9 CLIN EXP IMMUNOL
JI Clin. Exp. Immunol.
PD MAY
PY 2011
VL 164
SU 1
BP 27
EP 30
DI 10.1111/j.1365-2249.2011.04363.x
PG 4
WC Immunology
SC Immunology
GA 748RT
UT WOS:000289409300009
PM 21447128
ER
PT J
AU Niles, J
McGrath, M
Laliberte, K
AF Niles, John
McGrath, Martina
Laliberte, Karen
TI Continuous RTX therapy for ANCA-AAV
SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY
LA English
DT Meeting Abstract
CT 15th International Vasculitis/ANCA Workshop
CY MAY 15-18, 2011
CL Chapel Hill, NC
C1 [Niles, John; McGrath, Martina; Laliberte, Karen] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 5
Z9 5
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0009-9104
J9 CLIN EXP IMMUNOL
JI Clin. Exp. Immunol.
PD MAY
PY 2011
VL 164
SU 1
BP 62
EP 62
PG 1
WC Immunology
SC Immunology
GA 748RT
UT WOS:000289409300060
ER
PT J
AU Specks, U
Stone, JH
AF Specks, Ulrich
Stone, John H.
CA RAVE-ITN Res Grp
TI Long-term efficacy and safety results of the RAVE trial
SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY
LA English
DT Meeting Abstract
CT 15th International Vasculitis/ANCA Workshop
CY MAY 15-18, 2011
CL Chapel Hill, NC
C1 [Specks, Ulrich] Mayo Clin, Rochester, MN USA.
[Stone, John H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 17
Z9 18
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0009-9104
J9 CLIN EXP IMMUNOL
JI Clin. Exp. Immunol.
PD MAY
PY 2011
VL 164
SU 1
BP 65
EP 65
PG 1
WC Immunology
SC Immunology
GA 748RT
UT WOS:000289409300066
ER
PT J
AU Tomasson, G
Boers, M
Walsh, M
Cuthbertson, D
Carette, S
Davis, JC
Hoffman, GS
Khalidi, NA
Langford, CA
McAlear, CA
McCune, WJ
Monach, PA
Seo, P
Specks, U
Spiera, R
St Clair, EW
Stone, JH
Ytterberg, SR
Merkel, PA
AF Tomasson, Gunnar
Boers, Maarten
Walsh, Michael
Cuthbertson, David
Carette, Simon
Davis, John C.
Hoffman, Gary S.
Khalidi, Nader A.
Langford, Carol A.
McAlear, Carol A.
McCune, W. Joseph
Monach, Paul A.
Seo, Philip
Specks, Ulrich
Spiera, Robert
St Clair, E. William
Stone, John H.
Ytterberg, Steven R.
Merkel, Peter A.
TI Measurement of health-related quality of life among patients with
ANCA-AAV using the SF-36
SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY
LA English
DT Meeting Abstract
CT 15th International Vasculitis/ANCA Workshop
CY MAY 15-18, 2011
CL Chapel Hill, NC
C1 [Tomasson, Gunnar; McAlear, Carol A.; Monach, Paul A.; Merkel, Peter A.] Boston Univ, Boston, MA 02215 USA.
[Boers, Maarten] Vrije Univ Amsterdam Med Ctr, Amsterdam, Netherlands.
[Walsh, Michael; Khalidi, Nader A.] McMaster Univ, Hamilton, ON, Canada.
[Cuthbertson, David] Univ S Florida, Tampa, FL USA.
[Carette, Simon] Univ Toronto, Toronto, ON, Canada.
[Davis, John C.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Hoffman, Gary S.; Langford, Carol A.] Cleveland Clin, Cleveland, OH 44106 USA.
[McCune, W. Joseph] Univ Michigan, Ann Arbor, MI 48109 USA.
[Seo, Philip] Johns Hopkins Univ, Baltimore, MD USA.
[Specks, Ulrich; Ytterberg, Steven R.] Mayo Clin, Rochester, MN USA.
[Spiera, Robert] Hosp Special Surg, New York, NY 10021 USA.
[St Clair, E. William] Duke Univ, Durham, NC USA.
[Stone, John H.] 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 0009-9104
J9 CLIN EXP IMMUNOL
JI Clin. Exp. Immunol.
PD MAY
PY 2011
VL 164
SU 1
BP 83
EP 83
PG 1
WC Immunology
SC Immunology
GA 748RT
UT WOS:000289409300100
ER
PT J
AU Monach, PA
Tomasson, G
Specks, U
Stone, J
Cuthbertson, D
Ding, L
Fervenza, F
Fessler, B
Hoffman, GS
Ikle, D
Kallenberg, C
Krischer, J
Langford, C
Mueller, M
Seo, P
St Clair, EW
Spiera, R
Tchao, N
Ytterberg, S
Merkel, PA
AF Monach, Paul A.
Tomasson, Gunnar
Specks, Ulrich
Stone, John
Cuthbertson, David
Ding, Linna
Fervenza, Fernando
Fessler, Barri
Hoffman, Gary S.
Ikle, David
Kallenberg, Cees
Krischer, Jeffrey
Langford, Carol
Mueller, Mark
Seo, Phillip
St Clair, E. William
Spiera, Robert
Tchao, Nadia
Ytterberg, Steven
Merkel, Peter A.
TI Circulating markers of vascular injury and angiogenesis in ANCA-AAV
SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY
LA English
DT Meeting Abstract
CT 15th International Vasculitis/ANCA Workshop
CY MAY 15-18, 2011
CL Chapel Hill, NC
C1 [Monach, Paul A.; Tomasson, Gunnar; Merkel, Peter A.] Boston Univ, Boston, MA 02215 USA.
[Specks, Ulrich; Fervenza, Fernando; Ytterberg, Steven] Mayo Clin, Rochester, MN USA.
[Stone, John] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Cuthbertson, David; Krischer, Jeffrey] Univ S Florida, Tampa, FL USA.
[Ding, Linna] NIAID, Bethesda, MD 20892 USA.
[Fessler, Barri] Univ Alabama Birmingham, Birmingham, AL USA.
[Hoffman, Gary S.; Langford, Carol] Cleveland Clin, Cleveland, OH 44106 USA.
[Kallenberg, Cees] Univ Groningen, Univ Med Ctr Groningen, NL-9713 AV Groningen, Netherlands.
[Mueller, Mark; Tchao, Nadia] Immune Tolerance Network, Seattle, WA USA.
[Seo, Phillip] Johns Hopkins Univ, Baltimore, MD USA.
[St Clair, E. William] Duke Univ, Durham, NC USA.
[Spiera, Robert] Hosp Special Surg, New York, NY 10021 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0009-9104
J9 CLIN EXP IMMUNOL
JI Clin. Exp. Immunol.
PD MAY
PY 2011
VL 164
SU 1
BP 92
EP 93
PG 2
WC Immunology
SC Immunology
GA 748RT
UT WOS:000289409300118
ER
PT J
AU Nelson, DR
Hummel, AM
Silva, F
Schroeder, D
Stone, JH
Hoffman, GS
Merkel, PA
Monach, PA
Spiera, RF
St Clair, EW
Davis, JC
McCune, WJ
Kelley, JM
Edberg, JC
Kimberly, RP
Specks, U
AF Nelson, Darlene R.
Hummel, Amber M.
Silva, Francisco
Schroeder, Darrell
Stone, John H.
Hoffman, Gary S.
Merkel, Peter A.
Monach, Paul A.
Spiera, Robert F.
St Clair, E. William
Davis, John C., Jr.
McCune, W. Joseph
Kelley, James M.
Edberg, Jeffrey C.
Kimberly, Robert P.
Specks, Ulrich
TI IgA-ANCA in WG
SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY
LA English
DT Meeting Abstract
CT 15th International Vasculitis/ANCA Workshop
CY MAY 15-18, 2011
CL Chapel Hill, NC
C1 [Nelson, Darlene R.; Hummel, Amber M.; Silva, Francisco; Schroeder, Darrell; Specks, Ulrich] Mayo Clin, Rochester, MN USA.
[Silva, Francisco] Pontificia Univ Catolica Chile, Santiago, Chile.
[Stone, John H.] Johns Hopkins Univ, Baltimore, MD USA.
[Stone, John H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Hoffman, Gary S.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Merkel, Peter A.; Monach, Paul A.] Boston Univ, Boston, MA 02215 USA.
[Spiera, Robert F.] Hosp Special Surg, New York, NY 10021 USA.
[St Clair, E. William] Duke Univ, Durham, NC USA.
[Davis, John C., Jr.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[McCune, W. Joseph] Univ Michigan, Ann Arbor, MI 48109 USA.
[Kelley, James M.; Edberg, Jeffrey C.; Kimberly, Robert P.] Univ Alabama, Birmingham, AL USA.
[Kelley, James M.] Brigham & Womens Hosp, Boston, MA 02115 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 0009-9104
J9 CLIN EXP IMMUNOL
JI Clin. Exp. Immunol.
PD MAY
PY 2011
VL 164
SU 1
BP 94
EP 94
PG 1
WC Immunology
SC Immunology
GA 748RT
UT WOS:000289409300120
ER
PT J
AU Kim, JY
Kamis, IK
Singh, B
Batra, S
Dixon, RH
Dighe, AS
AF Kim, Ji Yeon
Kamis, Irina K.
Singh, Balaji
Batra, Shalini
Dixon, Roberta H.
Dighe, Anand S.
TI Implementation of computerized add-on testing for hospitalized patients
in a large academic medical center
SO CLINICAL CHEMISTRY AND LABORATORY MEDICINE
LA English
DT Article
DE clinical chemistry; laboratory management; order entry
ID PHYSICIAN ORDER-ENTRY; INTENSIVE-CARE; IMPACT; PHLEBOTOMY; SYSTEM;
SERVICES; SAFETY
AB Background: Physician requests for additional testing on an existing laboratory specimen (add-ons) are resource intensive and generally require a phone call to the laboratory. Verbal orders such as these have been noted to be associated with errors in accuracy. The aim of this study was to compare a novel computerized system for add-on requests to the prior verbal system.
Method: We compare the computerized add-on request system to the verbal system with respect to order completeness and workflow.
Results: We demonstrate that the computerized add-on system resulted in the complete in-laboratory documentation of the add-on request 100% of the time, compared to 58% with the verbal add-on system. In addition, we show that documentation of a verbal add-on request in the electronic medical record (EMR) occurred for 4% of requests, while in the computerized system EMR documentation occurred 100% of the time. We further demonstrate that the computerized add-on request process was well accepted by providers and did not significantly change the test mix of the add-on requests.
Conclusions: In computerized physician order entry (CPOE) implementations, add-on order functionality should be considered so these orders are documented in the EMR.
C1 [Kim, Ji Yeon; Dighe, Anand S.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Kamis, Irina K.; Singh, Balaji; Batra, Shalini; Dixon, Roberta H.] Partners HealthCare Syst Inc, Dept Informat Syst, Constitut Ctr 1, Charlestown, MA USA.
RP Dighe, AS (reprint author), Massachusetts Gen Hosp, Dept Pathol, Bigelow Bldg,Room 510,55 Fruit St, Boston, MA 02114 USA.
EM asdighe@partners.org
NR 19
TC 5
Z9 5
U1 0
U2 2
PU WALTER DE GRUYTER & CO
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1434-6621
J9 CLIN CHEM LAB MED
JI Clin. Chem. Lab. Med.
PD MAY
PY 2011
VL 49
IS 5
BP 845
EP 850
DI 10.1515/CCLM.2011.140
PG 6
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 749KS
UT WOS:000289465700013
PM 21303296
ER
PT J
AU Wu, YC
Rosenberg, JE
Taplin, ME
AF Wu, Yichao
Rosenberg, Jonathan E.
Taplin, Mary-Ellen
TI Novel agents and new therapeutics in castration-resistant prostate
cancer
SO CURRENT OPINION IN ONCOLOGY
LA English
DT Review
DE abiraterone acetate; cabazitaxel; castration-resistant prostate cancer;
immunotherapy; intermittent androgen deprivation therapy; MDV3100
ID ANDROGEN-DEPRIVATION THERAPY; INHIBITOR ABIRATERONE ACETATE; I
CLINICAL-TRIAL; LEUKEMIA GROUP-B; PHASE-I; SIPULEUCEL-T;
ANTITUMOR-ACTIVITY; PLUS PREDNISONE; DOCETAXEL; MEN
AB Purpose of review
This review highlights recent therapeutic advances in systemic therapies for prostate cancer (PCa).
Recent findings
Progress in PCa therapeutics has been made during the past year with the approval of a vaccine therapy, second-line chemotherapy, and reported survival advantage for a CYP (17,20) lyase inhibitor in castration-resistant prostate cancer (CRPC). This report will summarize the recently reported and expected data for PCa trials including an evaluation of intermittent vs. continuous androgen deprivation therapy. Denosumab is shown to support bone mineral density in hormonal sensitive PCa patients. Targeting of androgen-dependent pathways in CRPC postchemotherapy has been shown to improve survival with the lyase inhibitor abiraterone, and lead to prostate-specific antigen and objective responses with an androgen receptor antagonist (MDV3100). However, the addition of bevacizumab to docetaxel/prednisone in treating metastatic CRPC failed to provide a survival benefit. Cabazitaxel in metastatic CRPC postdocetaxel did demonstrate a survival benefit. Provenge, an autologous dendritic cell-based vaccine, demonstrated a reduction in the risk of death in metastatic CRPC. Other immunotherapy agents, including Prostvac and ipilimumab are under investigation. We also discuss the receptor tyrosine kinase inhibitor XL184 and poly (ADP-ribose) polymerase inhibitors which are in early clinical trials.
Summary
Recent advances in androgen targeting, chemotherapy, immunotherapy, and other targeted therapies have led to significant improvements in the care of CRPC patients.
C1 [Wu, Yichao; Rosenberg, Jonathan E.; Taplin, Mary-Ellen] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02215 USA.
RP Taplin, ME (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02215 USA.
EM Mary_Taplin@dfci.harvard.edu
NR 45
TC 18
Z9 18
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-8746
J9 CURR OPIN ONCOL
JI Curr. Opin. Oncol.
PD MAY
PY 2011
VL 23
IS 3
BP 290
EP 296
DI 10.1097/CCO.0b013e3283449400
PG 7
WC Oncology
SC Oncology
GA 749YM
UT WOS:000289507900010
PM 21311328
ER
PT J
AU Hazin, R
Barazi, MK
Summerfield, M
AF Hazin, Ribhi
Barazi, Mohammed K.
Summerfield, Michael
TI Challenges to establishing nationwide diabetic retinopathy screening
programs
SO CURRENT OPINION IN OPHTHALMOLOGY
LA English
DT Article
DE diabetic retinopathy; macular edema; photocoagulation; retinal
screening; screening; telemedicine; teleophthalmology
ID UNITED-STATES; MACULAR EDEMA; FUNDUS PHOTOGRAPHY; AFRICAN-AMERICANS; EYE
CARE; PHOTOCOAGULATION; PREVALENCE; MELLITUS; ADULTS; OPHTHALMOLOGY
AB Purpose of review
To review the results of recently published studies on diabetic retinopathy screening.
Recent findings
Despite numerous public health campaigns and the existence of guidelines designed to promote annual retinal exams for diabetes patients, an unacceptably high number of patients are not screened for diabetic retinopathy. Current findings suggest the need for novel methods to improve compliance with retinal screening exams among diabetes patients to preserve vision functionality in this population.
Summary
Diabetic retinopathy represents a major cause of acquired vision loss. The following review addresses the factors that contribute to inadequate retinopathy screenings among diabetes patients and proposes solutions that have the potential to increase the quality and accessibility of screening programs for diabetes patients.
C1 [Summerfield, Michael] Georgetown Univ, Washington Hosp Ctr, Washington, DC 20057 USA.
[Hazin, Ribhi] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA USA.
[Barazi, Mohammed K.] Retina Grp Washington, Washington, DC USA.
RP Summerfield, M (reprint author), Georgetown Univ, Washington Hosp Ctr, Washington, DC 20057 USA.
EM michaelsummerfield@hotmail.com
NR 54
TC 10
Z9 10
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-8738
EI 1531-7021
J9 CURR OPIN OPHTHALMOL
JI Curr. Opin. Ophthalmol.
PD MAY
PY 2011
VL 22
IS 3
BP 174
EP 179
DI 10.1097/ICU.0b013e32834595e8
PG 6
WC Ophthalmology
SC Ophthalmology
GA 749YQ
UT WOS:000289508400006
PM 21460726
ER
PT J
AU Hivert, MF
Sullivan, LM
Shrader, P
Fox, CS
Nathan, DM
D'Agostino, RB
Wilson, PWF
Kowall, B
Herder, C
Meisinger, C
Thorand, B
Rathmann, W
Meigs, JB
AF Hivert, M. -F.
Sullivan, L. M.
Shrader, P.
Fox, C. S.
Nathan, D. M.
D'Agostino, R. B., Sr.
Wilson, P. W. F.
Kowall, B.
Herder, C.
Meisinger, C.
Thorand, B.
Rathmann, W.
Meigs, J. B.
TI Insulin resistance influences the association of adiponectin levels with
diabetes incidence in two population-based cohorts: the Cooperative
Health Research in the Region of Augsburg (KORA) S4/F4 study and the
Framingham Offspring Study
SO DIABETOLOGIA
LA English
DT Article
DE Adiponectin; Insulin resistance; Diabetes incidence; Prospective cohorts
ID PLASMA ADIPONECTIN; TYPE-2; RISK; GLUCOSE
AB Lower adiponectin levels are associated with higher risk of incident type 2 diabetes. Most analyses have been adjusted for confounding factors, but few have taken into account insulin resistance per se. We tested the hypothesis that the association of adiponectin levels with incident type 2 diabetes differs between insulin-resistant and insulin-sensitive individuals.
We studied two prospective cohorts: the Framingham Offspring Study (n = 2,023) and the Cooperative Health Research in the Region of Augsburg (KORA) S4/F4 study (n = 887) cohorts. Insulin resistance was estimated by HOMA-insulin resistance (HOMA-IR). We used logistic regression analysis to test the association between adiponectin and incident type 2 diabetes overall and in insulin-resistant vs insulin-sensitive individuals (defined by a parts per thousand yen vs < 75th percentile of HOMA-IR).
At baseline, Framingham's participants were 60 +/- 9 years old and 56% were women; KORA's participants were 63 +/- 5 years old and 49% were women. Type 2 diabetes incidence was 5.4% over 6.5 years (n = 109) in Framingham and 10.5% over 8 years (n = 93) in KORA. Lower adiponectin levels were associated with type 2 diabetes incidence in both cohorts. In insulin-resistant individuals, lower adiponectin levels were associated with higher risk of type 2 diabetes incidence (OR 1.60 [95% CI 1.10-2.31] per SD decrease in Framingham, p = 0.01; and OR 2.34 [95% CI 1.16-4.73] in KORA, p = 0.02); while this was not observed in insulin-sensitive individuals (OR 1.10 [95% CI 0.73-1.67] in Framingham, p = 0.64; and OR 1.34 [95%CI: 0.88-2.03] in KORA, p = 0.18).
We conclude that lower adiponectin levels are associated with higher risk of type 2 diabetes in insulin-resistant but not in insulin-sensitive individuals. This suggests that some level of insulin resistance is needed to see deleterious effects of low adiponectin.
C1 [Hivert, M. -F.; Shrader, P.; Meigs, J. B.] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[Hivert, M. -F.; Nathan, D. M.; Meigs, J. B.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Sullivan, L. M.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Fox, C. S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Fox, C. S.] Brigham & Womens Hosp, Dept Endocrinol & Metab, Boston, MA 02115 USA.
[Nathan, D. M.] Massachusetts Gen Hosp, Dept Med, Ctr Diabet, Boston, MA 02114 USA.
[D'Agostino, R. B., Sr.] Boston Univ, Dept Math & Stat, Consulting Unit, Boston, MA 02215 USA.
[Wilson, P. W. F.] Emory Univ, Sch Med, Emory Clin Cardiovasc Res Inst, Atlanta, GA USA.
[Kowall, B.; Rathmann, W.] Univ Dusseldorf, German Diabet Ctr, Leibniz Ctr Diabet Res, Inst Biometr & Epidemiol, Dusseldorf, Germany.
[Herder, C.] Univ Dusseldorf, German Diabet Ctr, Leibniz Ctr Diabet Res, Inst Clin Diabetol, Dusseldorf, Germany.
[Meisinger, C.; Thorand, B.] Helmholtz Zentrum Munchen, Inst Epidemiol 2, Neuherberg, Germany.
RP Meigs, JB (reprint author), Massachusetts Gen Hosp, Div Gen Med, 50 Staniford St,9th Floor, Boston, MA 02114 USA.
EM jmeigs@partners.org
RI Library, Woodruff Health/A-6096-2012; Meisinger, Christine/B-5358-2014;
Thorand, Barbara/B-5349-2014;
OI Thorand, Barbara/0000-0002-8416-6440; Meisinger,
Christa/0000-0002-9026-6544; Sullivan, Lisa/0000-0003-0726-7149
FU National Heart, Lung and Blood Institute's Framingham Heart Study
[N01-HC-25195]; National Institutes of Health, National Center for
Research Resources, NIH [RO1 HL064753, RO1 HL076784, R01 AG028321];
General Clinical Research Centers Program [M01-RR-01066]; American
Diabetes Association; NIDDK [K24 DK080140]; Earle Charlton Fund for
Innovative Diabetes Research; GlaxoSmithKline; German Research
Foundation [RA 459/2-1]; German Federal Ministry of Health; Ministry of
School, Science and Research of the State of North-Rhine-Westfalia;
Helmholtz Zentrum Munchen; German Research Center for Environmental
Health; German Federal Ministry of Education, Science, Research and
Technology; State of Bavaria
FX The study was supported by the National Heart, Lung and Blood
Institute's Framingham Heart Study (Contract No. N01-HC-25195) the
National Institutes of Health, National Center for Research Resources,
NIH grants RO1 HL064753; RO1 HL076784; R01 AG028321; General Clinical
Research Centers Program (Grant Number M01-RR-01066), and by a Career
Development Award from the American Diabetes Association and NIDDK K24
DK080140 (J. B. Meigs). D. M. Nathan is supported in part by the Earle
Charlton Fund for Innovative Diabetes Research. J. B. Meigs currently
has research grants from GlaxoSmithKline, and has a consulting agreement
with Interleukin Genetics. The KORA S4/F4 Diabetes Cohort Study was
funded by a German Research Foundation project grant to W. Rathmann
(DFG; RA 459/2-1). The German Diabetes Center is funded by the German
Federal Ministry of Health, and the Ministry of School, Science and
Research of the State of North-Rhine-Westfalia. The KORA research
platform and the KORA Augsburg studies are financed by the Helmholtz
Zentrum Munchen, German Research Center for Environmental Health, which
is funded by the German Federal Ministry of Education, Science, Research
and Technology and by the State of Bavaria. We thank the field staff in
Augsburg who were involved in the conduct of the studies.
NR 14
TC 20
Z9 26
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0012-186X
J9 DIABETOLOGIA
JI Diabetologia
PD MAY
PY 2011
VL 54
IS 5
BP 1019
EP 1024
DI 10.1007/s00125-011-2067-y
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 746NL
UT WOS:000289253900006
PM 21336532
ER
PT J
AU Jazwinski, CH
Walcheski, CH
AF Jazwinski, Christine H.
Walcheski, Christina H.
TI At the Mall With Children: Group Size and Pedestrian Economy of Movement
SO ENVIRONMENT AND BEHAVIOR
LA English
DT Article
DE pedestrian traffic patterns; pedestrian locomotion; groups; walking
speed; behavior in shopping malls; movement in public places
ID SOCIAL FACILITATION; BEHAVIOR; WALKING; CHOICE; CROWDS
AB The study of pedestrian locomotion in public environments includes both velocity and trajectory of movement. Within public settings such as shopping malls, pedestrians display economy of movement by minimizing the distance (trajectory) walked to arrive at a destination (Bitgood & Dukes, 2006). Although groups of pedestrians have been found to walk more slowly than individuals (Finnis & Walton, 2008), there has been little systematic investigation of how the size of a group and the presence of accompanying children independently affect pedestrian trajectory and velocity. Five naturalistic observational studies with 1,050 observations were conducted at an enclosed retail shopping mall. Neither the size of groups nor the number of children had a significant effect on trajectory of movement. However, both group size and number of children independently predicted pedestrian velocity. Results have implications for predictions of pedestrian facility throughput.
C1 [Jazwinski, Christine H.] St Cloud State Univ, Dept Psychol, St Cloud, MN 56301 USA.
[Walcheski, Christina H.] St Paul Reg Off, US Dept Vet Affairs, St Paul, MN USA.
RP Jazwinski, CH (reprint author), St Cloud State Univ, Dept Psychol, St Cloud, MN 56301 USA.
EM chjazwinski@stcloudstate.edu
NR 29
TC 2
Z9 2
U1 2
U2 7
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0013-9165
EI 1552-390X
J9 ENVIRON BEHAV
JI Environ. Behav.
PD MAY
PY 2011
VL 43
IS 3
BP 363
EP 386
DI 10.1177/0013916510364461
PG 24
WC Environmental Studies; Psychology, Multidisciplinary
SC Environmental Sciences & Ecology; Psychology
GA 749KB
UT WOS:000289463500004
ER
PT J
AU Delforge, M
Terpos, E
Richardson, PG
Shpilberg, O
Khuageva, NK
Schlag, R
Dimopoulos, MA
Kropff, M
Spicka, I
Petrucci, MT
Samoilova, OS
Mateos, MV
Magen-Nativ, H
Goldschmidt, H
Esseltine, DL
Ricci, DS
Liu, K
Deraedt, W
Cakana, A
van de Velde, H
Miguel, JFS
AF Delforge, Michel
Terpos, Evangelos
Richardson, Paul G.
Shpilberg, Ofer
Khuageva, Nuriet K.
Schlag, Rudolf
Dimopoulos, Meletios A.
Kropff, Martin
Spicka, Ivan
Petrucci, Maria T.
Samoilova, Olga S.
Mateos, Maria-Victoria
Magen-Nativ, Hila
Goldschmidt, Hartmut
Esseltine, Dixie-Lee
Ricci, Deborah S.
Liu, Kevin
Deraedt, William
Cakana, Andrew
van de Velde, Helgi
Miguel, Jesus F. San
TI Fewer bone disease events, improvement in bone remodeling, and evidence
of bone healing with bortezomib plus melphalan-prednisone vs.
melphalan-prednisone in the phase III VISTA trial in multiple myeloma
SO EUROPEAN JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE VISTA; bone; myeloma; bortezomib; melphalan-prednisone
ID HISTONE DEACETYLASE INHIBITOR; STEM-CELL TRANSPLANTATION;
DIFFERENTIATION IN-VITRO; OSTEOBLAST DIFFERENTIATION; PROTEASOME
INHIBITOR; ALKALINE-PHOSPHATASE; SERUM CONCENTRATIONS;
RELAPSED/REFRACTORY MYELOMA; OSTEOLYTIC LESIONS; DEXAMETHASONE
AB Objectives:
Bone disease is a key presenting feature of myeloma. This post hoc analysis of the phase III VISTA trial of bortezomib plus melphalan-prednisone (VMP) vs. MP in previously untreated myeloma patients assessed clinical bone disease events and changes in alkaline phosphatase (ALP), a marker for osteoblast activation, and serum Dickkopf-1 (DKK-1), an inhibitor of osteoblast differentiation, during treatment.
Methods:
Patients received nine 6-wk cycles of VMP (bortezomib 1.3 mg/m2, days 1, 4, 8, 11, 22, 25, 29, 32, cycles 1-4, days 1, 8, 22, 29, cycles 5-9, plus melphalan 9 mg/m2 and prednisone 60 mg/m2, days 1-4, cycles 1-9; N = 344) or MP alone (N = 338).
Results:
Rates of bisphosphonates use during treatment (73% vs. 82%), progression because of worsening bone disease (3% vs. 11%), and requirement for subsequent radiotherapy (3% vs. 8%) were lower with VMP vs. MP. Median maximum ALP increase was significantly higher with VMP vs. MP overall (49.7% vs. 30.3%, P = 0.029), and higher by response group (complete response [CR]: 68.7% vs. 43.9%; partial response [PR]: 41.5% vs. 31.2%). Greater maximum ALP increase was strongly associated with achievement of CR (P < 0.0001) and CR/PR (P < 0.01). Median DKK-1 decreased with VMP by 694.4 pg/mL and increased with MP by 1273.3 pg/mL from baseline to day 4 (P = 0.0069). Available radiologic data revealed evidence of bone healing in 6/11 VMP-treated patients, who achieved best responses of three CR, one PR, and two stable disease.
Conclusions:
These results suggest a positive effect of bortezomib on bone metabolism and potentially bone healing in myeloma.
C1 [Terpos, Evangelos; Dimopoulos, Meletios A.] Univ Athens, Sch Med, GR-11527 Athens, Greece.
[Richardson, Paul G.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Shpilberg, Ofer; Magen-Nativ, Hila] Rabin Med Ctr, Petah Tiqwa, Israel.
[Khuageva, Nuriet K.] SP Botkin Moscow City Clin Hosp, Moscow, Russia.
[Schlag, Rudolf] Praxisklin Dr Schlag, Wurzburg, Germany.
[Kropff, Martin] Univ Munster, Munster, Germany.
[Spicka, Ivan] Univ Hosp, Prague, Czech Republic.
[Petrucci, Maria T.] Univ Roma La Sapienza, Rome, Italy.
[Samoilova, Olga S.] Nizhnii Novgorod Reg Clin Hosp, Nizhnii Novgorod, Russia.
[Mateos, Maria-Victoria; Miguel, Jesus F. San] Hosp Univ Salamanca, IBMCC, CIC, USAL CSIC, Salamanca, Spain.
[Goldschmidt, Hartmut] Heidelberg Univ, Heidelberg, Germany.
[Goldschmidt, Hartmut] Natl Ctr Tumour Dis, Heidelberg, Germany.
[Esseltine, Dixie-Lee] Millennium Pharmaceut Inc, Cambridge, MA USA.
[Ricci, Deborah S.; Liu, Kevin] Johnson & Johnson Pharmaceut R&D LLC, Raritan, NJ USA.
[Deraedt, William; van de Velde, Helgi] Johnson & Johnson Pharmaceut R&D, Beerse, Belgium.
[Cakana, Andrew] Johnson & Johnson Pharmaceut R&D, High Wycombe, Bucks, England.
RP Delforge, M (reprint author), Univ Hosp Leuven, Dept Hematol, Herestr 49, B-3000 Louvain, Belgium.
EM michel.delforge@uzleuven.be
RI 2011, Secribsal/D-9425-2012;
OI SAN MIGUEL, JESUS/0000-0002-9183-4857
FU Flanders Fund for Scientific Research; Millennium Pharmaceuticals, Inc;
Johnson & Johnson Pharmaceutical Research & Development, L.L.C.;
Millennium Pharmaceuticals
FX The authors would like to acknowledge the Flanders Fund for Scientific
Research for whom Michel Delforge is a clinical professor. The authors
would also like to acknowledge the writing assistance of Steve Hill and
Catherine Crookes of FireKite during the development of this
publication, which was funded by Millennium Pharmaceuticals, Inc and
Johnson & Johnson Pharmaceutical Research & Development, L.L.C. In
addition, the authors would like to thank Jhilik De and Sudha
Visvanathan for technical assistance with the DKK-1 analysis.; MD:
consultancy and honoraria with Janssen-Cilag, Celgene, and Novartis. ET:
consultancy, honoraria, and membership with Janssen-Cilag. PGR: research
funding from Millennium Pharmaceuticals, and membership of advisory
boards for Millennium Pharmaceuticals, Celgene, Bristol-Myers Squibb,
Johnson & Johnson, and Keryx Pharmaceuticals. OS: membership of advisory
board for Janssen-Cilag. NKK: none. RS: none. MAD: consultancy and
honoraria with Millennium Pharmaceuticals and OrthoBiotech. MK:
consultancy and honoraria with OrthoBiotech and Celgene as well as
membership of various speakers' bureaus and advisory committees. IS:
honoraria for data analysis of patients treated with bortezomib in Czech
Republic, and membership of speakers bureau at Czech Haematological
Society Meetings, on myeloma therapy (any), and myeloma therapy with new
drugs (thalidomide, bortezomib, lenalidomide). MTP: honoraria with
Janssen-Cilag and Celgene. OSS: none. M-VM: honoraria and membership
with OrthoBiotech and Millennium Pharmaceuticals. HM-N: none. HG:
consultancy with Janssen-Cilag, plus research support for clinical
studies, and honoraria support for educational talks. D-LE: employment
with Millennium Pharmaceuticals, and ownership interest in Johnson &
Johnson and Millennium/Takeda. DSR, WD and HvdV: employment and
ownership interest with Johnson & Johnson. KL: employment with Johnson &
Johnson, and ownership interest in Johnson & Johnson and Merck. AC:
employment with Johnson & Johnson. JFSM: honoraria and membership with
Celgene, Millennium Pharmaceuticals, and Janssen-Cilag.
NR 53
TC 31
Z9 35
U1 1
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0902-4441
EI 1600-0609
J9 EUR J HAEMATOL
JI Eur. J. Haematol.
PD MAY
PY 2011
VL 86
IS 5
BP 372
EP 384
DI 10.1111/j.1600-0609.2011.01599.x
PG 13
WC Hematology
SC Hematology
GA 749NI
UT WOS:000289474500002
PM 21366694
ER
PT J
AU Buhl, AM
James, DF
Neuberg, D
Jain, S
Rassenti, LZ
Kipps, TJ
AF Buhl, Anne Mette
James, Danelle F.
Neuberg, Donna
Jain, Sonia
Rassenti, Laura Z.
Kipps, Thomas J.
TI Analysis of CLLU1 expression levels before and after therapy in patients
with chronic lymphocytic leukemia
SO EUROPEAN JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE chronic lymphocytic leukemia; minimal residual disease; real-time
quantitative PCR; chronic lymphocytic leukemia upregulated gene 1
ID MINIMAL RESIDUAL DISEASE; CALCULATING CORRELATION-COEFFICIENTS; MUTATION
STATUS; RITUXIMAB; FLUDARABINE; CYCLOPHOSPHAMIDE; SURVIVAL;
CHEMOIMMUNOTHERAPY; TRIAL; GOAL
AB Objective:
Chronic lymphocytic leukemia (CLL) is incurable, but therapy leading to eradication of minimal residual disease (MRD) in CLL is associated with improved clinical outcomes. CLL upregulated gene 1 (CLLU1) is solely upregulated in CLL patient samples. We hypothesized that CLLU1 could be used to monitor for residual disease in CLL patient samples after therapy.
Methods:
We examined whether the CLLU1 real-time quantitative PCR (RQ-PCR) could detect small numbers of CLL cells in mixtures of normal peripheral blood mononuclear (PBMC) cells. We then performed a retrospective analysis on time-matched cryo-preserved specimens from patients who achieved MRD-negative remissions that underwent serial marrow biopsies for evaluation of residual disease by 4-color flow cytometry. RNA from PBMC samples collected at the time of the marrow assessments was analyzed for CLLU1. Nine patients underwent a total of 46 paired blood and marrow evaluations (median 5 assessments per patient).
Results:
CLLU1 RQ-PCR on PBMCs of healthy donors reconstituted with varying amounts of CLL cells demonstrated leukemia cells could be reliably detected with high sensitivities depending on the CLLU1 expression level. Analysis of time-matched samples assessed for CLLU1 levels in the blood by RQ-PCR and residual disease of the marrow determined by 4-color flow cytometry revealed a correlation coefficient of 0.96 (P < 0.0001).
Conclusion:
The CLLU1 RQ-PCR is a sensitive and specific assay for detecting residual CLL cells after therapy. Assessment of blood CLLU1 levels can be used as a reliable marker of tumor burden and has the potential to complement currently used techniques for MRD monitoring in patients with CLL.
C1 [Buhl, Anne Mette] Rigshosp, Dept Hematol, DK-2100 Copenhagen, Denmark.
[Buhl, Anne Mette; James, Danelle F.; Rassenti, Laura Z.; Kipps, Thomas J.] Univ Calif San Diego, Dept Med, Div Hematol Oncol, Moores UCSD Canc Ctr, La Jolla, CA 92093 USA.
[Neuberg, Donna] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA USA.
[Jain, Sonia] UCSD, Div Biostat & Bioinformat, La Jolla, CA USA.
RP Buhl, AM (reprint author), Rigshosp, Dept Hematol, L4041,Blegdamsvej 9, DK-2100 Copenhagen, Denmark.
EM annemette.buhl@gmail.com
FU The Alfred Benzon Foundation; CLL Research Consortium (CRC); NIH
[PO1-CA081534]; Lymphoma Research Foundation; TACF-ASP
FX The authors would like to thank the CRC Tissue Core, E. Avery for
technical assistance, F. He for data analysis, M. Cook for assistance
with database searches, L. B. Pedersen for helpful discussions, and C.
Geisler for comments to the manuscript. This work was supported by
grants from The Alfred Benzon Foundation, the CLL Research Consortium
(CRC) and NIH PO1-CA081534. DFJ is supported by a Lymphoma Research
Foundation Fellowship and a TACF-ASP Young Investigator Award.
NR 27
TC 4
Z9 4
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0902-4441
EI 1600-0609
J9 EUR J HAEMATOL
JI Eur. J. Haematol.
PD MAY
PY 2011
VL 86
IS 5
BP 405
EP 411
DI 10.1111/j.1600-0609.2011.01588.x
PG 7
WC Hematology
SC Hematology
GA 749NI
UT WOS:000289474500005
PM 21323738
ER
PT J
AU Merfeld, DM
AF Merfeld, Daniel M.
TI Signal detection theory and vestibular thresholds: I. Basic theory and
practical considerations
SO EXPERIMENTAL BRAIN RESEARCH
LA English
DT Review
DE Detection theory; Spatial orientation; Vestibular; Perception;
Threshold; Psychophysics
ID PSYCHOMETRIC FUNCTION; ANGULAR ACCELERATION; VERTICAL AXIS; WHOLE-BODY;
PERCEPTION; MOTION; DISCRIMINATION; MOVEMENT; VECTION
AB Detection theory has been applied to the measurement of vestibular thresholds and vestibular sensory integration. Yet, a formal detection theory analysis of vestibular responses has not been published. Such a de novo analysis seems warranted because the vestibular system has characteristics that differ from other sensory systems, which impacts the application of detection theory. For example, the physical stimuli evoking vestibular responses are typically bidirectional (e.g., leftward/rightward); this bidirectional nature of vestibular responses leads to another characteristic-what is sometimes called vestibular bias-that must also be considered, since it can impact threshold measurements, including thresholds found using staircase procedures. This paper develops a basic model of vestibular noise and then analyzes this model for four standard paradigms-one-interval recognition, one-interval detection, two-interval detection, and two-interval recognition. While any of these paradigms might be justified for a specific application, it is concluded that one-interval recognition paradigms have advantages over other paradigms for many vestibular applications. One-interval recognition is favored over one-interval detection because it lends itself to a fixed detection boundary, is more efficient, and is less impacted by device vibration. One-interval recognition is generally favored over two-interval recognition because it assesses vestibular bias and can require substantially less time than two-interval tasks.
C1 Massachusetts Eye & Ear Infirm, Jenks Vestibular Res Lab, Boston, MA 02114 USA.
RP Merfeld, DM (reprint author), Massachusetts Eye & Ear Infirm, Jenks Vestibular Res Lab, Boston, MA 02114 USA.
EM dan_merfeld@meei.harvard.edu
FU NIH [NIDCD R01 04158]
FX Funding for this experiment was provided in part by the NIH (NIDCD R01
04158). We would also like to thank Margaret Lankow for administrative
assistance, Csilla Haburcakova and Saori Fukuda for help with the
graphics, and Shomesh Chaudhuri, Michael Barnett-Cowan, Luzia Grabherr,
Tim Hullar, Faisal Karmali, Koeun Lim, Fred Mast, Chuck Oman, and
Florian Soyka, who provided comments on preliminary drafts. Thanks also
to Jay Goldberg, who has inspired the use of such theoretical analyses
in the vestibular sciences alongside thorough experimental evaluations
of such analyses.
NR 36
TC 27
Z9 27
U1 1
U2 9
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0014-4819
EI 1432-1106
J9 EXP BRAIN RES
JI Exp. Brain Res.
PD MAY
PY 2011
VL 210
IS 3-4
BP 389
EP 405
DI 10.1007/s00221-011-2557-7
PG 17
WC Neurosciences
SC Neurosciences & Neurology
GA 749QQ
UT WOS:000289484300006
PM 21359662
ER
PT J
AU Krivickas, LS
Dorer, DJ
Ochala, J
Frontera, WR
AF Krivickas, Lisa S.
Dorer, David J.
Ochala, Julien
Frontera, Walter R.
TI Relationship between force and size in human single muscle fibres
SO EXPERIMENTAL PHYSIOLOGY
LA English
DT Article
ID OLDER MEN; CONTRACTILE PROPERTIES; SHORTENING VELOCITY; WOMEN; YOUNG;
FROG; PRESERVATION; STRENGTH; CALCIUM; MYOSIN
AB When the contractile properties of single muscle fibres are studied, force is typically normalized by fibre cross-sectional area and expressed as specific force. We studied a set of 2725 chemically skinned human single muscle fibres from 119 healthy adults to determine whether specific force is the optimal way to express the relationship between single-fibre force and size. A linear mixed effects model was used to estimate the slope and slope variability among individuals of log-log plots of force and diameter. For type I fibres, the slope estimate was 0.99 (95% confidence interval 0.36-1.62), and for type IIa fibres it was 0.94 (95% confidence interval 0.77-1.11), indicating that force is proportional to fibre diameter, rather than to cross-sectional area. If force were proportional to cross-sectional area, the slope estimate would be 2.0. In future studies using the chemically skinned single fibre preparation, force may be normalized to fibre diameter rather than cross-sectional area. We propose that a new term, 'normalized force', be used for this variable, with units of newtons per metre. We demonstrate using our data set that when populations of single fibres are compared with one another, the determination of whether the size and force relationship is the same or different is dependent upon the method used to account for fibre size (i.e. specific force versus 'normalized force').
C1 [Frontera, Walter R.] Univ Puerto Rico, Sch Med, Dept Phys Med & Rehabil, San Juan, PR 00936 USA.
[Frontera, Walter R.] Univ Puerto Rico, Sch Med, Dept Physiol, San Juan, PR 00936 USA.
[Krivickas, Lisa S.; Frontera, Walter R.] Spaulding Rehabil Hosp, Dept Phys Med & Rehabil, Boston, MA USA.
[Krivickas, Lisa S.; Frontera, Walter R.] Harvard Univ, Sch Med, Boston, MA USA.
[Dorer, David J.] Massachusetts Gen Hosp, Ctr Biostat, Boston, MA 02114 USA.
[Ochala, Julien] Univ Uppsala Hosp, Dept Neurosci, Uppsala, Sweden.
RP Frontera, WR (reprint author), Univ Puerto Rico, Sch Med, Dept Phys Med & Rehabil, Off A-880,POB 365067, San Juan, PR 00936 USA.
EM walter.frontera@upr.edu
OI Ochala, Julien/0000-0002-6358-2920
NR 28
TC 6
Z9 6
U1 3
U2 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0958-0670
J9 EXP PHYSIOL
JI Exp. Physiol.
PD MAY 1
PY 2011
VL 96
IS 5
BP 539
EP 547
DI 10.1113/expphysiol.2010.055269
PG 9
WC Physiology
SC Physiology
GA 750CO
UT WOS:000289522100008
PM 21317219
ER
PT J
AU Guey, LT
Kravic, J
Melander, O
Burtt, NP
Laramie, JM
Lyssenko, V
Jonsson, A
Lindholm, E
Tuomi, T
Isomaa, B
Nilsson, P
Almgren, P
Kathiresan, S
Groop, L
Seymour, AB
Altshuler, D
Voight, BF
AF Guey, Lin T.
Kravic, Jasmina
Melander, Olle
Burtt, Noel P.
Laramie, Jason M.
Lyssenko, Valeriya
Jonsson, Anna
Lindholm, Eero
Tuomi, Tiinamaija
Isomaa, Bo
Nilsson, Peter
Almgren, Peter
Kathiresan, Sekar
Groop, Leif
Seymour, Albert B.
Altshuler, David
Voight, Benjamin F.
TI Power in the Phenotypic Extremes: A Simulation Study of Power in
Discovery and Replication of Rare Variants
SO GENETIC EPIDEMIOLOGY
LA English
DT Article
DE liability ascertainment; next-generation sequencing; variant discovery;
replication of association; phenotype extremes
ID GENOME-WIDE ASSOCIATION; QUANTITATIVE TRAIT LOCI;
CORONARY-HEART-DISEASE; DISCORDANT SIB PAIRS; COMMON DISEASES;
PLASMA-LEVELS; RISK-FACTORS; PREDICTION; CONTRIBUTE; ALLELES
AB Next-generation sequencing technologies are making it possible to study the role of rare variants in human disease. Many studies balance statistical power with cost-effectiveness by (a) sampling from phenotypic extremes and (b) utilizing a two-stage design. Two-stage designs include a broad-based discovery phase and selection of a subset of potential causal genes/variants to be further examined in independent samples. We evaluate three parameters: first, the gain in statistical power due to extreme sampling to discover causal variants; second, the informativeness of initial (Phase I) association statistics to select genes/variants for follow-up; third, the impact of extreme and random sampling in (Phase 2) replication. We present a quantitative method to select individuals from the phenotypic extremes of a binary trait, and simulate disease association studies under a variety of sample sizes and sampling schemes. First, we find that while studies sampling from extremes have excellent power to discover rare variants, they have limited power to associate them to phenotype-suggesting high false-negative rates for upcoming studies. Second, consistent with previous studies, we find that the effect sizes estimated in these studies are expected to be systematically larger compared with the overall population effect size; in a well-cited lipids study, we estimate the reported effect to be twofold larger. Third, replication studies require large samples from the general population to have sufficient power; extreme sampling could reduce the required sample size as much as fourfold. Our observations offer practical guidance for the design and interpretation of studies that utilize extreme sampling. Genet. Epidemiol. 35: 236-246, 2011. (c) 2011 Wiley-Liss, Inc.
C1 [Voight, Benjamin F.] Broad Inst Harvard, Cambridge Ctr 7, Cambridge, MA 02144 USA.
[Burtt, Noel P.; Kathiresan, Sekar; Altshuler, David; Voight, Benjamin F.] MIT, Cambridge, MA 02139 USA.
[Guey, Lin T.; Laramie, Jason M.; Seymour, Albert B.] Pfizer Biotherapeut, Appl Quantitat Genotherapeut, Cambridge, MA USA.
[Kravic, Jasmina; Lyssenko, Valeriya; Jonsson, Anna; Lindholm, Eero; Almgren, Peter; Groop, Leif] Lund Univ, Dept Clin Sci Diabet & Endocrinol, Malmo, Sweden.
[Kravic, Jasmina; Lyssenko, Valeriya; Jonsson, Anna; Lindholm, Eero; Almgren, Peter; Groop, Leif] Lund Univ, Ctr Diabet, Malmo, Sweden.
[Melander, Olle] Lund Univ, Lund Univ Diabet Ctr, Clin Res Ctr, Malmo Univ Hosp, S-22100 Lund, Sweden.
[Tuomi, Tiinamaija] Univ Helsinki, Dept Med, Helsinki Univ Hosp, Helsinki, Finland.
[Tuomi, Tiinamaija; Isomaa, Bo] Folkhalsan Res Ctr, Helsinki, Finland.
[Isomaa, Bo] Malmska Municipal Hlth Ctr & Hosp, Pietarsaari, Finland.
[Nilsson, Peter] Lund Univ, Dept Clin Sci, Malmo, Sweden.
[Kathiresan, Sekar; Altshuler, David; Voight, Benjamin F.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Kathiresan, Sekar] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Kathiresan, Sekar; Altshuler, David; Voight, Benjamin F.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Altshuler, David] Harvard Univ, Sch Med, Dept Genet, Boston, MA USA.
[Altshuler, David] Massachusetts Gen Hosp, Diabet Unit, Boston, MA 02114 USA.
RP Voight, BF (reprint author), Broad Inst Harvard, Cambridge Ctr 7, Cambridge, MA 02144 USA.
EM bvoight@broadinstitute.org
RI Voight, Benjamin/F-1775-2011; Altshuler, David/A-4476-2009;
OI Altshuler, David/0000-0002-7250-4107; Tuomi,
Tiinamaija/0000-0002-8306-6202
FU Marianne and Marcus Wallenberg Foundation; The Swedish Research Council
(Scania Diabetes Registry); The Sigrid Juselius Foundation; Folkhalsan
Foundation (Botnia Study)
FX Contract grant sponsors: Marianne and Marcus Wallenberg Foundation; The
Swedish Research Council (Scania Diabetes Registry); The Sigrid Juselius
Foundation; Folkhalsan Foundation (Botnia Study).
NR 47
TC 44
Z9 44
U1 1
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0741-0395
EI 1098-2272
J9 GENET EPIDEMIOL
JI Genet. Epidemiol.
PD MAY
PY 2011
VL 35
IS 4
BP 236
EP 246
DI 10.1002/gepi.20572
PG 11
WC Genetics & Heredity; Mathematical & Computational Biology
SC Genetics & Heredity; Mathematical & Computational Biology
GA 748FM
UT WOS:000289375400004
PM 21308769
ER
PT J
AU Blendea, D
Singh, JP
AF Blendea, Dan
Singh, Jagmeet P.
TI Lead positioning strategies to enhance response to cardiac
resynchronization therapy
SO HEART FAILURE REVIEWS
LA English
DT Article
DE Cardiac resynchronization therapy; Lead positioning; Dyssynchrony
ID LEFT-VENTRICULAR LEAD; BUNDLE-BRANCH BLOCK; CORONARY VENOUS ANATOMY;
CONGESTIVE-HEART-FAILURE; VIDEO-ASSISTED THORACOSCOPY; RESYNCHRONISATION
THERAPY; ISCHEMIC CARDIOMYOPATHY; PREDICTS RESPONSE; ELECTRICAL DELAY;
CONDUCTION DELAY
AB Left ventricular lead position is one of the main determinants of CRT response. There are several approaches in LV lead positioning that include favoring an optimal anatomical position or targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay. The conventional LV lead implantation faces several technical difficulties that may prevent the obtaining of a stable position and good performance of the LV lead without phrenic nerve stimulation. In addition, implant of the LV pacing lead in areas with myocardial scar may result in less than optimal cardiac resynchronization. Several strategies have been proposed to overcome all these obstacles including multimodality cardiac imaging to help in preprocedural or intraprocedural identification of the latest activated areas of the LV and the potential anatomical constraints. In selected patients, the surgical implant may be a solution to overcome these constraints. In the future, LV endocardial or epicardial multisite pacing may deliver an enhanced response to CRT.
C1 [Blendea, Dan; Singh, Jagmeet P.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Heart,Cardiac Arrhythmia Serv, Boston, MA 02163 USA.
RP Singh, JP (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Heart,Cardiac Arrhythmia Serv, Boston, MA 02163 USA.
EM Jsingh@partners.org
NR 74
TC 5
Z9 6
U1 0
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1382-4147
EI 1573-7322
J9 HEART FAIL REV
JI Heart Fail. Rev.
PD MAY
PY 2011
VL 16
IS 3
BP 291
EP 303
DI 10.1007/s10741-010-9212-4
PG 13
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 750FY
UT WOS:000289532300008
PM 21184174
ER
PT J
AU Gupta, V
Kawahara, G
Gundry, SR
Chen, AT
Lencer, WI
Zhou, Y
Zon, LI
Kunkel, LM
Beggs, AH
AF Gupta, Vandana
Kawahara, Genri
Gundry, Stacey R.
Chen, Aye T.
Lencer, Wayne I.
Zhou, Yi
Zon, Leonard I.
Kunkel, Louis M.
Beggs, Alan H.
TI The zebrafish dag1 mutant: a novel genetic model for
dystroglycanopathies
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID WALKER-WARBURG-SYNDROME; CONGENITAL MUSCULAR-DYSTROPHY; FUKUTIN-RELATED
PROTEIN; ALPHA-DYSTROGLYCAN; SKELETAL-MUSCLE; SARCOPLASMIC-RETICULUM;
EMBRYONIC-DEVELOPMENT; GLYCOPROTEIN COMPLEX; POMT1 GENE; MUTATIONS
AB In a forward genetic approach to identify novel genes for congenital muscle diseases, a zebrafish mutant, designated patchytail, was identified that exhibits degenerating muscle fibers with impaired motility behavior. Genetic mapping identified a genomic locus containing the zebrafish ortholog of the dystroglycan gene (DAG1). Patchytail fish contain a point mutation (c.1700T > A) in dag1, resulting in a missense change p.V567D. This change is associated with reduced transcripts and a complete absence of protein. The absence of alpha-dystroglycan and beta-dystroglycan caused destabilization of dystroglycan complex, resulting in membrane damages. Membrane damage was localized on the extracellular matrix at myosepta as well as basement membrane between adjacent myofibers. These studies also identified structural abnormalities in triads at 3 days post fertilization (dpf) of dystroglycan-deficient muscles, significantly preceding sarcolemmal damage that becomes evident at 7 dpf. Immunofluorescence studies identified a subpopulation of dystroglycan that is expressed at t-tubules in normal skeletal muscles. In dag1-mutated fish, smaller and irregular-shaped t-tubule vesicles, as well as highly disorganized terminal cisternae of sarcoplasmic reticulum, were common. In addition to skeletal muscle defects, dag1-mutated fish have brain abnormalities and ocular defects in posterior as well as anterior chambers. These phenotypes of dystroglycan-deficient fish are highly reminiscent of the phenotypes observed in the human conditions muscle-eye-brain disease and Walker-Warburg syndrome. This animal model will provide unique opportunities in the understanding of biological functions of dystroglycan in a wide range of dystroglycanopathies, as disruption of this gene in higher vertebrates results in early embryonic lethality.
C1 [Gupta, Vandana; Kawahara, Genri; Gundry, Stacey R.; Kunkel, Louis M.; Beggs, Alan H.] Childrens Hosp, Div Genet, Manton Ctr Orphan Dis Res, Boston, MA 02115 USA.
[Gupta, Vandana; Kawahara, Genri; Gundry, Stacey R.; Kunkel, Louis M.; Beggs, Alan H.] Childrens Hosp, Genom Program, Manton Ctr Orphan Dis Res, Boston, MA 02115 USA.
[Chen, Aye T.; Zhou, Yi; Zon, Leonard I.] Childrens Hosp, Stem Cell Program & Pediat Hematol Oncol, Boston, MA 02115 USA.
[Chen, Aye T.; Zhou, Yi; Zon, Leonard I.] Dana Farber Canc Inst, Harvard Stem Cell Inst, Boston, MA 02115 USA.
[Lencer, Wayne I.] Harvard Univ, Sch Med, Childrens Hosp Boston, Gastroenterol Div,Harvard Digest Dis Ctr, Boston, MA 02115 USA.
[Gundry, Stacey R.] Northeastern Univ, Coll Sci, Boston, MA 02115 USA.
[Zon, Leonard I.] Howard Hughes Med Inst, Chevy Chase, MD 20815 USA.
RP Beggs, AH (reprint author), Childrens Hosp, Div Genet, Manton Ctr Orphan Dis Res, CLSB 15026,300 Longwood Ave, Boston, MA 02115 USA.
EM beggs@enders.tch.harvard.edu
OI Beggs, Alan/0000-0001-8818-0568
FU National Institute of Arthritis and Musculoskeletal and Skin Diseases
[R01 AR044345]; National Institute of Neurological Disorders and Strokes
[P50 NS040828]; Lee and Penny Anderson Family Foundation; William
Randolph Hearst Fund; National Institute of Child Health and Human
Development [P30HD18655]
FX This work was supported by National Institute of Health grants from the
National Institute of Arthritis and Musculoskeletal and Skin Diseases
(R01 AR044345 to A.H.B.); National Institute of Neurological Disorders
and Strokes (P50 NS040828 to A.H.B.); by the Lee and Penny Anderson
Family Foundation (to A.H.B.); and the William Randolph Hearst Fund (to
V.G.). DNA sequencing was performed by the Children's Hospital Boston
Genomics Program Molecular Genetics Core supported in part by National
Institute of Child Health and Human Development grant (P30HD18655).
NR 62
TC 53
Z9 53
U1 3
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD MAY
PY 2011
VL 20
IS 9
BP 1712
EP 1725
DI 10.1093/hmg/ddr047
PG 14
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 747HR
UT WOS:000289311400005
PM 21296866
ER
PT J
AU Jehl, SP
Doling, AM
Giddings, KS
Phalipon, A
Sansonetti, PJ
Goldberg, MB
Starnbach, MN
AF Jehl, Stephanie P.
Doling, Amy M.
Giddings, Kara S.
Phalipon, Armelle
Sansonetti, Philippe J.
Goldberg, Marcia B.
Starnbach, Michael N.
TI Antigen-Specific CD8(+) T Cells Fail To Respond to Shigella flexneri
SO INFECTION AND IMMUNITY
LA English
DT Article
ID LYMPHOCYTIC CHORIOMENINGITIS VIRUS; TOXIN-MEDIATED DELIVERY; ANTHRAX
TOXIN; IN-VIVO; INFECTED MACROPHAGES; IMMUNE-RESPONSES;
YERSINIA-ENTEROCOLITICA; PROTECTIVE IMMUNITY; VACCINE DEVELOPMENT;
INDUCED APOPTOSIS
AB CD8(+) T lymphocytes often play a primary role in adaptive immunity to cytosolic microbial pathogens. Surprisingly, CD8(+) T cells are not required for protective immunity to the enteric pathogen Shigella flexneri, despite the ability of Shigella to actively secrete proteins into the host cytoplasm, a location from which antigenic peptides are processed for presentation to CD8(+) T cells. To determine why CD8(+) T cells fail to play a role in adaptive immunity to S. flexneri, we investigated whether antigen-specific CD8(+) T cells are primed during infection but are unable to confer protection or, alternatively, whether T cells fail to be primed. To test whether Shigella is capable of stimulating an antigen-specific CD8(+) T-cell response, we created an S. flexneri strain that constitutively secretes a viral CD8(+) T-cell epitope via the Shigella type III secretion system and characterized the CD8(+) T-cell response to this strain both in mice and in cultured cells. Surprisingly, no T cells specific for the viral epitope were stimulated in mice infected with this strain, and cells infected with the recombinant strain were not targeted by epitope-specific T cells. Additionally, we found that the usually robust T-cell response to antigens artificially introduced into the cytoplasm of cultured cells was significantly reduced when the antigen-presenting cell was infected with Shigella. Collectively, these results suggest that antigen-specific CD8(+) T cells are not primed during S. flexneri infection and, as a result, afford little protection to the host during primary or subsequent infection.
C1 [Jehl, Stephanie P.; Doling, Amy M.; Giddings, Kara S.; Goldberg, Marcia B.; Starnbach, Michael N.] Harvard Univ, Sch Med, Dept Microbiol & Mol Genet, Boston, MA 02115 USA.
[Phalipon, Armelle; Sansonetti, Philippe J.] Inst Pasteur, INSERM, Unite Pathogenie Microbienne Mol, U786, F-75724 Paris 15, France.
[Goldberg, Marcia B.] Massachusetts Gen Hosp, Div Infect Dis, Cambridge, MA 02139 USA.
RP Starnbach, MN (reprint author), Harvard Univ, Sch Med, Dept Microbiol & Mol Genet, 200 Longwood Ave, Boston, MA 02115 USA.
EM starnbach@hms.harvard.edu
FU National Institutes of Health [AI055962, AI043562]
FX This work was supported by National Institutes of Health grant AI055962
to M.N.S. and grant AI043562 to M.B.G.
NR 53
TC 6
Z9 6
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0019-9567
EI 1098-5522
J9 INFECT IMMUN
JI Infect. Immun.
PD MAY
PY 2011
VL 79
IS 5
BP 2021
EP 2030
DI 10.1128/IAI.00939-10
PG 10
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 752EP
UT WOS:000289672700024
PM 21357720
ER
PT J
AU Zella, GC
Hait, EJ
Glavan, T
Gevers, D
Ward, DV
Kitts, CL
Korzenik, JR
AF Zella, Garrett C.
Hait, Elizabeth J.
Glavan, Tiffany
Gevers, Dirk
Ward, Doyle V.
Kitts, Christopher L.
Korzenik, Joshua R.
TI Distinct Microbiome in Pouchitis Compared to Healthy Pouches in
Ulcerative Colitis and Familial Adenomatous Polyposis
SO INFLAMMATORY BOWEL DISEASES
LA English
DT Article
DE pouchitis; microbiome; ulcerative colitis; familial adenomatous
polyposis; ileal pouch-anal anastomosis
ID INFLAMMATORY-BOWEL-DISEASE; PLACEBO-CONTROLLED TRIAL; CROHNS-DISEASE;
ANAL ANASTOMOSIS; DOUBLE-BLIND; AKKERMANSIA-MUCINIPHILA; BACTERIAL
FLAGELLIN; IMMUNE-RESPONSE; MUCIN; GENE
AB Background: Pouchitis occurs in up to 50% of patients with ulcerative colitis (UC) undergoing ileal pouch anal anastomosis (IPAA). Pouchitis rarely occurs in patients with familial adenomatous polyposis (FAP) who undergo IPAA. Our aim was to compare mucosal and luminal flora in patients with UC-associated pouchitis (UCP), healthy UC pouches (HUC), and healthy FAP pouches (FAP).
Methods: Nineteen patients were enrolled in this cross-sectional study (nine UCP, three HUC, seven FAP). Patients with active pouchitis were identified using the Pouchitis Disease Activity Index (PDAI). Ileal pouch mucosal biopsies and fecal samples were analyzed with a 16S rDNA-based terminal restriction fragment length polymorphism (TRFLP) approach. Pooled fecal DNA from four UCP and four FAP pouches were sequenced for further speciation.
Results: TRFLP data revealed statistically significant differences in the mucosal and fecal microbiota between each group of patients. UCP samples exhibited significantly more TRFLP peaks matching Clostridium and Eubacterium genera compared to HUC and FAP pouches and fewer peaks matching Lactobacillus and Streptococcus genera compared to FAP. DNA Sanger sequencing of a subset of luminal samples revealed UCP having more identifiable sequences of Firmicutes (51.2% versus 21.2%) and Verrucomicrobia (20.2% versus 3.2%), and fewer Bacteroidetes (17.9% versus 60.5%) and Proteobacteria (9.8% versus 14.7%) compared to FAP.
Conclusions: The pouch microbial environment appears to be distinctly different in the settings of UC pouchitis, healthy UC, and FAP. These findings suggest that a dysbiosis may exist in pouchitis which may be central to understanding the disease. (Inflamm Bowel Dis 2011;17:1092-1100)
C1 [Zella, Garrett C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pediat,Div Pediat Gastroenterol, Boston, MA 02114 USA.
[Hait, Elizabeth J.] Childrens Hosp, Div Gastroenterol & Nutr, Boston, MA 02115 USA.
[Glavan, Tiffany] Univ Calif Davis, Dept Med Microbiol & Immunol, Davis, CA 95616 USA.
[Gevers, Dirk] Broad Inst MIT & Harvard, Microbial Sequencing Ctr, Cambridge, MA USA.
[Gevers, Dirk] Univ Ghent, Microbiol Lab, B-9000 Ghent, Belgium.
[Ward, Doyle V.] Broad Inst MIT & Harvard, Genome Sequencing & Anal Program, Cambridge, MA USA.
[Kitts, Christopher L.] Calif Polytech State Univ San Luis Obispo, Dept Biol Sci, Environm Biotechnol Inst, San Luis Obispo, CA 93407 USA.
[Korzenik, Joshua R.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Gastrointestinal Unit,Dept Med, Boston, MA 02114 USA.
RP Zella, GC (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pediat,Div Pediat Gastroenterol, 175 Cambridge St,5th Fl, Boston, MA 02114 USA.
EM gzella@partners.org
FU Fund for Scientific Research Flanders (Belgium)
FX Supported by the Fund for Scientific Research Flanders (Belgium),
postdoctoral fellowship (to D.G.).
NR 46
TC 27
Z9 27
U1 0
U2 12
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1078-0998
EI 1536-4844
J9 INFLAMM BOWEL DIS
JI Inflamm. Bowel Dis.
PD MAY
PY 2011
VL 17
IS 5
BP 1092
EP 1100
DI 10.1002/ibd.21460
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 748CH
UT WOS:000289367100005
PM 20845425
ER
PT J
AU Ananthakrishnan, AN
McGinley, EL
Binion, DG
Saeian, K
AF Ananthakrishnan, Ashwin N.
McGinley, Emily L.
Binion, David G.
Saeian, Kia
TI Ambient Air Pollution Correlates with Hospitalizations for Inflammatory
Bowel Disease: An Ecologic Analysis
SO INFLAMMATORY BOWEL DISEASES
LA English
DT Article
DE inflammatory bowel disease; IBD; air pollution; environment;
hospitalizations
ID CROHNS-DISEASE; ULCERATIVE-COLITIS; ENVIRONMENTAL-FACTORS; PASSIVE
SMOKING; OLMSTED COUNTY; PREVALENCE; FRANCE; EPIDEMIOLOGY; ASSOCIATION;
PARTICULATE
AB Background: Known genetic loci account for less than 25% of the risk for inflammatory bowel disease (IBD), suggesting a potential role for environmental triggers. The association between ambient air pollution and IBD hospitalizations has not been previously studied.
Methods: Data from the Wisconsin Hospital Association (WHA) for the year 2002 was used to identify the number of IBD-related hospitalizations for each of the 72 counties in Wisconsin. Average annual emissions density (2002) for each of the six criteria pollutants were obtained for each county from the Environmental Protection Agency. Pearson correlation and Poisson regression analysis were performed at the level of the county.
Results: There was a mean of 81.3 IBD hospitalizations/100,000 population per county (range 0-174). The total criteria pollutant emissions density correlated significantly with adult IBD hospitalizations (Pearson's correlation coefficient (rho) 0.28, P = 0.02). On Poisson regression, a 1-log increase in the density of total criteria pollutant emission was associated with a 40% increase in the rate of IBD hospitalizations (incidence rate ratio [IRR] 1.40, 95% confidence interval [CI] 1.31-1.50) This was similar for both ulcerative colitis (UC) (IRR 1.48, 95% CI 1.27-1.73) and Crohn's disease (CD) hospitalizations (IRR 1.39, 95% CI 1.26-1.52). Analysis of each of the individual criteria pollutant emission densities revealed a significant association for all the component criteria pollutants.
Conclusions: In this ecologic analysis, total air emissions of criteria pollutants appear to be associated with hospitalizations for IBD in adults. The ecologic design precludes drawing firm conclusions about association or causality and further research is needed. (Inflamm Bowel Dis 2011;17:1138-1145)
C1 [Ananthakrishnan, Ashwin N.; Saeian, Kia] Med Coll Wisconsin, Div Gastroenterol & Hepatol, Milwaukee, WI 53226 USA.
[McGinley, Emily L.] Med Coll Wisconsin, Div Epidemiol, Milwaukee, WI 53226 USA.
[Binion, David G.] Univ Pittsburgh, Sch Med, Div Gastroenterol Hepatol & Nutr, Pittsburgh, PA USA.
RP Ananthakrishnan, AN (reprint author), Massachusetts Gen Hosp, Gastrointestinal Unit, 165 Cambridge St, Boston, MA 02114 USA.
EM aananthakrishnan@partners.org
NR 41
TC 31
Z9 31
U1 2
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1078-0998
EI 1536-4844
J9 INFLAMM BOWEL DIS
JI Inflamm. Bowel Dis.
PD MAY
PY 2011
VL 17
IS 5
BP 1138
EP 1145
DI 10.1002/ibd.21455
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 748CH
UT WOS:000289367100011
PM 20806342
ER
PT J
AU Bunin, GR
Felice, MA
Davidson, W
Friedman, DL
Shields, CL
Maidment, A
O'Shea, M
Nichols, KE
Leahey, A
Dunkel, IJ
Jubran, R
Rodriguez-Galindo, C
Schmidt, ML
Weinstein, JL
Goldman, S
Abramson, DH
Wilson, MW
Gallie, BL
Chan, HSL
Shapiro, M
Cnaan, A
Ganguly, A
Meadows, AT
AF Bunin, Greta R.
Felice, Marc A.
Davidson, William
Friedman, Debra L.
Shields, Carol L.
Maidment, Andrew
O'Shea, Michael
Nichols, Kim E.
Leahey, Ann
Dunkel, Ira J.
Jubran, Rima
Rodriguez-Galindo, Carlos
Schmidt, Mary Lou
Weinstein, Joanna L.
Goldman, Stewart
Abramson, David H.
Wilson, Matthew W.
Gallie, Brenda L.
Chan, Helen S. L.
Shapiro, Michael
Cnaan, Avital
Ganguly, Arupa
Meadows, Anna T.
TI Medical radiation exposure and risk of retinoblastoma resulting from new
germline RB1 mutation
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE germline mutation; ionizing radiation; retinoblastoma; case-control
studies; pediatric cancer
ID CELL MUTAGENESIS; IONIZING-RADIATION; PATERNAL ALLELE; GENETIC RISK;
KINETICS; MICE
AB Although ionizing radiation induces germline mutations in animals, human studies of radiation-exposed populations have not detected an effect. We conducted a case-control study of sporadic bilateral retinoblastoma, which results from a new germline RB1 mutation, to investigate gonadal radiation exposure of parents from medical sources before their child's conception. Parents of 206 cases from nine North American institutions and 269 controls participated; fathers of 184 cases and 223 friend and relative controls and mothers of 204 cases and 260 controls provided information in telephone interviews on their medical radiation exposure. Cases provided DNA for RB1 mutation testing. Of common procedures, lower gastrointestinal (GI) series conferred the highest estimated dose to testes and ovaries. Paternal history of lower GI series was associated with increased risk of retinoblastoma in the child [matched odds ratio (OR) = 3.6, 95% confidence interval (CI) = 1.2-11.2, two-sided p = 0.02], as was estimated total testicular dose from all procedures combined (OR for highest dose=3.9, 95% CI = 1.2-14.4, p = 0.02). Maternal history of lower GI series was also associated with increased risk (OR = 7.6, 95% CI = 2.8-20.7, p < 0.001) as was the estimated total dose (OR for highest dose = 3.0, 95% CI = 1.4-7.0, p = 0.005). The RB1 mutation spectrum in cases of exposed parents did not differ from that of other cases. Some animal and human data support our findings of an association of gonadal radiation exposure in men and women with new germline RB1 mutation detectable in their children, although bias, confounding, and/or chance may also explain the results.
C1 [Bunin, Greta R.; Nichols, Kim E.; Leahey, Ann; Meadows, Anna T.] Childrens Hosp Philadelphia, Div Oncol, Philadelphia, PA 19104 USA.
[Bunin, Greta R.; Nichols, Kim E.; Leahey, Ann; Meadows, Anna T.] Childrens Hosp Philadelphia, Ctr Childhood Canc Res, Philadelphia, PA 19104 USA.
[Felice, Marc A.; Davidson, William] Univ Penn, Off Environm Hlth & Radiat Safety, Philadelphia, PA 19104 USA.
[Friedman, Debra L.] Vanderbilt Univ, Sch Med, Dept Pediat, Vanderbilt Ingram Canc Ctr, Nashville, TN 37212 USA.
[Shields, Carol L.] Wills Eye Inst, Ocular Oncol Serv, Philadelphia, PA USA.
[Maidment, Andrew; O'Shea, Michael] Hosp Univ Penn, Dept Radiol, Philadelphia, PA 19104 USA.
[Dunkel, Ira J.] Mem Sloan Kettering Canc Ctr, Dept Pediat, New York, NY 10021 USA.
[Jubran, Rima] Univ So Calif, Keck Sch Med, Childrens Hosp Los Angeles, Div Pediat Hematol Oncol, Los Angeles, CA 90033 USA.
[Rodriguez-Galindo, Carlos] Harvard Univ, Childrens Hosp, Sch Med, Boston, MA 02115 USA.
[Rodriguez-Galindo, Carlos] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Schmidt, Mary Lou] Univ Illinois, Coll Med, Dept Pediat, Chicago, IL USA.
[Weinstein, Joanna L.] Northwestern Univ, Childrens Mem Hosp, Feinberg Sch Med, Div Hematol Oncol Stem Cell Transplantat, Chicago, IL 60614 USA.
[Goldman, Stewart] Childrens Mem Hosp, Northwestern Feinberg Sch Med, Dept Neurooncol, Chicago, IL 60614 USA.
[Abramson, David H.] Mem Sloan Kettering Canc Ctr, Ophthalm Oncol Serv, New York, NY 10021 USA.
[Wilson, Matthew W.] Univ Tennessee, Ctr Hlth Sci, Hamilton Eye Inst, Memphis, TN 38163 USA.
[Wilson, Matthew W.] St Jude Childrens Hosp, Dept Surg & Pathol, Memphis, TN 38105 USA.
[Gallie, Brenda L.] Univ Toronto, Hosp Sick Children, Dept Ophthalmol & Visual Sci, Toronto, ON M5G 1X8, Canada.
[Gallie, Brenda L.] Univ Toronto, Ontario Canc Inst, Campbell Family Canc Inst, Toronto, ON M5G 1X8, Canada.
[Chan, Helen S. L.] Hosp Sick Children, Div Hematol Oncol, Toronto, ON M5G 1X8, Canada.
[Shapiro, Michael] Univ Illinois, Dept Ophthalmol, Chicago, IL 60680 USA.
[Shapiro, Michael] Retina Consultants Ltd, Des Plaines, IL USA.
[Cnaan, Avital] Childrens Natl Med Ctr, Childrens Res Inst, Washington, DC 20010 USA.
[Ganguly, Arupa] Univ Penn, Genet Diagnost Lab, Dept Genet, Philadelphia, PA 19104 USA.
RP Bunin, GR (reprint author), Childrens Hosp Philadelphia, Div Oncol, 3535 Market St,Room 1472, Philadelphia, PA 19104 USA.
EM bunin@email.chop.edu
OI Dunkel, Ira/0000-0001-8091-6067
FU US National Institutes of Health [R01CA081012]
FX Grant sponsor: US National Institutes of Health; Grant number:
R01CA081012
NR 26
TC 12
Z9 12
U1 1
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD MAY 1
PY 2011
VL 128
IS 10
BP 2393
EP 2404
DI 10.1002/ijc.25565
PG 12
WC Oncology
SC Oncology
GA 740SZ
UT WOS:000288816000015
PM 20648557
ER
PT J
AU Shanmugam, R
Kusumanchi, P
Appaiah, H
Cheng, LA
Crooks, P
Neelakantan, S
Peat, T
Klaunig, J
Matthews, W
Nakshatri, H
Sweeney, CJ
AF Shanmugam, Rajasubramaniam
Kusumanchi, Praveen
Appaiah, Hitesh
Cheng, Liang
Crooks, Peter
Neelakantan, Sundar
Peat, Tyler
Klaunig, James
Matthews, William
Nakshatri, Harikrishna
Sweeney, Christopher J.
TI A water soluble parthenolide analog suppresses in vivo tumor growth of
two tobacco-associated cancers, lung and bladder cancer, by targeting
NF-kappa B and generating reactive oxygen species
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE dimethylaminoparthenolide; cell cycle; apoptosis; cancer
ID INDUCED APOPTOSIS; BREAST-CANCER; SESQUITERPENE LACTONES; THERAPEUTIC
TARGET; ACTIVATES P53; UP-REGULATION; CELLS; INHIBITION; CHEMOTHERAPY;
LEUKEMIA
AB Dimethylaminoparthenolide (DMAPT) is a water soluble parthenolide analog with preclinical activity in hematologic malignancies. Using non-small lung cancer (NSCLC) cell lines (A549 and H522) and an immortalized human bronchial epithelial cell line (BEAS2B) and TCC cell lines (UMUC-3, HT-1197 and HT-1376) and a bladder papilloma (RT-4), we aimed to characterize DMAPT's anticancer activity in tobacco-associated neoplasms. Flow cytometric, electrophoretic mobility gel shift assays (EMSA), and Western blot studies measured generation of reactive oxygen species (ROS), inhibition of NF kappa B DNA binding, and changes in cell cycle distribution and apoptotic proteins. DMAPT generated ROS with subsequent JNK activation and also decreased NF kappa B DNA binding and antiapoptotic proteins, TRAF-2 and XIAP. DMAPT-induced apoptotic cell death and altered cell cycle distribution with upregulation of p21 and p73 levels in a cell type-dependent manner. DMAPT suppressed cyclin D1 in BEAS2B. DMAPT retained NF kappa B and cell cycle inhibitory activity in the presence of the tobacco carcinogen nitrosamine ketone, 4(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Using a BrdU accumulation assay, 5-20 mu M of DMAPT was shown to inhibit cellular proliferation of all cell lines by more than 95%. Oral dosing of DMAPT suppressed in vivo A549 and UMUC-3 subcutaneous xenograft growth by 54% (p = 0.015) and 63% (p < 0.01), respectively, and A549 lung metastatic volume by 28% (p = 0.043). In total, this data demonstrates DMAPT's novel anticancer properties in both early and late stage tobacco-associated neoplasms as well as its significant in vivo activity. The data provides support for the conduct of clinical trials in TCC and NSCLC.
C1 [Sweeney, Christopher J.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Shanmugam, Rajasubramaniam; Kusumanchi, Praveen; Sweeney, Christopher J.] Indiana Univ, Dept Med, Indianapolis, IN USA.
[Appaiah, Hitesh; Nakshatri, Harikrishna] Indiana Univ, Dept Surg, Indianapolis, IN USA.
[Cheng, Liang] Indiana Univ, Dept Pathol, Indianapolis, IN USA.
[Crooks, Peter; Neelakantan, Sundar] Univ Kentucky, Coll Pharm, Lexington, KY USA.
[Peat, Tyler; Klaunig, James] Indiana Univ, Dept Pharmacol & Toxicol, Indianapolis, IN 46204 USA.
[Matthews, William] Leuchemix Inc, Woodside, CA USA.
[Nakshatri, Harikrishna] Walther Canc Inst, Indianapolis, IN USA.
[Nakshatri, Harikrishna] Indiana Univ, Dept Biochem & Mol Biol, Indianapolis, IN 46204 USA.
RP Sweeney, CJ (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St,DA-1230, Boston, MA 02115 USA.
EM christopher_sweeney@dfci.harvard.edu
RI Nidumanda, HITESH/B-5744-2015
FU FAMRI [052319]; NIH [R03 CA137796]; Walther Cancer Institute; Kentucky
Foundation; Gerry Gillette and Family
FX Grant sponsor: FAMRI Clinical Investigator Award; Grant number: 052319;
Grant sponsor: NIH; Grant number: R03 CA137796; Grant sponsors: Walther
Cancer Institute, Kentucky Foundation; We acknowledge Dr. Craig Jordan,
PhD (University of Rochester), for his suggestions and constructive
review of the manuscript. This work was supported, in part, by grants
from donations from Gerry Gillette and Family, Walther Cancer Institute
(to C.J.S.), NIH (to H.N.) and Kentucky Foundation (to P.C.).
NR 47
TC 32
Z9 35
U1 1
U2 9
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD MAY 1
PY 2011
VL 128
IS 10
BP 2481
EP 2494
DI 10.1002/ijc.25587
PG 14
WC Oncology
SC Oncology
GA 740SZ
UT WOS:000288816000024
PM 20669221
ER
PT J
AU Abushahin, N
Zhang, TG
Chiang, S
Zhang, XS
Hatch, K
Zheng, WX
AF Abushahin, Nisreen
Zhang, Tingguo
Chiang, Sarah
Zhang, Xiangsheng
Hatch, Kenneth
Zheng, Wenxin
TI Serous Endometrial Intraepithelial Carcinoma Arising in Adenomyosis: A
Report of 5 Cases
SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY
LA English
DT Article
DE Endometrial serous carcinoma; Serous endometrial intraepithelial
carcinoma; Adenomyosis; Endometrial glandular dysplasia
ID GLANDULAR DYSPLASIA; FALLOPIAN-TUBE; ADENOCARCINOMA; P53; OVARY;
PERITONEUM; PRECURSOR; UTERUS; CANCER; LESION
AB Serous endometrial intraepithelial carcinoma (serous EIC) arising in adenomysis is rare. It may be underrecognized because of its deceiving morphology when embedded in the foci of adenomysis. Although there is no connection to peritoneal cavity, some cases may be associated with extrauterine disease. It is currently unknown what the etiology for such a disease is. More studies are in need to elucidate the pathogenesis of such a grave malady. We report a series of 5 cases of serous EIC, which may arise in adenomyosis. The 5 cases are in 5 different patients or whom on histopathological examination of their hysterectomy specimens, the finding of adenomyosis involved with serous intraepithelial neoplasia was identified. The finding of interest was the presence of multifoci of adenomyosis; some of those foci were involved in serous EIC. In addition to EIC, lesions of endometrial glandular dysplasia were present in the foci of adenomyosis. To rule out the possibility of endometrial serous carcinoma (ESC) invading into the areas of the adenomyosis, all of the 5 uteri were extensively examined. Among the 5 uteri, the eutopic endometirum showed 1 invasive ESC, 2 serous EIC, and 2 benign resting endometrium without any cancer or precancerous lesions. In 1 uterus with ESC, we did not see any direct spatial connection between the invasive component of ESC and the areas of EIC in the foci of adenomyosis. In 2 uteri with serous EIC within the endometrial cavity, there was a distance of at least 0.5 cm between the lesions within the endometrial cavity and the serous EIC in adenomyosis. The remaining 2 uteri showed no evidence of endometrial malignancy in the endometrial cavity, whereas serous EIC was present only in areas of adenomyosis. Clinicopathologic data including characterized immunohistochemical stainings and p53 gene sequence analysis are presented and clinical significance is discussed.
C1 [Abushahin, Nisreen; Zheng, Wenxin] Univ Arizona, Coll Med, Dept Pathol, Tucson, AZ 85724 USA.
[Hatch, Kenneth; Zheng, Wenxin] Univ Arizona, Dept Obstet & Gynecol, Tucson, AZ 85724 USA.
[Zheng, Wenxin] Univ Arizona, Arizona Canc Ctr, Tucson, AZ 85724 USA.
[Zhang, Tingguo; Zheng, Wenxin] Shandong Univ, Qilu Hosp, Dept Pathol, Jinan 250100, Peoples R China.
[Chiang, Sarah] Harvard Univ, Sch Med, Dept Pathol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Zheng, WX (reprint author), Univ Arizona, Coll Med, Dept Pathol, Tucson, AZ 85724 USA.
EM zhengw@email.arizona.edu
OI Abu Shahin, Nisreen/0000-0003-3044-3569
NR 35
TC 7
Z9 7
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0277-1691
EI 1538-7151
J9 INT J GYNECOL PATHOL
JI Int. J. Gynecol. Pathol.
PD MAY
PY 2011
VL 30
IS 3
BP 271
EP 281
DI 10.1097/PGP.0b013e318200868e
PG 11
WC Obstetrics & Gynecology; Pathology
SC Obstetrics & Gynecology; Pathology
GA 749YK
UT WOS:000289507700008
PM 21464726
ER
PT J
AU Lin, NH
Smeaton, LM
Giguel, F
Novitsky, V
Moyo, S
Mitchell, RM
Makhema, J
Essex, M
Lockman, S
Kuritzkes, DR
AF Lin, Nina H.
Smeaton, Laura M.
Giguel, Francoise
Novitsky, Vladimir
Moyo, Sikhulile
Mitchell, Rebecca M.
Makhema, Joseph
Essex, Myron
Lockman, Shahin
Kuritzkes, Daniel R.
TI Prevalence and Clinical Associations of CXCR4-Using HIV-1 Among
Treatment-Naive Subtype C-Infected Women in Botswana
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE AIDS; HIV-1 tropism; CCR5; CXCR4; subtype C; antiretroviral therapy
ID HUMAN-IMMUNODEFICIENCY-VIRUS; SYNCYTIUM-INDUCING PHENOTYPE; CHEMOKINE
RECEPTOR USE; DISEASE PROGRESSION; CORECEPTOR USAGE; ANTIRETROVIRAL
THERAPY; EXPERIENCED PATIENTS; SOUTH-AFRICA; AIDS; CXCR4
AB HIV-1 coreceptor use was determined using a phenotypic assay in plasma samples from treatment-naive women infected with subtype C virus who had CD4 cell counts below 200 cells/mm(3). Of 148 women, 14.9% were infected with dual/mixed virus; the remainder had R5 virus. A greater proportion of women in the lowest CD4 cell count stratum had dual/mixed virus ( P = 0.026); change in coreceptor use after antiretroviral therapy exposure was uncommon. CXCR4-using HIV-1 was less common in subtype C-infected women than reported in subtype B cohorts but was most prevalent in women with the lowest CD4 cell counts.
C1 [Giguel, Francoise; Lockman, Shahin; Kuritzkes, Daniel R.] Brigham & Womens Hosp, Sect Retroviral Therapeut, Cambridge, MA 02139 USA.
[Lin, Nina H.; Giguel, Francoise] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
[Lin, Nina H.; Lockman, Shahin; Kuritzkes, Daniel R.] Harvard Univ, Sch Med, Boston, MA USA.
[Smeaton, Laura M.; Novitsky, Vladimir; Mitchell, Rebecca M.; Essex, Myron; Lockman, Shahin] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Smeaton, Laura M.; Novitsky, Vladimir; Mitchell, Rebecca M.; Essex, Myron; Lockman, Shahin] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
[Smeaton, Laura M.; Novitsky, Vladimir; Moyo, Sikhulile; Mitchell, Rebecca M.; Makhema, Joseph; Essex, Myron; Lockman, Shahin] Botswana Harvard AIDS Inst, Gaborone, Botswana.
RP Kuritzkes, DR (reprint author), Brigham & Womens Hosp, Sect Retroviral Therapeut, 65 Landsdowne St,Room 449, Cambridge, MA 02139 USA.
EM dkuritzkes@partners.org
RI Moyo, Sikhulile/E-1464-2015
OI Moyo, Sikhulile/0000-0003-3821-4592
FU National Institutes of Health (NIH) [K24 RR016482, U01 AI068636,
R24TW007988]; Harvard Center for AIDS Research (CFAR) [P30 AI060354];
Harvard Institute for Global Health International; Bristol-Myer's
Squibb; American Society of Tropical Medicine and Hygiene; CFAR
[2P30AI060354-06]; [R01 HD037793]; [R01 HD044391]
FX This work was supported in part by Public Health Services grants from
the National Institutes of Health (NIH) including K24 RR016482 and U01
AI068636 (an ACTG Virology Support Laboratory contract) (D. R. K.); R01
HD037793 (M. E.); R01 HD044391 (S. L.); a Scholar Award from the Harvard
Center for AIDS Research (CFAR) (P30 AI060354), a Harvard Institute for
Global Health International Fellowship, a Bristol-Myer's Squibb Virology
Fellowship, and a Burroughs Wellcome Fund/American Society of Tropical
Medicine and Hygiene post-doctoral fellowship (N.H.L.); the NIH Fogarty
grant R24TW007988 (R. M. M); and the CFAR Biostatistical core grant
award 2P30AI060354-06 (L. M. S.).
NR 37
TC 9
Z9 9
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD MAY 1
PY 2011
VL 57
IS 1
BP 46
EP 50
DI 10.1097/QAI.0b013e318214fe27
PG 5
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 749YU
UT WOS:000289509100013
PM 21346588
ER
PT J
AU Spencer, TJ
Mick, E
Surman, CBH
Hammerness, P
Doyle, R
Aleardi, M
Kotarski, M
Williams, CG
Biederman, J
AF Spencer, Thomas J.
Mick, Eric
Surman, Craig B. H.
Hammerness, Paul
Doyle, Robert
Aleardi, Megan
Kotarski, Meghan
Williams, Courtney G.
Biederman, Joseph
TI A Randomized, Single-Blind, Substitution Study of OROS Methylphenidate
(Concerta) in ADHD Adults Receiving Immediate Release Methylphenidate
SO JOURNAL OF ATTENTION DISORDERS
LA English
DT Article
DE ADHD; adult; clinical trial; methylphenidate
ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DEFICIT HYPERACTIVITY
DISORDER; ONCE-A-DAY; CONTROLLED TRIAL
AB Objective: The main aim of this study was to examine the efficacy, tolerability, and compliance of an extended-release formulation of methylphenidate (OROS-MPH) in adults with ADHD receiving immediate-release methylphenidate (IR-MPH). Method: Participants were outpatient adults with ADHD who were stable on IR-MPH-administered TID. Participants were randomized (4:1) to equipotent doses of OROS-MPH or to continue IR-MPH and were assessed weekly for 6 weeks with the Adult ADHD Investigator System Symptom Report Scale (AISRS). Results: Randomization of 53 IR-MPH responders to IR- or OROS-MPH had no effect on AISRS score at endpoint (11.2 +/- 6.9 vs. 10.7 +/- 5.1, p = .8). Participants stabilized on IR-MPH and switched to OROS-MPH remained satisfied over 71% of the time. However, the IR-MPH group missed more doses (7.3 +/- 6.8 vs. 3.3 +/- 4.2, p = .02) than the OROS-MPH group. Conclusion: Findings showed that adults with ADHD can be successfully switched from an effective regimen of IR-MPH TID to once-daily OROS-MPH. Results also demonstrated better compliance with OROS-MPH than with IR-MPH treatment. (J. of Att. Dis. 2011; 15(4) 286-294)
C1 [Spencer, Thomas J.; Mick, Eric] Massachusetts Gen Hosp, Clin & Res Program Pediat Psychopharmacol, Boston, MA 02114 USA.
[Surman, Craig B. H.] Massachusetts Gen Hosp, Adult ADHD Res Program, Boston, MA 02114 USA.
[Hammerness, Paul] Massachusetts Gen Hosp, Clin & Res Program Pediat Psychopharmacol & Adult, Boston, MA 02114 USA.
[Doyle, Robert] Massachusetts Gen Hosp, Child & Adolescent Psychiat Clin, Boston, MA 02114 USA.
[Aleardi, Megan; Kotarski, Meghan; Biederman, Joseph] Massachusetts Gen Hosp, Clin & Res Programs Pediat Psychopharmacol & Adul, Boston, MA 02114 USA.
[Williams, Courtney G.] Massachusetts Gen Hosp, Pediat Psychopharmacol & Adult Adhd Res Program, Boston, MA 02114 USA.
[Spencer, Thomas J.; Mick, Eric; Hammerness, Paul; Biederman, Joseph] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Doyle, Robert] Harvard Univ, Hlth Serv, Boston, MA 02114 USA.
RP Spencer, TJ (reprint author), Massachusetts Gen Hosp, Clin & Res Program Pediat Psychopharmacol, 6th Floor Yawkee Bldg, Boston, MA 02114 USA.
EM tspencer@partners.org
OI Mick, Eric/0000-0001-8505-8145
FU McNeil Pediatrics; Shire Laboratories, Inc.; Eli Lilly Company;
Glaxo-Smith Kline; Janssen Pharmaceutical; McNeil Pharmaceutical;
Novartis Pharmaceuticals; Cephalon; Pfizer; National Institute of Mental
Health; Ortho-McNeil Janssen Scientific Affairs; Shire Pharmaceuticals;
Abbott; Eli Lilly; Forest; McNeil; Shire; Elminda Ltd; Bristol Myers
Squibb; Johnson Johnson; Merck; New River; Organon; Takeda; Alza;
AstraZeneca; Janssen Pharmaceuticals Inc.; Otsuka; NICHD; Fundacion
Areces; Medice Pharmaceuticals; Spanish Child Psychiatry Association;
Celltech; Esai; Glaxo; Gliatech; Janssen; NARSAD; NIDA; Noven;
Neurosearch; Pharmacia; Prechter Foundation; Stanley Foundation; UCB
Pharma, Inc.; Wyeth; ElMinda; Hilda and Preston Davis Foundation;
National Institutes of Health; Janssen-Ortho; MGH Academy/Reed Medical
Education
FX Dr. Thomas Spencer has received research support from, has been a
speaker for, or has been a speaker on a speaker bureau, or has been on
an Advisory Board of the following sources: Shire Laboratories, Inc.,
Eli Lilly & Company, Glaxo-Smith Kline, Janssen Pharmaceutical, McNeil
Pharmaceutical, Novartis Pharmaceuticals, Cephalon, Pfizer, and the
National Institute of Mental Health.; Dr. Eric Mick receives research
support from the following sources and is on an advisory board for the
following sources: McNeil Pediatrics, Ortho-McNeil Janssen Scientific
Affairs, Pfizer, Shire Pharmaceuticals, and the National Institute of
Mental Health (NIMH) and has had an advisory or consulting relationship
with Pfizer and Shire Pharmaceutical.; In the past 2 years, Dr.
Hammerness has received research funds or participated in CME
activities/professional talks supported by the following pharmaceutical
companies: Abbott, Eli Lilly, Forest, McNeil, Shire. Dr. Hammerness has
also received research funds from Elminda Ltd and has participated in
speaker training and served on the advisory board for Shire. In the past
2 years, Dr. Hammerness has participated, as an investigator, in
research studies funded by the following pharmaceutical companies:
Abbott, Bristol Myers Squibb, Cephalon, Eli Lilly, Glaxo-SmithKline,
Johnson & Johnson, McNeil, Merck, New River, Organon, Pfizer, Shire,
Takeda. Dr. Hammerness has also received honoraria from Reed Medical
Education (a logistics collaborator for the MGH Psychiatry Academy).
Commercial entities supporting the MGH Psychiatry Academy are listed on
the Academy's website, www.mghcme.org.; Dr. Joseph Biederman is
currently receiving research support from the following sources: Alza,
AstraZeneca, Bristol Myers Squibb, Eli Lilly and Co., Janssen
Pharmaceuticals Inc., McNeil, Merck, Organon, Otsuka, Shire, NIMH, and
NICHD; In 2009, Dr. Joseph Biederman received a speaker's fee from the
following sources: Fundacion Areces, Medice Pharmaceuticals, and the
Spanish Child Psychiatry Association; In previous years, Dr. Joseph
Biederman received research support, consultation fees, or speaker's
fees for/from the following additional sources: Abbott, AstraZeneca,
Celltech, Cephalon, Eli Lilly and Co., Esai, Forest, Glaxo, Gliatech,
Janssen, McNeil, NARSAD, NIDA, New River, Novartis, Noven, Neurosearch,
Pfizer, Pharmacia, The Prechter Foundation, Shire, The Stanley
Foundation, UCB Pharma, Inc. and Wyeth; Dr. Surman has received research
support from Abbott, Alza, Cephalon, Eli Lilly, ElMinda the Hilda and
Preston Davis Foundation, McNeil, Merck, New River, National Institutes
of Health, Organon, Pfizer, Shire, and Takeda; has been a speaker for
Janssen-Ortho, McNeil, Novartis, Shire, and MGH Academy/Reed Medical
Education (which received funding from multiple pharmaceutical
companies); and has been a consultant/advisor for McNeil, Shire and
Takeda.
NR 18
TC 13
Z9 13
U1 0
U2 6
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1087-0547
EI 1557-1246
J9 J ATTEN DISORD
JI J. Atten. Disord.
PD MAY
PY 2011
VL 15
IS 4
BP 286
EP 294
DI 10.1177/1087054710367880
PG 9
WC Psychology, Developmental; Psychiatry
SC Psychology; Psychiatry
GA 745VK
UT WOS:000289197800003
PM 20495161
ER
PT J
AU Sudore, RL
Covinsky, KE
AF Sudore, Rebecca L.
Covinsky, Kenneth E.
TI Respecting Elders by Respecting Their Paid Caregivers
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Editorial Material
ID LIMITED HEALTH LITERACY; SELF-MANAGEMENT; CONTROLLED-TRIAL; PATIENT
C1 [Sudore, Rebecca L.; Covinsky, Kenneth E.] San Francisco VA Med Ctr, San Francisco, CA 94122 USA.
[Sudore, Rebecca L.; Covinsky, Kenneth E.] Univ Calif San Francisco, Div Geriatr, San Francisco, CA 94143 USA.
RP Sudore, RL (reprint author), San Francisco VA Med Ctr, 4150 Clement St,181G, San Francisco, CA 94122 USA.
EM rebecca.sudore@ucsf.edu
FU NIA NIH HHS [K24 AG029812]
NR 13
TC 3
Z9 3
U1 2
U2 3
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 MAY
PY 2011
VL 26
IS 5
BP 464
EP 465
DI 10.1007/s11606-011-1667-z
PG 2
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 750QI
UT WOS:000289562700004
PM 21424164
ER
PT J
AU Bhatnagar, D
Morris, JL
Rodriguez, M
Centor, RM
Estrada, CA
Willett, LL
AF Bhatnagar, Deepa
Morris, Jason L.
Rodriguez, Martin
Centor, Robert M.
Estrada, Carlos A.
Willett, Lisa L.
TI A Middle-Age Woman with Sudden Onset Dyspnea
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Editorial Material
ID STRATEGIES; MEDICINE
C1 [Bhatnagar, Deepa; Morris, Jason L.; Centor, Robert M.; Estrada, Carlos A.; Willett, Lisa L.] Univ Alabama, Birmingham, AL 35294 USA.
[Bhatnagar, Deepa; Rodriguez, Martin] Univ Alabama, Birmingham, AL USA.
[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 Willett, LL (reprint author), Univ Alabama, BDB 341,1530 3rd Ave, Birmingham, AL 35294 USA.
EM lwillett@uab.edu
NR 6
TC 2
Z9 2
U1 0
U2 0
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 MAY
PY 2011
VL 26
IS 5
BP 551
EP 554
DI 10.1007/s11606-011-1636-6
PG 4
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 750QI
UT WOS:000289562700020
PM 21301984
ER
PT J
AU Shang, SB
Ordway, D
Henao-Tamayo, M
Bai, XY
Oberley-Deegan, R
Shanley, C
Orme, IM
Case, S
Minor, M
Ackart, D
Hascall-Dove, L
Ovrutsky, AR
Kandasamy, P
Voelker, DR
Lambert, C
Freed, BM
Iseman, MD
Basaraba, RJ
Chan, ED
AF Shang, Shaobin
Ordway, Diane
Henao-Tamayo, Marcela
Bai, Xiyuan
Oberley-Deegan, Rebecca
Shanley, Crystal
Orme, Ian M.
Case, Stephanie
Minor, Maisha
Ackart, David
Hascall-Dove, Laurel
Ovrutsky, Alida R.
Kandasamy, Pitchaimani
Voelker, Dennis R.
Lambert, Cherie
Freed, Brian M.
Iseman, Michael D.
Basaraba, Randall J.
Chan, Edward D.
TI Cigarette Smoke Increases Susceptibility to Tuberculosis-Evidence From
In Vivo and In Vitro Models
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID NICOTINIC ACETYLCHOLINE-RECEPTORS; MYCOBACTERIUM-TUBERCULOSIS; PULMONARY
TUBERCULOSIS; TOBACCO-SMOKE; CYTOKINE PRODUCTION; DENDRITIC CELLS;
IMMUNE-RESPONSE; PASSIVE SMOKING; RISK-FACTOR; MICE
AB Methods. We exposed C57BL/6 mice to CS for 14 weeks and examined their ability to control an aerosol infection of Mycobacterium tuberculosis Erdman.
Results. CS-exposed mice had more M. tuberculosis isolated from the lungs and spleens after 14 and 30 d, compared with control mice. The CS-exposed mice had worse lung lesions and less lung and splenic macrophages and dendritic cells (DCs) producing interleukin12 and tumor necrosis factor alpha (TNF-alpha). There were significantly more interleukin 10-producing macrophages and DCs in the spleens of infected CS-exposed mice than in non-CS-exposed controls. CS-exposed mice also showed a diminished influx of interferon gamma-producing and TNF-alpha-producing CD4(+) and CD8(+) effector and memory T cells into the lungs and spleens. There was a trend toward an increased number of viable intracellular M. tuberculosis in macrophages isolated from humans who smoke compared with nonsmokers. THP-1 human macrophages and primary human alveolar macrophages exposed to CS extract, nicotine, or acrolein showed an increased burden of intracellular M. tuberculosis.
Conclusion. CS suppresses the protective immune response to M. tuberculosis in mice, human THP-1 cells, and primary human alveolar macrophages.
C1 [Shang, Shaobin; Ordway, Diane; Henao-Tamayo, Marcela; Shanley, Crystal; Orme, Ian M.; Ackart, David; Hascall-Dove, Laurel; Basaraba, Randall J.] Colorado State Univ, Dept Microbiol Immunol & Pathol, Mycobacteria Res Labs, Ft Collins, CO 80523 USA.
[Bai, Xiyuan; Ovrutsky, Alida R.; Chan, Edward D.] Denver Vet Affairs Med Ctr, Denver, CO USA.
[Oberley-Deegan, Rebecca; Case, Stephanie; Minor, Maisha; Kandasamy, Pitchaimani; Voelker, Dennis R.; Iseman, Michael D.; Chan, Edward D.] Natl Jewish Hlth, Dept Med, Denver, CO USA.
[Oberley-Deegan, Rebecca; Case, Stephanie; Minor, Maisha; Kandasamy, Pitchaimani; Voelker, Dennis R.; Iseman, Michael D.; Chan, Edward D.] Natl Jewish Hlth, Dept Acad Affairs, Denver, CO USA.
[Bai, Xiyuan; Ovrutsky, Alida R.; Iseman, Michael D.; Chan, Edward D.] Univ Colorado Denver, Div Pulm Sci & Crit Care Med, Denver, CO USA.
[Lambert, Cherie; Freed, Brian M.] Univ Colorado Denver, Div Clin Immunol & Allergy, Denver, CO USA.
RP Ordway, D (reprint author), Colorado State Univ, Dept Microbiol Immunol & Pathol, Mycobacteria Res Labs, Ft Collins, CO 80523 USA.
EM d.ordway-rodriguez@colostate.edu
RI Shang, Shaobin/K-5669-2015; Henao-Tamayo, Marcela/D-8189-2017
OI Shang, Shaobin/0000-0003-4407-1911; Henao-Tamayo,
Marcela/0000-0002-4249-9650
FU College of Veterinary Medicine and Biomedical Sciences Research Council,
Colorado State University [149106]
FX This work was supported by the College of Veterinary Medicine and
Biomedical Sciences Research Council, Colorado State University (grant
number 149106).
NR 49
TC 36
Z9 36
U1 1
U2 10
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1537-6613
J9 J INFECT DIS
JI J. Infect. Dis.
PD MAY 1
PY 2011
VL 203
IS 9
BP 1240
EP 1248
DI 10.1093/infdis/jir009
PG 9
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 747FQ
UT WOS:000289306100007
PM 21357942
ER
PT J
AU Kim, AY
Timm, J
Bloom, AK
Allen, TM
AF Kim, Arthur Y.
Timm, Joerg
Bloom, Allyson K.
Allen, Todd M.
TI Two Years' Persistence of Naturally Present Substitution R155K Within
Hepatitis C Virus NS3 Protease in the Absence of Protease
Inhibitor-based Therapy Reply
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Letter
C1 [Kim, Arthur Y.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Bloom, Allyson K.; Allen, Todd M.] MGH MIT & Harvard, Ragon Inst, Boston, MA USA.
[Timm, Joerg] Univ Duisburg Essen, Essen, Germany.
RP Kim, AY (reprint author), MGH, Partners AIDS Res Ctr, Infect Dis Unit, 149 13th St,5th Floor, Charlestown, MA 02129 USA.
EM akim1@partners.org
RI Allen, Todd/F-5473-2011
NR 4
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1537-6613
J9 J INFECT DIS
JI J. Infect. Dis.
PD MAY 1
PY 2011
VL 203
IS 9
BP 1342
EP 1343
DI 10.1093/infdis/jir022
PG 2
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 747FQ
UT WOS:000289306100021
ER
PT J
AU Rowell, SL
Oral, E
Muratoglu, OK
AF Rowell, Shannon L.
Oral, Ebru
Muratoglu, Orhun K.
TI Comparative Oxidative Stability of alpha-Tocopherol Blended and Diffused
UHMWPEs at 3 Years of Real-Time Aging
SO JOURNAL OF ORTHOPAEDIC RESEARCH
LA English
DT Article
DE total hip arthroplasty; highly cross-linked polyethylene; oxidation
resistance; vitamin E; alpha-tocopherol
ID MOLECULAR-WEIGHT POLYETHYLENE; IRRADIATED UHMWPE; VITAMIN-E;
MECHANICAL-PROPERTIES; CROSS-LINKING; FREE-RADICALS; WEAR;
STABILIZATION; COMPONENTS
AB Vitamin E (alpha-tocopherol) is a free-radical stabilizing antioxidant used to maintain oxidative stability in radiation cross-linked ultra-high molecular weight polyethylene (UHMWPE) used in total joint replacements. We investigated the oxidative resistance of vitamin E-stabilized UHMWPE in (i) postirradiation vitamin E-diffused UHMWPE, (ii) vitamin E blended and irradiated UHMWPE, and (iii) unstabilized, irradiated UHMWPE after accelerated aging and real-time aging in an aqueous environment at 40 degrees C for 36 months. Unstabilized samples exhibited substantial oxidation throughout the surface and bulk with both types of aging. While vitamin E-stabilized, radiation cross-linked UHMWPEs were all superior to unstabilized samples, irradiated blends showed surface oxidation and subsurface oxidation potential beginning at ten months in real-time aging. In contrast, postirradiation vitamin E-diffused UHMWPEs showed no detectable oxidation and no increase in oxidation potential despite elution of some vitamin E. We also showed that current thermal accelerated aging methods were unable to differentiate among the oxidative stability of vitamin E-stabilized, radiation cross-linked UHMWPEs prepared by different processes. (C) 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 29:773-780, 2011
C1 [Rowell, Shannon L.; Oral, Ebru; Muratoglu, Orhun K.] Massachusetts Gen Hosp, Harris Orthopaed Lab, Boston, MA 02114 USA.
[Oral, Ebru; Muratoglu, Orhun K.] Harvard Univ, Sch Med, Dept Orthopaed Surg, Boston, MA USA.
RP Oral, E (reprint author), Massachusetts Gen Hosp, Harris Orthopaed Lab, Boston, MA 02114 USA.
EM eoral@partners.org
FU NIH [AR051142]; Biomet, Inc.; Zimmer, Inc.
FX This work was funded by NIH (AR051142), Biomet, Inc., Zimmer, Inc., and
laboratory funds. Dr. Muratoglu receives royalties from Zimmer and
Biomet, and he is a non-paid consultant for Biomet. Dr. Oral receives
royalties from Zimmer.
NR 21
TC 12
Z9 14
U1 1
U2 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0736-0266
EI 1554-527X
J9 J ORTHOP RES
JI J. Orthop. Res.
PD MAY
PY 2011
VL 29
IS 5
BP 773
EP 780
DI 10.1002/jor.21288
PG 8
WC Orthopedics
SC Orthopedics
GA 748XA
UT WOS:000289425100021
PM 21437958
ER
PT J
AU Cypess, AM
AF Cypess, Aaron M.
TI A New Connection between Muscle and Brown Fat
SO JOURNAL OF PEDIATRICS
LA English
DT Editorial Material
ID ADIPOSE-TISSUE; ADULT HUMANS; HOMEOSTASIS
C1 Joslin Diabet Ctr, Boston, MA 02215 USA.
RP Cypess, AM (reprint author), Joslin Diabet Ctr, 1 Joslin Pl, Boston, MA 02215 USA.
EM aaron.cypess@joslin.harvard.edu
FU NCRR NIH HHS [KL2 RR025757, UL1 RR025758]; NIDDK NIH HHS [RC1 DK087317,
K23 DK081604, R01 DK082659]
NR 15
TC 0
Z9 1
U1 0
U2 1
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 MAY
PY 2011
VL 158
IS 5
BP 696
EP 698
DI 10.1016/j.jpeds.2011.01.001
PG 4
WC Pediatrics
SC Pediatrics
GA 746YH
UT WOS:000289286100003
PM 21353245
ER
PT J
AU Kemper, AR
Knapp, AA
Metterville, DR
Comeau, AM
Green, NS
Perrin, JM
AF Kemper, Alex R.
Knapp, Alixandra A.
Metterville, Danielle R.
Comeau, Anne Marie
Green, Nancy S.
Perrin, James M.
TI Weighing the Evidence for Newborn Screening for Hemoglobin H Disease
SO JOURNAL OF PEDIATRICS
LA English
DT Article
ID CLINICAL-FEATURES; COMMITTEE REPORT; CALIFORNIA; SARDINIA
AB Objective To conduct a systematic review to assist the United States Secretary of Health and Human Services Advisory Committee on Heritable Disorders in Newborns and Children (SACHDNC) to determine whether Hemoglobin H screening should be included among the core recommended conditions for newborn screening.
Study design We identified 21 articles in MEDLINE from 1989 to March 2010 that provided evidence regarding screening, treatment, and outcomes associated with Hemoglobin H disease.
Results In California, newborn screening has identified 9 cases per 100 000 of deletional hemoglobin H disease and 0.6 cases per 100 000 of nondeletional hemoglobin H disease. Five cases of hemoglobin Bart's hydrops fetalis syndrome were also identified in over ten years of screening for Hemoglobin H disease. Although Hemoglobin H disease is associated with a wide range of morbidity, no studies were found that evaluated the benefits of early identification and treatment.
Conclusions The SACHDNC found the data insufficient to recommend that states adopt newborn screening for Hemoglobin H disease. (J Pediatr 2011; 158: 780-3).
C1 [Kemper, Alex R.] Duke Univ, Duke Clin Res Inst, Durham, NC 27705 USA.
[Kemper, Alex R.; Metterville, Danielle R.; Perrin, James M.] MassGen Hosp Children, Ctr Child & Adolescent Hlth Policy, Boston, MA USA.
[Comeau, Anne Marie] Univ Massachusetts, Sch Med, New England Newborn Screening Program, Worcester, MA USA.
[Comeau, Anne Marie] Univ Massachusetts, Sch Med, Dept Pediat, Worcester, MA USA.
[Green, Nancy S.] Columbia Univ, Dept Pediat, New York, NY 10027 USA.
RP Kemper, AR (reprint author), Duke Univ, Duke Clin Res Inst, 2400 Pratt St,Room 0311 Terrace Level, Durham, NC 27705 USA.
EM alex.kemper@duke.edu
OI Green, Nancy/0000-0002-9877-1561
FU HHS; HRSA; Maternal and Child Health Bureau (MCHB)
FX Supported by subcontracts to Columbia University, Duke University, and
MassGeneral Hospital for Children under prime contract
(HHSP23320045014XI) to Altarum Institute, from HHS, HRSA, Maternal and
Child Health Bureau (MCHB). The authors declare no conflicts of
interest.
NR 18
TC 9
Z9 10
U1 0
U2 0
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 MAY
PY 2011
VL 158
IS 5
BP 780
EP 783
DI 10.1016/j.jpeds.2010.10.042
PG 4
WC Pediatrics
SC Pediatrics
GA 746YH
UT WOS:000289286100018
PM 21167500
ER
PT J
AU Gould, MK
Schultz, EM
Wagner, TH
Xu, XY
Ghaus, SJ
Wallace, RB
Provenzale, D
Au, DH
AF Gould, Michael K.
Schultz, Ellen M.
Wagner, Todd H.
Xu, Xiangyan
Ghaus, Sharfun J.
Wallace, Robert B.
Provenzale, Dawn
Au, David H.
TI Disparities in Lung Cancer Staging with Positron Emission Tomography in
the Cancer Care Outcomes Research and Surveillance (CanCORS) Study
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Article
DE Lung neoplasms; Carcinoma; Non-small cell lung; Neoplasm staging;
Tomography; Emission-computed; Healthcare disparities
ID FORTHCOMING 7TH EDITION; GUIDELINES 2ND EDITION; MEDICARE BENEFICIARIES;
RACIAL DISPARITIES; TNM CLASSIFICATION; MALIGNANT-TUMORS;
RANDOMIZED-TRIAL; COMORBIDITY; PROPOSALS; GROUPINGS
AB Introduction: Disparities in treatment exist for nonwhite and Hispanic patients with non-small cell lung cancer, but little is known about disparities in the use of staging tests or their underlying causes.
Methods: Prospective, observational cohort study of 3638 patients with newly diagnosed non-small cell lung cancer from 4 large, geographically defined regions, 5 integrated health care systems, and 13 VA health care facilities.
Results: Median age was 69 years, 62% were men, 26% were Hispanic or nonwhite, 68% graduated high school, 50% had private insurance, and 41% received care in the VA or another integrated health care system. After adjustment, positron emission tomography (PET) use was 13% lower among nonwhites and Hispanics than non-Hispanic whites (risk ratio [RR] 0.87, 95% confidence interval [CI] 0.77-0.97), 13% lower among those with Medicare than those with private insurance (RR 0.87, 95% CI 0.76-0.99), and 24% lower among those with an elementary school education than those with a graduate degree (RR 0.76, 95% CI 0.57-0.98). Disparate use of PET was not observed among patients who received care in an integrated health care setting, but the association between race/ethnicity and PET use was similar in magnitude across all other subgroups. Further analysis showed that income, education, insurance, and health care setting do not explain the association between race/ethnicity and PET use.
Conclusions: Hispanics and nonwhites with non-small cell lung cancer are less likely to receive PET imaging. This finding is consistent across subgroups and not explained by differences in income, education, or insurance coverage.
C1 [Gould, Michael K.] Univ So Calif, Keck Sch Med, Los Angeles, CA 90033 USA.
[Gould, Michael K.; Wagner, Todd H.; Ghaus, Sharfun J.] VA Palo Alto Hlth Care Syst, Palo Alto, CA USA.
[Gould, Michael K.; Schultz, Ellen M.] Stanford Univ, Ctr Primary Care & Outcomes Res, Stanford, CA 94305 USA.
[Wagner, Todd H.] VA Hlth Econ Res Ctr, Menlo Pk, CA USA.
[Xu, Xiangyan] Palo Alto Inst Res & Educ, Palo Alto, CA USA.
[Wallace, Robert B.] Univ Iowa, Iowa City, IA USA.
[Provenzale, Dawn] Durham VA Med Ctr, Durham Epidemiol Res & Informat Ctr, Durham, NC USA.
[Provenzale, Dawn] Duke Univ, Durham, NC USA.
[Au, David H.] Univ Washington, Hlth Serv Res & Dev Serv, VA Puget Sound Hlth Care Syst, Seattle, WA 98195 USA.
[Au, David H.] Univ Washington, Dept Med, Seattle, WA USA.
RP Gould, MK (reprint author), Univ So Calif, Keck Sch Med, 2020 Zonal Ave,IRD 715, Los Angeles, CA 90033 USA.
EM mgould@usc.edu
FU NCI NIH HHS [U01 CA093344-01, U01 CA093324, P30 CA014089-34S4, U01
CA093348, U01 CA093339, P30 CA014089, U01 CA093326, U01 CA093332, U01
CA093344, U01 CA093329]
NR 31
TC 4
Z9 4
U1 2
U2 2
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 MAY
PY 2011
VL 6
IS 5
BP 875
EP 883
DI 10.1097/JTO.0b013e31821671b6
PG 9
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA 750NF
UT WOS:000289554100006
PM 21572580
ER
PT J
AU Ou, SHI
Kwak, EL
Siwak-Tapp, C
Dy, J
Bergethon, K
Clark, JW
Camidge, DR
Solomon, BJ
Maki, RG
Bang, YJ
Kim, DW
Christensen, J
Tan, WW
Wilner, KD
Salgia, R
Iafrate, AJ
AF Ou, Sai-Hong Ignatius
Kwak, Eunice L.
Siwak-Tapp, Christina
Dy, Joni
Bergethon, Kristin
Clark, Jeffrey W.
Camidge, D. Ross
Solomon, Benjamin J.
Maki, Robert G.
Bang, Yung-Jue
Kim, Dong-Wan
Christensen, James
Tan, Weiwei
Wilner, Keith D.
Salgia, Ravi
Iafrate, A. John
TI Activity of Crizotinib (PF02341066), a Dual Mesenchymal-Epithelial
Transition (MET) and Anaplastic Lymphoma Kinase (ALK) Inhibitor, in a
Non-small Cell Lung Cancer Patient with De Novo MET Amplification
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Article
DE Non-small cell lung cancer; De novo MET amplification NSCLC; 18(F)-FDG
PET/CT; Crizotinib (PF02341066); MET polysomy; Anaplastic lymphoma
kinase (ALK) re-arranged NSCLC
ID GENE COPY NUMBER; RESISTANCE; MUTATIONS; GEFITINIB; ERLOTINIB; SURVIVAL;
TUMORS; LEADS
AB Crizotinib is a dual MET and ALK inhibitor. Currently, clinical development of crizotinib is focused primarily on ALK rearranged non-small cell lung cancer (NSCLC). Here we report an NSCLC patient with de novo MET amplification but no ALK rearrangement who achieved a rapid and durable response to crizotinib indicating is also a bona fide MET inhibitor.
C1 [Ou, Sai-Hong Ignatius] Univ Calif Irvine, Med Ctr, Div Hematol Oncol, Dept Internal Med,Chao Family Comprehens Canc Ctr, Orange, CA 92868 USA.
[Kwak, Eunice L.; Bergethon, Kristin; Clark, Jeffrey W.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
[Camidge, D. Ross] Univ Colorado, Ctr Canc, Aurora, CO USA.
[Solomon, Benjamin J.] Peter MacCallum Canc Ctr, Melbourne, Vic, Australia.
[Maki, Robert G.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Bang, Yung-Jue; Kim, Dong-Wan] Seoul Natl Univ Hosp, Dept Internal Med, Seoul 110744, South Korea.
[Christensen, James; Tan, Weiwei; Wilner, Keith D.] Pfizer Global Res & Dev, La Jolla, CA USA.
[Salgia, Ravi] Univ Chicago, Med Ctr, Chicago, IL 60637 USA.
[Iafrate, A. John] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
RP Ou, SHI (reprint author), Univ Calif Irvine, Med Ctr, Div Hematol Oncol, Dept Internal Med,Chao Family Comprehens Canc Ctr, 101 City Dr,Bldg 56,RT 81,Rm 241, Orange, CA 92868 USA.
EM Ignatius.ou@uci.edu
RI Bang, Yung Jue/J-2759-2012
FU Pfizer, Inc. [A8081001]; [5RO1CA125541-05]
FX Supported by (A8081001, ClinicalTrials.gov identifier NCT00585195)
Pfizer, Inc. Ravi Salgia, MD, PhD, is supported by grant
5RO1CA125541-05.
NR 19
TC 181
Z9 191
U1 6
U2 24
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 MAY
PY 2011
VL 6
IS 5
BP 942
EP 946
DI 10.1097/JTO.0b013e31821528d3
PG 5
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA 750NF
UT WOS:000289554100015
PM 21623265
ER
PT J
AU Choi, WW
Williams, SB
Gu, XM
Lipsitz, SR
Nguyen, PL
Hu, JC
AF Choi, Wesley W.
Williams, Stephen B.
Gu, Xiangmei
Lipsitz, Stuart R.
Nguyen, Paul L.
Hu, Jim C.
TI Overuse of Imaging for Staging Low Risk Prostate Cancer
SO JOURNAL OF UROLOGY
LA English
DT Article
DE diagnostic imaging; health services misuse; prostatic neoplasms; health
expenditures
ID COMPUTED-TOMOGRAPHY; BONE-SCAN; CONTEMPORARY TRENDS; ANTIGEN;
STATISTICS; QUALITY; CARE; MEN
AB Purpose: Routine imaging for staging low risk prostate cancer is not recommended according to current guidelines. We characterized patterns of care and factors associated with imaging overuse.
Materials and Methods: We used SEER-Medicare linked data to identify men diagnosed with low risk prostate cancer from 2004 to 2005, and determined if imaging (computerized tomography, magnetic resonance imaging, bone scan, abdominal ultrasound) was obtained following prostate cancer diagnosis before treatment.
Results: Of the 6,444 men identified with low risk disease 2,330 (36.2%) underwent imaging studies. Of these men 1,512 (23.5%), 1,710 (26.5%) and 118 (1.8%) underwent cross-sectional imaging (computerized tomography or magnetic resonance imaging), bone scan and abdominal ultrasound, respectively. Radiation therapy vs surgery was associated with greater odds of imaging (OR 1.99, 95% CI 1.68-2.35, p < 0.01), while active surveillance vs surgery was associated with lower odds of imaging (OR 0.44, 95% CI 0.34-0.56, p < 0.01). Associated with increased odds of imaging was median household income greater than $60,000 (OR 1.41, 95% CI 1.11-1.79, p < 0.01), and men from New Jersey vs San Francisco (OR 3.11, 95% CI 2.24-4.33, p < 0.01) experienced greater odds of imaging. Men living in areas with greater than 90% vs less than 75% high school education experienced lower odds of imaging (OR 0.76, 95% CI 0.6-0.95, p = 0.02).
Conclusions: There is widespread overuse and significant geographic variation in the use of imaging to stage low risk prostate cancer. Moreover treatment associated variation in imaging was noted with the greatest vs lowest imaging use observed for radiation therapy vs active surveillance.
C1 [Choi, Wesley W.; Williams, Stephen B.; Hu, Jim C.] Harvard Univ, Sch Med, Div Urol Surg, Boston, MA USA.
[Gu, Xiangmei; Lipsitz, Stuart R.; Hu, Jim C.] Harvard Univ, Ctr Surg & Publ Hlth, Sch Med, Boston, MA USA.
[Nguyen, Paul L.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Radiat Oncol, Boston, MA 02115 USA.
[Nguyen, Paul L.; Hu, Jim C.] Dana Farber Canc Inst, Lank Ctr Genitourinary Oncol, Boston, MA 02115 USA.
RP Hu, JC (reprint author), Brigham & Womens Faulkner Hosp, 1153 Ctr St,Ste 4420, Boston, MA 02130 USA.
EM jhu2@partners.org
FU Robert and Kathy Salipante Minimally Invasive Urologic Oncology
Fellowship; Department of Defense [W81XWH-08-1-0283]
FX Supported by the Robert and Kathy Salipante Minimally Invasive Urologic
Oncology Fellowship.; Recipient of Department of Defense Physician
Training Award W81XWH-08-1-0283.
NR 30
TC 30
Z9 30
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
EI 1527-3792
J9 J UROLOGY
JI J. Urol.
PD MAY
PY 2011
VL 185
IS 5
BP 1645
EP 1649
DI 10.1016/j.juro.2010.12.033
PG 5
WC Urology & Nephrology
SC Urology & Nephrology
GA 746WQ
UT WOS:000289279600031
PM 21419444
ER
PT J
AU Jura, YH
Townsend, MK
Curhan, GC
Resnick, NM
Grodstein, F
AF Jura, Ying H.
Townsend, Mary K.
Curhan, Gary C.
Resnick, Neil M.
Grodstein, Francine
TI Caffeine Intake, and the Risk of Stress, Urgency and Mixed Urinary
Incontinence
SO JOURNAL OF UROLOGY
LA English
DT Article
DE urinary incontinence; stress; urinary incontinence; urge; caffeine;
epidemiology; female
ID LIFE-STYLE FACTORS; QUESTIONNAIRE; VALIDITY; BLADDER; WOMEN
AB Purpose: Although caffeine consumption is common and generally believed to affect bladder function, little is known about caffeine intake and incident urinary incontinence.
Materials and Methods: We performed a prospective cohort study in 65,176 women 37 to 79 years old without incontinence in the Nurses' Health Study and the Nurses' Health Study II. Incident incontinence was identified from questionnaires during 4 years of followup. Caffeine intake was measured using food frequency questionnaires administered before incontinence development. The multivariate adjusted relative risk of the relation between caffeine intake and incontinence risk as well as attributable risk were calculated.
Results: Caffeine was not associated with incontinence monthly or more. However, there was a modest, significantly increased risk of incontinence at least weekly in women with the highest (greater than 450 mg) vs the lowest (less than 150 mg) daily intake (RR 1.19, 95% CI 1.06-1.34) and a significant trend of increasing risk with increasing intake (p for trend = 0.01). This risk appeared focused on incident urgency incontinence (greater than 450 vs less than 150 mg daily, RR 1.34, 95% CI 1.00-1.80, p for trend = 0.05) but not on stress or mixed incontinence (p for trend = 0.75 and 0.19, respectively). The attributable risk of urgency incontinence associated with high caffeine intake was 25%.
Conclusions: Findings suggest that high but not lower caffeine intake is associated with a modest increase in the incidence of frequent urgency incontinence. A fourth of the cases with the highest caffeine consumption would be eliminated if high caffeine intake were eliminated. Confirmation of these findings in other studies is needed before recommendations can be made.
C1 [Townsend, Mary K.; Curhan, Gary C.; Grodstein, Francine] Harvard Univ, Channing Lab, Sch Publ Hlth, Boston, MA 02115 USA.
[Jura, Ying H.] Harvard Univ, Sch Publ Hlth, Massachusetts Gen Hosp, Dept Urol, Boston, MA 02115 USA.
[Curhan, Gary C.] Harvard Univ, Sch Publ Hlth, Div Renal, Boston, MA 02115 USA.
[Townsend, Mary K.; Curhan, Gary C.; Grodstein, Francine] Harvard Univ, Sch Publ Hlth, Dept Med, Brigham & Womens Hosp,Dept Epidemiol, Boston, MA 02115 USA.
[Jura, Ying H.; Townsend, Mary K.; Curhan, Gary C.; Grodstein, Francine] Harvard Univ, Sch Med, Boston, MA USA.
[Resnick, Neil M.] Univ Pittsburgh, Sch Med, Div Geriatr Med, Pittsburgh, PA USA.
RP Townsend, MK (reprint author), Harvard Univ, Channing Lab, Sch Publ Hlth, 181 Longwood Ave, Boston, MA 02115 USA.
EM nhmkt@channing.harvard.edu
FU National Institutes of Health [DK62438, CA87969, CA50385]; Harvard
School of Public Health (MKT); Up-To-Date, Takeda; Clinical Journal of
the American Society of Nephrology
FX Supported by National Institutes of Health Grants DK62438, CA87969 and
CA50385, and the Yerby Postdoctoral Fellowship Program at Harvard School
of Public Health (MKT).; Financial interest and/or other relationship
with Up-To-Date, Takeda and Clinical Journal of the American Society of
Nephrology.
NR 17
TC 31
Z9 32
U1 0
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5347
EI 1527-3792
J9 J UROLOGY
JI J. Urol.
PD MAY
PY 2011
VL 185
IS 5
BP 1775
EP 1780
DI 10.1016/j.juro.2011.01.003
PG 6
WC Urology & Nephrology
SC Urology & Nephrology
GA 746WQ
UT WOS:000289279600073
PM 21420114
ER
PT J
AU Allen, SJ
Hamrah, P
Gate, D
Mott, KR
Mantopoulos, D
Zheng, LX
Town, T
Jones, C
von Andrian, UH
Freeman, GJ
Sharpe, AH
BenMohamed, L
Ahmed, R
Wechsler, SL
Ghiasi, H
AF Allen, Sariah J.
Hamrah, Pedram
Gate, David
Mott, Kevin R.
Mantopoulos, Dimosthenis
Zheng, Lixin
Town, Terrence
Jones, Clinton
von Andrian, Ulrich H.
Freeman, Gordon J.
Sharpe, Arlene H.
BenMohamed, Lbachir
Ahmed, Rafi
Wechsler, Steven L.
Ghiasi, Homayon
TI The Role of LAT in Increased CD8(+) T Cell Exhaustion in Trigeminal
Ganglia of Mice Latently Infected with Herpes Simplex Virus 1
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID CHRONIC VIRAL-INFECTION; HEPATITIS-C-VIRUS; TYPE-1 LATENCY; SPONTANEOUS
REACTIVATION; PD-1 EXPRESSION; TRANSCRIPT GENE; ELEVATED FREQUENCIES;
DISEASE PROGRESSION; STROMAL KERATITIS; SENSORY GANGLIA
AB Herpes simplex virus (HSV) infection is a classic example of latent viral infection in humans and experimental animal models. The HSV-1 latency-associated transcript (LAT) plays a major role in the HSV-1 latency reactivation cycle and thus in recurrent disease. Whether the presence of LAT leads to generation of dysfunctional T cell responses in the trigeminal ganglia (TG) of latently infected mice is not known. To address this issue, we used LAT-positive [LAT(+)] and LAT-deficient [LAT(-)] viruses to evaluate the effect of LAT on CD8 T cell exhaustion in TG of latently infected mice. The amount of latency as determined by quantitative reverse transcription-PCR (qRT-PCR) of viral DNA in total TG extracts was 3-fold higher with LAT(+) than with LAT(-) virus. LAT expression and increased latency correlated with increased mRNA levels of CD8, PD-1, and Tim-3. PD-1 is both a marker for exhaustion and a primary factor leading to exhaustion, and Tim-3 can also contribute to exhaustion. These results suggested that LAT(+) TG contain both more CD8(+) T cells and more CD8(+) T cells expressing the exhaustion markers PD-1 and Tim-3. This was confirmed by flow cytometry analyses of expression of CD3/CD8/PD-1/Tim-3, HSV-1, CD8(+) T cell pentamer (specific for a peptide derived from residues 498 to 505 of glycoprotein B [gB(498-505)]), interleukin-2 (IL-2), and tumor necrosis factor alpha (TNF-alpha). The functional significance of PD-1 and its ligands in HSV-1 latency was demonstrated by the significantly reduced amount of HSV-1 latency in PD-1- and PD-L1-deficient mice. Together, these results may suggest that both PD-1 and Tim-3 are mediators of CD8(+) T cell exhaustion and latency in HSV-1 infection.
C1 [Allen, Sariah J.; Mott, Kevin R.; Ghiasi, Homayon] Cedars Sinai Burns & Allen Res Inst, Ctr Neurobiol & Vaccine Dev, Dept Surg, Los Angeles, CA 90048 USA.
[Hamrah, Pedram; Mantopoulos, Dimosthenis; Zheng, Lixin] Harvard Univ, Sch Med, Dept Ophthalmol, Massachusetts Eye & Ear Infirm, Boston, MA USA.
[Gate, David; Town, Terrence] Cedars Sinai Med Ctr, Dept Neurosurg, Maxine Dunitz Neurosurg Inst, Los Angeles, CA 90048 USA.
[Gate, David; Town, Terrence] Cedars Sinai Med Ctr, Dept Biomed Sci, Maxine Dunitz Neurosurg Inst, Los Angeles, CA 90048 USA.
[Jones, Clinton] Univ Nebraska, Nebraska Ctr Virol, Dept Vet & Biomed Sci, Lincoln, NE USA.
[von Andrian, Ulrich H.; Sharpe, Arlene H.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Freeman, Gordon J.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med,Dept Med Oncol, Boston, MA 02115 USA.
[Sharpe, Arlene H.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[BenMohamed, Lbachir; Wechsler, Steven L.] Univ Calif Irvine, Sch Med, Dept Ophthalmol, Irvine, CA 92717 USA.
[BenMohamed, Lbachir; Wechsler, Steven L.] Univ Calif Irvine, Sch Med, Gavin Herbert Eye Inst, Irvine, CA 92717 USA.
[Ahmed, Rafi] Emory Univ, Sch Med, Dept Microbiol & Immunol, Atlanta, GA 30322 USA.
[Ahmed, Rafi] Emory Univ, Sch Med, Emory Vaccine Ctr, Atlanta, GA 30322 USA.
[Wechsler, Steven L.] Univ Calif Irvine, Sch Med, Dept Microbiol & Mol Genet, Irvine, CA 92717 USA.
[Wechsler, Steven L.] Univ Calif Irvine, Ctr Virus Res, Irvine, CA USA.
RP Ghiasi, H (reprint author), Cedars Sinai Burns & Allen Res Inst, Ctr Neurobiol & Vaccine Dev, Dept Surg, D2024,8700 Beverly Blvd, Los Angeles, CA 90048 USA.
EM ghiasih@cshs.org
RI von Andrian, Ulrich/A-5775-2008
FU PHS [EY13615, EY13191, 1P20RR15635]; Discovery Eye Foundation; Henry L.
Guenther Foundation; Research to Prevent Blindness; USDA Agriculture and
Food Research Initiative [08-00891, 09-01653]; [P01 56299]
FX This work was supported by PHS grants EY13615 (H. G.) and EY13191 (S. L.
W.), The Discovery Eye Foundation, The Henry L. Guenther Foundation,
Research to Prevent Blindness, and grant P01 56299 to A. H. S., G.J.F.,
and R. A. S. L. Wechsler is an RPB Senior Scientific Investigator.
Support was also provided by the USDA Agriculture and Food Research
Initiative Competitive Grants Program (08-00891 and 09-01653) and a PHS
grant to the Nebraska Center for Virology (1P20RR15635).
NR 83
TC 40
Z9 41
U1 1
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD MAY
PY 2011
VL 85
IS 9
BP 4184
EP 4197
DI 10.1128/JVI.02290-10
PG 14
WC Virology
SC Virology
GA 751LG
UT WOS:000289618600013
PM 21307196
ER
PT J
AU Kasprowicz, V
zur Wiesch, JS
Kuntzen, T
Nolan, BE
Longworth, S
Berical, A
Blum, J
McMahon, C
Reyor, LL
Elias, N
Kwok, WW
McGovern, BG
Freeman, G
Chung, RT
Klenerman, P
Lewis-Ximenez, L
Walker, BD
Allen, TM
Kim, AY
Lauer, GM
AF Kasprowicz, Victoria
zur Wiesch, Julian Schulze
Kuntzen, Thomas
Nolan, Brian E.
Longworth, Steven
Berical, Andrew
Blum, Jenna
McMahon, Cory
Reyor, Laura L.
Elias, Nahel
Kwok, William W.
McGovern, Barbara G.
Freeman, Gordon
Chung, Raymond T.
Klenerman, Paul
Lewis-Ximenez, Lia
Walker, Bruce D.
Allen, Todd M.
Kim, Arthur Y.
Lauer, Georg M.
TI High Level of PD-1 Expression on Hepatitis C Virus (HCV)-Specific CD8(+)
and CD4(+) T Cells during Acute HCV Infection, Irrespective of Clinical
Outcome (vol 82, pg 3154, 2008)
SO JOURNAL OF VIROLOGY
LA English
DT Correction
C1 [Kasprowicz, Victoria] Harvard Univ, Partners AIDS Res Ctr, Massachusetts Gen Hosp, Sch Med, Charlestown, MA 02129 USA.
Univ Hamburg, Med Klin 1, Hamburg, Germany.
Massachusetts Gen Hosp, Transplantat Unit, Dept Surg, Boston, MA 02114 USA.
Benaroya Res Inst Virginia Mason, Seattle, WA USA.
Lemuel Shattuck Hosp, Boston, MA USA.
Tufts Univ, Sch Med, Boston, MA 02111 USA.
Harvard Univ, Sch Med, Dept Med Oncol, Dana Farber Canc Inst,Dept Med, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Gastrointestinal Unit, Dept Med, Boston, MA 02114 USA.
Univ Oxford, Nuffield Dept Med, Oxford OX1 3SY, England.
Fiocruz MS, Inst Oswaldo Cruz, Dept Virol, BR-21045900 Rio De Janeiro, Brazil.
Howard Hughes Med Inst, Chevy Chase, MD USA.
RP Kasprowicz, V (reprint author), Harvard Univ, Partners AIDS Res Ctr, Massachusetts Gen Hosp, Sch Med, 149 13th St,6th Floor,Room 6001, Charlestown, MA 02129 USA.
RI Allen, Todd/F-5473-2011
NR 1
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD MAY
PY 2011
VL 85
IS 9
BP 4633
EP 4633
DI 10.1128/JVI.00376-11
PG 1
WC Virology
SC Virology
GA 751LG
UT WOS:000289618600061
ER
PT J
AU Matthews, PC
Leslie, AJ
Katzourakis, A
Crawford, H
Payne, R
Prendergast, A
Power, K
Kelleher, AD
Klenerman, P
Carlson, J
Heckerman, D
Ndung'u, T
Walker, BD
Allen, TM
Pybus, OG
Goulder, PJR
AF Matthews, Philippa C.
Leslie, Alasdair J.
Katzourakis, Aris
Crawford, Hayley
Payne, Rebecca
Prendergast, Andrew
Power, Karen
Kelleher, Anthony D.
Klenerman, Paul
Carlson, Jonathan
Heckerman, David
Ndung'u, Thumbi
Walker, Bruce D.
Allen, Todd M.
Pybus, Oliver G.
Goulder, Philip J. R.
TI HLA Footprints on Human Immunodeficiency Virus Type 1 Are Associated
with Interclade Polymorphisms and Intraclade Phylogenetic Clustering
(vol 83, pg 4605, 2009)
SO JOURNAL OF VIROLOGY
LA English
DT Correction
C1 [Matthews, Philippa C.] Peter Medawar Bldg Pathogen Res, Nuffield Dept Med, Dept Paediat, Oxford OX1 3SY, England.
Univ Oxford, Dept Zool, Oxford OX1 3SY, England.
Harvard Univ, Massachusetts Gen Hosp, Sch Med, Partners AIDS Res Ctr, Boston, MA USA.
St Vincents Hosp, Ctr Immunol, Sydney, NSW 2010, Australia.
Microsoft Res, Redmond, WA 98055 USA.
Univ KwaZulu Natal, HIV Pathogenesis Programme, Doris Duke Med Res Inst, Durban, South Africa.
Howard Hughes Med Inst, Chevy Chase, MD USA.
RP Matthews, PC (reprint author), Peter Medawar Bldg Pathogen Res, Nuffield Dept Med, Dept Paediat, S Parks Rd, Oxford OX1 3SY, England.
RI Allen, Todd/F-5473-2011
NR 1
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD MAY
PY 2011
VL 85
IS 9
BP 4635
EP 4635
DI 10.1128/JVI.00375-11
PG 1
WC Virology
SC Virology
GA 751LG
UT WOS:000289618600063
ER
PT J
AU Kasprowicz, V
Kang, YH
Lucas, M
zur Wiesch, JS
Kuntzen, T
Fleming, V
Nolan, BE
Longworth, S
Berical, A
Bengsch, B
Thimme, R
Lewis-Ximenez, L
Allen, TM
Kim, AY
Klenerman, P
Lauer, GM
AF Kasprowicz, Victoria
Kang, Yu-Hoi
Lucas, Michaela
zur Wiesch, Julian Schulze
Kuntzen, Thomas
Fleming, Vicki
Nolan, Brian E.
Longworth, Steven
Berical, Andrew
Bengsch, Bertram
Thimme, Robert
Lewis-Ximenez, Lia
Allen, Todd M.
Kim, Arthur Y.
Klenerman, Paul
Lauer, Georg M.
TI Hepatitis C Virus (HCV) Sequence Variation Induces an HCV-Specific
T-Cell Phenotype Analogous to Spontaneous Resolution (vol 84, pg 1656,
2010)
SO JOURNAL OF VIROLOGY
LA English
DT Correction
C1 [Kasprowicz, Victoria] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ragon Inst Massachusetts Gen Hosp Massachusetts I, Boston, MA 02115 USA.
Harvard Univ, Gastrointestinal Unit, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
Univ Oxford, Nuffield Dept Med, Oxford, England.
Univ Freiburg, Med Klin, D-7800 Freiburg, Germany.
Fiocruz MS, Dept Virol, Inst Oswaldo Cruz, BR-21045900 Rio De Janeiro, Brazil.
RP Kasprowicz, V (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ragon Inst Massachusetts Gen Hosp Massachusetts I, Boston, MA 02115 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD MAY
PY 2011
VL 85
IS 9
BP 4636
EP 4636
DI 10.1128/JVI.00374-11
PG 1
WC Virology
SC Virology
GA 751LG
UT WOS:000289618600064
ER
PT J
AU Barnes, JL
Gorin, Y
AF Barnes, Jeffrey L.
Gorin, Yves
TI Myofibroblast differentiation during fibrosis: role of NAD(P)H oxidases
SO KIDNEY INTERNATIONAL
LA English
DT Review
DE extracellular matrix; fibrosis; Nox4; reactive oxygen species; smooth
muscle actin
ID SMOOTH-MUSCLE-CELLS; GROWTH-FACTOR-BETA; EPITHELIAL-MESENCHYMAL
TRANSITION; MESSENGER-RNA TRANSLATION; OXYGEN SPECIES PRODUCTION; RAT
MESANGIAL CELLS; RENAL TUBULOINTERSTITIAL FIBROSIS; FIBRONECTIN ISOFORM
DISTRIBUTION; UNILATERAL URETERAL OBSTRUCTION; FIBROBLAST-SPECIFIC
PROTEIN-1
AB Progression of fibrosis involves interstitial hypercellularity, matrix accumulation, and atrophy of epithelial structures, resulting in loss of normal function and ultimately organ failure. There is common agreement that the fibroblast/myofibroblast is the cell type most responsible for interstitial matrix accumulation and consequent structural deformations associated with fibrosis. During wound healing and progressive fibrotic events, fibroblasts transform into myofibroblasts acquiring smooth muscle features, most notably the expression of alpha-smooth muscle actin and synthesis of mesenchymal cell-related matrix proteins. In renal disease, glomerular mesangial cells also acquire a myofibroblast phenotype and synthesize the same matrix proteins. The origin of interstitial myofibroblasts during fibrosis is a matter of debate, where the cells are proposed to derive from resident fibroblasts, pericytes, perivascular adventitial, epithelial, and/or endothelial sources. Regardless of the origin of the cells, transforming growth factor-beta1 (TGF-beta 1) is the principal growth factor responsible for myofibroblast differentiation to a profibrotic phenotype and exerts its effects via Smad signaling pathways involving mitogen-activated protein kinase and Akt/protein kinase B. Additionally, reactive oxygen species (ROS) have important roles in progression of fibrosis. ROS are derived from a variety of enzyme sources, of which the nicotinamide adenine dinucleotide phosphate (NAD(P) H) oxidase family has been identified as a major source of superoxide and hydrogen peroxide generation in the cardiovasculature and kidney during health and disease. Recent evidence indicates that the NAD(P) H oxidase homolog Nox4 is most accountable for ROS-induced fibroblast and mesangial cell activation, where it has an essential role in TGF-beta 1 signaling of fibroblast activation and differentiation into a profibrotic myofibroblast phenotype and matrix production. Information on the role of ROS in mesangial cell and fibroblast signaling is incomplete, and further research on myofibroblast differentiation during fibrosis is warranted. Kidney International (2011) 79, 944-956; doi:10.1038/ki.2010.516; published online 9 February 2011
C1 [Barnes, Jeffrey L.; Gorin, Yves] Univ Texas Hlth Sci Ctr San Antonio, Div Nephrol, Dept Med, San Antonio, TX 78229 USA.
[Barnes, Jeffrey L.] S Texas Vet Hlth Care Syst, Med Res Serv, Audie Murphy Mem Vet Adm Hosp, San Antonio, TX USA.
RP Barnes, JL (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Div Nephrol, Dept Med, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA.
EM barnesj@uthscsa.edu
OI Gorin, Yves/0000-0003-4048-6925
FU NIDDK NIH HHS [R01 DK079996, R01 DK080106]
NR 221
TC 154
Z9 164
U1 3
U2 30
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0085-2538
J9 KIDNEY INT
JI Kidney Int.
PD MAY
PY 2011
VL 79
IS 9
BP 944
EP 956
DI 10.1038/ki.2010.516
PG 13
WC Urology & Nephrology
SC Urology & Nephrology
GA 750AD
UT WOS:000289514400004
PM 21307839
ER
PT J
AU Chen, CH
Gadikota, HR
Gill, TJ
Li, GA
AF Chen, Chih-Hui
Gadikota, Hemanth R.
Gill, Thomas J.
Li, Guoan
TI The effect of graft fixation sequence on force distribution in
double-bundle anterior cruciate ligament reconstruction
SO KNEE SURGERY SPORTS TRAUMATOLOGY ARTHROSCOPY
LA English
DT Article
DE Anterior cruciate ligament (ACL); Double-bundle reconstruction; Graft
fixation; Sequence; Force distribution
ID FEMORAL TUNNEL PLACEMENT; KNEE FLEXION ANGLES; IN-SITU FORCES; HAMSTRING
TENDONS; ANATOMIC RECONSTRUCTION; SEMITENDINOSUS TENDON; SINGLE-BUNDLE;
POSTEROLATERAL BUNDLES; BIOMECHANICAL ANALYSIS; ACL RECONSTRUCTION
AB This paper investigated the effect of graft fixation sequence on knee joint biomechanics after a double-bundle ACL reconstruction.
Two independently published biomechanical studies that investigated the biomechanics of double-bundle ACL reconstructions using similar robotic testing systems were compared. In each study, ten human cadaveric knees were tested under three different conditions: intact, ACL deficient, and ACL reconstructed using a double-bundle technique with the anteromedial (AM) graft fixed at 60A degrees of flexion and the posterolateral (PL) graft fixed at full extension. In one study (Study A), the AM graft was fixed first; while in another study (Study B), the PL graft was fixed first. Knee kinematics, in situ forces of the ACL and the ACL grafts were measured under two loading conditions: an anterior tibial load of 134 N and a combined tibial torques (10 N center dot m valgus and 5 N center dot m internal tibial torques) in both studies.
When AM graft was fixed first, the in situ force of the AM graft was lower than the native AM bundle at all flexion angles. The in situ force in the PL graft, however, was higher than the native PL bundle at all flexion angles. When the PL graft was fixed first, the in situ force of the AM graft was higher than the native AM bundle, while the in situ forces of the PL graft were lower than the native PL bundle at all flexion angles. Both studies demonstrated that the double-bundle ACL reconstructions can closely restore the normal knee joint kinematics.
Even though the grafts were fixed using similar initial tensions and at same flexion angles, the sequence of fixing the two grafts in a double-bundle ACL reconstruction could alter the in situ forces in the grafts and affect the knee kinematics. These data imply that in clinical application of a double-bundle ACL reconstruction, the sequence of graft fixation should be an important surgical parameter.
C1 [Chen, Chih-Hui; Gadikota, Hemanth R.; Gill, Thomas J.; Li, Guoan] Massachusetts Gen Hosp, Dept Orthopaed Surg, Bioengn Lab, Boston, MA 02114 USA.
[Chen, Chih-Hui; Gadikota, Hemanth R.; Gill, Thomas J.; Li, Guoan] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Chen, Chih-Hui] Taichung Vet Gen Hosp, Dept Orthopaed Surg, Taichung, Taiwan.
[Chen, Chih-Hui] Natl Yang Ming Univ, Inst Biomed Engn, Taipei 112, Taiwan.
RP Li, GA (reprint author), Massachusetts Gen Hosp, Dept Orthopaed Surg, Bioengn Lab, 55 Fruit St,GRJ 1215, Boston, MA 02114 USA.
EM gli1@partners.org
FU National Institutes of Health [R01AR055612]
FX The authors gratefully acknowledge the support of the National
Institutes of Health (R01AR055612).
NR 48
TC 4
Z9 4
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0942-2056
EI 1433-7347
J9 KNEE SURG SPORT TR A
JI Knee Surg. Sports Traumatol. Arthrosc.
PD MAY
PY 2011
VL 19
IS 5
BP 712
EP 718
DI 10.1007/s00167-010-1319-6
PG 7
WC Orthopedics; Sport Sciences; Surgery
SC Orthopedics; Sport Sciences; Surgery
GA 750FD
UT WOS:000289529700004
PM 21082163
ER
PT J
AU Liu, F
Gadikota, HR
Kozanek, M
Hosseini, A
Yue, B
Gill, TJ
Rubash, HE
Li, GA
AF Liu, Fang
Gadikota, Hemanth R.
Kozanek, Michal
Hosseini, Ali
Yue, Bing
Gill, Thomas J.
Rubash, Harry E.
Li, Guoan
TI In vivo length patterns of the medial collateral ligament during the
stance phase of gait
SO KNEE SURGERY SPORTS TRAUMATOLOGY ARTHROSCOPY
LA English
DT Article
DE Knee kinematics; Gait; Stance phase; Medial collateral ligament (MCL)
ID TOTAL KNEE ARTHROPLASTY; NON-OPERATIVE TREATMENT; ANTERIOR CRUCIATE;
POSTEROMEDIAL CORNER; DOUBLE-BUNDLE; RECONSTRUCTION; INJURIES; LAXITY;
VARUS; RESTRAINTS
AB The function of the medial collateral ligament (MCL) during gait has not been investigated. Our objective was to measure the kinematics of the medial collateral ligament during the stance phase of gait on a treadmill using a combined dual fluoroscopic imaging system (DFIS) and MRI technique.
Three-dimensional models of the knee were constructed using magnetic resonance images of 7 healthy human knees. The contours of insertion areas of the superficial MCL (sMCL) and deep MCL (dMCL) on the femur and tibia were constructed using the coronal plane MR images of each knee. Both the sMCL and the dMCL were separated into 3 portions: the anterior, mid, and posterior bundles. The relative elongation of the bundles was calculated using the bundle length at heel strike (or 0% of the stance phase) as a reference.
The lengths of the anterior bundles were positively correlated with the knee flexion angle. The mid-bundles of the sMCL and dMCL were found to function similarly in trend with the anterior bundles during the stance phase of the gait and their lengths had weak correlations with the knee flexion angles. The elongations of the posterior bundles of sMCL and dMCL were peaked at mid-stance and terminal extension/pre-swing stance phase. The lengths of the posterior bundles were negatively correlated with the knee flexion during the stance phase.
The data of this study demonstrated that the anterior and posterior bundles of the sMCL and dMCL have a reciprocal function during the stance phase of gait. This data provide insight into the function of the MCL and a normal reference for the study of physiology and pathology of the MCL. The data may be useful in designing reconstruction techniques to better reproduce the native biomechanical behavior of the MCL.
IV.
C1 [Li, Guoan] Massachusetts Gen Hosp, Dept Orthopaed Surg, Bioengn Lab, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Li, GA (reprint author), Massachusetts Gen Hosp, Dept Orthopaed Surg, Bioengn Lab, 55 Fruit St, Boston, MA 02114 USA.
EM gli1@partners.org
FU NIAMS NIH HHS [R01 AR055612, R01 AR055612-02]
NR 34
TC 17
Z9 20
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0942-2056
EI 1433-7347
J9 KNEE SURG SPORT TR A
JI Knee Surg. Sports Traumatol. Arthrosc.
PD MAY
PY 2011
VL 19
IS 5
BP 719
EP 727
DI 10.1007/s00167-010-1336-5
PG 9
WC Orthopedics; Sport Sciences; Surgery
SC Orthopedics; Sport Sciences; Surgery
GA 750FD
UT WOS:000289529700005
PM 21153541
ER
PT J
AU Mcloughlin, MJ
Colbert, LH
Stegner, AJ
Cook, DB
AF Mcloughlin, Michael J.
Colbert, Lisa H.
Stegner, Aaron J.
Cook, Dane B.
TI Are Women with Fibromyalgia Less Physically Active than Healthy Women?
SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
LA English
DT Article
DE EXERCISE; CHRONIC PAIN; MUSCLE; ACTIGRAPHY; ACCELEROMETER; SELF-REPORT
ID CHRONIC-FATIGUE-SYNDROME; ACTIVITY QUESTIONNAIRE; EXERCISE;
ACCELEROMETER; PAIN; RELIABILITY; CALIBRATION; DEPRESSION; PREVALENCE;
VALIDATION
AB MCLOUGHLIN, M. J., L. H. COLBERT, A. J. STEGNER, and D. B. COOK. Are Women with Fibromyalgia Less Physically Active than Healthy Women? Med. Sci. Sports Exerc., Vol. 43, No. 5, pp. 905-912, 2011. Purpose: The primary purpose was to quantify and compare physical activity in fibromyalgia (FM) patients to age-matched healthy controls using both objective and self-report measures. Secondary purposes were to compare self-reported and objective measurement of physical activity and to evaluate the relationship between physical activity and pain and mood. Method: Patients with FM (n = 39) and healthy controls (n = 40) completed the International Physical Activity Questionnaire and wore an accelerometer at the hip for 7 d. Pain and mood were measured using the McGill Pain Questionnaire, Pain Catastrophizing Scale, Beck Depression Inventory, State-Trait Anxiety Inventory, Profile of Mood States, and Fibromyalgia Impact Questionnaire. Results: FM patients had significantly lower physical activity than controls measured by both the International Physical Activity Questionnaire and accelerometer (P < 0.05). Both groups self-reported significantly greater moderate and vigorous physical activities than were measured by the accelerometer (P < 0.05). Self-reported and objective measures of time spent in different intensities of activity showed significant correlations in healthy controls (r = 0.41-0.51, rho = 0.41, P < 0.05). No significant correlations between measures were found in FM patients (P > 0.05). Finally, physical activity levels were negatively related (r = -0.37, P < 0.05) to depressed mood for FM patients and positively related (r = -0.41, P < 0.05) to self-reported vigor for healthy controls. Conclusions: This controlled study objectively demonstrates that FM patients are less physically active than healthy controls, thus extending on two earlier investigations that did not show differences in total physical activity levels using wrist-mounted actigraphy methods. Physical activity levels were not predictive of pain in FM but were significantly related to depressed mood. FM patients may also have a greater variability in their manner of self-report than healthy controls. Therefore, physical activity measurement in FM patients should not be limited solely to self-report measures.
C1 [Cook, Dane B.] Univ Wisconsin, Unit Gymnasium Natatorium 2, Dept Kinesiol, Madison, WI 53706 USA.
[Mcloughlin, Michael J.] Univ Iowa, Carver Coll Med, Iowa City, IA USA.
[Cook, Dane B.] William S Middleton Mem Vet Adm Med Ctr, Madison, WI USA.
RP Cook, DB (reprint author), Univ Wisconsin, Unit Gymnasium Natatorium 2, Dept Kinesiol, 2000 Observ Dr, Madison, WI 53706 USA.
EM dcook@education.wisc.edu
FU National Institutes of Health (National Institute of Arthritis and
Musculoskeletal and Skin Disorders) [ROI 5R01AR050969]
FX This research was supported by National Institutes of Health grant ROI
5R01AR050969 (the National Institute of Arthritis and Musculoskeletal
and Skin Disorders).
NR 35
TC 55
Z9 56
U1 3
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0195-9131
EI 1530-0315
J9 MED SCI SPORT EXER
JI Med. Sci. Sports Exerc.
PD MAY
PY 2011
VL 43
IS 5
BP 905
EP 912
DI 10.1249/MSS.0b013e3181fca1ea
PG 8
WC Sport Sciences
SC Sport Sciences
GA 750OF
UT WOS:000289557100023
PM 20881881
ER
PT J
AU Feinstein, TN
Wehbi, VL
Ardura, JA
Wheeler, DS
Ferrandon, S
Gardella, TJ
Vilardaga, JP
AF Feinstein, Timothy N.
Wehbi, Vanessa L.
Ardura, Juan A.
Wheeler, David S.
Ferrandon, Sebastien
Gardella, Thomas J.
Vilardaga, Jean-Pierre
TI Retromer terminates the generation of cAMP by internalized PTH receptors
SO NATURE CHEMICAL BIOLOGY
LA English
DT Article
ID PARATHYROID-HORMONE RECEPTOR; PROTEIN-COUPLED-RECEPTOR; SPECTRAL
IMAGING-SYSTEMS; BONE-MINERAL DENSITY; BETA-ARRESTIN; KINASE-C;
BETA(2)-ADRENERGIC RECEPTORS; BETA-2-ADRENERGIC RECEPTOR; MAMMALIAN
RETROMER; DESENSITIZATION
AB The generation of cAMP by G protein-coupled receptors (GPCRs) and its termination are currently thought to occur exclusively at the plasma membrane of cells. Under existing models of receptor regulation, this signal is primarily restricted by desensitization of the receptors through their binding to beta-arrestins. However, this paradigm is not consistent with recent observations that the parathyroid hormone receptor type 1 (PTHR) continues to stimulate cAMP production even after receptor internalization, as beta-arrestins are known to rapidly bind and internalize activated PTHR. Here we show that binding to beta-arrestin1 prolongs rather than terminates the generation of cAMP by PTHR, and that cAMP generation correlates with the persistence of arrestin-receptor complexes on endosomes. PTHR signaling is instead turned off by the retromer complex, which regulates the movement of internalized receptor from endosomes to the Golgi apparatus. Thus, binding by the retromer complex regulates the sustained generation of cAMP triggered by an internalized GPCR.
C1 [Feinstein, Timothy N.; Wehbi, Vanessa L.; Ardura, Juan A.; Wheeler, David S.; Vilardaga, Jean-Pierre] Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, Lab GPCR Biol, Pittsburgh, PA 15260 USA.
[Ferrandon, Sebastien; Gardella, Thomas J.; Vilardaga, Jean-Pierre] Massachusetts Gen Hosp, Dept Med, Endocrine Unit, Boston, MA 02114 USA.
[Ferrandon, Sebastien; Gardella, Thomas J.; Vilardaga, Jean-Pierre] Harvard Univ, Sch Med, Boston, MA USA.
RP Vilardaga, JP (reprint author), Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, Lab GPCR Biol, Pittsburgh, PA 15260 USA.
EM jpv@pitt.edu
RI Feinstein, Timothy/G-3110-2011; Ardura, Juan /L-8139-2014;
OI Ardura, Juan /0000-0002-8881-4775; Feinstein,
Timothy/0000-0002-9801-9708
FU US National Institutes of Health [R01DK087688]
FX This work was supported by the US National Institutes of Health award
R01DK087688 (to J.-P.V.). We thank J. Bonifacino for plasmids encoding
retromer subunits Vps26 and Vps29YFP and L. Traub for
plasmids encoding beta-arrestin1tom and beta-arrestin1[I386A,
V387A]tom.
NR 49
TC 82
Z9 82
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1552-4450
J9 NAT CHEM BIOL
JI Nat. Chem. Biol.
PD MAY
PY 2011
VL 7
IS 5
BP 278
EP 284
DI 10.1038/nchembio.545
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 751KZ
UT WOS:000289617800011
PM 21445058
ER
PT J
AU Tritos, NA
Biller, BMK
Swearingen, B
AF Tritos, Nicholas A.
Biller, Beverly M. K.
Swearingen, Brooke
TI Management of Cushing disease
SO NATURE REVIEWS ENDOCRINOLOGY
LA English
DT Review
ID TERM-FOLLOW-UP; CORTICOTROPIN-RELEASING HORMONE; GAMMA-KNIFE
RADIOSURGERY; BILATERAL LAPAROSCOPIC ADRENALECTOMY; TRANSSPHENOIDAL
PITUITARY SURGERY; DEXAMETHASONE-SUPPRESSION TEST; ECTOPIC ACTH
SYNDROME; LOW-DOSE ETOMIDATE; DOPAMINE AGONISTS; NELSONS-SYNDROME
AB Cushing disease is caused by a corticotroph tumor of the pituitary gland. Patients with Cushing disease are usually treated with transsphenoidal surgery, as this approach leads to remission in 70-90% of cases and is associated with low morbidity when performed by experienced pituitary gland surgeons. Nonetheless, among patients in postoperative remission, the risk of recurrence of Cushing disease could reach 20-25% at 10 years after surgery. Patients with persistent or recurrent Cushing disease might, therefore, benefit from a second pituitary operation (which leads to remission in 50-70% of cases), radiation therapy to the pituitary gland or bilateral adrenalectomy. Remission after radiation therapy occurs in similar to 85% of patients with Cushing disease after a considerable latency period. Interim medical therapy is generally advisable after patients receive radiation therapy because of the long latency period. Bilateral adrenalectomy might be considered in patients who do not improve following transsphenoidal surgery, particularly patients who are very ill and require rapid control of hypercortisolism, or those wishing to avoid the risk of hypopituitarism associated with radiation therapy. Adrenalectomized patients require lifelong adrenal hormone replacement and are at risk of Nelson syndrome. The development of medical therapies with improved efficacy might influence the management of this challenging condition.
C1 [Tritos, Nicholas A.; Biller, Beverly M. K.] Massachusetts Gen Hosp, Neuroendocrine Unit, Boston, MA 02114 USA.
[Swearingen, Brooke] Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02114 USA.
RP Tritos, NA (reprint author), Massachusetts Gen Hosp, Neuroendocrine Unit, 0 Emerson Pl,Suite 112, Boston, MA 02114 USA.
EM ntritos@partners.org
NR 123
TC 83
Z9 92
U1 0
U2 8
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-5029
EI 1759-5037
J9 NAT REV ENDOCRINOL
JI Nat. Rev. Endocrinol.
PD MAY
PY 2011
VL 7
IS 5
BP 279
EP 289
DI 10.1038/nrendo.2011.12
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 752DT
UT WOS:000289669900007
PM 21301487
ER
PT J
AU Schacht, JP
Anton, RF
Randall, PK
Li, XB
Henderson, S
Myrick, H
AF Schacht, Joseph P.
Anton, Raymond F.
Randall, Patrick K.
Li, Xingbao
Henderson, Scott
Myrick, Hugh
TI Stability of fMRI striatal response to alcohol cues: A hierarchical
linear modeling approach
SO NEUROIMAGE
LA English
DT Article
DE Alcohol; fMRI; Cue reactivity; Ventral striatum; Dorsal striatum; HLM
ID TEST-RETEST RELIABILITY; INDUCED BRAIN ACTIVATION; ABSTINENT ALCOHOLICS;
VENTRAL STRIATUM; DORSAL STRIATUM; NUCLEUS-ACCUMBENS; FUNCTIONAL MRI;
PREFRONTAL CORTEX; BOLD RESPONSE; DOPAMINE
AB In functional magnetic resonance imaging (fMRI) studies of alcohol-dependent individuals, alcohol cues elicit activation of the ventral and dorsal aspects of the striatum (VS and DS), which are believed to underlie aspects of reward learning critical to the initiation and maintenance of alcohol dependence. Cue-elicited striatal activation may represent a biological substrate through which treatment efficacy may be measured. However, to be useful for this purpose, VS or DS activation must first demonstrate stability across time. Using hierarchical linear modeling (HLM), this study tested the stability of cue-elicited activation in anatomically and functionally defined regions of interest in bilateral VS and DS. Nine non-treatment-seeking alcohol-dependent participants twice completed an alcohol cue reactivity task during two fMRI scans separated by 14 clays. HLM analyses demonstrated that, across all participants, alcohol cues elicited significant activation in each of the regions of interest. At the group level, these activations attenuated slightly between scans, but session-wise differences were not significant. Within-participants stability was best in the anatomically defined right VS and DS and in a functionally defined region that encompassed right caudate and putamen (intraclass correlation coefficients of .75, .81, and .76, respectively). Thus, within this small sample, alcohol cue-elicited fMRI activation had good reliability in the right striatum, though a larger sample is necessary to ensure generalizability and further evaluate stability. This study also demonstrates the utility of FILM analytic techniques for serial fMRI studies, in which separating within-participants variance (individual changes in activation) from between-participants factors (time or treatment) is critical. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Schacht, Joseph P.; Anton, Raymond F.; Randall, Patrick K.; Li, Xingbao; Henderson, Scott; Myrick, Hugh] Med Univ S Carolina, Charleston Alcohol Res Ctr, Dept Psychiat & Behav Sci, Charleston, SC 29425 USA.
[Li, Xingbao] Med Univ S Carolina, Ctr Adv Imaging Res, Charleston, SC 29425 USA.
[Myrick, Hugh] Ralph H Johnson Dept Vet Affairs Med Ctr, Charleston, SC USA.
RP Schacht, JP (reprint author), Med Univ S Carolina, Charleston Alcohol Res Ctr, Dept Psychiat & Behav Sci, Charleston, SC 29425 USA.
EM schacht@musc.edu
FU Oldham Research Fund; NIAAA [T32 AA007474, K05 AA017435]; Charleston
Alcohol Research Center [NIAAA P50 AA10761]
FX This work was funded by the Oldham Research Fund (Myrick). Dr. Schacht
was supported by NIAAA T32 AA007474, Dr. Anton by NIAAA K05 AA017435,
and Dr. Myrick by the Charleston Alcohol Research Center (NIAAA P50
AA10761). These funding sources had no role in the study design,
collection, analysis and interpretation of data, writing of the paper,
or decision to submit the paper for publication. Portions of this work
were presented as an oral presentation and poster at the Research
Society or Alcoholism annual meeting (June 2010).
NR 65
TC 21
Z9 23
U1 6
U2 13
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
EI 1095-9572
J9 NEUROIMAGE
JI Neuroimage
PD MAY 1
PY 2011
VL 56
IS 1
BP 61
EP 68
DI 10.1016/j.neuroimage.2011.02.004
PG 8
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 749HK
UT WOS:000289454900008
PM 21316465
ER
PT J
AU Kilpatrick, LA
Suyenobu, BY
Smith, SR
Bueller, JA
Goodman, T
Creswell, JD
Tillisch, K
Mayer, EA
Naliboff, BD
AF Kilpatrick, Lisa A.
Suyenobu, Brandall Y.
Smith, Suzanne R.
Bueller, Joshua A.
Goodman, Trudy
Creswell, J. David
Tillisch, Kirsten
Mayer, Emeran A.
Naliboff, Bruce D.
TI Impact of mindfulness-based stress reduction training on intrinsic brain
connectivity
SO NEUROIMAGE
LA English
DT Article
DE Mindfulness; Meditation; Functional connectivity; Resting state fMRI;
Auditory; Attention
ID STATE FUNCTIONAL CONNECTIVITY; HUMAN VISUAL-CORTEX; PREFRONTAL CORTEX;
FMRI; MEDITATION; FLUCTUATIONS; ATTENTION; NETWORKS; SELF; ORGANIZATION
AB The beneficial effects of mindful awareness and mindfulness meditation training on physical and psychological health are thought to be mediated in part through changes in underlying brain processes. Functional connectivity MRI (fcMRI) allows identification of functional networks in the brain. It has been used to examine state-dependent activity and is well suited for studying states such as meditation. We applied fcMRI to determine if Mindfulness-Based Stress Reduction (MBSR) training is effective in altering intrinsic connectivity networks (ICNs). Healthy women were randomly assigned to participate in an 8-week Mindfulness-Based Stress Reduction (MBSR) training course or an 8-week waiting period. After 8 weeks, fMRI data (1.5 T) was acquired while subjects rested with eyes closed, with the instruction to pay attention to the sounds of the scanner environment. Group independent component analysis was performed to investigate training-related changes in functional connectivity. Significant MBSR-related differences in functional connectivity were found mainly in auditory/salience and medial visual networks. Relative to findings in the control group, MBSR subjects showed (1) increased functional connectivity within auditory and visual networks, (2) increased functional connectivity between auditory cortex and areas associated with attentional and self-referential processes, (3) stronger anticorrelation between auditory and visual cortex, and (4) stronger anticorrelation between visual cortex and areas associated with attentional and self-referential processes. These findings suggest that 8 weeks of mindfulness meditation training alters intrinsic functional connectivity in ways that may reflect a more consistent attentional focus, enhanced sensory processing, and reflective awareness of sensory experience. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Kilpatrick, Lisa A.; Suyenobu, Brandall Y.; Smith, Suzanne R.; Bueller, Joshua A.; Tillisch, Kirsten; Mayer, Emeran A.; Naliboff, Bruce D.] Univ Calif Los Angeles, Ctr Neurobiol Stress, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Naliboff, Bruce D.] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Kilpatrick, Lisa A.; Suyenobu, Brandall Y.; Smith, Suzanne R.; Bueller, Joshua A.; Tillisch, Kirsten; Mayer, Emeran A.] Univ Calif Los Angeles, Dept Med, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Mayer, Emeran A.] Univ Calif Los Angeles, David Geffen Sch Med, Brain Res Inst, Los Angeles, CA 90095 USA.
[Naliboff, Bruce D.] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Creswell, J. David] Carnegie Mellon Univ, LA, Los Angeles, CA USA.
[Goodman, Trudy] LA, Insight, Los Angeles, CA USA.
RP Kilpatrick, LA (reprint author), Univ Calif Los Angeles, Ctr Neurobiol Stress, David Geffen Sch Med, Peter V Ueberroth Bldg,Room 2338C1,10945 Le Conte, Los Angeles, CA 90095 USA.
EM lakilpatrick@mednet.ucla.edu
RI Kilpatrick, Lisa/E-6995-2015
FU G. Oppenheimer Family Foundation; National Institutes of Health [AT
00268, DK64531]; UCLA Ahmanson-Lovelace Brain Mapping Center
FX This study is supported by funds from G. Oppenheimer Family Foundation,
National Institutes of Health grants AT 00268 and DK64531, and the UCLA
Ahmanson-Lovelace Brain Mapping Center.
NR 63
TC 86
Z9 88
U1 6
U2 59
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
EI 1095-9572
J9 NEUROIMAGE
JI Neuroimage
PD MAY 1
PY 2011
VL 56
IS 1
BP 290
EP 298
DI 10.1016/j.neuroimage.2011.02.034
PG 9
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 749HK
UT WOS:000289454900029
PM 21334442
ER
PT J
AU Mandeville, JB
Choi, JK
Jarraya, B
Rosen, BR
Jenkins, BG
Vanduffel, W
AF Mandeville, Joseph B.
Choi, Ji-Kyung
Jarraya, Bechir
Rosen, Bruce R.
Jenkins, Bruce G.
Vanduffel, Wim
TI fMRI of Cocaine Self-Administration in Macaques Reveals Functional
Inhibition of Basal Ganglia
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE cocaine; self-administration; fMRI; CBV; NHP; monkey
ID POSITRON-EMISSION-TOMOGRAPHY; STRIATAL DOPAMINE TRANSPORTER;
CEREBRAL-BLOOD-FLOW; DRUG-ABUSE RESEARCH; RHESUS-MONKEYS; HUMAN BRAIN;
PHARMACOLOGICAL MRI; CONTRAST AGENT; D2 RECEPTORS; IN-VIVO
AB Disparities in cocaine-induced neurochemical and metabolic responses between human beings and rodents motivate the use of non-human primates (NHP) to model consequences of repeated cocaine exposure in human subjects. To characterize the functional response to cocaine infusion in NHP brain, we employed contrast-enhanced fMRI during both non-contingent injection of drug and self-administration of cocaine in the magnet. Cocaine robustly decreased cerebral blood volume (CBV) throughout basal ganglia and motor/pre-motor cortex and produced subtle functional inhibition of prefrontal cortex. No brain regions exhibited significant elevation of CBV in response to cocaine challenge. Theses effects in NHP brain are opposite in sign to the cocaine-induced fMRI response in rats, but consistent with previous measurements in NHP based on glucose metabolism. Because the striatal ratio of D2 to D1 receptors is larger in human beings and NHP than rats, we hypothesize that the inhibitory effects of D2 receptor binding dominate the functional response in primates, whereas excitatory D1 receptor stimulation predominates in the rat. If the NHP accurately models the human response to cocaine, downregulation of D2 receptors in human cocaine-abusing populations can be expected to blunt cocaine-induced functional responses, contributing to the weak and variable fMRI responses reported in human basal ganglia following cocaine infusion. Neuropsychopharmacology (2011) 36, 1187-1198; doi: 10.1038/npp.2011.1; published online 9 February 2011
C1 [Mandeville, Joseph B.; Choi, Ji-Kyung; Jarraya, Bechir; Rosen, Bruce R.; Jenkins, Bruce G.; Vanduffel, Wim] Massachusetts Gen Hosp, Dept Radiol, Charlestown, MA 02129 USA.
[Mandeville, Joseph B.; Choi, Ji-Kyung; Jarraya, Bechir; Rosen, Bruce R.; Jenkins, Bruce G.; Vanduffel, Wim] Massachusetts Gen Hosp, MIT, HMS, Athinoula Martinos Ctr Biomed Imaging, Boston, MA 02114 USA.
[Jarraya, Bechir] Neurospin CEA Saclay Ctr, INSERM, Avenir Lab, Gif Sur Yvette, France.
[Vanduffel, Wim] Katholieke Univ Leuven, Lab Neuro Psychofysiol, Louvain, Belgium.
RP Mandeville, JB (reprint author), Massachusetts Gen Hosp, Dept Radiol, Bldg 149,Room 2301,13th St, Charlestown, MA 02129 USA.
EM jbm@nmr.mgh.harvard.edu
OI Jarraya, Bechir/0000-0003-0878-763X
FU National Center for Biomedical Imaging and Bioengineering [R01EB001782,
R03EB008134]; National Center for Drug Abuse [R01DA016187, R21DA021773];
National Institute of Neurological Disorders and Stroke [R21NS064432];
National Science Foundation in the USA [0745436]; Fondation Bettencourt
Schueller; Inserm Avenir program in France
FX We gratefully acknowledge financial support from the National Center for
Biomedical Imaging and Bioengineering (R01EB001782, R03EB008134), the
National Center for Drug Abuse (R01DA016187, R21DA021773), the National
Institute of Neurological Disorders and Stroke (R21NS064432), and the
National Science Foundation (0745436) in the USA, as well as the
Fondation Bettencourt Schueller and the Inserm Avenir program in France.
Helen Deng, MD, provided invaluable assistance in training animals,
maintaining venous catheters, and coordinating procedures with the
veterinary staff.
NR 91
TC 27
Z9 27
U1 1
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD MAY
PY 2011
VL 36
IS 6
BP 1187
EP 1198
DI 10.1038/npp.2011.1
PG 12
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 749ZJ
UT WOS:000289511800007
PM 21307843
ER
PT J
AU Barry, DT
Goulet, JL
Kerns, RK
Becker, WC
Gordon, AJ
Justice, AC
Fiellin, DA
AF Barry, Declan T.
Goulet, Joseph L.
Kerns, Robert K.
Becker, William C.
Gordon, Adam J.
Justice, Amy C.
Fiellin, David A.
TI Nonmedical use of prescription opioids and pain in veterans with and
without HIV
SO PAIN
LA English
DT Article
DE Opioids; Pain; HIV; Veterans
ID UNITED-STATES; USE DISORDERS; ABUSE; DEPENDENCE; ALCOHOL
AB Few studies have systematically evaluated nonmedical use of prescription opioids (NMU) among U. S. military veterans, those who report pain, and those with human immunodeficiency virus (HIV). An increased understanding of the factors associated with NMU may help providers to balance maintaining patient access to prescription opioids for legitimate medical reasons and reducing the risks of addiction. We analyzed self-report data and electronic medical and pharmacy record data from 4122 participants in the Veterans Aging Cohort Study. Bivariate associations were analyzed using chi-squared tests, t tests, and median tests, and multivariable associations were assessed using logistic regression. Median participant age was 52 years; 95% were men; 65% were black, and 53% were HIV infected. NMU was reported by 13% of participants. In multivariable analysis, NMU was associated with: being Hispanic (adjusted odds ratio [AOR] 1.8); aged 40-44 years (AOR 1.6); Alcohol Use Disorders Identification Test score >= 20 (AOR 2.0); drug use disorder (AOR 1.9); opioid use disorder (AOR 2.7); past month cigarette use (AOR 1.3); receiving a past-year Veterans Health Administration opioid prescription (AOR 1.9); hepatitis C (AOR 1.5); and pain interference (AOR 1.1). Being overweight (AOR 0.6) or obese (AOR 0.5) and having a higher 12-Item Short-Form Health Survey (SF-12) Mental Component Summary (AOR 0.98) were associated with less NMU. Patients with and without NMU did not differ on HIV status or SF-12 Physical Component Summary. Veterans in care have a high prevalence of NMU that is associated with substance use, medical status, and pain interference, but not HIV status. (C) 2011 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
C1 [Barry, Declan T.] Yale Univ, Sch Med, CMHC SAC, New Haven, CT 06519 USA.
[Barry, Declan T.] APT Fdn Pain Treatment Serv, New Haven, CT USA.
[Goulet, Joseph L.; Kerns, Robert K.; Justice, Amy C.] VA Connecticut Healthcare Syst, New Haven, CT USA.
[Goulet, Joseph L.; Justice, Amy C.; Fiellin, David A.] Yale Univ, Sch Publ Hlth, Ctr Interdisciplinary Res AIDS, New Haven, CT 06519 USA.
[Gordon, Adam J.] Univ Pittsburgh, Pittsburgh, PA USA.
[Gordon, Adam J.] VA Pittsburgh Healthcare Syst, MIRECC, Pittsburgh, PA USA.
[Gordon, Adam J.] VA Pittsburgh Healthcare Syst, CHERP, Pittsburgh, PA USA.
RP Barry, DT (reprint author), Yale Univ, Sch Med, CMHC SAC, 34 Pk St,Room 220, New Haven, CT 06519 USA.
EM declan.barry@yale.edu
RI barry, declan/G-4462-2011;
OI Becker, William/0000-0002-0788-1467; Goulet, Joseph/0000-0002-0842-804X;
Fiellin, David/0000-0002-4006-010X
FU National Institute on Alcohol Abuse and Alcoholism [U10 AA 13566]; VHA
Public Health Strategic Health Core Group; National Institute on Alcohol
and Alcohol Abuse [U01 AA 13566]; Department of Veterans Affairs,
Veterans Health Administration, Office of Health Services Research and
Development [REA 08-266]; National Institute on Mental Health (NIMH)
[P30MH062294]; National Institute on Drug Abuse (NIDA) [R01 DA019511-03,
R01 DA025991, R01 DA020576-01A1, K23 DA024050-02]
FX The Veterans Aging Cohort Study is funded by the National Institute on
Alcohol Abuse and Alcoholism (U10 AA 13566) and the VHA Public Health
Strategic Health Core Group. The material presented in this study is
based upon work supported in part by funding from the National Institute
on Alcohol and Alcohol Abuse (U01 AA 13566); the Department of Veterans
Affairs, Veterans Health Administration, Office of Health Services
Research and Development (REA 08-266); the National Institute on Mental
Health (NIMH P30MH062294); and the National Institute on Drug Abuse
(NIDA R01 DA019511-03, R01 DA025991, R01 DA020576-01A1, K23
DA024050-02). The views expressed in this article are those of the
authors and do not necessarily reflect the position or policy of any of
the funding agencies, including the Department of Veterans Affairs, or
the United States Government. The funding agencies had no further role
in study design; in the collection, analysis, and interpretation of
data; in the writing of the report; or in the decision to submit the
paper for publication.
NR 24
TC 20
Z9 20
U1 0
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-3959
J9 PAIN
JI Pain
PD MAY
PY 2011
VL 152
IS 5
BP 1133
EP 1138
DI 10.1016/j.pain.2011.01.038
PG 6
WC Anesthesiology; Clinical Neurology; Neurosciences
SC Anesthesiology; Neurosciences & Neurology
GA 749YI
UT WOS:000289507500027
PM 21354703
ER
PT J
AU Leung, FW
AF Leung, Felix W.
TI A hypothesis-generating review of the water method for difficult
colonoscopy
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Difficult colonoscopy; water method
ID RANDOMIZED CONTROLLED-TRIAL; UNSEDATED COLONOSCOPY; INCOMPLETE
COLONOSCOPY; TECHNICAL PERFORMANCE; CO2 INSUFFLATION; US VETERANS;
SEDATION; COMPLICATION; SATISFACTION; DISCOMFORT
AB Objective. Several factors such as significant procedure-related discomfort, excessive intubation time or failed cecal intubation have been associated with difficult colonoscopy. An update of these factors and colonoscopy techniques reported to be efficacious in enhancing completion of cecal intubation in difficult colonoscopy patients is provided in this review. Material and methods. A Medline search (January 2006 to July 2010) was conducted using the following search terms: colonoscopy, difficult, abdominal pain, and discomfort. Results. Reviewed data are tabulated for presentation. Several water-related techniques have been described separately as adjuncts to usual air insufflation to minimize discomfort, reduce intubation time and improve success rate of cecal intubation. A combination of these techniques was subjected to trial-and-error modifications followed by randomized controlled comparisons. Progressive improvement in colonoscopy outcomes that paralleled stepwise incorporation of exclusion of air insufflation, removal of residual colonic air by suction and removal of residual feces by water exchange during the insertion phase has been described. Conclusions. The water method is potentially important for improving results of colonoscopy (cecal intubation) especially in unsedated patients. The unsedated option may lower costs. The success of the water method in difficult cases should be evaluated in randomized controlled trials. The call should be considered and explored by endoscopists interested in improving the quality of colonoscopy. A multicenter study to optimize the number of cases will be most desirable. In pragmatic terms, the use of the water method in difficult (unsedated) colonoscopy in the United States did receive recent editorial endorsement.
C1 [Leung, Felix W.] Vet Affairs Greater Los Angeles Healthcare Syst, Sepulveda Ambulatory Care Ctr, N Hill, CA USA.
[Leung, Felix W.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
RP Leung, FW (reprint author), Vet Affairs Greater Los Angeles Healthcare Syst, Sepulveda Ambulatory Care Ctr, 111G,16111 Plummer St, North Hills, CA 91343 USA.
EM felix.leung@va.gov
FU Veterans Affairs Medical Research Funds; American College of
Gastroenterology
FX The study is supported in part by Veterans Affairs Medical Research
Funds at Veterans Affairs Greater Los Angeles Healthcare System and an
American College of Gastroenterology Clinical Research Award (FWL).
NR 41
TC 9
Z9 11
U1 0
U2 0
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0036-5521
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PD MAY
PY 2011
VL 46
IS 5
BP 517
EP 521
DI 10.3109/00365521.2011.551885
PG 5
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 749BN
UT WOS:000289437200002
PM 21288188
ER
PT J
AU Nordenstedt, H
El-Serag, H
AF Nordenstedt, Helena
El-Serag, Hashem
TI The influence of age, sex, and race on the incidence of esophageal
cancer in the United States (1992--2006)
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Age; esophageal cancer; male predominance; SEER; sex ratio
ID GASTROESOPHAGEAL-REFLUX SYMPTOMS; ABDOMINAL OBESITY; HISTOLOGIC TYPES;
GASTRIC CARDIA; HORMONES; WOMEN; RISK; ADENOCARCINOMA; COHORT; MEN
AB Background. There is a striking male predominance in esophageal cancer patients. Sex hormones have been suggested as a contributing factor and these are influenced by age and race. In this study, we examined the male-to-female incidence rate ratios of esophageal cancer in the United States. Methods. We used data from 13 registries in the Surveillance, Epidemiology, and End Results (SEER) database to calculate male-to-female incidence rate ratios of esophageal adenocarcinoma (EA) and esophageal squamous cell carcinoma (ESCC) diagnosed during 1992--2006 in different age and race groups. Results. For EA, all races had similar sex and age-specific incidence patterns showing a peak in the male-to-female incidence rate ratio in the age group 50--59, and an age-related decline thereafter. The highest male-to-female ratio was seen in Hispanics (20.5) and the lowest in Blacks (7.0) compared with 10.8 in Whites. By contrast, the male-to-female incidence rate ratios were low and fairly stable throughout the different age groups in ESCC. Conclusion. The male-to-female incidence rate ratios in esophageal cancer vary considerably according to histology, age, and race. The highest sex ratios were seen in EA in the age group 50--59, rendering plausibility to the hypothesis that female sex hormone exposure may play a protective role in the development of this cancer.
C1 [Nordenstedt, Helena] Karolinska Inst, Dept Mol Med & Surg, S-17176 Stockholm, Sweden.
[Nordenstedt, Helena; El-Serag, Hashem] Baylor Coll Med, Houston Ctr Qual Care & Utilizat Studies, Houston, TX 77030 USA.
[Nordenstedt, Helena; El-Serag, Hashem] Michael E DeBakey Vet Adm Med Ctr, Houston, TX USA.
RP Nordenstedt, H (reprint author), Karolinska Inst, Dept Mol Med & Surg, S-17176 Stockholm, Sweden.
EM helena.nordenstedt@ki.se
FU Public Health Service [DK078154-03, DK56338]; Houston VA HSR&D Center of
Excellence [HFP90-020]
FX This work was in part supported by Public Health Service Grant
DK078154-03 to Dr. El-Serag, by Public Health Service Grant DK56338,
which funds the Texas Medical Center Digestive Diseases Center, and in
part by the Houston VA HSR&D Center of Excellence (HFP90-020).
NR 28
TC 21
Z9 22
U1 1
U2 4
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0036-5521
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PD MAY
PY 2011
VL 46
IS 5
BP 597
EP 602
DI 10.3109/00365521.2011.551890
PG 6
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 749BN
UT WOS:000289437200012
PM 21271900
ER
PT J
AU Emmons, RR
Garber, CE
Cirnigliaro, CM
Kirshblum, SC
Spungen, AM
Bauman, WA
AF Emmons, Racine R.
Garber, Carol Ewing
Cirnigliaro, Christopher M.
Kirshblum, Steven C.
Spungen, Ann M.
Bauman, William A.
TI ASSESSMENT OF MEASURES FOR ABDOMINAL ADIPOSITY IN PERSONS WITH SPINAL
CORD INJURY
SO ULTRASOUND IN MEDICINE AND BIOLOGY
LA English
DT Article
DE Spinal cord injury; Abdominal adiposity; Abdominal ultrasonography
ID X-RAY ABSORPTIOMETRY; BODY-MASS INDEX; CORONARY-HEART-DISEASE; VISCERAL
FAT; METABOLIC SYNDROME; WAIST CIRCUMFERENCE; COMPUTED-TOMOGRAPHY;
SERUM-LIPIDS; RISK-FACTORS; ULTRASONOGRAPHY
AB Ultrasound may be a useful tool to assess abdominal adiposity, but it has not been validated in the spinal cord injury (SCI) population. This study evaluated associations between abdominal ultrasound and other methods to assess adiposity in 24 men with SCI and 20 able-bodied (AB) men. Waist (WC) and hip circumference (HC) and waist-to-hip ratio (WHR) were measured. Trunk (TRK%), android (A%) and waist fat (W%) were determined by dual energy x-ray absorptiometry (DXA); ultrasonography determined abdominal subcutaneous (SF) and visceral fat (VF). The SCI group had greater TRK% (40.0 +/- 9.6 vs. 32.0 +/- 10.3), W%(47.0 +/- 9.7 vs. 40.6 +/- 9.4), A% (43.0 +/- 9.8 vs. 35.8 +/- 10.6) and WHR(0.99 +/- 0.1 vs. 0.92 +/- 0.06) than the AB group. WC and WHR correlated with VF in the SCI group. These associations suggest that ultrasound may be a useful tool in clinical practice for the measurement of VF in weight loss programs and for the assessment of cardiometabolic disorders. (E-mail: racine.emmons@va.gov) Published by Elsevier Inc. on behalf of World Federation for Ultrasound in Medicine & Biology.
C1 [Emmons, Racine R.; Cirnigliaro, Christopher M.; Spungen, Ann M.; Bauman, William A.] James J Peters VA Med Ctr, Dept Vet Affairs, Rehabil Res & Dev Ctr Excellence Med Consequences, Bronx, NY 10468 USA.
[Kirshblum, Steven C.] Kessler Inst Rehabil, W Orange, NJ USA.
[Emmons, Racine R.; Garber, Carol Ewing] Columbia Univ, Teachers Coll, New York, NY 10027 USA.
[Kirshblum, Steven C.] Univ Med Sch New Jersey, Dept Phys Med & Rehabil, Newark, NJ USA.
[Spungen, Ann M.; Bauman, William A.] Mt Sinai Sch Med, Dept Med, New York, NY USA.
[Spungen, Ann M.; Bauman, William A.] Mt Sinai Sch Med, Dept Rehabil Med, New York, NY USA.
RP Emmons, RR (reprint author), James J Peters VA Med Ctr, VA Ctr Excellence Med Consequences SCI, Room 7A-13,130 W Kingsbridge Rd, Bronx, NY 10468 USA.
EM racine.emmons@va.gov
OI Garber, Carol/0000-0002-1268-576X
FU Department of Veterans Affairs Rehabilitation Research & Development
Center of Excellence for the Medical Consequences of Spinal Cord Injury
[B4162C]
FX This work was supported by the Department of Veterans Affairs
Rehabilitation Research & Development Center of Excellence for the
Medical Consequences of Spinal Cord Injury (#B4162C).
NR 29
TC 11
Z9 12
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0301-5629
EI 1879-291X
J9 ULTRASOUND MED BIOL
JI Ultrasound Med. Biol.
PD MAY
PY 2011
VL 37
IS 5
BP 734
EP 741
DI 10.1016/j.ultrasmedbio.2011.02.002
PG 8
WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
GA 750PY
UT WOS:000289561700009
PM 21439716
ER
PT J
AU Lee, AF
Hayes, MM
LeBrun, D
Espinosa, I
Nielsen, GP
Rosenberg, AE
Lee, CH
AF Lee, Anna F.
Hayes, Malcolm M.
LeBrun, David
Espinosa, Inigo
Nielsen, G. Petur
Rosenberg, Andrew E.
Lee, Cheng-Han
TI FLI-1 Distinguishes Ewing Sarcoma From Small Cell Osteosarcoma and
Mesenchymal Chondrosarcoma
SO APPLIED IMMUNOHISTOCHEMISTRY & MOLECULAR MORPHOLOGY
LA English
DT Article
DE FLI-1; ewing sarcoma; small cell osteosarcoma; mesenchymal
chondrosarcoma; small round blue cell tumor; immunohistochemistry
ID SARCOMA/PRIMITIVE NEUROECTODERMAL TUMOR; ROUND-CELL; IMMUNOHISTOCHEMICAL
DETECTION; MONOCLONAL-ANTIBODY; EXPRESSION; LYMPHOMA; DIAGNOSIS; BONE;
RHABDOMYOSARCOMA; UTILITY
AB Small cell osteosarcoma and mesenchymal chondrosarcoma are 2 primary bone tumors with a small round blue cell component, which can mimic the appearance of Ewing sarcoma. Distinguishing these tumors from each other on biopsy material is important clinically, as optimal therapy differs according to the tumor type. However, separating these entities on morphology alone can be challenging. FLI-1 has been described to be a useful marker for Ewing sarcoma, particularly when hematolymphoid markers are negative. In small cell osteosarcoma and mesenchymal chondrosarcoma, the FLI-1 staining pattern has not been adequately characterized. Using a monoclonal FLI-1 antibody, nuclear immunoreactivity in tumor cells was evaluated in 10 small cell osteosarcomas, 10 mesenchymal chondrosarcomas, and 8 Ewing sarcomas, together with a number of other small, round, blue cell tumors. None of the small cell osteosarcomas or mesenchymal chondrosarcomas exhibited FLI-1 staining in the tumor cells, in contrast to the positive nuclear FLI-1 staining in the stromal endothelial cells. In comparison, 6 of the 8 Ewing sarcomas showed moderate-to-strong nuclear FLI-1 staining of the tumor cells in addition to strong staining of the stromal endothelial cell nuclei. With the exception of lymphoblastic lymphomas, FLI-1 positivity was not seen in the other small round blue cell tumors examined. These findings show that, in contrast to Ewing sarcoma, small cell osteosarcoma and mesenchymal chondrosarcoma lack FLI-1 immunoreactivity. FLI-1 is therefore useful in the differential diagnosis of small round blue cell tumors of the bone.
C1 [Lee, Anna F.; Lee, Cheng-Han] Vancouver Gen Hosp, Dept Anat Pathol, Vancouver, BC V5Z 1M9, Canada.
[Hayes, Malcolm M.] British Columbia Canc Agcy, Dept Pathol, Vancouver, BC V5Z 4E6, Canada.
[LeBrun, David] Queens Univ, Queens Canc Res Inst, Dept Pathol & Mol Med, Kingston, ON, Canada.
[Espinosa, Inigo] Autonomous Univ Barcelona, Hosp Santa Creu & St Pau, Dept Pathol, Barcelona, Spain.
[Nielsen, G. Petur; Rosenberg, Andrew E.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
RP Lee, CH (reprint author), Vancouver Gen Hosp, Dept Anat Pathol, 1415 Jim Pattison Pavill N,899 W 12th Ave, Vancouver, BC V5Z 1M9, Canada.
EM chenghan@interchange.ubc.ca
OI Lee, Anna/0000-0002-6703-0656
NR 21
TC 13
Z9 15
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1062-3345
J9 APPL IMMUNOHISTO M M
JI Appl. Immunohistochem.
PD MAY
PY 2011
VL 19
IS 3
BP 233
EP 238
DI 10.1097/PAI.0b013e3181fd6697
PG 6
WC Anatomy & Morphology; Medical Laboratory Technology; Pathology
SC Anatomy & Morphology; Medical Laboratory Technology; Pathology
GA 746WS
UT WOS:000289279800006
PM 21084965
ER
PT J
AU Hao, XB
Wang, YY
Ren, FL
Zhu, SS
Ren, YM
Jia, BQ
Li, YP
Shi, YG
Chang, ZJ
AF Hao, Xinbao
Wang, Yinyin
Ren, Fangli
Zhu, Shanshan
Ren, Yongming
Jia, Baoqing
Li, Yi-Ping
Shi, Yuguang
Chang, Zhijie
TI SNX25 regulates TGF-beta signaling by enhancing the receptor degradation
SO CELLULAR SIGNALLING
LA English
DT Article
DE TGF-beta; SNX25; Sorting nexin; Endocytosis; Receptor degradation
ID SORTING NEXIN; MEDIATED ENDOCYTOSIS; ENDOTHELIAL-CELLS; EARLY ENDOSOMES;
FYVE DOMAIN; I RECEPTOR; PX DOMAIN; INTERNALIZATION; PATHWAY; FAMILY
AB SNXs (sorting nexin), a family of proteins playing roles in cargo sorting and signaling from compartments within the endocytic network, regulate traffic of membrane proteins including TGF-beta receptors. Here we report that the full length human and mouse SNX25, a SNX member with PX, PXA and RGS domains, colocalizes with TGF-beta receptors, and forms internalized cytosolic punctae upon treatment with TGF-beta. While overexpression of SNX25 inhibits TGF-beta induced luciferase reporter activity, knocking down endogenous SNX25 by siRNA in NIH3T3 cells elevates the TGF-beta receptor levels and facilitates TGF-beta signaling. Immunoprecipitation experiments demonstrate that SNX25 interacts with T beta RI. Western blot analyses indicate that SNX25 enhances the degradation of TGF-beta receptors. SNX25 induced TGF-beta receptor degradation is shown via the clathrin dependent endocytosis pathway into lysosome. We have characterized that PXA domain of SNX25 is required for the degradation of T beta RI. Our findings demonstrate that SNX25 negatively regulates TGF-beta signaling by enhancing the receptor degradation through lysosome pathway. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Wang, Yinyin; Ren, Fangli; Zhu, Shanshan; Ren, Yongming; Chang, Zhijie] Tsinghua Univ, Sch Med, Dept Biol Sci & Biotechnol, State Key Lab Biomembrane & Membrane Biotechnol, Beijing 100084, Peoples R China.
[Hao, Xinbao; Chang, Zhijie] Hainan Med Coll, Affiliated Hosp, Dept Hematol Oncol, Hainan 570102, Peoples R China.
[Jia, Baoqing] Chinese Peoples Liberat Army Gen Hosp, Dept Gen Surg, Beijing 100853, Peoples R China.
[Li, Yi-Ping] Harvard Univ, Sch Dent Med, Forsyth Res Inst, Boston, MA 02115 USA.
[Shi, Yuguang] Penn State Univ, Sch Med, Dept Cellular & Mol Physiol, Hershey, PA 17033 USA.
RP Chang, ZJ (reprint author), Tsinghua Univ, Sch Med, Dept Biol Sci & Biotechnol, State Key Lab Biomembrane & Membrane Biotechnol, Beijing 100084, Peoples R China.
EM zhijiec@mail.tsinghua.edu.cn
FU NSFC [30530420, 30660205, 30871286, 30611120522]; 863 project
[2007AA021505]; Ministry of Education, China [207093]; National
Supporting Projects [2006CB910102]
FX This work was supported by the Tsinghua Yu-Yuan Medical Sciences Fund
and grants from the NSFC (No. 30530420, 30660205, 30871286 and
30611120522), the 863 project (2007AA021505), the Supporting Fund of the
Ministry of Education, China (207093), and the National Supporting
Projects (2006CB910102). We thank Dr. Xin-Yuan Fu at Indiana University
for providing pGL2-M67/sie construct, helpful comments and suggestions.
We thank Xiaofan Wang at Duke University for kindly providing the
BMPRI(QD) construct and helpful suggestions. We thank Drs. Xin-Hua Feng,
Yang Shi, Yeguang Chen, and Michael B. Yaffe for kindly providing the
related vectors. We also thank Dr. Masahiro Kawabata for the great gifts
of Luc reporter system, (CAGA)12-MLP-Luc. We thank Dr.
Duanqing Pei for his providing us the GFP-SNX1 and GFP-SNX6 expression
vectors. We thank Miss Mengyao Feng for her technical assistance in the
protein purification. We thank Dr. David M. Irwin at University of
Toronto for his reading the manuscript and suggestions.
NR 48
TC 12
Z9 13
U1 2
U2 11
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 MAY
PY 2011
VL 23
IS 5
BP 935
EP 946
DI 10.1016/j.cellsig.2011.01.022
PG 12
WC Cell Biology
SC Cell Biology
GA 742XA
UT WOS:000288977400022
PM 21266196
ER
PT J
AU McDonough, A
Matura, LA
Carroll, DL
AF McDonough, Annette
Matura, Lea Ann
Carroll, Diane L.
TI Symptom Experience of Pulmonary Arterial Hypertension Patients
SO CLINICAL NURSING RESEARCH
LA English
DT Article
DE cardiovascular diseases; clinical research areas; specialty clinic;
health care settings; physical function; syndromes
ID QUALITY-OF-LIFE; DIAGNOSIS
AB Purpose: To describe symptoms experienced by pulmonary arterial hypertension (PAH) patients and the impact these symptoms have had on their lives. Method: Qualitative descriptive methodology was chosen incorporating semistructured interviews to investigate the symptom experience of ten patients with PAH. Results: All patients were diagnosed with WHO Group I PAH and 70% were WHO functional Class III. Two overarching themes emerged: holding back and redefining life. Holding back was represented by three sub-themes: fear, anticipation of worsening symptoms, and treatment effects. Redefining life was characterized by uncertainty, activity restrictions, and making the best of it. Conclusion: This study revealed specific concerns related to the symptom experience of PAH patients and how they redefined their lives to accommodate these symptoms. These findings provide a basis for larger, quantitative studies to examine the extent of symptom impact as well as a framework for development of self management interventions to improve the symptom experience and QOL.
C1 [McDonough, Annette] Univ Massachusetts, BS Complet Program, Lowell, MA 01854 USA.
[Matura, Lea Ann] Northeastern Univ, Boston, MA 02115 USA.
[Carroll, Diane L.] Massachusetts Gen Hosp, Munn Ctr Nursing Res, Inst Patient Care, Boston, MA 02114 USA.
RP McDonough, A (reprint author), Univ Massachusetts, BS Complet Program, 3 Solomont Way,Suite 2, Lowell, MA 01854 USA.
EM ajm0928@yahoo.com
NR 28
TC 20
Z9 20
U1 0
U2 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1054-7738
J9 CLIN NURS RES
JI Clin. Nurs. Res.
PD MAY
PY 2011
VL 20
IS 2
BP 120
EP 134
DI 10.1177/1054773810391249
PG 15
WC Nursing
SC Nursing
GA 746JL
UT WOS:000289242300002
PM 21131430
ER
PT J
AU Smith, JT
Johnson, AH
Heckman, JD
AF Smith, Jeremy T.
Johnson, Anne H.
Heckman, James D.
TI Nonoperative Treatment of an Os Peroneum Fracture in a High-level
Athlete: A Case Report
SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH
LA English
DT Article
ID CLINICAL RATING SYSTEMS; LONGUS TENDON; ANKLE INSTABILITY; RUPTURE;
FOOT; INJURIES; HINDFOOT; REPAIR; PAIN
AB The os peroneum is a sesamoid bone in the peroneus longus tendon. Fractures of the os peroneum are rare. Some authors recommend surgery for active patients.
A 41-year-old male professional tennis coach sustained a minimally displaced fracture of the os peroneum. He was treated with restricted weightbearing for 2 weeks, followed by physical therapy and gradual return to activities. He returned to tennis 8 weeks after injury. Followup 7 years after the injury showed he had full strength, full motion, and a radiographically healed os peroneum. The American Orthopaedic Foot and Ankle Society (AOFAS) Ankle-Hindfoot Scale score was 100 and Ankle Activity Score and Tegner Activity Level Scale were unchanged from those before injury.
Fracture of the os peroneum is a rare injury and treatment recommendations are based largely on very small series and case reports. Proposed treatment strategies for fracture of the os peroneum include nonoperative treatment, fixation of the fracture, excision of the bone with direct repair of the tendon, and tenodesis of the peroneus longus to the peroneus brevis.
Although some surgeons suggest fracture of the os peroneum should be treated operatively in active patients, this case shows nonoperative treatment allowed pain-free return to activities in a high-level athlete with a minimally-displaced fracture.
C1 [Smith, Jeremy T.] Massachusetts Gen Hosp, Harvard Combined Orthopaed Residency Program, Boston, MA 02114 USA.
[Johnson, Anne H.; Heckman, James D.] Massachusetts Gen Hosp, Dept Orthopaed Surg, Boston, MA 02114 USA.
RP Smith, JT (reprint author), Massachusetts Gen Hosp, Harvard Combined Orthopaed Residency Program, White 535, Boston, MA 02114 USA.
EM jsmith42@partners.org
NR 30
TC 7
Z9 7
U1 0
U2 2
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 MAY
PY 2011
VL 469
IS 5
BP 1498
EP 1501
DI 10.1007/s11999-011-1812-3
PG 4
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 744QO
UT WOS:000289109600042
PM 21328020
ER
PT J
AU Krajewski, KM
Guo, MY
Van den Abbeele, AD
Yap, J
Ramaiya, N
Jagannathan, J
Heng, DYC
Atkins, MB
McDermott, DF
Schutz, FAB
Pedrosa, I
Choueiri, TK
AF Krajewski, Katherine M.
Guo, Mengye
Van den Abbeele, Annick D.
Yap, Jeffrey
Ramaiya, Nikhil
Jagannathan, Jyothi
Heng, Daniel Y. C.
Atkins, Michael B.
McDermott, David F.
Schutz, Fabio A. B.
Pedrosa, Ivan
Choueiri, Toni K.
TI Comparison of Four Early Posttherapy Imaging Changes (EPTIC; RECIST 1.0,
Tumor Shrinkage, Computed Tomography Tumor Density, Choi Criteria) in
Assessing Outcome to Vascular Endothelial Growth Factor-Targeted Therapy
in Patients With Advanced Renal Cell Carcinoma
SO EUROPEAN UROLOGY
LA English
DT Article
DE Renal cell carcinoma; VEGF-targeted therapy; RECIST 1.0; Choi; Tumor
shrinkage
ID CONTRAST-ENHANCED CT; ANTIANGIOGENIC THERAPY; RESPONSE CRITERIA;
SUNITINIB; SIZE; CANCER; ATTENUATION
AB Background: Vascular endothelial growth factor (VEGF)-targeted therapy has become standard treatment for patients with metastatic renal cell cancer (mRCC). Since these therapies can induce tumor necrosis and minimal tumor shrinkage, Response Evaluation Criteria in Solid Tumors (RECIST) may not be optimal for predicting clinical outcome.
Objective: To systematically determine the optimal early posttherapy imaging changes (EPTIC) to separate responders and nonresponders at the first posttreatment follow-up computed tomography (CT).
Design, setting, and participants: Seventy mRCC patients with 155 target lesions treated with first-line sunitinib, sorafenib, or bevacizumab at academic medical centers underwent contrast-enhanced thoracic and abdominal CT at baseline and first follow-up after therapy initiation (median: 78 d after therapy initiation; range: 31-223 d).
Measurements: Evaluations were performed according to (1) RECIST 1.0; (2) Choi criteria; (3) tumor shrinkage (TS) of >= 10% decrease in sum of the longest unidimensional diameter (SLD); and (4) 15% or 20% decrease in mean CT tumor density. Correlation with time to treatment failure (TTF) and overall survival (OS) were compared and stratified by response to each of the radiologic criteria.
Results and limitations: Eleven patients were considered responders by RECIST 1.0; 49 based on Choi criteria; 31 patients had >= 10% decrease in the SLD; and 36 and 32 patients had >= 15% and >= 20% decrease, respectively, in mean tumor density on CT. Only the threshold of 10% decrease in the SLD was statistically significant in predicting TTF (10.4 vs 5.1 mo; p = 0.02) and OS (32.5 vs 15.8 mo; p = 0.002). Receiver operating characteristic analysis yielded a 10% decrease in SLD as the optimal size change threshold for responders. The retrospective nature of the study and measurements by a single oncoradiologist are inherent limitations.
Conclusions: In the retrospectively analyzed study population of mRCC patients receiving VEGF-targeted agents, a 10% reduction in the SLD on the first follow-up CT was an optimal early predictor of outcome. (C) 2011 European Association of Urology. Published by Elsevier B.V. All rights reserved.
C1 [Krajewski, Katherine M.; Guo, Mengye; Van den Abbeele, Annick D.; Yap, Jeffrey; Ramaiya, Nikhil; Jagannathan, Jyothi] Dana Farber Canc Inst, Dept Imaging, Boston, MA 02115 USA.
[Krajewski, Katherine M.; Guo, Mengye; Van den Abbeele, Annick D.; Yap, Jeffrey; Ramaiya, Nikhil; Jagannathan, Jyothi] Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA.
[Krajewski, Katherine M.; Guo, Mengye; Van den Abbeele, Annick D.; Yap, Jeffrey; Ramaiya, Nikhil; Jagannathan, Jyothi] Harvard Univ, Sch Med, Boston, MA USA.
[Heng, Daniel Y. C.] Tom Baker Canc Clin, Calgary, AB, Canada.
[Atkins, Michael B.; McDermott, David F.; Pedrosa, Ivan] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Schutz, Fabio A. B.; Choueiri, Toni K.] Dana Farber Canc Inst, Kidney Canc Ctr, Boston, MA 02115 USA.
RP Choueiri, TK (reprint author), 44 Binney St, Boston, MA 02115 USA.
EM Toni_Choueiri@DFCI.HARVARD.EDU
FU Bayer HealthCare Pharmaceuticals; Onyx Pharmaceuticals; Genentech;
Pfizer; Philanthropic Trust Family Research Fund for Kidney Cancer
FX I certify 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: Michael B. Atkins
received honoraria as a consultant for Bayer HealthCare Pharmaceuticals
and Onyx Pharmaceuticals, Genentech, and Aveo and received research
support from Bayer HealthCare Pharmaceuticals and Onyx Pharmaceuticals,
Genentech, and Pfizer. Toni K. Choueiri received honoraria as an
advisory board member of Bayer HealthCare Pharmaceuticals and Onyx
Pharmaceuticals, Novartis, GlaxoSmithKline, Abbot, Genentech, and
Agennix and as a consultant for Bayer HealthCare Pharmaceuticals and
Onyx Pharmaceuticals, Novartis, GlaxoSmithKline, and Pfizer.; The
Philanthropic Trust Family Research Fund for Kidney Cancer was involved
in the preparation of this research.
NR 18
TC 62
Z9 62
U1 1
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 MAY
PY 2011
VL 59
IS 5
BP 856
EP 862
DI 10.1016/j.eururo.2011.01.038
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA 743BT
UT WOS:000288991500033
PM 21306819
ER
PT J
AU Donati, OF
Alkadhi, H
Scheffel, H
Kuehnel, C
Hennemuth, A
Wyss, C
Azemaj, N
Plass, A
Kozerke, S
Falk, V
Leschka, S
Stolzmann, P
AF Donati, Olivio F.
Alkadhi, Hatem
Scheffel, Hans
Kuehnel, Caroline
Hennemuth, Anja
Wyss, Christophe
Azemaj, Naim
Plass, Andre
Kozerke, Sebastian
Falk, Volkmar
Leschka, Sebastian
Stolzmann, Paul
TI 3D Fusion of Functional Cardiac Magnetic Resonance Imaging and Computed
Tomography Coronary Angiography Accuracy and Added Clinical Value
SO INVESTIGATIVE RADIOLOGY
LA English
DT Article
DE computed tomography; magnetic resonance imaging; myocardial perfusion;
coronary artery disease; image fusion
ID DUAL-SOURCE CT; ARTERY-DISEASE; DIAGNOSTIC PERFORMANCE; COMBINED
VISUALIZATION; SHOOT MODE; K-SPACE; REVASCULARIZATION; EXPERIENCE;
HEART; METAANALYSIS
AB Purpose: To evaluate the accuracy and added diagnostic value of 3-dimensional (3D) image fusion of computed tomography coronary angiography (CTCA) and functional cardiac magnetic resonance (CMR) for assessing hemodynamically relevant coronary artery disease (CAD).
Methods: Twenty-seven patients with significant coronary stenoses on prospectively electrocardiography-gated dual-source CTCA, confirmed by catheter angiography and perfusion defects on CMR at 1.5 T were included. Surface representations and volume-rendered images from 3D-fused CTCA/ CMR data were generated using a software prototype. Fusion accuracy was evaluated by calculating surface distances of blood pools and Dice similarity coefficients. Two independent, blinded readers assigned myocardial defects to culprit coronary arteries with side-by side analysis of CTCA and CMR and using fused CTCA/CMR. Added value of fused CTCA/CMR was defined as change in assignment of culprit coronary artery to myocardial defect compared with side-by-side analysis.
Results: 3D fusion of CTCA/CMR was feasible and accurate (surface distance of blood pools: 4.1 +/- 1.3 mm, range: 2.4-7.1 mm; Dice similarity coefficients: 0.78 +/- 0.08, range: 0.51-0.86) in all patients. Side-by-side analysis of CTCA and CMR allowed no assignment of a single culprit artery to a myocardial defect in 6 of 27 (22%) patients. Fused CTCA/CMR allowed further confinement of culprit coronary arteries in 3 of these 6 patients (11%). Myocardial defects were reassigned in 2 of 27 (7%) patients using fused CTCA/CMR, whereas the results remained unchanged in 22 of 27 (81%) patients. Interobserver agreement for assignment of culprit arteries to myocardial defects increased with fused CTCA/CMR (k = 0.66-0.89).
Conclusion: 3D fusion of low-dose CTCA and functional CMR is feasible and accurate, and adds, at a low radiation dose, diagnostic value for the assessment of hemodynamically relevant CAD as compared with side-byside analysis alone. This technique can be clinically useful for the following: planning of surgical or interventional procedures in patients having a high prevalence of CAD and for improved topographic assignment of coronary stenoses to corresponding myocardial perfusion defects.
C1 [Alkadhi, Hatem; Stolzmann, Paul] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cardiac MR PET CT Program, Boston, MA 02114 USA.
[Donati, Olivio F.; Alkadhi, Hatem; Scheffel, Hans; Azemaj, Naim; Leschka, Sebastian; Stolzmann, Paul] Univ Zurich Hosp, Inst Diagnost & Intervent Radiol, CH-8091 Zurich, Switzerland.
[Kuehnel, Caroline; Hennemuth, Anja] Fraunhofer MEVIS, Bremen, Germany.
[Wyss, Christophe] Univ Zurich Hosp, Ctr Cardiovasc, CH-8091 Zurich, Switzerland.
[Azemaj, Naim; Plass, Andre; Falk, Volkmar] Univ Zurich Hosp, Cardiovasc Surg Clin, CH-8091 Zurich, Switzerland.
[Kozerke, Sebastian] Univ Zurich, Inst Biomed Engn, Zurich, Switzerland.
[Kozerke, Sebastian] ETH, Zurich, Switzerland.
RP Alkadhi, H (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cardiac MR PET CT Program, 165 Cambridge St,Suite 400, Boston, MA 02114 USA.
EM halkadhi@partners.org
RI Kozerke, Sebastian/J-3209-2015
OI Kozerke, Sebastian/0000-0003-3725-8884
NR 40
TC 3
Z9 3
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0020-9996
J9 INVEST RADIOL
JI Invest. Radiol.
PD MAY
PY 2011
VL 46
IS 5
BP 331
EP 340
DI 10.1097/RLI.0b013e3182056caf
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 746GK
UT WOS:000289231100007
PM 21285891
ER
PT J
AU Moriguchi, Y
Negreira, A
Weierich, M
Dautoff, R
Dickerson, BC
Wright, CI
Barrett, LF
AF Moriguchi, Yoshiya
Negreira, Alyson
Weierich, Mariann
Dautoff, Rebecca
Dickerson, Bradford C.
Wright, Christopher I.
Barrett, Lisa Feldman
TI Differential Hemodynamic Response in Affective Circuitry with Aging: An
fMRI Study of Novelty, Valence, and Arousal
SO JOURNAL OF COGNITIVE NEUROSCIENCE
LA English
DT Article
ID AGE-RELATED DIFFERENCES; MEDIAL PREFRONTAL CORTEX; CEREBRAL-BLOOD-FLOW;
HUMAN AMYGDALA; ORBITOFRONTAL CORTEX; ELDERLY ADULTS; RHESUS-MONKEY;
SENSORY STIMULATION; ALZHEIMER-DISEASE; EMOTIONAL STIMULI
AB Emerging evidence indicates that stimulus novelty is affectively potent and reliably engages the amygdala and other portions of the affective workspace in the brain. Using fMRI, we examined whether novel stimuli remain affectively salient across the lifespan, and therefore, whether novelty processing-a potentially survival-relevant function-is preserved with aging. Nineteen young and 22 older healthy adults were scanned during observing novel and familiar affective pictures while estimating their own subjectively experienced aroused levels. We investigated age-related difference of magnitude of activation, hemodynamic time course, and functional connectivity of BOLD responses in the amygdala. Although there were no age-related differences in the peak response of the amygdala to novelty, older individuals showed a narrower, sharper (i.e., "peakier") hemodynamic time course in response to novel stimuli, as well as decreased connectivity between the left amygdala and the affective areas including orbito-frontal regions. These findings have relevance for understanding age-related differences in memory and affect regulation.
C1 [Moriguchi, Yoshiya] Massachusetts Gen Hosp, Neuroimaging Res Program, Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Moriguchi, Yoshiya; Negreira, Alyson; Weierich, Mariann; Dautoff, Rebecca; Dickerson, Bradford C.; Wright, Christopher I.; Barrett, Lisa Feldman] Harvard Univ, Sch Med, Charlestown, MA 02129 USA.
[Barrett, Lisa Feldman] Boston Coll, Chestnut Hill, MA 02167 USA.
RP Moriguchi, Y (reprint author), Massachusetts Gen Hosp, Neuroimaging Res Program, Martinos Ctr Biomed Imaging, 13th St,Bldg 149,CNY-9, Charlestown, MA 02129 USA.
EM ymorigu@ncnp.go.jp
FU National Institutes of Health [DP1OD003312]; National Institute on Aging
[AG030311]
FX We thank Mary Foley and Larry White for their technical assistance. This
work was supported in part by the National Institutes of Health
Director's Pioneer Award (DP1OD003312) and a National Institute on Aging
grant (AG030311) to Lisa Feldman Barrett.
NR 102
TC 16
Z9 16
U1 1
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 MAY
PY 2011
VL 23
IS 5
BP 1027
EP 1041
DI 10.1162/jocn.2010.21527
PG 15
WC Neurosciences; Psychology, Experimental
SC Neurosciences & Neurology; Psychology
GA 743ZZ
UT WOS:000289062000001
PM 20521849
ER
PT J
AU Kuperberg, GR
Paczynski, M
Ditman, T
AF Kuperberg, Gina R.
Paczynski, Martin
Ditman, Tali
TI Establishing Causal Coherence across Sentences: An ERP Study
SO JOURNAL OF COGNITIVE NEUROSCIENCE
LA English
DT Article
ID EVENT-RELATED POTENTIALS; LATENT SEMANTIC ANALYSIS; LONG-TERM-MEMORY;
LANGUAGE COMPREHENSION; TEXT COMPREHENSION; BRAIN POTENTIALS;
INDIVIDUAL-DIFFERENCES; LEXICAL DECISION; DISCOURSE COMPREHENSION;
PREDICTIVE INFERENCES
AB This study examined neural activity associated with establishing causal relationships across sentences during on-line comprehension. ERPs were measured while participants read and judged the relatedness of three-sentence scenarios in which the final sentence was highly causally related, intermediately related, and causally unrelated to its context. Lexico-semantic co-occurrence was matched across the three conditions using a Latent Semantic Analysis. Critical words in causally unrelated scenarios evoked a larger N400 than words in both highly causally related and intermediately related scenarios, regardless of whether they appeared before or at the sentence-final position. At midline sites, the N400 to intermediately related sentence-final words was attenuated to the same degree as to highly causally related words, but otherwise the N400 to intermediately related words fell in between that evoked by highly causally related and intermediately related words. Nomodulation of the late positivity/P600 component was observed across conditions. These results indicate that both simple and complex causal inferences can influence the earliest stages of semantically processing an incoming word. Further, they suggest that causal coherence, at the situation level, can influence incremental word-by-word discourse comprehension, even when semantic relationships between individual words are matched.
C1 [Kuperberg, Gina R.] Tufts Univ, Dept Psychol, Medford, MA 02155 USA.
[Kuperberg, Gina R.; Ditman, Tali] Massachusetts Gen Hosp, Charlestown, MA USA.
RP Kuperberg, GR (reprint author), Tufts Univ, Dept Psychol, 490 Boston Ave, Medford, MA 02155 USA.
EM kuperber@nmr.mgh.harvard.edu
FU National Institute of Mental Health [RO1 MH02034]; National Alliance for
Research in Schizophrenia and Depression (NARSAD); Sidney J. Baer Trust
FX This work was funded by National Institute of Mental Health (RO1 MH02034
to G. R. K.), and the National Alliance for Research in Schizophrenia
and Depression (NARSAD) with the Sidney J. Baer Trust (G. R. K.). We
thank Mante Nieuwland and Ellen Lau for their insightful comments on the
manuscript. We are also grateful to Abigail Swain for her assistance in
analyzing data and to Eric Fields for his help with manuscript
preparation.
NR 124
TC 36
Z9 38
U1 2
U2 26
PU MIT PRESS
PI CAMBRIDGE
PA 55 HAYWARD STREET, CAMBRIDGE, MA 02142 USA
SN 0898-929X
EI 1530-8898
J9 J COGNITIVE NEUROSCI
JI J. Cogn. Neurosci.
PD MAY
PY 2011
VL 23
IS 5
BP 1230
EP 1246
DI 10.1162/jocn.2010.21452
PG 17
WC Neurosciences; Psychology, Experimental
SC Neurosciences & Neurology; Psychology
GA 743ZZ
UT WOS:000289062000018
PM 20175676
ER
PT J
AU van Diepen, JA
Wong, MC
Guigas, B
Bos, J
Stienstra, R
Hodson, L
Shoelson, SE
Berbee, JFP
Rensen, PCN
Romijn, JA
Havekes, LM
Voshol, PJ
AF van Diepen, Janna A.
Wong, Man C.
Guigas, Bruno
Bos, Jasper
Stienstra, Rinke
Hodson, Leanne
Shoelson, Steven E.
Berbee, Jimmy F. P.
Rensen, Patrick C. N.
Romijn, Johannes A.
Havekes, Louis M.
Voshol, Peter J.
TI Hepatocyte-specific IKK-beta activation enhances VLDL-triglyceride
production in APOE(star)3-Leiden mice
SO JOURNAL OF LIPID RESEARCH
LA English
DT Article
DE nuclear factor kappa B; lipid metabolism; liver; very low density
lipoprotein; I kappa B kinase beta
ID LIVER PARENCHYMAL-CELLS; ELEMENT-BINDING PROTEIN; FATTY-ACID SYNTHESIS;
NF-KAPPA-B; INSULIN-RESISTANCE; KUPFFER CELLS; LIPOPROTEIN PRODUCTION;
HEPATIC STEATOSIS; SYNTHESIS INVIVO; PPAR-ALPHA
AB Low-grade inflammation in different tissues, including activation of the nuclear factor kappa B pathway in liver, is involved in metabolic disorders such as type 2 diabetes and cardiovascular diseases (CVDs). In this study, we investigated the relation between chronic hepatocyte-specific overexpression of IkB kinase (IKK)-beta and hypertriglyceridemia, an important risk factor for CVD, by evaluating whether activation of IKK-beta only in the hepatocyte affects VLDL-triglyceride (TG) metabolism directly. Transgenic overexpression of constitutively active human IKK-beta specifically in hepatocytes of hyperlipidemic APOE*3-Leiden mice clearly induced hypertriglyceridemia. Mechanistic in vivo studies revealed that the hypertriglyceridemia was caused by increased hepatic VLDL-TG production rather than a change in plasma VLDL-TG clearance. Studies in primary hepatocytes showed that IKK-beta overexpression also enhances TG secretion in vitro, indicating a direct relation between IKK-beta activation and TG production within the hepatocyte. Hepatic lipid analysis and hepatic gene expression analysis of pathways involved in lipid metabolism suggested that hepatocyte- specific IKK-beta overexpression increases VLDL production not by increased steatosis or decreased FA oxidation, but most likely by carbohydrate-responsive element binding protein-mediated upregulation of Fas expression.jlr These findings implicate that specific activation of inflammatory pathways exclusively within hepatocytes induces hypertriglyceridemia. Furthermore, we identify the hepatocytic IKK-beta pathway as a possible target to treat hypertriglyceridemia. van Diepen, J. A., M. C. Wong, B. Guigas, J. Bos, R. Stienstra, L. Hodson, S. E. Shoelson, J. F. P. Berbee, P. C. N. Rensen, J. A. Romijn, L. M. Havekes, and P. J. Voshol. Hepatocyte-specific IKK-beta activation enhances VLDL-triglyceride production in APOE*3-Leiden mice. J. Lipid Res. 2011. 52: 942-950.
C1 [van Diepen, Janna A.; Bos, Jasper; Berbee, Jimmy F. P.; Rensen, Patrick C. N.; Romijn, Johannes A.; Havekes, Louis M.; Voshol, Peter J.] Leiden Univ, Med Ctr, Dept Gen Internal Med Endocrinol & Metab Dis, Leiden, Netherlands.
[Wong, Man C.] Leiden Univ, Med Ctr, Dept Pulmonol, Leiden, Netherlands.
[Guigas, Bruno] Leiden Univ, Med Ctr, Dept Mol Cell Biol, Leiden, Netherlands.
[Havekes, Louis M.] Leiden Univ, Med Ctr, Dept Cardiol, Leiden, Netherlands.
[Stienstra, Rinke] Radboud Univ Nijmegen, Med Ctr, Dept Gen Internal Med, NL-6525 ED Nijmegen, Netherlands.
[Hodson, Leanne] Univ Oxford, Churchill Hosp, Oxford Ctr Diabet Endocrinol & Metab, Oxford, England.
[Shoelson, Steven E.] Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02115 USA.
[Shoelson, Steven E.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Havekes, Louis M.] Netherlands Org Appl Sci Res Biosci, Gaubius Lab, Leiden, Netherlands.
RP van Diepen, JA (reprint author), Leiden Univ, Med Ctr, Dept Gen Internal Med Endocrinol & Metab Dis, Leiden, Netherlands.
EM J.A.van_Diepen@lumc.nl
RI Stienstra, Rinke/A-4763-2015; Guigas, Bruno/M-2515-2015; van Diepen,
Janna/E-9485-2010
OI Stienstra, Rinke/0000-0001-6729-7193; Guigas, Bruno/0000-0002-8856-5799;
van Diepen, Janna/0000-0001-9091-1075
FU Netherlands Organization for Scientific Research (NWO) [917.76.301];
Dutch Diabetes Research Foundation [2005.01.003]; Dutch Organization for
Scientific Research (NWO) [017.003.83]; Netherlands Heart Foundation
[2009T038]
FX This work was supported by grants from the Netherlands Organization for
Scientific Research (NWO Zon-MW; 917.76.301 to P.J.V.) and the Dutch
Diabetes Research Foundation (2005.01.003 to P.J.V.). M.C.W. is
supported by a Mosaic grant of the Dutch Organization for Scientific
Research (NWO 017.003.83). P.C.N.R. is an Established Investigator of
the Netherlands Heart Foundation (2009T038).
NR 38
TC 12
Z9 12
U1 0
U2 0
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 MAY
PY 2011
VL 52
IS 5
BP 942
EP 950
DI 10.1194/jlr.M010405
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 746XB
UT WOS:000289281000008
PM 21357939
ER
PT J
AU Factor, SA
Steenland, NK
Higgins, DS
Molho, ES
Kay, DM
Montimurro, J
Rosen, AR
Zabetian, CP
Payami, H
AF Factor, Stewart A.
Steenland, N. Kyle
Higgins, Donald S.
Molho, Eric S.
Kay, Denise M.
Montimurro, Jennifer
Rosen, Ami R.
Zabetian, Cyrus P.
Payami, Haydeh
TI Postural instability/gait disturbance in Parkinson's disease has
distinct subtypes: an exploratory analysis
SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY
LA English
DT Article
ID QUALITY-OF-LIFE; ALPHA-SYNUCLEIN; DATATOP COHORT; DEMENTIA; FALLS; GAIT;
RISK; ASSOCIATION; AGE; FREQUENCY
AB Objective To test the hypothesis that postural instability with falling (PIF) and freezing of gait (FOG) are distinct subtypes of the postural instability/gait disturbance (PIGD) form of Parkinson's disease (PD).
Methods 499 PD subjects from the NeuroGenetics Research Consortium were studied using logistic regression to examine, in a cross sectional analysis, predictors of FOG and PIF. Potential predictors were from four spheres; demographic, clinical motor, clinical non-motor and genetic.
Results FOG and PIF were both associated with greater gait subscores and lower tremor subscores on the Unified Parkinson's Disease Rating Scale (p <= 0.02). However, they differed with regard to demographic, non-motor and genetic predictors. FOG was associated with greater duration of disease, with ORs of 3.01 (95% CI 1.35 to 6.72) and 4.91 (95% CI 2.29 to 10.54) for third and fourth quartiles of duration, respectively, versus the lowest half of duration. The risk of having psychotic symptoms was also significantly increased (OR 3.02, 95% CI 1.41 to 6.49; p=0.004). FOG was inversely associated with the presence of the CYP2D6*4 allele (OR 0.41, 95% CI 0.21 to 0.80; p=0.009) suggesting a protective effect. PIF was associated with depression (OR 1.08, 95% CI 1.01 to 1.15; p<0.02) and was inversely associated with APOE 34 (OR 0.21, 95% CI 0.05 to 0.87; p=0.03), again suggesting a protective effect.
Conclusion FOG and PIF have different demographic, non-motor and genetic predictors suggesting that they may be pathophysiologically distinct subtypes of PIGD. These findings have implications in the discovery of therapeutic targets for these disabling features as well as for predicting outcomes of PD.
C1 [Factor, Stewart A.] Emory Univ, Dept Neurol, Sch Med, Atlanta, GA 30329 USA.
[Higgins, Donald S.; Molho, Eric S.] Albany Med Ctr, New York, NY USA.
[Kay, Denise M.; Montimurro, Jennifer; Payami, Haydeh] New York State Dept Hlth, New York, NY USA.
[Zabetian, Cyrus P.] VA Puget Sound Hlth Care Syst, Washington, DC USA.
[Zabetian, Cyrus P.] Univ Washington, Washington, DC USA.
RP Factor, SA (reprint author), Emory Univ, Dept Neurol, Sch Med, 1841 Clifton Rd NE, Atlanta, GA 30329 USA.
EM sfactor@emory.edu
OI Kay, Denise/0000-0002-9928-2698; Zabetian, Cyrus/0000-0002-7739-4306
FU Michael J Fox Foundation; Close to a Cure Foundation; NIH, Washington,
DC USA [R01-NS36960]; Department of Veterans Affairs; New York State
Department of Health Wadsworth Center, Albany, NY, USA; Sartain Lanier
Family Foundation, Atlanta, GA, USA; TEVA Neurosciences; Ipsen; Schering
Plough; TEVA-speakers bureau; Allergan; Merz;
Boehringer-Ingelheim-speakers bureau
FX Michael J Fox Foundation: Edmond J Safra Global Genetics Consortia
Grant, New York, NY USA. Close to a Cure Foundation: A Fund for
Parkinson's Research of Foundation for the Carolinas, North Carolina
USA. NIH: R01-NS36960, Washington, DC USA. Department of Veterans
Affairs Merit Review Award. New York State Department of Health
Wadsworth Center, Albany, NY, USA. The Sartain Lanier Family Foundation,
Atlanta, GA, USA. The content is solely the responsibility of the
authors and does not necessarily represent the official views of the
funding agencies. The funding agencies had no role in design of this
study. The authors had full access to all of the data in the study and
SAF takes responsibility for the integrity of the data and accuracy of
the data analysis; SAF has research grants from TEVA Neurosciences,
Ipsen and Schering Plough. He is also a consultant for
Boehringer-Ingelheim, Allergan, UCB and Lundbeck. ESM has the following
disclosures: TEVA-speakers bureau, research grant support;
Allergan-research grant support, speakers bureau, consulting fee;
Merz-research grant, consulting fee; Ipsen-research grant, consulting
fee; Boehringer-Ingelheim-speakers bureau.
NR 40
TC 38
Z9 40
U1 0
U2 8
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-3050
J9 J NEUROL NEUROSUR PS
JI J. Neurol. Neurosurg. Psychiatry
PD MAY
PY 2011
VL 82
IS 5
BP 564
EP 568
DI 10.1136/jnnp.2010.222042
PG 5
WC Clinical Neurology; Psychiatry; Surgery
SC Neurosciences & Neurology; Psychiatry; Surgery
GA 746HL
UT WOS:000289234500021
PM 20884673
ER
PT J
AU Baum, NM
DesRoches, C
Campbell, EG
Goold, SD
AF Baum, Nancy M.
DesRoches, Catherine
Campbell, Eric G.
Goold, Susan Dorr
TI Resource Allocation in Public Health Practice: A National Survey of
Local Public Health Officials
SO JOURNAL OF PUBLIC HEALTH MANAGEMENT AND PRACTICE
LA English
DT Article
DE local public health officials; priority setting; resource allocation
ID PERFORMANCE; SYSTEMS
AB Objectives: The purpose of this study was to gain an empirical understanding of the types of allocation decisions local health officials (LHOs) make and the factors that influence those allocation decisions. Design: We conducted a national survey of LHOs in the United States in 2008 to 2009. The sample was stratified by the size of the population served by the department. We merged our data with data from the 2008 National Association of County and City Health Officials Profile survey. Descriptive statistics were generated using weighted data. Results: Our final sample size was 608 respondents, with an average of 10 years experience. The LHOs reported little shifting of resources among population groups but greater capacity to redirect staffing time. Less than half of LHOs reported using economic analyses or conducting needs assessments when setting priorities. Having sole provider status in a community strongly influenced LHOs' allocation decisions. In addition, the effectiveness of activities, previous budget allocations, and input from boards of health were influential factors in allocation decisions. Public expectations were moderately to very influential, but direct public input had a low impact on allocation decisions. Conclusions: Survey findings provide a clearer understanding of how LHOs fulfill their obligations as stewards of public health resources and ensure effective activities and access to needed services. It may be useful to assess the value of more structured allocation methods (eg, decision frameworks) in the allocation process. Expanding opportunities for public engagement in priority setting may also be valuable for difficult allocation decisions.
C1 [Baum, Nancy M.; Goold, Susan Dorr] Univ Michigan, Sch Publ Hlth, Dept Hlth Management & Policy, Ann Arbor, MI 48109 USA.
[Goold, Susan Dorr] Univ Michigan, Ctr Bioeth & Social Sci Med, Ann Arbor, MI 48109 USA.
[Goold, Susan Dorr] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
[DesRoches, Catherine; Campbell, Eric G.] Harvard Univ, Sch Med, Boston, MA USA.
[DesRoches, Catherine; Campbell, Eric G.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Baum, NM (reprint author), Univ Michigan, Sch Publ Hlth, Dept Hlth Management & Policy, 1415 Washington Hts,M-3141,SPH-2, Ann Arbor, MI 48109 USA.
EM nmbaum@umich.edu
OI Goold, Susan Dorr/0000-0002-0258-9774
NR 26
TC 12
Z9 12
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1078-4659
J9 J PUBLIC HEALTH MAN
JI J. Public Health Manag. Pract.
PD MAY-JUN
PY 2011
VL 17
IS 3
BP 265
EP 274
DI 10.1097/PHH.0b013e318207599c
PG 10
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 745ES
UT WOS:000289149200013
PM 21464688
ER
PT J
AU Groessl, EJ
Weingart, KR
Stepnowsky, CJ
Gifford, AL
Asch, SM
Ho, SB
AF Groessl, E. J.
Weingart, K. R.
Stepnowsky, C. J.
Gifford, A. L.
Asch, S. M.
Ho, S. B.
TI The hepatitis C self-management programme: a randomized controlled trial
SO JOURNAL OF VIRAL HEPATITIS
LA English
DT Article
DE behavioural interventions; health-related quality of life; hepatitis C;
self-management; US veterans
ID QUALITY-OF-LIFE; DISORDERS IDENTIFICATION TEST; WELL-BEING SCALE;
VIRUS-INFECTION; CHRONIC DISEASE; PLUS RIBAVIRIN; PRIMARY-CARE;
ANTIVIRAL THERAPY; WEIGHT-REDUCTION; UNITED-STATES
AB Chronic hepatitis C (HCV) infection afflicts millions of people worldwide. While antiviral treatments are effective for some patients, many either cannot or choose not to receive antiviral treatment. Education about behavioural changes like alcohol avoidance and symptom management, in contrast, is universally recommended, particularly in HCV-infected persons from disadvantaged groups where liver risk factors are most prevalent. Self-management interventions are one option for fostering improved HCV knowledge and health-related quality of life (HRQOL). One hundred and thirty-two patients with VA with HCV (mean age of 54.6, 95% men, 41% ethnic minority, 83% unmarried, 72% unemployed/disabled, 48% homeless in last 5 years) were randomized to either a 6-week self-management workshop or an information-only intervention. The weekly 2-h self-management sessions were based on cognitive-behavioural principles and were adapted from an existing self-management programme that has been efficacious with other chronic diseases. HCV-specific modules were added. Outcomes including HRQOL, HCV knowledge, self-efficacy, depression, energy and health distress were measured at baseline and 6 weeks later. Data were analysed using ANOVA. When compared to the information-only group, participants attending the self-management workshop improved more on HCV knowledge (P < 0.001), HCV self-efficacy (P = 0.011), and SF-36 energy/vitality (P = 0.040). Similar trends were found for SF-36 physical functioning (P = 0.055) and health distress (P = 0.055). Attending the self-management programme improved disease knowledge and HRQOL 6 weeks later in this disadvantaged population. The intervention can improve the health of people with hepatitis C, independent of antiviral therapy. Future research will study longer-term outcomes, effects on antiviral treatment and costs.
C1 [Groessl, E. J.] VA San Diego Healthcare Syst, Hlth Serv Res & Dev, La Jolla, CA 92161 USA.
[Groessl, E. J.; Stepnowsky, C. J.; Ho, S. B.] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Gifford, A. L.] Edith Nourse Rogers Mem Vet Hosp, Bedford, MA USA.
[Gifford, A. L.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Asch, S. M.] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Asch, S. M.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
RP Groessl, EJ (reprint author), VA San Diego Healthcare Syst, Hlth Serv Res & Dev, 3350 Jolla Village Dr 111 N-1, La Jolla, CA 92161 USA.
EM egroessl@ucsd.edu
FU VA HSRD [IAC 05-067]
FX This study is funded by a research grant from the VA HSR&D, Project #
IAC 05-067. This project is registered at clinical Trails. gov,
registration # NCT00328042.
NR 71
TC 9
Z9 9
U1 1
U2 11
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1352-0504
J9 J VIRAL HEPATITIS
JI J. Viral Hepatitis
PD MAY
PY 2011
VL 18
IS 5
BP 358
EP 368
DI 10.1111/j.1365-2893.2010.01328.x
PG 11
WC Gastroenterology & Hepatology; Infectious Diseases; Virology
SC Gastroenterology & Hepatology; Infectious Diseases; Virology
GA 746MR
UT WOS:000289251900007
PM 20529203
ER
PT J
AU Zhang, ZP
Tongchusak, S
Mizukami, Y
Kang, YJ
Ioji, T
Touma, M
Reinhold, B
Keskin, DB
Reinherz, EL
Sasada, T
AF Zhang, Zhiping
Tongchusak, Songsak
Mizukami, Yo
Kang, Yoon Joong
Ioji, Tetsuya
Touma, Maki
Reinhold, Bruce
Keskin, Derin B.
Reinherz, Ellis L.
Sasada, Tetsuro
TI Induction of anti-tumor cytotoxic T cell responses through
PLGA-nanoparticle mediated antigen delivery
SO BIOMATERIALS
LA English
DT Article
DE Nanoparticle; Peptide; Toll-like receptor 4 agonist; Tumor immunity;
Interferon-gamma; Immune escape
ID TUMOR REJECTION ANTIGEN; DENDRITIC CELLS; IMMUNE-RESPONSES; B16
MELANOMA; BIODEGRADABLE NANOPARTICLES; ACTIVE IMMUNOTHERAPY; VACCINE
DELIVERY; CO-DELIVERY; CANCER; ENHANCEMENT
AB Nanotechnology-based antigen delivery has been developing as a vaccine strategy due to its dose-sparing and prolonged antigen presentation features. In the current study, we examined the feasibility of nanoparticle (NP)-mediated delivery of antigenic peptides to efficiently induce cytotoxic T lymphocyte responses against tumor-associated self-antigens in C57BL/6 mouse models. The biodegradable poly(e, L-lactide-co-glycolide) nanoparticle (PLGA-NP) carrying murine melanoma antigenic peptides, hgp100(25-33) and TRP2(180-188), were prepared by double emulsion method. Efficient uptake of PLGA-NP by murine dendritic cells was shown in vitro and in vivo, using NP labeled with the fluorescent dye DiD. Intradermal injection of peptide-loaded PLGA-NP into mice induced antigen-specific T cell responses more strongly than the peptides mixed with Freund's adjuvant. More importantly, vaccination with PLGA-NP carrying both TRP2(180-188) and a toll-like receptor 4 agonist, monophosphoryl lipid A, significantly delayed growth of subcutaneously inoculated B16 melanoma cells in a prophylactic setting. Furthermore, the anti-tumor activity of NP-mediated peptide vaccination was significantly augmented by combined treatment with interferon-gamma, which might prevent tumor escape through up-regulation of MHC class I expression on tumor cells. Our findings demonstrate the feasibility of NP-mediated antigen delivery for cancer immunotherapy, in particular when immune escape mechanisms of tumor cells are blocked simultaneously. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Zhang, Zhiping; Tongchusak, Songsak; Mizukami, Yo; Kang, Yoon Joong; Reinhold, Bruce; Reinherz, Ellis L.; Sasada, Tetsuro] Dana Farber Canc Inst, Canc Vaccine Ctr, Boston, MA 02115 USA.
[Touma, Maki; Reinhold, Bruce; Keskin, Derin B.; Reinherz, Ellis L.] Dana Farber Canc Inst, Immunobiol Lab, Boston, MA 02115 USA.
[Zhang, Zhiping; Tongchusak, Songsak; Kang, Yoon Joong; Touma, Maki; Reinhold, Bruce; Keskin, Derin B.; Reinherz, Ellis L.; Sasada, Tetsuro] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[Zhang, Zhiping] Huazhong Univ Sci & Technol, Tongji Sch Pharm, Wuhan 430030, Peoples R China.
[Ioji, Tetsuya; Sasada, Tetsuro] Kurume Univ, Sch Med, Dept Immunol & Immunotherapy, Fukuoka 8300011, Japan.
RP Sasada, T (reprint author), Dana Farber Canc Inst, Canc Vaccine Ctr, HIM 418,Ave Louis Pasteur, Boston, MA 02115 USA.
EM tsasada@med.kurume-u.ac.jp
RI zhang, zhiping/H-1786-2011
FU DFCI Cancer Vaccine Center
FX We thank Drs. Wanyong Zeng, Mei Sue, Vladmir Brusic, Mans Handley
(Dana-Farber Cancer Institute), and Ray Surajit (Boston University) for
their helpful discussion and technical help; Drs. Anna Bershteyn and
Darrel Irvine (Department of Materials Science and Engineering, MIT,
Boston) for their helpful discussion and kindly providing us with
particle sizer; Dr. Lihong Bu (Department of Neurobiology, Children's
Hospital Boston) for confocal microscope; and the staffs of Department
of Cell Biology in Harvard Medical School for their assistance on TEM.
This study was supported by the DFCI Cancer Vaccine Center funding.
NR 49
TC 83
Z9 85
U1 12
U2 92
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0142-9612
J9 BIOMATERIALS
JI Biomaterials
PD MAY
PY 2011
VL 32
IS 14
BP 3666
EP 3678
DI 10.1016/j.biomaterials.2011.01.067
PG 13
WC Engineering, Biomedical; Materials Science, Biomaterials
SC Engineering; Materials Science
GA 743LU
UT WOS:000289020600014
PM 21345488
ER
PT J
AU Celano, CM
Huffman, JC
AF Celano, Christopher M.
Huffman, Jeff C.
TI Depression and Cardiac Disease A Review
SO CARDIOLOGY IN REVIEW
LA English
DT Review
DE depression; cardiac disease; coronary artery disease; congestive heart
failure; collaborative care
ID CORONARY-HEART-DISEASE; ACUTE MYOCARDIAL-INFARCTION;
RANDOMIZED-CONTROLLED-TRIAL; C-REACTIVE PROTEIN; SEROTONIN REUPTAKE
INHIBITORS; AUTONOMIC NERVOUS-SYSTEM; PLACEBO-CONTROLLED TRIAL;
ARTERY-BYPASS SURGERY; QUALITY-OF-LIFE; MAJOR DEPRESSION
AB Depression is highly prevalent in cardiac patients, with 20% to 40% of patients meeting criteria for major depressive disorder or experiencing an elevation in depressive symptoms. These depressive symptoms are often chronic and persistent, and they have been associated with the development and progression of coronary artery disease, worse health-related quality of life, poor physical functioning, recurrent cardiac events, and a 2- to 2.5-fold increased risk of mortality. Impaired adherence to health behaviors and adverse physiological effects of depression, including inflammation, endothelial dysfunction, platelet hyperactivity, and autonomic nervous system abnormalities, may link depression with adverse cardiac outcomes. Pharmacologic and psychotherapeutic interventions appear to be safe and effective at reducing depressive symptoms in patients with cardiovascular disease and may impact cardiac outcomes. Unfortunately, depression often is unrecognized and untreated in this population, despite the availability of brief screening tools that can be used for this purpose. We recommend the routine screening of cardiac patients for depression when there are adequate mechanisms for management and referral, such as available consulting psychiatrists or care management programs that facilitate the delivery of pharmacologic and psychotherapeutic treatments in this vulnerable population.
C1 [Celano, Christopher M.; Huffman, Jeff C.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Celano, Christopher M.; Huffman, Jeff C.] Harvard Univ, Sch Med, Boston, MA USA.
RP Celano, CM (reprint author), Massachusetts Gen Hosp, Dept Psychiat, 55 Fruit St,WACC 812, Boston, MA 02114 USA.
EM ccelano@partners.org
NR 127
TC 82
Z9 90
U1 4
U2 25
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1061-5377
EI 1538-4683
J9 CARDIOL REV
JI Cardiol. Rev.
PD MAY-JUN
PY 2011
VL 19
IS 3
BP 130
EP 142
DI 10.1097/CRD.0b013e31820e8106
PG 13
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 745CS
UT WOS:000289142100005
PM 21464641
ER
PT J
AU Yoon, JH
Jang, IK
AF Yoon, Joo Heung
Jang, Ik-Kyung
TI Heparin-Induced Thrombocytopenia in Cardiovascular Patients
Pathophysiology, Diagnosis, and Treatment
SO CARDIOLOGY IN REVIEW
LA English
DT Review
DE heparin-induced thrombocytopenia; HIT; cardiovascular patients;
PF4/heparin antibody
ID CORONARY-ARTERY-BYPASS; ECARIN CLOTTING TIME; VENOUS LIMB GANGRENE;
CARDIOPULMONARY BYPASS; CARDIAC-SURGERY; ARGATROBAN THERAPY; CLINICAL
SETTINGS; GRAFT OCCLUSION; ILL PATIENTS; ANTIBODIES
AB Heparin-induced thrombocytopenia is a life-threatening immunemediated platelet activation condition that can cause arterial and venous thromboembolism. The triggering complex, platelet factor 4/heparin antibody, has several unique immunologic characteristics that have not been well elucidated until recently. In patients undergoing cardiovascular procedures such as percutaneous coronary intervention and coronary artery bypass graft surgery, the prevalence of platelet factor 4/heparin antibody is significantly higher than that in the general population. The acuity and graveness of the thromboembolic phenomenon requires early diagnosis and empirical initiation of treatment, even before confirmatory test results are available. Also, although multiple therapeutic modalities exist, the safety and efficacy of each option depends upon the clinical setting. Therefore, this review will focus on the updated pathophysiology of heparin-induced thrombocytopenia, new diagnostic criteria, and the various treatment options for cardiovascular patients with different conditions.
C1 [Yoon, Joo Heung; Jang, Ik-Kyung] Harvard Univ, Dept Med, Div Cardiol, Massachusetts Gen Hosp,Sch Med, Boston, MA 02114 USA.
RP Jang, IK (reprint author), Harvard Univ, Dept Med, Div Cardiol, Massachusetts Gen Hosp,Sch Med, 55 Fruit St,GRB 800, Boston, MA 02114 USA.
EM ijang@partners.org
NR 126
TC 5
Z9 5
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1061-5377
EI 1538-4683
J9 CARDIOL REV
JI Cardiol. Rev.
PD MAY-JUN
PY 2011
VL 19
IS 3
BP 143
EP 153
DI 10.1097/CRD.0b013e318211f7c0
PG 11
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 745CS
UT WOS:000289142100006
PM 21464642
ER
PT J
AU Piris, A
Mihm, MC
Duncan, LM
AF Piris, Adriano
Mihm, Martin C., Jr.
Duncan, Lyn M.
TI AJCC melanoma staging update: impact on dermatopathology practice and
patient management
SO JOURNAL OF CUTANEOUS PATHOLOGY
LA English
DT Article
DE cancer; dermatopathology; melanoma
ID AMERICAN JOINT COMMITTEE; SENTINEL LYMPH-NODES; CUTANEOUS MELANOMA;
MITOTIC RATE; PROGNOSTIC-SIGNIFICANCE; ULCERATION; BIOPSY
AB Piris A, Mihm MC Jr, Duncan LM. AJCC melanoma staging update: impact on dermatopathology practice and patient management.
C1 [Piris, Adriano; Duncan, Lyn M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dermatopathol Unit,Pathol Serv, Boston, MA USA.
[Mihm, Martin C., Jr.] Harvard Univ, Sch Med, Dept Dermatol, Brigham & Womens Hosp, Boston, MA 02115 USA.
RP Duncan, LM (reprint author), MGH Dermatopathol Unit, WRN 825,55 Fruit St, Boston, MA 02114 USA.
EM duncan@helix.mgh.harvard.edu
NR 17
TC 29
Z9 30
U1 1
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0303-6987
J9 J CUTAN PATHOL
JI J. Cutan. Pathol.
PD MAY
PY 2011
VL 38
IS 5
BP 394
EP 400
DI 10.1111/j.1600-0560.2011.01699.x
PG 7
WC Dermatology; Pathology
SC Dermatology; Pathology
GA 741MH
UT WOS:000288867300004
PM 21385199
ER
PT J
AU Bragg, DC
Armata, IA
Nery, FC
Breakefield, XO
Sharma, N
AF Bragg, D. Cristopher
Armata, Ioanna A.
Nery, Flavia C.
Breakefield, Xandra O.
Sharma, Nutan
TI Molecular pathways in dystonia
SO NEUROBIOLOGY OF DISEASE
LA English
DT Review
DE Dystonia; TorsinA; THAP1; PACT; PRKRA; Dopamine; Endoplasmic reticulum;
Transcription; Stress
ID ONSET TORSION DYSTONIA; THAP-ZINC-FINGER; TRANSGENIC MOUSE MODEL;
DELTA-E-TORSINA; ENDOPLASMIC-RETICULUM STRESS; PROTEIN-KINASE PKR; DYT1
DYSTONIA; NUCLEAR-ENVELOPE; MUTANT TORSINA; PC12 CELLS
AB The hereditary dystonias comprise a set of diseases defined by a common constellation of motor deficits. These disorders are most likely associated with different molecular etiologies, many of which have yet to be elucidated. Here we discuss recent advances in three forms of hereditary dystonia, DYT1, DYT6 and DYT16, which share a similar clinical picture: onset in childhood or adolescence, progressive spread of symptoms with generalized involvement of body regions and a steady state affliction without treatment. Unlike DYT1, the genes responsible for DYT6 and DYT16 have only recently been identified, with relatively little information about the function of the encoded proteins. Nevertheless. recent data suggest that these proteins may fit together within interacting pathways involved in dopaminergic signaling, transcriptional regulation, and cellular stress responses. This review focuses on these molecular pathways, highlighting potential common themes among these dystonias which may serve as areas for future research. This article is part of a Special Issue entitled "Advances in dystonia". (C) 2010 Elsevier Inc. All rights reserved.
C1 [Bragg, D. Cristopher; Armata, Ioanna A.; Nery, Flavia C.; Breakefield, Xandra O.; Sharma, Nutan] Massachusetts Gen Hosp, Dept Neurol, Charlestown, MA 02129 USA.
[Bragg, D. Cristopher; Armata, Ioanna A.; Nery, Flavia C.; Breakefield, Xandra O.] Harvard Univ, Sch Med, Program Neurosci, Boston, MA 02115 USA.
[Breakefield, Xandra O.] Massachusetts Gen Hosp, Dept Radiol, Charlestown, MA 02129 USA.
RP Bragg, DC (reprint author), Massachusetts Gen Hosp, Dept Neurol, Bldg 149,13th St, Charlestown, MA 02129 USA.
EM bragg@helix.mgh.harvard.edu
FU NIH/NINDS [NS064450, NS069973, NS037409]; Tyler's Hope for a Dystonia
Cure, Inc.; Dystonia Medical Research Foundation
FX The authors gratefully acknowledge Dr. John R. Engen, for assistance
with structural modeling of THAP1, Ms. Emily Mills and Millstone Design
(www.millstone.com) for preparation of Figs. 2 and 4, and Ms. Suzanne
McDavitt, for the skilled editorial assistance with this manuscript.
This work supported by NIH/NINDS grants NS064450 (DCB), NS069973 (DCB),
NS037409 (XOB, NS), as well as grants from Tyler's Hope for a Dystonia
Cure, Inc. (DCB) and the Dystonia Medical Research Foundation (FCN).
NR 154
TC 41
Z9 41
U1 0
U2 7
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0969-9961
J9 NEUROBIOL DIS
JI Neurobiol. Dis.
PD MAY
PY 2011
VL 42
IS 2
SI SI
BP 136
EP 147
DI 10.1016/j.nbd.2010.11.015
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 743LE
UT WOS:000289019000003
PM 21134457
ER
PT J
AU Castellino, S
Keller, F
Dunphy, C
McCarten, K
Thomson, J
Voss, S
Nachman, J
Constine, L
Chen, L
Schwartz, C
AF Castellino, S.
Keller, F.
Dunphy, C.
McCarten, K.
Thomson, J.
Voss, S.
Nachman, J.
Constine, L.
Chen, Lu
Schwartz, C.
TI CHILDREN AND ADOLESCENTS WITH LOW RISK HODGKIN LYMPHOMA (HL)
SO PEDIATRIC BLOOD & CANCER
LA English
DT Meeting Abstract
C1 [Castellino, S.] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
[Keller, F.] Emory Univ, Atlanta, GA 30322 USA.
[Dunphy, C.] Univ N Carolina, Chapel Hill, NC USA.
[McCarten, K.; Schwartz, C.] Rhode Isl Hosp, Providence, RI USA.
[Thomson, J.] Primary Childrens Med Ctr, Salt Lake City, UT 84103 USA.
[Voss, S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Nachman, J.] Univ Chicago, Chicago, IL 60637 USA.
[Constine, L.] Univ Rochester, Rochester, NY USA.
[Chen, Lu] Childrens Oncol Grp Operat, Arcadia, CA USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
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 MAY
PY 2011
VL 56
IS 5
MA IV-2
BP 883
EP 883
PG 1
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA 731TK
UT WOS:000288132100069
ER
PT J
AU Yan-Meier, L
Eberhart, NK
Hammen, CL
Gitlin, M
Sokolski, K
Altshuler, L
AF Yan-Meier, Leslie
Eberhart, Nicole K.
Hammen, Constance L.
Gitlin, Michael
Sokolski, Kenneth
Altshuler, Lori
TI Stressful life events predict delayed functional recovery following
treatment for mania in bipolar disorder
SO PSYCHIATRY RESEARCH
LA English
DT Article
DE Bipolar; Mania; Stress; Functional recovery
ID UNIPOLAR DEPRESSION; SOCIAL-ADJUSTMENT; I DISORDER; STEP-BD; IMPAIRMENT;
HOSPITALIZATION; RECURRENCE; OUTCOMES; DISABILITY; REACTIVITY
AB Identifying predictors of functional recovery in bipolar disorder is critical to treatment efforts to help patients re-establish premorbid levels of role adjustment following an acute manic episode. The current study examined the role of stressful life events as potential obstacles to recovery of functioning in various roles. 65 patients with bipolar I disorder participated in a longitudinal study of functional recovery following clinical recovery from a manic episode. Stressful life events were assessed as predictors of concurrent vs. delayed recovery of role functioning in 4 domains (friends, family, home duties, work/school). Despite clinical recovery, a subset of patients experienced delayed functional recovery in various role domains. Moreover, delayed functional recovery was significantly associated with presence of one or more stressors in the prior 3 months, even after controlling for mood symptoms. Presence of a stressor predicted longer time to functional recovery in life domains, up to 112 days in work/school. Interventions that provide monitoring, support, and problem-solving may be needed to help prevent or mitigate the effects of stress on functional recovery. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
C1 [Yan-Meier, Leslie; Hammen, Constance L.] Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90024 USA.
[Eberhart, Nicole K.] RAND Corp, Santa Monica, CA USA.
[Hammen, Constance L.; Gitlin, Michael; Altshuler, Lori] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA.
[Sokolski, Kenneth] Vet Adm Long Beach Healthcare Syst, Mental Hlth Care Grp, Long Beach, CA USA.
[Sokolski, Kenneth] Univ Calif Irvine, Dept Psychiat, Irvine, CA 92717 USA.
[Altshuler, Lori] W Los Angeles Healthcare Ctr, VA Greater Los Angeles Healthcare System, Dept Psychiat, Los Angeles, CA USA.
RP Hammen, CL (reprint author), 1285 Franz Hall,Box 951563, Los Angeles, CA 90095 USA.
EM hammen@psych.ucla.edu
FU National Institute of Mental Health [1R01MH057762]
FX Funding for this study was provided by the National Institute of Mental
Health 1R01MH057762, awarded to Dr. Altshuler.
NR 50
TC 10
Z9 10
U1 1
U2 4
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0165-1781
J9 PSYCHIAT RES
JI Psychiatry Res.
PD APR 30
PY 2011
VL 186
IS 2-3
BP 267
EP 271
DI 10.1016/j.psychres.2010.08.028
PG 5
WC Psychiatry
SC Psychiatry
GA 744YS
UT WOS:000289131700018
PM 20888051
ER
PT J
AU Chen, DC
Zhou, MA
Zhou, DH
Xiu, MH
Wu, GY
Kosten, TR
Zhang, XY
AF Chen, Da Chun
Zhou, Ming Ai
Zhou, Dong Hao
Xiu, Mel Hong
Wu, Gui Ying
Kosten, Thomas R.
Zhang, Xiang Yang
TI Gender differences in the prevalence of diabetes mellitus in chronic
hospitalized patients with schizophrenia on long-term antipsychotics
SO PSYCHIATRY RESEARCH
LA English
DT Article
DE Schizophrenia; Gender differences; Diabetes mellitus
ID HORMONE REPLACEMENT THERAPY; IMPAIRED FASTING GLUCOSE; 2ND-GENERATION
ANTIPSYCHOTICS; METABOLIC ABNORMALITIES; TOLERANCE; INSULIN; RISK
AB Gender-specific relationships between diabetes mellitus (DM) and schizophrenia have previously received little systematic study. The results showed that the overall DM prevalence was 20% with rates of 17% (58/343) in males and 27% (46/172) in females (p<0.01). Furthermore, increased body mass index (BMI), abdominal obesity and antipsychotic types were predictors of diabetes in these chronic schizophrenic patients. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
C1 [Wu, Gui Ying; Kosten, Thomas R.; Zhang, Xiang Yang] Baylor Coll Med, Menninger Dept Psychiat & Behav Sci, Houston, TX 77030 USA.
[Zhou, Ming Ai; Zhou, Dong Hao] LinYi Chinese Med Hosp, Dept Immunol & Allergol, Linyi, Shandong, Peoples R China.
[Chen, Da Chun; Xiu, Mel Hong; Zhang, Xiang Yang] Beijing HuiLongGuan Hosp, Ctr Biol Psychiat, Beijing, Peoples R China.
RP Kosten, TR (reprint author), VA Med Ctr, Res Bldg 110,Room 229,2002 Holcombe Blvd, Houston, TX 77030 USA.
EM kosten@bcm.edu; xyzhang@bcm.edu
FU Stanley Medical Research Institute [03T-459, 05T-726]; Department of
Veterans Affairs; VISN 16; Mental Illness Research, Education, and
Clinical Center, United States National Institute of Health [K05-DA0454,
P50-DA18827, U01-MH79639]
FX This study was supported by grants from the Stanley Medical Research
Institute (03T-459 and 05T-726), and the Department of Veterans Affairs,
VISN 16, Mental Illness Research, Education, and Clinical Center, United
States National Institute of Health K05-DA0454, P50-DA18827, and
U01-MH79639.
NR 20
TC 5
Z9 8
U1 0
U2 0
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0165-1781
J9 PSYCHIAT RES
JI Psychiatry Res.
PD APR 30
PY 2011
VL 186
IS 2-3
BP 451
EP 453
DI 10.1016/j.psychres.2010.07.054
PG 3
WC Psychiatry
SC Psychiatry
GA 744YS
UT WOS:000289131700052
PM 20797801
ER
PT J
AU Walterfang, M
Looi, JCL
Styner, M
Walker, RH
Danek, A
Niethammer, M
Evans, A
Kotschet, K
Rodrigues, GR
Hughes, A
Velakoulis, D
AF Walterfang, Mark
Looi, Jeffrey Chee Leong
Styner, Martin
Walker, Ruth H.
Danek, Adrian
Niethammer, Marc
Evans, Andrew
Kotschet, Katya
Rodrigues, Guilherme R.
Hughes, Andrew
Velakoulis, Dennis
TI Shape alterations in the striatum in chorea-acanthocytosis
SO PSYCHIATRY RESEARCH-NEUROIMAGING
LA English
DT Article
DE Neuroacanthocytosis; Chorea-acanthocytosis; Chorea; Caudate; Striatum;
Neurodegeneration
ID OBSESSIVE-COMPULSIVE DISORDER; VOXEL-BASED MORPHOMETRY; CAUDATE-NUCLEUS;
BASAL GANGLIA; HUNTINGTONS-DISEASE; NEUROACANTHOCYTOSIS; CIRCUITS;
PROTEIN; IMAGES; BRAIN
AB Chorea-acanthocytosis (ChAc) is an uncommon autosomal recessive disorder due to mutations of the VPS13A gene, which encodes for the membrane protein chorein. ChAc presents with progressive limb and orobuccal chorea, but there is often a marked dysexecutive syndrome. ChAc may first present with neuropsychiatric disturbance such as obsessive-compulsive disorder (OCD), suggesting a particular role for disruption to striatal structures involved in non-motor frontostriatal loops, such as the head of the caudate nucleus. Two previous studies have suggested a marked reduction in volume in the caudate nucleus and putamen, but did not examine morphometric change. We investigated morphometric change in 13 patients with genetically or biochemically confirmed ChAc and 26 age- and gender-matched controls. Subjects underwent magnetic resonance imaging and manual segmentation of the caudate nucleus and putamen, and shape analysis using a non-parametric spherical harmonic technique. Both structures showed significant and marked reductions in volume compared with controls, with reduction greatest in the caudate nucleus. Both structures showed significant shape differences, particularly in the head of the caudate nucleus. No significant correlation was shown between duration of illness and striatal volume or shape, suggesting that much structural change may have already taken place at the time of symptom onset. Our results suggest that striatal neuron loss may occur early in the disease process, and follows a dorsal-ventral gradient that may correlate with early neuropsychiatric and cognitive presentations of the disease. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
C1 [Walterfang, Mark; Evans, Andrew; Velakoulis, Dennis] Royal Melbourne Hosp, Neuropsychiat Unit, Melbourne, Vic 3050, Australia.
[Looi, Jeffrey Chee Leong] Australian Natl Univ, Sch Med, Dept Neurosci Ageing, Canberra, ACT, Australia.
[Styner, Martin] Univ N Carolina, Neuroimaging Res & Anal Labs, Chapel Hill, NC USA.
[Walker, Ruth H.] James J Peters Vet Affairs Med Ctr, Dept Neurol, Bronx, NY 10468 USA.
[Walker, Ruth H.] Mt Sinai Sch Med, Dept Neurol, New York, NY 10029 USA.
[Danek, Adrian] Univ Munich, Dept Neurol, D-8000 Munich, Germany.
[Niethammer, Marc] Univ N Carolina, Biomed Res Imaging Ctr, Chapel Hill, NC USA.
[Kotschet, Katya] St Vincents Hosp, Dept Neurol, Melbourne, Vic, Australia.
[Rodrigues, Guilherme R.] Univ Sao Paulo, Ribeirao Preto Sch Med, Dept Neurol, Sao Paulo, Brazil.
[Hughes, Andrew] Austin Hosp, Dept Neurol, Melbourne, Vic 3084, Australia.
RP Walterfang, M (reprint author), Royal Melbourne Hosp, Neuropsychiat Unit, Level 2,Joan Cade Bldg, Melbourne, Vic 3050, Australia.
EM mark.walterfang@mh.org.au
RI Rodrigues, Guilherme/D-3547-2009; Walterfang, Mark/H-4930-2011; Danek,
Adrian/G-7339-2011;
OI Rodrigues, Guilherme/0000-0002-4296-1016; Walterfang,
Mark/0000-0002-1389-3691; Danek, Adrian/0000-0001-8857-5383; Styner,
Martin/0000-0002-8747-5118; Looi, Jeffrey/0000-0003-3351-6911
FU Advocacy for Neuroacanthocytosis Patients; UNC Neurodevelopmental
Disorders Research Centre [HD 03110]; NIH [U54 EB005149-01]; National
Alliance for Medical Image Computing; Melbourne Neuropsychiatry Centre
FX Dr Walterfang was supported by a grant from the Advocacy for
Neuroacanthocytosis Patients (www.naadvocacy.org). Dr Walterfang takes
responsibility for the integrity of the data and the accuracy of the
data analysis. Furthermore, Dr Styner's work was funded by the UNC
Neurodevelopmental Disorders Research Centre HD 03110, and the NIH
Roadmap Grant U54 EB005149-01, National Alliance for Medical Image
Computing. Dr. B. Bader performed the chorein Western blot with the help
of G. Kwiatkowski at the Zentrum fur Neuropathologie und Prionforschung,
University of Munich (director: Prof. Dr. H. Kretzschmar), financially
supported by the Advocacy for Neuroacanthocytosis Patients. Dr. Looi
self-funded travel and accommodation for his contribution to this
project at Melbourne Neuropsychiatry Centre.
NR 36
TC 19
Z9 20
U1 1
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0925-4927
EI 1872-7506
J9 PSYCHIAT RES-NEUROIM
JI Psychiatry Res. Neuroimaging
PD APR 30
PY 2011
VL 192
IS 1
BP 29
EP 36
DI 10.1016/j.pscychresns.2010.10.006
PG 8
WC Clinical Neurology; Neuroimaging; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 751FG
UT WOS:000289602300004
PM 21377843
ER
PT J
AU PosthumaDeBoer, J
Wurdinger, T
Graat, HCA
van Beusechem, VW
Helder, MN
van Royen, BJ
Kaspers, GJL
AF PosthumaDeBoer, Jantine
Wurdinger, Thomas
Graat, Harm C. A.
van Beusechem, Victor W.
Helder, Marco N.
van Royen, Barend J.
Kaspers, Gertjan J. L.
TI WEE1 inhibition sensitizes osteosarcoma to radiotherapy
SO BMC CANCER
LA English
DT Article
ID HIGH-GRADE OSTEOSARCOMA; DNA-DAMAGE; IONIZING-RADIATION; ION
RADIOTHERAPY; CELLS; BONE; KINASE; RADIOSENSITIZATION; CHEMOTHERAPY;
EXTREMITIES
AB Background: The use of radiotherapy in osteosarcoma (OS) is controversial due to its radioresistance. OS patients currently treated with radiotherapy generally are inoperable, have painful skeletal metastases, refuse surgery or have undergone an intralesional resection of the primary tumor. After irradiation-induced DNA damage, OS cells sustain a prolonged G(2) cell cycle checkpoint arrest allowing DNA repair and evasion of cell death. Inhibition of WEE1 kinase leads to abrogation of the G(2) arrest and could sensitize OS cells to irradiation induced cell death.
Methods: WEE1 expression in OS was investigated by gene-expression data analysis and immunohistochemistry of tumor samples. WEE1 expression in OS cell lines and human osteoblasts was investigated by Western blot. The effect of WEE1 inhibition on the radiosensitivity of OS cells was assessed by cell viability and caspase activation analyses after combination treatment. The presence of DNA damage was visualized using immunofluorescence microscopy. Cell cycle effects were investigated by flow cytometry and WEE1 kinase regulation was analyzed by Western blot.
Results: WEE1 expression is found in the majority of tested OS tissue samples. Small molecule drug PD0166285 inhibits WEE1 kinase activity. In the presence of WEE1-inhibitor, irradiated cells fail to repair their damaged DNA, and show higher levels of caspase activation. The inhibition of WEE1 effectively abrogates the irradiation-induced G(2) arrest in OS cells, forcing the cells into premature, catastrophic mitosis, thus enhancing cell death after irradiation treatment.
Conclusion: We show that PD0166285, a small molecule WEE1 kinase inhibitor, can abrogate the G(2) checkpoint in OS cells, pushing them into mitotic catastrophe and thus sensitizing OS cells to irradiation-induced cell death. This suggests that WEE1 inhibition may be a promising strategy to enhance the radiotherapy effect in patients with OS.
C1 [PosthumaDeBoer, Jantine; Graat, Harm C. A.; Helder, Marco N.; van Royen, Barend J.; Kaspers, Gertjan J. L.] Vrije Univ Amsterdam Med Ctr, Dept Orthopaed Surg, NL-1007 MB Amsterdam, Netherlands.
[Wurdinger, Thomas] Vrije Univ Amsterdam Med Ctr, Neurooncol Res Grp, Dept Neurosurg, NL-1007 MB Amsterdam, Netherlands.
[Wurdinger, Thomas] Vrije Univ Amsterdam Med Ctr, Neurooncol Res Grp, Dept Paediat Oncol Haematol, NL-1007 MB Amsterdam, Netherlands.
[Wurdinger, Thomas] Massachusetts Gen Hosp, Mol Neurogenet Unit, Dept Neurol, Charlestown, MA 02129 USA.
[Wurdinger, Thomas] Harvard Univ, Sch Med, Charlestown, MA 02129 USA.
[van Beusechem, Victor W.] Vrije Univ Amsterdam Med Ctr, Dept Med Oncol, RIFOL, NL-1007 MB Amsterdam, Netherlands.
[Helder, Marco N.; van Royen, Barend J.] STEGA, Res Inst MOVE, NL-1007 MB Amsterdam, Netherlands.
RP Kaspers, GJL (reprint author), Vrije Univ Amsterdam Med Ctr, Dept Orthopaed Surg, POB 7057, NL-1007 MB Amsterdam, Netherlands.
EM gjl.kaspers@vumc.nl
FU Individualised Musculoskeletal Regeneration and Reconstruction Network
(Danish Research Council) Aarhus, Denmark; VONK: VUmc Onderzoek naar
Kinderkanker (Stichting Research Fonds Kindergeneeskunde VUmc)
Amsterdam, the Netherlands
FX JP is supported by the Individualised Musculoskeletal Regeneration and
Reconstruction Network (Danish Research Council) Aarhus, Denmark and by
VONK: VUmc Onderzoek naar Kinderkanker (Stichting Research Fonds
Kindergeneeskunde VUmc) Amsterdam, the Netherlands.
NR 36
TC 33
Z9 37
U1 0
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD APR 29
PY 2011
VL 11
AR 156
DI 10.1186/1471-2407-11-156
PG 8
WC Oncology
SC Oncology
GA 769NQ
UT WOS:000291023100001
PM 21529352
ER
PT J
AU Massimini, DF
Warner, JJP
Li, GA
AF Massimini, Daniel F.
Warner, Jon J. P.
Li, Guoan
TI Non-invasive determination of coupled motion of the scapula and
humerus-An in-vitro validation (vol 44, pg 408, 2011)
SO JOURNAL OF BIOMECHANICS
LA English
DT Correction
C1 [Massimini, Daniel F.; Warner, Jon J. P.; Li, Guoan] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Bioengn Lab, Boston, MA 02114 USA.
[Massimini, Daniel F.] MIT, Dept Mech Engn, Cambridge, MA 02139 USA.
RP Li, GA (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Bioengn Lab, GRJ-1215,55 Fruit St, Boston, MA 02114 USA.
EM gli1@partners.org
NR 1
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0021-9290
J9 J BIOMECH
JI J. Biomech.
PD APR 29
PY 2011
VL 44
IS 7
BP 1428
EP 1428
DI 10.1016/j.jbiomech.2011.03.021
PG 1
WC Biophysics; Engineering, Biomedical
SC Biophysics; Engineering
GA 770GU
UT WOS:000291075800033
ER
PT J
AU Goichberg, P
Bai, YN
D'Amario, D
Ferreira-Martins, J
Fiorini, C
Zheng, HQ
Signore, S
del Monte, F
Ottolenghi, S
D'Alessandro, DA
Michler, RE
Hosoda, T
Anversa, P
Kajstura, J
Rota, M
Leri, A
AF Goichberg, Polina
Bai, Yingnan
D'Amario, Domenico
Ferreira-Martins, Joao
Fiorini, Claudia
Zheng, Hanqiao
Signore, Sergio
del Monte, Federica
Ottolenghi, Sergio
D'Alessandro, David A.
Michler, Robert E.
Hosoda, Toru
Anversa, Piero
Kajstura, Jan
Rota, Marcello
Leri, Annarosa
TI The Ephrin A1-EphA2 System Promotes Cardiac Stem Cell Migration After
Infarction
SO CIRCULATION RESEARCH
LA English
DT Article
DE ephrin; cardiac stem cells; myocardial regeneration; cell migration
ID PROGENITOR CELLS; GROWTH-FACTOR; MYOCARDIAL REGENERATION; MOUSE HEART;
ACTIVATION; PROLIFERATION; INHIBITION; PHENOTYPE; FAILURE; EPHA2
AB Rationale: Understanding the mechanisms that regulate trafficking of human cardiac stem cells (hCSCs) may lead to development of new therapeutic approaches for the failing heart.
Objective: We tested whether the motility of hCSCs in immunosuppressed infarcted animals is controlled by the guidance system that involves the interaction of Eph receptors with ephrin ligands.
Methods and Results: Within the cardiac niches, cardiomyocytes expressed preferentially the ephrin A1 ligand, whereas hCSCs possessed the EphA2 receptor. Treatment of hCSCs with ephrin A1 resulted in the rapid internalization of the ephrin A1-EphA2 complex, posttranslational modifications of Src kinases, and morphological changes consistent with the acquisition of a motile cell phenotype. Ephrin A1 enhanced the motility of hCSCs in vitro, and their migration in vivo following acute myocardial infarction. At 2 weeks after infarction, the volume of the regenerated myocardium was 2-fold larger in animals injected with ephrin A1-activated hCSCs than in animals receiving control hCSCs; this difference was dictated by a greater number of newly formed cardiomyocytes and coronary vessels. The increased recovery in myocardial mass with ephrin A1-treated hCSCs was characterized by further restoration of cardiac function and by a reduction in arrhythmic events.
Conclusions: Ephrin A1 promotes the motility of EphA2-positive hCSCs, facilitates their migration to the area of damage, and enhances cardiac repair. Thus, in situ stimulation of resident hCSCs with ephrin A1 or their ex vivo activation before myocardial delivery improves cell targeting to sites of injury, possibly providing a novel strategy for the management of the diseased heart. (Circ Res. 2011;108:1071-1083.)
C1 [Goichberg, Polina; Bai, Yingnan; D'Amario, Domenico; Ferreira-Martins, Joao; Zheng, Hanqiao; Signore, Sergio; Hosoda, Toru; Anversa, Piero; Kajstura, Jan; Rota, Marcello; Leri, Annarosa] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Anesthesia,Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA.
[Goichberg, Polina; Bai, Yingnan; D'Amario, Domenico; Ferreira-Martins, Joao; Zheng, Hanqiao; Signore, Sergio; Hosoda, Toru; Anversa, Piero; Kajstura, Jan; Rota, Marcello; Leri, Annarosa] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA.
[Goichberg, Polina; Bai, Yingnan; D'Amario, Domenico; Ferreira-Martins, Joao; Zheng, Hanqiao; Signore, Sergio; Hosoda, Toru; Anversa, Piero; Kajstura, Jan; Rota, Marcello; Leri, Annarosa] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Cardiovasc Med,Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA.
[del Monte, Federica] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Cardiovasc Inst, Boston, MA 02115 USA.
[Fiorini, Claudia; D'Alessandro, David A.; Michler, Robert E.] Albert Einstein Coll Med, Montefiore Med Ctr, New York, NY USA.
[Ottolenghi, Sergio] Univ Milano Bicocca, Dept Biosci & Biotechnol, Milan, Italy.
RP Leri, A (reprint author), Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Anesthesia,Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA.
EM aleri@partners.org
RI Hosoda, Toru/G-1873-2010;
OI Hosoda, Toru/0000-0002-7273-0630; Ferreira-Martins,
Joao/0000-0002-5491-9421; Fiorini, Claudia/0000-0003-4878-2438
FU NIH
FX This work was supported by the NIH.
NR 44
TC 44
Z9 47
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7330
J9 CIRC RES
JI Circ.Res.
PD APR 29
PY 2011
VL 108
IS 9
BP 1071
EP U114
DI 10.1161/CIRCRESAHA.110.239459
PG 30
WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Hematology
GA 756AL
UT WOS:000289983600007
PM 21415392
ER
PT J
AU Jacobson, EM
Concepcion, E
Ho, K
Kopp, P
Toniolo, JV
Tomer, Y
AF Jacobson, Eric M.
Concepcion, Erlinda
Ho, Kenneth
Kopp, Peter
Toniolo, Jussara Vono
Tomer, Yaron
TI cDNA Immunization of Mice with Human Thyroglobulin Generates Both
Humoral and T Cell Responses: A Novel Model of Thyroid Autoimmunity
SO PLOS ONE
LA English
DT Article
ID RECEPTOR A-SUBUNIT; HASHIMOTOS-THYROIDITIS; GENE-TRANSFER; IN-VIVO;
ANTITHYROGLOBULIN AUTOANTIBODIES; THYROTROPIN RECEPTOR; SKELETAL-MUSCLE;
INTRAMUSCULAR INJECTION; GRAVES HYPERTHYROIDISM; DNA ELECTROTRANSFER
AB Thyroglobulin (Tg) represents one of the largest known self-antigens involved in autoimmunity. Numerous studies have implicated it in triggering and perpetuating the autoimmune response in autoimmune thyroid diseases (AITD). Indeed, traditional models of autoimmune thyroid disease, experimental autoimmune thyroiditis (EAT), are generated by immunizing mice with thyroglobulin protein in conjunction with an adjuvant, or by high repeated doses of Tg alone, without adjuvant. These extant models are limited in their experimental flexibility, i.e. the ability to make modifications to the Tg used in immunizations. In this study, we have immunized mice with a plasmid cDNA encoding the full-length human Tg (hTG) protein, in order to generate a model of Hashimoto's thyroiditis which is closer to the human disease and does not require adjuvants to breakdown tolerance. Human thyroglobulin cDNA was injected and subsequently electroporated into skeletal muscle using a square wave generator. Following hTg cDNA immunizations, the mice developed both B and T cell responses to Tg, albeit with no evidence of lymphocytic infiltration of the thyroid. This novel model will afford investigators the means to test various hypotheses which were unavailable with the previous EAT models, specifically the effects of hTg sequence variations on the induction of thyroiditis.
C1 [Jacobson, Eric M.] Univ Cincinnati, Coll Med, Div Endocrinol, Cincinnati, OH 45221 USA.
[Concepcion, Erlinda; Ho, Kenneth; Tomer, Yaron] Mt Sinai Sch Med, Dept Med, Div Endocrinol, New York, NY USA.
[Kopp, Peter; Toniolo, Jussara Vono] Northwestern Univ, Div Endocrinol Metab & Mol Med, Feinberg Sch Med, Chicago, IL 60611 USA.
[Tomer, Yaron] James J Peters VA Med Ctr, Bronx, NY USA.
RP Jacobson, EM (reprint author), Univ Cincinnati, Coll Med, Div Endocrinol, Cincinnati, OH 45221 USA.
EM Eric.Jacobson@uc.edu
FU National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
[DK061659, DK067555, DK073681, DK063024]; American Thyroid Association
FX This work was supported in part by grants DK061659, DK067555, DK073681
(to YT) and DK063024 (to PK) from the National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK). EMJ was supported by a grant from
the American Thyroid Association (http://www.thyroid.org). The funders
had no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript. No additional external
funding was received for this study.
NR 67
TC 5
Z9 5
U1 0
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 29
PY 2011
VL 6
IS 4
AR e19200
DI 10.1371/journal.pone.0019200
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 756OZ
UT WOS:000290024700100
PM 21559421
ER
PT J
AU Kajiya, M
Komatsuzawa, H
Papantonakis, A
Seki, M
Makihira, S
Ouhara, K
Kusumoto, Y
Murakami, S
Taubman, MA
Kawai, T
AF Kajiya, Mikihito
Komatsuzawa, Hitoshi
Papantonakis, Annatoula
Seki, Makoto
Makihira, Seicho
Ouhara, Kazuhisa
Kusumoto, Yutaka
Murakami, Shinya
Taubman, Martin A.
Kawai, Toshihisa
TI Aggregatibacter actinomycetemcomitans Omp29 Is Associated with Bacterial
Entry to Gingival Epithelial Cells by F-Actin Rearrangement
SO PLOS ONE
LA English
DT Article
ID OUTER-MEMBRANE PROTEIN; PATHOGEN ACTINOBACILLUS-ACTINOMYCETEMCOMITANS;
EXPERIMENTAL PERIODONTAL-DISEASE; INFLAMMATORY BONE-RESORPTION;
BLOOD-BRAIN-BARRIER; ESCHERICHIA-COLI; PORPHYROMONAS-GINGIVALIS;
YERSINIA-ENTEROCOLITICA; BACTEROIDES-GINGIVALIS; JUNCTIONAL EPITHELIUM
AB The onset and progressive pathogenesis of periodontal disease is thought to be initiated by the entry of Aggregatibacter actinomycetemcomitans (Aa) into periodontal tissue, especially gingival epithelium. Nonetheless, the mechanism underlying such bacterial entry remains to be clarified. Therefore, this study aimed to investigate the possible role of Aa outer membrane protein 29 kD (Omp29), a homologue of E. coli OmpA, in promoting bacterial entry into gingival epithelial cells. To accomplish this, Omp29 expression vector was incorporated in an OmpA-deficient mutant of E. coli. Omp29(+)/OmpA(-) 2 E. coli demonstrated 22-fold higher entry into human gingival epithelial line cells (OBA9) than Omp29(-)/OmpA(-) E. coli. While the entry of Aa and Omp29(+)/OmpA(-) E. coli into OBA9 cells were inhibited by anti-Omp29 antibody, their adherence to OBA9 cells was not inhibited. Stimulation of OBA9 cells with purified Omp29 increased the phosphorylation of focal adhesion kinase (FAK), a pivotal cell-signaling molecule that can up-regulate actin rearrangement. Furthermore, Omp29 increased the formation of F-actin in OBA9 cells. The internalization of Omp29-coated beads and the entry of Aa into OBA9 were partially inhibited by treatment with PI3-kinase inhibitor (Wortmannin) and Rho GTPases inhibitor (EDIN), both known to convey FAK-signaling to actin-rearrangement. These results suggest that Omp29 is associated with the entry of Aa into gingival epithelial cells by up-regulating F-actin rearrangement via the FAK signaling pathway.
C1 [Kajiya, Mikihito; Papantonakis, Annatoula; Seki, Makoto; Makihira, Seicho; Ouhara, Kazuhisa; Taubman, Martin A.; Kawai, Toshihisa] Forsyth Inst, Dept Immunol, Boston, MA USA.
[Kajiya, Mikihito; Kawai, Toshihisa] Harvard Univ, Sch Dent Med, Dept Oral Med Infect & Immun, Boston, MA 02115 USA.
[Komatsuzawa, Hitoshi] Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Oral Microbiol, Kagoshima 890, Japan.
[Kusumoto, Yutaka] Osaka Ohtani Univ, Fac Pharm, Immunol Lab, Osaka, Japan.
[Murakami, Shinya] Osaka Univ, Grad Sch Dent, Dept Periodontol, Div Oral Biol & Dis Control, Osaka, Japan.
RP Kajiya, M (reprint author), Forsyth Inst, Dept Immunol, Boston, MA USA.
EM tkawai@forsyth.org
FU National Institute of Dental and Craniofacial Research [DE-03420,
DE-18499, DE-19917]
FX The study reported herein was supported in part by grants DE-03420,
DE-18499 and DE-19917 from the National Institute of Dental and
Craniofacial Research (http://www.nidcr.nih.gov). The funders had no
role in study design, data collection and analysis, decision to publish,
or preparation of the manuscript.
NR 36
TC 12
Z9 12
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 29
PY 2011
VL 6
IS 4
AR e18287
DI 10.1371/journal.pone.0018287
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 756OZ
UT WOS:000290024700010
PM 21559515
ER
PT J
AU Ran, CZ
Zhao, W
Moir, RD
Moore, A
AF Ran, Chongzhao
Zhao, Wei
Moir, Robert D.
Moore, Anna
TI Non-Conjugated Small Molecule FRET for Differentiating Monomers from
Higher Molecular Weight Amyloid Beta Species
SO PLOS ONE
LA English
DT Article
ID THIOFLAVIN-T BINDING; ALZHEIMERS-DISEASE; A-BETA; CEREBROSPINAL-FLUID;
OLIGOMERS; PEPTIDE; FIBRILS; MEMORY; FIBRILLOGENESIS; MECHANISM
AB Background: Systematic differentiation of amyloid (A beta) species could be important for diagnosis of Alzheimer's disease (AD). In spite of significant progress, controversies remain regarding which species are the primary contributors to the AD pathology, and which species could be used as the best biomarkers for its diagnosis. These controversies are partially caused by the lack of reliable methods to differentiate the complicated subtypes of A beta species. Particularly, differentiation of A beta monomers from toxic higher molecular weight species (HrMW) would be beneficial for drug screening, diagnosis, and molecular mechanism studies. However, fast and cheap methods for these specific aims are still lacking.
Principal Findings: We demonstrated the feasibility of a non-conjugated FRET (Forster resonance energy transfer) technique that utilized amyloid beta (A beta) species as intrinsic platforms for the FRET pair assembly. Mixing two structurally similar curcumin derivatives that served as the small molecule FRET pair with A beta 40 aggregates resulted in a FRET signal, while no signal was detected when using A beta 40 monomer solution. Lastly, this FRET technique enabled us to quantify the concentrations of A beta monomers and high molecular weight species in solution.
Significance: We believe that this FRET technique could potentially be used as a tool for screening for inhibitors of A beta aggregation. We also suggest that this concept could be generalized to other misfolded proteins/peptides implicated in various pathologies including amyloid in diabetes, prion in bovine spongiform encephalopathy, tau protein in AD, and alpha-synuclein in Parkinson disease.
C1 [Ran, Chongzhao; Zhao, Wei; Moore, Anna] Harvard Univ, MGH MIT HMS Athinoula A Martinos Ctr Biomed Imagi, Massachusetts Gen Hosp, Mol Imaging Lab,Dept Radiol,Sch Med, Charlestown, MA USA.
[Moir, Robert D.] Massachusetts Gen Hosp, Dept Neurol, Alzheimers Dis Res Unit, Charlestown, MA USA.
RP Ran, CZ (reprint author), Harvard Univ, MGH MIT HMS Athinoula A Martinos Ctr Biomed Imagi, Massachusetts Gen Hosp, Mol Imaging Lab,Dept Radiol,Sch Med, Charlestown, MA USA.
EM amoore@helix.mgh.harvard.edu
FU NIA [K25AG036760]
FX This work was supported in part by K25AG036760 award from NIA to C.R. No
additional external funding was received for this study. The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 28
TC 14
Z9 16
U1 3
U2 18
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 29
PY 2011
VL 6
IS 4
AR e19362
DI 10.1371/journal.pone.0019362
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 756OZ
UT WOS:000290024700148
PM 21559413
ER
PT J
AU Salehi-Had, H
Roh, MI
Giani, A
Hisatomi, T
Nakao, S
Kim, IK
Gragoudas, ES
Vavvas, D
Guccione, S
Miller, JW
AF Salehi-Had, Hani
Roh, Mi In
Giani, Andrea
Hisatomi, Toshio
Nakao, Shintaro
Kim, Ivana K.
Gragoudas, Evangelos S.
Vavvas, Demetrios
Guccione, Samira
Miller, Joan W.
TI Utilizing Targeted Gene Therapy with Nanoparticles Binding Alpha v Beta
3 for Imaging and Treating Choroidal Neovascularization
SO PLOS ONE
LA English
DT Article
ID MACULAR DEGENERATION; INTEGRIN ALPHA(V)BETA(3); PHOTODYNAMIC THERAPY;
RETINAL NEOVASCULARIZATION; VISUAL IMPAIRMENT; TUMOR-REGRESSION;
CELL-SURVIVAL; ANGIOGENESIS; DELIVERY; MODEL
AB Purpose: The integrin avb3 is differentially expressed on neovascular endothelial cells. We investigated whether a novel intravenously injectable avb3 integrin-ligand coupled nanoparticle (NP) can target choroidal neovascular membranes (CNV) for imaging and targeted gene therapy.
Methods: CNV lesions were induced in rats using laser photocoagulation. The utility of NP for in vivo imaging and gene delivery was evaluated by coupling the NP with a green fluorescing protein plasmid (NP-GFPg). Rhodamine labeling (Rd-NP) was used to localize NP in choroidal flatmounts. Rd-NP-GFPg particles were injected intravenously on weeks 1, 2, or 3. In the treatment arm, rats received NP containing a dominant negative Raf mutant gene (NP-ATP mu-Raf) on days 1, 3, and 5. The change in CNV size and leakage, and TUNEL positive cells were quantified.
Results: GFP plasmid expression was seen in vivo up to 3 days after injection of Rd-NP-GFPg. Choroidal flatmounts confirmed the localization of the NP and the expression of GFP plasmid in the CNV. Treating the CNV with NP-ATP mu-Raf decreased the CNV size by 42% (P < 0.001). OCT analysis revealed that the reduction of CNV size started on day 5 and reached statistical significance by day 7. Fluorescein angiography grading showed significantly less leakage in the treated CNV (P < 0.001). There were significantly more apoptotic (TUNEL-positive) nuclei in the treated CNV.
Conclusion: Systemic administration of avb3 targeted NP can be used to label the abnormal blood vessels of CNV for imaging. Targeted gene delivery with NP-ATP mu-Raf leads to a reduction in size and leakage of the CNV by induction of apoptosis in the CNV.
C1 [Salehi-Had, Hani; Roh, Mi In; Giani, Andrea; Hisatomi, Toshio; Nakao, Shintaro; Kim, Ivana K.; Gragoudas, Evangelos S.; Vavvas, Demetrios; Miller, Joan W.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol,Angiogenesis Lab, Boston, MA 02115 USA.
[Guccione, Samira] Stanford Univ, Lucas Ctr, Radiol Sci Lab, Palo Alto, CA 94304 USA.
RP Salehi-Had, H (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol,Angiogenesis Lab, Boston, MA 02115 USA.
EM guccione@stanford.edu
OI Hisatomi, Toshio/0000-0003-2552-9595; Vavvas,
Demetrios/0000-0002-8622-6478
FU Research to Prevent Blindness (NY); Neovascular Research Fund; AMD
Center of Excellence
FX This work was supported by: Research to Prevent Blindness (NY)
Unrestricted Grant to the Harvard Department of Ophthalmology and
Neovascular Research Fund; AMD Center of Excellence. The funders had no
role in study design, data collection and analysis, decision to publish,
or preparation of the manuscript.
NR 45
TC 11
Z9 12
U1 0
U2 14
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 29
PY 2011
VL 6
IS 4
AR e18864
DI 10.1371/journal.pone.0018864
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 756OZ
UT WOS:000290024700029
PM 21559527
ER
PT J
AU Tucker, BA
Park, IH
Qi, SD
Klassen, HJ
Jiang, CH
Yao, J
Redenti, S
Daley, GQ
Young, MJ
AF Tucker, Budd A.
Park, In-Hyun
Qi, Sara D.
Klassen, Henry J.
Jiang, Caihui
Yao, Jing
Redenti, Stephen
Daley, George Q.
Young, Michael J.
TI Transplantation of Adult Mouse iPS Cell-Derived Photoreceptor Precursors
Restores Retinal Structure and Function in Degenerative Mice
SO PLOS ONE
LA English
DT Article
ID PLURIPOTENT STEM-CELLS; MACULAR DEGENERATION; PROGENITOR CELLS;
POLYCISTRONIC VECTOR; HUMAN FIBROBLASTS; HEAD INDUCTION; GENERATION;
DIFFERENTIATION; EXPRESSION; PROMOTE
AB This study was designed to determine whether adult mouse induced pluripotent stem cells (iPSCs), could be used to produce retinal precursors and subsequently photoreceptor cells for retinal transplantation to restore retinal function in degenerative hosts. iPSCs were generated using adult dsRed mouse dermal fibroblasts via retroviral induction of the transcription factors Oct4, Sox2, KLF4 and c-Myc. As with normal mouse ES cells, adult dsRed iPSCs expressed the pluripotency genes SSEA1, Oct4, Sox2, KLF4, c-Myc and Nanog. Following transplantation into the eye of immunecompromised retinal degenerative mice these cells proceeded to form teratomas containing tissue comprising all three germ layers. At 33 days post-differentiation a large proportion of the cells expressed the retinal progenitor cell marker Pax6 and went on to express the photoreceptor markers, CRX, recoverin, and rhodopsin. When tested using calcium imaging these cells were shown to exhibit characteristics of normal retinal physiology, responding to delivery of neurotransmitters. Following subretinal transplantation into degenerative hosts differentiated iPSCs took up residence in the retinal outer nuclear layer and gave rise to increased electro retinal function as determined by ERG and functional anatomy. As such, adult fibroblast-derived iPSCs provide a viable source for the production of retinal precursors to be used for transplantation and treatment of retinal degenerative disease.
C1 [Tucker, Budd A.; Jiang, Caihui; Redenti, Stephen] Univ Iowa, Dept Ophthalmol, Carver Coll Med, Inst Vis Res, Iowa City, IA 52242 USA.
[Qi, Sara D.; Yao, Jing; Young, Michael J.] Harvard Univ, Sch Med, Dept Ophthalmol, Schepens Eye Res Inst, Boston, MA USA.
[Park, In-Hyun] Childrens Hosp, Div Pediat Hematol Oncol, Boston, MA 02115 USA.
[Park, In-Hyun] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Daley, George Q.] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Daley, George Q.] Childrens Hosp, Howard Hughes Med Inst, Harvard Stem Cell Inst, Manton Ctr Orphan Dis Res, Boston, MA 02115 USA.
[Klassen, Henry J.] Univ Calif Irvine, Gavin Herbert Eye Inst, Sch Med, Dept Ophthalmol, Orange, CA 92668 USA.
[Yao, Jing] Fudan Univ, Shanghai Med Sch, Eye & ENT Hosp, Dept Ophthalmol, Shanghai 200433, Peoples R China.
RP Tucker, BA (reprint author), Univ Iowa, Dept Ophthalmol, Carver Coll Med, Inst Vis Res, Iowa City, IA 52242 USA.
EM budd-tucker@uiowa.edu
OI Tucker, Budd/0000-0003-2178-1742
FU National Institutes of Health (NIH); Foundation Fighting Blindness;
Lincy and Discovery Eye Foundations; Research to Prevent Blindness
FX BAT is supported by grants from the National Institutes of Health (NIH)
(DP2 new innovators award) and the Foundation Fighting Blindness; MJY is
supported by grants from the Lincy and Discovery Eye Foundations and
Research to Prevent Blindness; GQD is supported by grants from the NIH,
and is an investigator of the Manton Center for Orphan Disease Research
and the Howard Hughes Medical Institute. The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 39
TC 105
Z9 113
U1 3
U2 27
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 29
PY 2011
VL 6
IS 4
AR e18992
DI 10.1371/journal.pone.0018992
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 756OZ
UT WOS:000290024700047
PM 21559507
ER
PT J
AU Zhang, L
Bhasin, M
Schor-Bardach, R
Wang, XE
Collins, MP
Panka, D
Putheti, P
Signoretti, S
Alsop, DC
Libermann, T
Atkins, MB
Mier, JW
Goldberg, SN
Bhatt, RS
AF Zhang, Liang
Bhasin, Manoj
Schor-Bardach, Rachel
Wang, Xiaoen
Collins, Michael P.
Panka, David
Putheti, Prabhakar
Signoretti, Sabina
Alsop, David C.
Libermann, Towia
Atkins, Michael B.
Mier, James W.
Goldberg, S. Nahum
Bhatt, Rupal S.
TI Resistance of Renal Cell Carcinoma to Sorafenib Is Mediated by
Potentially Reversible Gene Expression
SO PLOS ONE
LA English
DT Article
ID PROBE LEVEL DATA; ANTIANGIOGENIC THERAPY; CANCER; BIOLOGY; TUMORS;
MICROARRAYS; METASTASIS; ALGORITHMS; SUMMARIES; GROWTH
AB Purpose: Resistance to antiangiogenic therapy is an important clinical problem. We examined whether resistance occurs at least in part via reversible, physiologic changes in the tumor, or results solely from stable genetic changes in resistant tumor cells.
Experimental Design: Mice bearing two human RCC xenografts were treated with sorafenib until they acquired resistance. Resistant 786-O cells were harvested and reimplanted into naive mice. Mice bearing resistant A498 cells were subjected to a 1 week treatment break. Sorafenib was then again administered to both sets of mice. Tumor growth patterns, gene expression, viability, blood vessel density, and perfusion were serially assessed in treated vs control mice.
Results: Despite prior resistance, reimplanted 786-O tumors maintained their ability to stabilize on sorafenib in sequential reimplantation steps. A transcriptome profile of the tumors revealed that the gene expression profile of tumors upon reimplantation reapproximated that of the untreated tumors and was distinct from tumors exhibiting resistance to sorafenib. In A498 tumors, revascularization was noted with resistance and cessation of sorafenib therapy and tumor perfusion was reduced and tumor cell necrosis enhanced with re-exposure to sorafenib.
Conclusions: In two RCC cell lines, resistance to sorafenib appears to be reversible. These results support the hypothesis that resistance to VEGF pathway therapy is not solely the result of a permanent genetic change in the tumor or selection of resistant clones, but rather is due to a great extent to reversible changes that likely occur in the tumor and/or its microenvironment.
C1 [Zhang, Liang; Panka, David; Atkins, Michael B.; Mier, James W.; Bhatt, Rupal S.] Beth Israel Deaconess Med Ctr, Div Hematol Oncol, Boston, MA 02215 USA.
[Bhasin, Manoj; Libermann, Towia] Beth Israel Deaconess Med Ctr, Div Interdisciplinary Med & Biotechnol, Boston, MA 02215 USA.
[Bhasin, Manoj] Beth Israel Deaconess Med Ctr, Genom & Prote Ctr, Boston, MA 02215 USA.
[Schor-Bardach, Rachel; Wang, Xiaoen; Alsop, David C.; Goldberg, S. Nahum] Beth Israel Deaconess Med Ctr, Dept Radiol, Boston, MA 02215 USA.
[Schor-Bardach, Rachel; Goldberg, S. Nahum] Hadassah Hebrew Univ, Med Ctr, Dept Radiol, Jerusalem, Israel.
[Collins, Michael P.; Signoretti, Sabina] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Putheti, Prabhakar] Beth Israel Deaconess Med Ctr, Dept Surg, Transplant Inst, Boston, MA 02215 USA.
[Putheti, Prabhakar] Beth Israel Deaconess Med Ctr, Dept Med, Transplant Inst, Boston, MA 02215 USA.
[Signoretti, Sabina] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Bhatt, Rupal S.] Dana Farber Harvard Canc Ctr, Kidney Canc Program, Boston, MA USA.
RP Zhang, L (reprint author), Beth Israel Deaconess Med Ctr, Div Hematol Oncol, Boston, MA 02215 USA.
EM rbhatt@bidmc.harvard.edu
RI Alsop, David/J-5764-2013;
OI Alsop, David/0000-0002-8206-1995; Libermann, Towia/0000-0002-4006-8179
FU DF/HCC Kidney Cancer SPORE [2 P50 CA101942]; National Comprehensive
Cancer Network, Jenkintown, PA
FX This work was supported by DF/HCC Kidney Cancer SPORE: 2 P50 CA101942, a
Career Development Award (RB), and the National Comprehensive Cancer
Network, Jenkintown, PA (JM). No additional external funding was
received for this study. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 34
TC 14
Z9 15
U1 0
U2 6
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 APR 29
PY 2011
VL 6
IS 4
AR e19144
DI 10.1371/journal.pone.0019144
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 756OZ
UT WOS:000290024700075
PM 21559452
ER
PT J
AU Sanchez-Alavez, M
Osborn, O
Tabarean, IV
Holmberg, KH
Eberwine, J
Kahn, CR
Bartfai, T
AF Sanchez-Alavez, Manuel
Osborn, Olivia
Tabarean, Iustin V.
Holmberg, Kristina H.
Eberwine, James
Kahn, C. Ronald
Bartfai, Tamas
TI Insulin-like Growth Factor 1-mediated Hyperthermia Involves Anterior
Hypothalamic Insulin Receptors
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID FACTOR-I RECEPTOR; IGF-I; BODY-TEMPERATURE; RAT-BRAIN; LIFE-SPAN;
TRANSGENIC MICE; HUMAN LONGEVITY; CELL-GROWTH; RESISTANCE; PROTEIN
AB The objective is to investigate the role of insulin-like growth factor 1 (IGF-1) in the regulation of core body temperature. Sequencing cDNA libraries from individual warm-sensitive neurons from the preoptic area (POA) of the hypothalamus, a region involved in the central control of thermoregulation, identified neurons that express both IGF-1 receptor (IGF-1R) and insulin receptor transcripts. The effects of administration of IGF-1 into the POA was measured by radiotelemetry monitoring of core temperature, brown adipose tissue (BAT) temperature, metabolic assessment, and imaging of BAT by positron emission tomography of 2-[F-18]fluoro-2-deoxyglucose uptake combined with computed tomography. IGF-1 injection into the POA caused dose-dependent hyperthermia that could be blocked by pretreatment with the IGF-1R tyrosine kinase inhibitor, PQ401. The IGF-1-evoked hyperthermia involved activation of brown adipose tissue and was accompanied by a switch from glycolysis to fatty acid oxidation as a source of energy as shown by lowered respiratory exchange ratio. Transgenic mice that lack neuronal insulin receptor expression in the brain (NIRKO mice) were unable to mount the full hyperthermic response to IGF-1, suggesting that the IGF-1 mediated hyperthermia is partly dependent on expression of functional neuronal insulin receptors. These data indicate a novel thermoregulatory role for both IGF-1R and neuronal insulin receptors in IGF-1 activation of BAT and hyperthermia. These central effects of IGF-1 signaling may play a role in regulation of metabolic rate, aging, and the risk of developing type 2 diabetes.
C1 [Osborn, Olivia] Univ Calif San Diego, Dept Med, Div Endocrinol & Metab, La Jolla, CA 92093 USA.
[Sanchez-Alavez, Manuel; Tabarean, Iustin V.; Bartfai, Tamas] Scripps Res Inst, Dept Mol & Integrat Neurosci, Harold Dorris Neurol Inst, La Jolla, CA 92037 USA.
[Holmberg, Kristina H.] Pfizer Ltd, Expt Biol Sci, Sandwich CT13 9NJ, Kent, England.
[Eberwine, James] Univ Penn, Sch Med, Dept Pharmacol, Philadelphia, PA 19104 USA.
[Kahn, C. Ronald] Joslin Diabet Ctr, Boston, MA 02215 USA.
[Kahn, C. Ronald] Harvard Univ, Sch Med, Boston, MA 02215 USA.
RP Osborn, O (reprint author), 10550 N Torrey Pines Rd, La Jolla, CA 92037 USA.
EM oosborn@ucsd.edu; tbartfai@scripps.edu
RI Eberwine, James/B-2247-2010
FU National Institutes of Health [R01NS043501, R01NS060799, DP1-OD-04117,
DK31036]; The Harold L. Dorris Neurological Research Institute; The
Skaggs Institute for Chemical Biology; The Ellison Medical Foundation;
Commonwealth of Pennsylvania
FX This work was supported, in whole or in part, by National Institutes of
Health Grants R01NS043501 (to T.B.), R01NS060799 (to I.V.T.),
DP1-OD-04117 (to J.E.), and DK31036 (to C.R.K.). This work was also
supported by The Harold L. Dorris Neurological Research Institute, The
Skaggs Institute for Chemical Biology, The Ellison Medical Foundation,
and by Health Research Formula Funds from the Commonwealth of
Pennsylvania. This is The Scripps Research Institute Manuscript 20540.
NR 54
TC 16
Z9 18
U1 0
U2 5
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 29
PY 2011
VL 286
IS 17
BP 14983
EP 14990
DI 10.1074/jbc.M110.188540
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 753OI
UT WOS:000289788300028
PM 21330367
ER
PT J
AU Wu, CWH
Vasalatiy, O
Liu, N
Wu, HT
Cheal, S
Chen, DY
Koretsky, AP
Griffiths, GL
Tootell, RBH
Ungerleider, LG
AF Wu, Carolyn W-H
Vasalatiy, Olga
Liu, Ning
Wu, Haitao
Cheal, Sarah
Chen, Der-Yow
Koretsky, Alan P.
Griffiths, Gary L.
Tootell, Roger B. H.
Ungerleider, Leslie G.
TI Development of a MR-Visible Compound for Tracing Neuroanatomical
Connections In Vivo
SO NEURON
LA English
DT Article
ID PRIMARY SOMATOSENSORY CORTEX; TOXIN SUBUNIT-B; MANGANESE-ENHANCED MRI;
WHITE-MATTER MICROSTRUCTURE; CENTRAL-NERVOUS-SYSTEM; SLOW
AXONAL-TRANSPORT; STANDING LIMB LOSS; RAT MOTOR CORTEX; CHOLERA-TOXIN;
DIFFUSION TENSOR
AB Traditional studies of neuroanatomical connections require injection of tracer compounds into living brains, then histology of the postmortem tissue. Here, we describe and validate a compound that reveals neuronal connections in vivo, using MRI. The classic anatomical tracer CTB (cholera-toxin subunit-B) was conjugated with a gadolinium-chelate to form GdDOTA-CTB. GdDOTA-CTB was injected into the primary somatosensory cortex (Si) or the olfactory pathway of rats. High-resolution MR images were collected at a range of time points at 11.71 and 7T. The transported GdDOTA-CTB was visible for at least 1 month post-injection, clearing within 2 months. Control injections of non-conjugated GdDOTA into Si were not transported and cleared within 1-2 days. Control injections of Gd-Albumin were not transported either, clearing within 7 days. These MR results were verified by classic immunohistochemical staining for CTB, in the same animals. The GdDOTA-CTB neuronal transport was target specific, monosynaptic, stable for several weeks, and reproducible.
C1 [Wu, Carolyn W-H; Chen, Der-Yow; Koretsky, Alan P.] NINDS, Lab Funct & Mol Imaging, NIH, Bethesda, MD 20814 USA.
[Vasalatiy, Olga; Wu, Haitao; Cheal, Sarah; Griffiths, Gary L.] NHLBI, Imaging Probe Dev Ctr, NIH, Bethesda, MD 20814 USA.
[Liu, Ning; Tootell, Roger B. H.; Ungerleider, Leslie G.] NIMH, Lab Brain & Cognit, NIH, Bethesda, MD 20814 USA.
[Wu, Carolyn W-H] CEA Saclay, Lab Integrated Biol, Unit Brain Plast, NeuroSpin I2BM, F-91191 Gif Sur Yvette, Ile de France, France.
[Tootell, Roger B. H.] Massachusetts Gen Hosp Charlestown, Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
RP Wu, CWH (reprint author), NINDS, Lab Funct & Mol Imaging, NIH, Bethesda, MD 20814 USA.
EM carolyn.wu@cea.fr
RI Koretsky, Alan/C-7940-2015
OI Koretsky, Alan/0000-0002-8085-4756
FU NIMH; NINDS IRP; NeuroSpin/CEA; Martinos Center for Biomedical Imaging;
NCRR; MIND Institute; NIH [R01 EY017081]; French L'Agence Nationale de
la Recherche [ANR-09-BLAN-0061-CSD8]
FX We are grateful to Steve Dodd for pulse sequence optimization, David Yu
for brain slicing, and Kathy Sharer for animal ordering and care. This
work was supported in part by the NIMH and NINDS IRP, NeuroSpin/CEA, the
Martinos Center for Biomedical Imaging, the NCRR, the MIND Institute,
NIH grant R01 EY017081 to R.B.H.T., and the French L'Agence Nationale de
la Recherche grant ANR-09-BLAN-0061-CSD8 to C.W.-H.W.
NR 97
TC 12
Z9 12
U1 0
U2 9
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
J9 NEURON
JI Neuron
PD APR 28
PY 2011
VL 70
IS 2
BP 229
EP 243
DI 10.1016/j.neuron.2011.03.010
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA 770FZ
UT WOS:000291073700006
PM 21521610
ER
PT J
AU Jakubikova, J
Adamia, S
Kost-Alimova, M
Klippel, S
Cervi, D
Daley, JF
Cholujova, D
Kong, SY
Leiba, M
Blotta, S
Ooi, M
Delmore, J
Laubach, J
Richardson, PG
Sedlak, J
Anderson, KC
Mitsiades, CS
AF Jakubikova, Jana
Adamia, Sophia
Kost-Alimova, Maria
Klippel, Steffen
Cervi, David
Daley, John F.
Cholujova, Dana
Kong, Sun-Young
Leiba, Merav
Blotta, Simona
Ooi, Melissa
Delmore, Jake
Laubach, Jacob
Richardson, Paul G.
Sedlak, Jan
Anderson, Kenneth C.
Mitsiades, Constantine S.
TI Lenalidomide targets clonogenic side population in multiple myeloma:
pathophysiologic and clinical implications
SO BLOOD
LA English
DT Article
ID STEM-LIKE CELLS; CANCER-CELLS; DRUG-RESISTANCE; THERAPEUTIC
IMPLICATIONS; THALIDOMIDE ANALOGS; BONE-MARROW; PHENOTYPE;
IDENTIFICATION; LINES; MODULATION
AB Recurrence of multiple myeloma (MM) after therapy suggests the presence of tumor-initiating subpopulations. In our study, we performed flow cytometry-based Hoechst 33342 staining to evaluate the existence of a MM population with stem-like features known as side population (SP) cells. SP cells exhibit substantial heterogeneity in MM cell lines and primary MM cells; express CD138 antigen in MM cell lines; display higher mRNA expression and functional activity of ABCG2 transporter; and have a higher proliferation index compared with non-SP cells. We observed evidence for clonogenic potential of SP cells, as well as the ability of SP cells to regenerate original population. Moreover, SP cells revealed higher tumorigenicity compared with non-SP cells. Importantly, lenalidomide decreased the percentage and clonogenicity of SP cells, and also induced phosphorylation changes in Akt, GSK-3 alpha/beta, MEK1, c-Jun, p53, and p70S6K in SP cells. Adherence to bone marrow stromal cells (BMSCs) increased the percentage, viability, and proliferation potential of SP cells. Lenalidomide and thalidomide abrogated this stimulatory effect of BMSCs and significantly decreased the percentage of SP cells. Our studies demonstrate a novel mechanism of action for lenalidomide, namely targeting SP fraction, providing the framework for new therapeutic strategies targeting subpopulations of MM cells including presumptive stem cells. (Blood. 2011; 117(17):4409-4419)
C1 [Anderson, Kenneth C.; Mitsiades, Constantine S.] Harvard Univ, Sch Med, Jerome Lipper Multiple Myeloma Ctr, Dept Med Oncol,Dana Farber Canc Inst, Boston, MA 02115 USA.
[Jakubikova, Jana; Adamia, Sophia; Klippel, Steffen; Cervi, David; Daley, John F.; Kong, Sun-Young; Leiba, Merav; Blotta, Simona; Ooi, Melissa; Delmore, Jake; Laubach, Jacob; Richardson, Paul G.; Anderson, Kenneth C.; Mitsiades, Constantine S.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Jakubikova, Jana; Cholujova, Dana; Sedlak, Jan] Slovak Acad Sci, Canc Res Inst, Dept Tumor Immunol, Bratislava, Slovakia.
[Kost-Alimova, Maria] Dana Farber Canc Inst, Belfer Inst Appl Canc Sci, Boston, MA 02115 USA.
RP Mitsiades, CS (reprint author), Harvard Univ, Sch Med, Jerome Lipper Multiple Myeloma Ctr, Dept Med Oncol,Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA.
EM Kenneth_Anderson@dfci.harvard.edu;
Constantine_Mitsiades@dfci.harvard.edu
FU Dana-Farber Cancer Institute; Chambers Medical Foundation; Stepanian
Fund; Richard J. Corman Fund; National Institute of Health [R01-50947,
P0-1-78378]; Slovak RD Agency [VVCE-0001-07]; Millennium and Celgene;
PharmaMar; Amgen Pharmaceuticals; AVEO Pharma; EMD Serono; Sunesis;
Gloucester; Genzyme; Johnson Johnson
FX This work was supported in part by the Dunkin Donuts Rising Stars
Program at the Dana-Farber Cancer Institute (C.S.M.), the Chambers
Medical Foundation (P.G.R, C.S.M.), the Stepanian Fund (P.G.R, C.S.M.),
the Richard J. Corman Fund (P.G.R., C.S.M.), National Institute of
Health grants R01-50947 (K.C.A, C.S.M.) and P0-1-78378 (K.C.A.), and the
Slovak R&D Agency grant VVCE-0001-07 (J.S.).; P.G.R. was in the
Speakers' Bureau (until 7/1/09) of Millennium and Celgene and received
honoraria from Millennium and Celgene. K.C.A. has received grants and
honoraria from Millennium and Celgene and was in the bureau (until
7/1/09) of Millennium and Celgene. C.S.M. has received in the past
consultant honoraria from Millennium Pharmaceuticals, Novartis
Pharmaceuticals, Bristol-Myers Squibb, Merck & Co, Kosan Pharmaceuticals
and Pharmion, licensing royalties from PharmaMar, and research funding
from Amgen Pharmaceuticals, AVEO Pharma, EMD Serono, Sunesis,
Gloucester, Genzyme, and Johnson & Johnson. The remaining authors
declare no competing financial interests.
NR 50
TC 89
Z9 95
U1 0
U2 8
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 APR 28
PY 2011
VL 117
IS 17
BP 4409
EP 4419
DI 10.1182/blood-2010-02-267344
PG 11
WC Hematology
SC Hematology
GA 756AV
UT WOS:000289984800005
PM 21321360
ER
PT J
AU Zhou, MY
Dong, XC
Baldauf, C
Chen, H
Zhou, YF
Springer, TA
Luo, XP
Zhong, C
Grater, F
Ding, JP
AF Zhou, Minyun
Dong, Xianchi
Baldauf, Carsten
Chen, Hua
Zhou, Yanfeng
Springer, Timothy A.
Luo, Xinping
Zhong, Chen
Graeter, Frauke
Ding, Jianping
TI A novel calcium-binding site of von Willebrand factor A2 domain
regulates its cleavage by ADAMTS13
SO BLOOD
LA English
DT Article
ID VONWILLEBRAND-FACTOR; CRYSTAL-STRUCTURE; SHEAR-STRESS; PROTEOLYSIS;
MUTATIONS; DISEASE; PLASMA; MODEL; THROMBOSIS; SUBSTRATE
AB The proteolysis of VWF by ADAMTS13 is an essential step in the regulation of its hemostatic and thrombogenic potential. Thecleavage occurs at strand beta 4 in the structural core of the A2 domain of VWF, so unfolding of the A2 domain is a prerequisite for cleavage. In the present study, we present the crystal structure of an engineered A2 domain that exhibits a significant difference in the alpha 3-beta 4 loop compared with the previously reported structure of wild-type A2. Intriguingly, a metal ion was detected at a site formed mainly by the C-terminal region of the alpha 3-beta 4 loop that was later identified as Ca(2+) after various biophysical and biochemical studies. Force-probe molecular dynamic simulations of a modeled structure of the wild-type A2 featuring the discovered Ca(2+)-binding site revealed that an increase in force was needed to unfold strand beta 4 when Ca(2+) was bound. Cleavage assays consistently demonstrated that Ca(2+)-binding stabilized the A2 domain and impeded its unfolding, and consequently protected it from cleavage by ADAMTS13. We have revealed a novel Ca(2+)-binding site at the A2 domain of VWF and demonstrated a relationship between Ca(2+) and force in the regulation of VWF and primary hemostasis. (Blood. 2011;117(17):4623-4631)
C1 [Zhou, Minyun; Dong, Xianchi; Zhong, Chen; Ding, Jianping] Chinese Acad Sci, State Key Lab Mol Biol, Shanghai, Peoples R China.
[Zhou, Minyun; Dong, Xianchi; Zhong, Chen; Ding, Jianping] Chinese Acad Sci, Res Ctr Struct Biol, Inst Biochem & Cell Biol, Shanghai Inst Biol Sci, Shanghai, Peoples R China.
[Zhou, Minyun; Dong, Xianchi] Chinese Acad Sci, Grad Sch, Shanghai, Peoples R China.
[Baldauf, Carsten; Graeter, Frauke] Chinese Acad Sci, Key Lab Computat Biol, Shanghai, Peoples R China.
[Baldauf, Carsten; Graeter, Frauke] Chinese Acad Sci, German Max Planck Soc Partner Inst, Inst Computat Biol, Shanghai Inst Biol Sci, Shanghai, Peoples R China.
[Chen, Hua; Luo, Xinping] Huashan Hosp, Fudan Med Sch, Shanghai, Peoples R China.
[Zhou, Yanfeng; Springer, Timothy A.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Zhou, Yanfeng; Springer, Timothy A.] Harvard Univ, Sch Med, Immune Dis Inst, Childrens Hosp Boston, Boston, MA 02115 USA.
[Graeter, Frauke] Heidelberg Inst Theoret Studies, Heidelberg, Germany.
RP Ding, JP (reprint author), 320 Yue Yang Rd, Shanghai 200031, Peoples R China.
EM jpding@sibs.ac.cn
RI Zhou, Yanfeng/B-3792-2012; Dong, Xianchi/C-1393-2015; Grater,
Frauke/D-3450-2009;
OI Dong, Xianchi/0000-0001-5121-1236; Grater, Frauke/0000-0003-2891-3381;
丁, 建平/0000-0001-7029-7346; Baldauf, Carsten/0000-0003-2637-6009
FU Ministry of Science and Technology of China [2007CB914302,
2011CB966301]; National Natural Science Foundation of China [30730028];
Chinese Academy of Sciences [KSCX2-YW-R-107, SIBS2008002]; Klaus Tschira
foundation; Alexander von Humboldt Foundation
FX This work was supported by grants from the Ministry of Science and
Technology of China (2007CB914302 and 2011CB966301), the National
Natural Science Foundation of China (30730028), the Chinese Academy of
Sciences (KSCX2-YW-R-107 and SIBS2008002), and the Klaus Tschira
foundation. C.B. is grateful for a Feodor Lynen fellowship from the
Alexander von Humboldt Foundation.
NR 40
TC 18
Z9 19
U1 1
U2 6
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 APR 28
PY 2011
VL 117
IS 17
BP 4623
EP 4631
DI 10.1182/blood-2010-11-321596
PG 9
WC Hematology
SC Hematology
GA 756AV
UT WOS:000289984800028
PM 21385852
ER
PT J
AU Pidala, J
Kurland, B
Chai, XY
Majhail, N
Weisdorf, DJ
Pavletic, S
Cutler, C
Jacobsohn, D
Palmer, J
Arai, S
Jagasia, M
Lee, SJ
AF Pidala, Joseph
Kurland, Brenda
Chai, Xiaoyu
Majhail, Navneet
Weisdorf, Daniel J.
Pavletic, Steven
Cutler, Corey
Jacobsohn, David
Palmer, Jeanne
Arai, Sally
Jagasia, Madan
Lee, Stephanie J.
TI Patient-reported quality of life is associated with severity of chronic
graft-versus-host disease as measured by NIH criteria: report on
baseline data from the Chronic GVHD Consortium
SO BLOOD
LA English
DT Article
ID CONSENSUS DEVELOPMENT PROJECT; WORKING GROUP-REPORT;
BONE-MARROW-TRANSPLANTATION; STEM-CELL TRANSPLANTATION; CLINICAL-TRIALS;
SYSTEMIC-SCLEROSIS; HEALTH; PREDICTORS; DIAGNOSIS; SURVIVORS
AB Quality of life (QOL) after hematopoietic cell transplantation (HCT) is compromised by chronic GVHD. In a prospectively assembled multicenter cohort of adults with chronic GVHD (n = 298), we examined the relationship between chronic GVHD severity defined by National Institutes of Health (NIH) criteria and QOL as measured by the SF-36 and FACT-BMT instruments at time of enrollment. Chronic GVHD severity was independently associated with QOL, adjusting for age. Compared with population normative data, SF-36 scores were more than a SD (10 points) lower on average for the summary physical component score (PCS) and role-physical subscale, and significantly lower (with magnitude 4-10 points) for several other subscales. Patients with moderate and severe cGVHD had PCS scores comparable with scores reported for systemic sclerosis, systemic lupus erythematosus, and multiple sclerosis, and greater impairment compared with common chronic conditions including diabetes, hypertension, and chronic lung disease. Moderate to severe cGVHD as defined by NIH criteria is associated with significant compromise in multiple QOL domains, with PCS scores in the range of other systemic autoimmune diseases. Compromised QOL provides a functional assessment of the effects of chronic GVHD, and may be measured in cGVHD clinical studies using either the SF-36 or the FACT-BMT. (Blood. 2011;117(17):4651-4657)
C1 [Pidala, Joseph] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
[Kurland, Brenda; Chai, Xiaoyu; Lee, Stephanie J.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Majhail, Navneet; Weisdorf, Daniel J.] Univ Minnesota, Minneapolis, MN USA.
[Pavletic, Steven] NCI, Bethesda, MD 20892 USA.
[Cutler, Corey] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Jacobsohn, David] Childrens Mem Hosp, Chicago, IL 60614 USA.
[Palmer, Jeanne] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Arai, Sally] Stanford Univ, Stanford, CA 94305 USA.
[Jagasia, Madan] Vanderbilt Univ, Nashville, TN USA.
RP Pidala, J (reprint author), H Lee Moffitt Canc Ctr & Res Inst, 12902 Magnolia Dr,FOB 3308, Tampa, FL 33612 USA.
EM joseph.pidala@moffitt.org
OI Kurland, Brenda/0000-0002-5669-0595
FU National Institutes of Health/National Cancer Institute [CA 118953-03]
FX This work was supported by National Institutes of Health/National Cancer
Institute grant CA 118953-03 (PI: S.J.L.).
NR 34
TC 103
Z9 106
U1 1
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 APR 28
PY 2011
VL 117
IS 17
BP 4651
EP 4657
DI 10.1182/blood-2010-11-319509
PG 7
WC Hematology
SC Hematology
GA 756AV
UT WOS:000289984800031
PM 21355084
ER
PT J
AU Kulkarni, S
Savan, R
Qi, Y
Gao, XJ
Yuki, Y
Bass, SE
Martin, MP
Hunt, P
Deeks, SG
Telenti, A
Pereyra, F
Goldstein, D
Wolinsky, S
Walker, B
Young, HA
Carrington, M
AF Kulkarni, Smita
Savan, Ram
Qi, Ying
Gao, Xiaojiang
Yuki, Yuko
Bass, Sara E.
Martin, Maureen P.
Hunt, Peter
Deeks, Steven G.
Telenti, Amalio
Pereyra, Florencia
Goldstein, David
Wolinsky, Steven
Walker, Bruce
Young, Howard A.
Carrington, Mary
TI Differential microRNA regulation of HLA-C expression and its association
with HIV control
SO NATURE
LA English
DT Article
ID HUMAN CELL-LINE; SURFACE EXPRESSION; MESSENGER-RNAS; GENES;
DEADENYLATION; ANTIGENS; GENOME
AB The HLA-C locus is distinct relative to the other classical HLA class I loci in that it has relatively limited polymorphism(1), lower expression on the cell surface(2,3), and more extensive ligand-receptor interactions with killer-cell immunoglobulin-like receptors(4). A single nucleotide polymorphism (SNP) 35 kb upstream of HLA-C (rs9264942; termed -35) associates with control of HIV(5-7), and with levels of HLA-C messenger RNA transcripts(8) and cell-surface expression(7), but the mechanism underlying its varied expression is unknown. We proposed that the -35 SNP is not the causal variant for differential HLA-C expression, but rather is marking another polymorphism that directly affects levels of HLA-C(7). Here we show that variation within the 3' untranslated region (UTR) of HLA-C regulates binding of the microRNA hsa-miR-148 to its target site, resulting in relatively low surface expression of alleles that bind this microRNA and high expression of HLA-C alleles that escape post-transcriptional regulation. The 3' UTR variant associates strongly with control of HIV, potentially adding to the effects of genetic variation encoding the peptide-binding region of the HLA class I loci. Variation in HLA-C expression adds another layer of diversity to this highly polymorphic locus that must be considered when deciphering the function of these molecules in health and disease.
C1 [Kulkarni, Smita; Qi, Ying; Gao, Xiaojiang; Yuki, Yuko; Bass, Sara E.; Martin, Maureen P.; Carrington, Mary] NCI, Canc & Inflammat Program, Expt Immunol Lab, SAIC Frederick Inc, Frederick, MD 21702 USA.
[Kulkarni, Smita; Qi, Ying; Gao, Xiaojiang; Yuki, Yuko; Martin, Maureen P.; Pereyra, Florencia; Walker, Bruce; Carrington, Mary] Harvard Univ, Boston, MA 02114 USA.
[Kulkarni, Smita; Qi, Ying; Gao, Xiaojiang; Yuki, Yuko; Martin, Maureen P.; Pereyra, Florencia; Walker, Bruce; Carrington, Mary] MIT, Ragon Inst, Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Hunt, Peter; Deeks, Steven G.] Univ Calif San Francisco, San Francisco Gen Hosp, Div Aids, San Francisco, CA 94110 USA.
[Telenti, Amalio] Univ Lausanne, Inst Microbiol, CH-1011 Lausanne, Switzerland.
[Goldstein, David] Duke Univ, Inst Genome Sci & Policy, Ctr Human Genome Variat, Durham, NC 27708 USA.
[Wolinsky, Steven] Northwestern Univ, Feinberg Sch Med, Div Infect Dis, Chicago, IL 60611 USA.
RP Carrington, M (reprint author), NCI, Canc & Inflammat Program, Expt Immunol Lab, SAIC Frederick Inc, Frederick, MD 21702 USA.
EM carringm@mail.nih.gov
RI Wolinsky, Steven/B-2893-2012; SHCS, int. coll. A/G-4083-2011; SHCS,
all/G-4072-2011;
OI Wolinsky, Steven/0000-0002-9625-6697; Young, Howard/0000-0002-3118-5111
FU National Cancer Institute, National Institutes of Health (NIH)
[HHSN261200800001E, N02-CP-55504, R01-DA04334, R01-DA12568]; NIH,
National Cancer Institute, Center for Cancer Research; Cancer
Inflammation Program Project Award; Bill & Melinda Gates Foundation;
Mark and Lisa Schwartz Foundation; National Institute of Allergy and
Infectious Diseases; National Cancer Institute; National Heart, Lung and
Blood Institute [UO1-AI-35042, 5-MO1-RR-00722, UO1-AI-35043,
UO1-AI-37984, UO1-AI-35039, UO1-AI-35040, UO1-AI-37613, UO1-AI-35041];
Swiss HIV Cohort Study; Swiss National Science Foundation
[33CSC0-108787]; [UL1 RR024131]; [P30 AI27763]
FX This project has been funded in part with federal funds from the
National Cancer Institute, National Institutes of Health (NIH), under
contracts HHSN261200800001E, N02-CP-55504, R01-DA04334 and R01-DA12568.
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 US Government. This research was supported in part by
the Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research and the Cancer Inflammation Program Project
Award for the year 2009, a grant from the Bill & Melinda Gates
Foundation as part of the Collaboration for AIDS Vaccine Discovery, and
the Mark and Lisa Schwartz Foundation. We would also like to thank the
patients and investigators involved in the Multicenter AIDS Cohort Study
(the MACS is funded by the National Institute of Allergy and Infectious
Diseases, with supplemental funding from the National Cancer Institute
and the National Heart, Lung and Blood Institute (grants UO1-AI-35042,
5-MO1-RR-00722 (GCRC), UO1-AI-35043, UO1-AI-37984, UO1-AI-35039,
UO1-AI-35040, UO1-AI-37613 and UO1-AI-35041), the Swiss HIV Cohort Study
(see Supplementary Note 4 for the list of members), supported by the
Swiss National Science Foundation grant number 33CSC0-108787, and the
SCOPE study, which was funded by the UL1 RR024131 (Clinical and
Translational Sciences Award) and P30 AI27763 (Center for AIDS Research)
grants. We thank S. Anderson, G. O'Connor and R. Thomas for advice, A.
Kronfli and K. Ramakrishnan for assistance in plasmid and genomic DNA
preparations, A. McFarland for western blots, V. Braud for the DT9
antibody, R. Johnson and G. Nelson for statistical advice and T. Covell
for administrative assistance.
NR 27
TC 148
Z9 158
U1 0
U2 13
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD APR 28
PY 2011
VL 472
IS 7344
BP 495
EP U548
DI 10.1038/nature09914
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 755QC
UT WOS:000289949600039
PM 21499264
ER
PT J
AU Gu, TL
Nardone, J
Wang, Y
Loriaux, M
Villen, J
Beausoleil, S
Tucker, M
Kornhauser, J
Ren, JM
MacNeill, J
Gygi, SP
Druker, BJ
Heinrich, MC
Rush, J
Polakiewicz, RD
AF Gu, Ting-lei
Nardone, Julie
Wang, Yi
Loriaux, Marc
Villen, Judit
Beausoleil, Sean
Tucker, Meghan
Kornhauser, Jon
Ren, Jianmin
MacNeill, Joan
Gygi, Steven P.
Druker, Brian J.
Heinrich, Michael C.
Rush, John
Polakiewicz, Roberto D.
TI Survey of Activated FLT3 Signaling in Leukemia
SO PLOS ONE
LA English
DT Article
ID ACUTE MYELOID-LEUKEMIA; ACUTE LYMPHOBLASTIC-LEUKEMIA; INTERNAL TANDEM
DUPLICATION; B-CELL DEVELOPMENT; RECEPTOR TYROSINE KINASE;
HEMATOPOIETIC-CELLS; ONCOGENIC FLT3; PHOSPHORYLATION; EXPRESSION;
MUTATIONS
AB Activating mutations of FMS-like tyrosine kinase-3 (FLT3) are found in approximately 30% of patients with acute myeloid leukemia (AML). FLT3 is therefore an attractive drug target. However, the molecular mechanisms by which FLT3 mutations lead to cell transformation in AML remain unclear. To develop a better understanding of FLT3 signaling as well as its downstream effectors, we performed detailed phosphoproteomic analysis of FLT3 signaling in human leukemia cells. We identified over 1000 tyrosine phosphorylation sites from about 750 proteins in both AML (wild type and mutant FLT3) and B cell acute lymphoblastic leukemia (normal and amplification of FLT3) cell lines. Furthermore, using stable isotope labeling by amino acids in cell culture (SILAC), we were able to quantified over 400 phosphorylation sites (pTyr, pSer, and pThr) that were responsive to FLT3 inhibition in FLT3 driven human leukemia cell lines. We also extended this phosphoproteomic analysis on bone marrow from primary AML patient samples, and identify over 200 tyrosine and 800 serine/threonine phosphorylation sites in vivo. This study showed that oncogenic FLT3 regulates proteins involving diverse cellular processes and affects multiple signaling pathways in human leukemia that we previously appreciated, such as Fc epsilon RI-mediated signaling, BCR, and CD40 signaling pathways. It provides a valuable resource for investigation of oncogenic FLT3 signaling in human leukemia.
C1 [Gu, Ting-lei; Nardone, Julie; Wang, Yi; Beausoleil, Sean; Tucker, Meghan; Kornhauser, Jon; Ren, Jianmin; MacNeill, Joan; Rush, John; Polakiewicz, Roberto D.] Cell Signaling Technol Inc, Danvers, MA USA.
[Loriaux, Marc] Oregon Hlth & Sci Univ, Dept Pathol, Portland, OR 97201 USA.
[Villen, Judit; Gygi, Steven P.] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA USA.
[Druker, Brian J.; Heinrich, Michael C.] Oregon Hlth & Sci Univ, Dept Hematol & Med Oncol, Portland, OR 97201 USA.
[Druker, Brian J.] Howard Hughes Med Inst, Portland, OR USA.
[Heinrich, Michael C.] Portland VA Med Ctr, Portland, OR USA.
RP Gu, TL (reprint author), Cell Signaling Technol Inc, Danvers, MA USA.
EM tgu@cellsignal.com; rpolakiewicz@cellsignal.com
OI Villen, Judit/0000-0002-1005-1739
NR 56
TC 18
Z9 18
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 28
PY 2011
VL 6
IS 4
AR e19169
DI 10.1371/journal.pone.0019169
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 756NX
UT WOS:000290020700034
PM 21552520
ER
PT J
AU Blaszkowsky, LS
Cusack, JC
Hong, TS
Chung, DC
Blake, MA
Lennerz, JK
AF Blaszkowsky, Lawrence S.
Cusack, James C., Jr.
Hong, Theodore S.
Chung, Daniel C.
Blake, Michael A.
Lennerz, Jochen K.
TI A Man with Adenocarcinoma of the Rectum Rectal adenocarcinoma associated
with the Lynch syndrome (hereditary nonpolyposis colorectal cancer), due
to an MSH6 mutation
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID TOTAL MESORECTAL EXCISION; PREOPERATIVE RADIOTHERAPY; MICROSATELLITE
INSTABILITY; POSTOPERATIVE CHEMORADIOTHERAPY; PATHOLOGICAL ASSESSMENT;
LOCAL RECURRENCE; COLON-CANCER; TRIAL; SURVIVAL; PREDISPOSITION
C1 [Blaszkowsky, Lawrence S.] Massachusetts Gen Hosp, Div Hematol Oncol, Boston, MA 02114 USA.
[Cusack, James C., Jr.] Massachusetts Gen Hosp, Div Surg Oncol, Boston, MA 02114 USA.
[Chung, Daniel C.] Massachusetts Gen Hosp, Div Gastroenterol, Boston, MA 02114 USA.
[Hong, Theodore S.] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
[Blake, Michael A.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Lennerz, Jochen K.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Blaszkowsky, Lawrence S.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Cusack, James C., Jr.] Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA.
[Hong, Theodore S.] Harvard Univ, Sch Med, Dept Radiat Oncol, Boston, MA 02115 USA.
[Blake, Michael A.] Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02115 USA.
[Lennerz, Jochen K.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
RP Blaszkowsky, LS (reprint author), Massachusetts Gen Hosp, Div Hematol Oncol, Boston, MA 02114 USA.
NR 39
TC 0
Z9 0
U1 0
U2 2
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD APR 28
PY 2011
VL 364
IS 17
BP 1658
EP 1668
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 755NW
UT WOS:000289940400014
PM 21524217
ER
PT J
AU Goldberg, NRS
Haack, AK
Lim, NS
Janson, OK
Meshul, CK
AF Goldberg, N. R. S.
Haack, A. K.
Lim, N. S.
Janson, O. K.
Meshul, C. K.
TI DOPAMINERGIC AND BEHAVIORAL CORRELATES OF PROGRESSIVE LESIONING OF THE
NIGROSTRIATAL PATHWAY WITH 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE
SO NEUROSCIENCE
LA English
DT Article
DE dopamine; progressive; tyrosine hydroxylase; motor control; Parkinson's
disease
ID PARKINSONS-DISEASE PATIENTS; MPTP-INDUCED PARKINSONISM; MULTIPLE SYSTEM
ATROPHY; NIGRA PARS COMPACTA; MOUSE MODEL; SUBSTANTIA-NIGRA;
CEREBROSPINAL-FLUID; ALPHA-SYNUCLEIN; TIME-COURSE; ORTHOSTATIC
HYPOTENSION
AB A number of neurotoxin- and gene-based rodent models of acute neurodegeneration of nigrostriatal dopamine (DA) neurons are used to study Parkinson's disease (PD). The rapid degeneration achieved by many of these current models limits the capacity of the model to develop pathogenic mechanisms and display the various stages of motor degradation representative of the human Parkinsonian condition. Chronic rodent models have been the only ones to reproduce these characteristics, yet do not show correlated progress of DA loss with multiple stepwise behavioral deficits as seen in humans. In the present study, we have developed a progressive model of increasing DA loss and motor dysfunction via progressively increased administration of the neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), in the C57BI/6J mouse. Mice were administered a daily (5 d/wk) dose of MPTP that increased weekly over the course of 4 weeks (4 mg/kg, 8 mg/kg, 16 mg/kg and 32 mg/kg). Each treatment group was tested for exploratory and motor behavioral changes after every week leading up to their final dose, as well as changes in tyrosine hydroxylase immunoreactivity (TH-ir) of the substantia nigra pars compacta (SNpc) and caudate putamen (CPu). We detected a 24% decrease in the mean number of TH-ir SNpc neurons/section after 1 week, and a 62% decrease after 4 weeks as compared to the vehicle group. CPu TH-ir began at a 35% loss after 1 week and increased to a 74% loss after 4 weeks compared to the vehicle group. CPu DA content showed an initial decrease of 20% after 1 week, and a final decrease of 70% following week 4 versus the vehicle group. Free-standing rears (versus wall-assisted rears, in a cylinder), decreased from 35% to 8% of total rears as the dose of MPTP increased from 4 mg/kg to 32 mg/kg, respectively. However, motor impairment as measured by a Parallel Rod Activity Chamber test was not significant until week 4 at 32 mg/kg compared to the vehicle group. The present study is the first to show stepwise progression of behavioral deficits which correlate with gradual dopaminergic decline in the nigrostriatal pathway. This progressive lesioning regiment may be appropriate for future investigation of pathogenic mechanisms and various intervention therapies in PD. Published by Elsevier Ltd on behalf of IBRO.
C1 [Goldberg, N. R. S.; Haack, A. K.; Lim, N. S.; Janson, O. K.; Meshul, C. K.] Portland VA Med Ctr, Portland, OR USA.
[Meshul, C. K.] Dept Behav Neurosci & Pathol, Portland, OR USA.
RP Meshul, CK (reprint author), Portland VA Med Ctr, Portland, OR USA.
EM meshulc@ohsu.edu
FU Department of Veterans Affairs Merit Review Program
FX Supported by the Department of Veterans Affairs Merit Review Program. We
also thank Dr. Deborah Finn for her consultation regarding the
statistical analysis.
NR 72
TC 24
Z9 25
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4522
EI 1873-7544
J9 NEUROSCIENCE
JI Neuroscience
PD APR 28
PY 2011
VL 180
BP 256
EP 271
DI 10.1016/j.neuroscience.2011.02.027
PG 16
WC Neurosciences
SC Neurosciences & Neurology
GA 748MV
UT WOS:000289395600027
PM 21335067
ER
PT J
AU Butler, MO
Friedlander, P
Milstein, MI
Mooney, MM
Metzler, G
Murray, AP
Tanaka, M
Berezovskaya, A
Imataki, O
Drury, L
Brennan, L
Flavin, M
Neuberg, D
Stevenson, K
Lawrence, D
Hodi, FS
Velazquez, EF
Jaklitsch, MT
Russell, SE
Mihm, M
Nadler, LM
Hirano, N
AF Butler, Marcus O.
Friedlander, Philip
Milstein, Matthew I.
Mooney, Mary M.
Metzler, Genita
Murray, Andrew P.
Tanaka, Makito
Berezovskaya, Alla
Imataki, Osamu
Drury, Linda
Brennan, Lisa
Flavin, Marisa
Neuberg, Donna
Stevenson, Kristen
Lawrence, Donald
Hodi, F. Stephen
Velazquez, Elsa F.
Jaklitsch, Michael T.
Russell, Sara E.
Mihm, Martin
Nadler, Lee M.
Hirano, Naoto
TI Establishment of Antitumor Memory in Humans Using in Vitro-Educated
CD8(+) T Cells
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Article
ID TUMOR-INFILTRATING LYMPHOCYTES; IN-VIVO PERSISTENCE; METASTATIC
MELANOMA; TRANSFER THERAPY; ADOPTIVE IMMUNOTHERAPY; IMMUNE-RESPONSE;
SOLID TUMORS; PHASE-I; ANTIGEN; REGRESSION
AB Although advanced-stage melanoma patients have a median survival of less than a year, adoptive T cell therapy can induce durable clinical responses in some patients. Successful adoptive T cell therapy to treat cancer requires engraftment of antitumor T lymphocytes that not only retain specificity and function in vivo but also display an intrinsic capacity to survive. To date, adoptively transferred antitumor CD8(+) T lymphocytes (CTLs) have had limited life spans unless the host has been manipulated. To generate CTLs that have an intrinsic capacity to persist in vivo, we developed a human artificial antigen-presenting cell system that can educate antitumor CTLs to acquire both a central memory and an effector memory phenotype as well as the capacity to survive in culture for prolonged periods of time. We examined whether antitumor CTLs generated using this system could function and persist in patients. We showed that MART1-specific CTLs, educated and expanded using our artificial antigen-presenting cell system, could survive for prolonged periods in advanced-stage melanoma patients without previous conditioning or cytokine treatment. Moreover, these CTLs trafficked to the tumor, mediated biological and clinical responses, and established antitumor immunologic memory. Therefore, this approach may broaden the availability of adoptive cell therapy to patients both alone and in combination with other therapeutic modalities.
C1 [Butler, Marcus O.; Friedlander, Philip; Milstein, Matthew I.; Mooney, Mary M.; Metzler, Genita; Murray, Andrew P.; Tanaka, Makito; Berezovskaya, Alla; Imataki, Osamu; Drury, Linda; Brennan, Lisa; Flavin, Marisa; Hodi, F. Stephen; Mihm, Martin; Nadler, Lee M.; Hirano, Naoto] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
[Butler, Marcus O.; Friedlander, Philip; Tanaka, Makito; Imataki, Osamu; Hodi, F. Stephen; Nadler, Lee M.; Hirano, Naoto] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Butler, Marcus O.; Friedlander, Philip; Tanaka, Makito; Imataki, Osamu; Lawrence, Donald; Hodi, F. Stephen; Mihm, Martin; Nadler, Lee M.; Hirano, Naoto] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[Neuberg, Donna; Stevenson, Kristen] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02215 USA.
[Lawrence, Donald] Brigham & Womens Hosp, Dept Thorac Surg, Boston, MA 02115 USA.
[Velazquez, Elsa F.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Velazquez, Elsa F.] Tufts Univ, Sch Med, Boston, MA 02111 USA.
[Jaklitsch, Michael T.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Jaklitsch, Michael T.; Russell, Sara E.] Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA.
[Russell, Sara E.] Brigham & Womens Hosp, Dept Surg, Boston, MA 02115 USA.
[Mihm, Martin] Brigham & Womens Hosp, Dept Dermatol, Boston, MA 02115 USA.
[Mihm, Martin] Harvard Univ, Sch Med, Dept Dermatol, Boston, MA 02115 USA.
[Hirano, Naoto] Princess Margaret Hosp, Ontario Canc Inst, Toronto, ON M5G 2M9, Canada.
[Hirano, Naoto] Univ Toronto, Toronto, ON M5S 1A8, Canada.
RP Butler, MO (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 450 Brookline Ave, Boston, MA 02215 USA.
EM marcus_butler@dfci.harvard.edu
FU Immunotherapy Fund 1; S. Craig Lindner Fund for Cancer Research; Rudolf
E. Rupert Foundation for Cancer Research; Cancer Research
Institute/Ludwig Institute for Cancer Research Cancer Vaccine
Collaborative; Friends of the Dana-Farber Cancer Institute; Dunkin'
Donuts Rising Stars Program; NIH [K22CA129240, R01CA148673]; American
Society; Center for Human Cell Therapy Boston [NIH 5U24HL074355];
Bristol-Myers Squibb
FX Funding was provided by the Immunotherapy Fund 1 (L.M.N.), the S. Craig
Lindner Fund for Cancer Research (L.M.N.), the Rudolf E. Rupert
Foundation for Cancer Research (L.M.N.), the Cancer Research
Institute/Ludwig Institute for Cancer Research Cancer Vaccine
Collaborative (M.O.B., L.M.N., and N.H.), Friends of the Dana-Farber
Cancer Institute (M.O.B. and N.H.), and Dunkin' Donuts Rising Stars
Program (M.O.B. and N.H.). N.H. was funded by NIH grants K22CA129240 and
R01CA148673 and the American Society of Hematology Scholar Award.
Preclinical scale-up was supported by the Center for Human Cell Therapy
Boston (NIH 5U24HL074355). Subjects received ipilimumab on clinical
trials supported by Bristol-Myers Squibb (F.S.H.).
NR 35
TC 56
Z9 59
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 APR 27
PY 2011
VL 3
IS 80
AR 80ra34
DI 10.1126/scitranslmed.3002207
PG 10
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 795MC
UT WOS:000292977300003
PM 21525398
ER
PT J
AU Gerszten, RE
Wang, TJ
AF Gerszten, Robert E.
Wang, Thomas J.
TI Two Roads Diverge: Weight Loss Interventions and Circulating Amino Acids
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Article
ID GASTRIC BYPASS-SURGERY; GLUCOSE-TOLERANCE TEST; INSULIN SECRETION;
PROFILES
AB In this issue of Science Translational Medicine, Laferrere and colleagues describe a metabolite pro ling approach to investigate changes in the circulating metabolome after equivalent weight loss spurred by either gastric bypass surgery (GBP) or dietary intervention. The results reveal that GBP enhances branched chain amino acid metabolism by mechanisms separate from weight loss. These observations raise the possibility that changes in circulating amino acids play a role in the correction of glycemic control observed shortly after GBP.
C1 [Gerszten, Robert E.] Massachusetts Gen Hosp East, Div Cardiol, Charlestown, MA 02129 USA.
Massachusetts Gen Hosp East, Ctr Immunol & Inflammatory Dis, Charlestown, MA 02129 USA.
Harvard Univ, Sch Med, Boston, MA 02114 USA.
Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
RP Gerszten, RE (reprint author), Massachusetts Gen Hosp East, Div Cardiol, Charlestown, MA 02129 USA.
EM rgerszten@partners.org
FU U.S. National Institutes of Health [NO1-HC-25195, R01-DK-HL081572];
Leducq Foundation; American Heart Association
FX The authors acknowledge support from the U.S. National Institutes of
Health (contracts NO1-HC-25195 and R01-DK-HL081572), the Leducq
Foundation, and the American Heart Association. Competing interests: The
authors are co-inventors on patent applications related to metabolite
predictors of diabetes.
NR 17
TC 6
Z9 6
U1 0
U2 4
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 APR 27
PY 2011
VL 3
IS 80
AR 80ps15
DI 10.1126/scitranslmed.3002377
PG 3
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 795MC
UT WOS:000292977300001
PM 21525396
ER
PT J
AU Wu, MF
Nienhuis, R
Maidment, N
Lam, HA
Siegel, JM
AF Wu, Ming-Fung
Nienhuis, Robert
Maidment, Nigel
Lam, Hoa A.
Siegel, Jerome M.
TI Role of the Hypocretin (Orexin) Receptor 2 (Hcrt-r2) in the Regulation
of Hypocretin Level and Cataplexy
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID LATERODORSAL TEGMENTAL NEURONS; LOCUS-COERULEUS NEURONS; BLOOD-PRESSURE
CHANGES; CANINE NARCOLEPSY; CHOLINERGIC SYSTEMS; MEDIAL MEDULLA;
KNOCKOUT MICE; HEART-RATE; SLEEP; PEPTIDES
AB Hypocretin receptor-2 (Hcrt-r2)-mutated dogs exhibit all the major symptoms of human narcolepsy and respond to drugs that increase or decrease cataplexy as do narcoleptic humans; yet, unlike narcoleptic humans, the narcoleptic dogs have normal hypocretin levels. We find that drugs that reduce or increase cataplexy in the narcoleptic dogs, greatly increase and decrease, respectively, hypocretin levels in normal dogs. The effects of these drugs on heart rate and blood pressure, which were considerable, were not correlated with their effects on cataplexy. Administration of these drugs to Hcrt-r2-mutated dogs produced indistinguishable changes in heart rate and blood pressure, indicating that neither central nor peripheral Hcrt-r2 is required for these cardiovascular effects. However, in contrast to the marked Hcrt level changes in the normal dogs, these drugs did not alter hypocretin levels in the Hcrt-r2 mutants. We conclude that Hcrt-r2 is a vital element in a feedback loop integrating Hcrt, acetylcholine, and norepinephrine function. In the absence of functional Hcrt-r2, Hcrt levels are not affected by monoaminergic and cholinergic drugs, despite the strong modulation of cataplexy by these drugs. Conversely, strong transient reductions of Hcrt level by these drugs do not produce episodes of cataplexy in normal dogs. The Hcrt-r2 mutation causes drug-induced cataplexy by virtue of its long-term effect on the functioning of other brain systems, rather than by increasing the magnitude of phasic changes in Hcrt level. A similar mechanism may be operative in spontaneous cataplexy in narcoleptic dogs as well as in narcoleptic humans.
C1 [Wu, Ming-Fung; Nienhuis, Robert; Siegel, Jerome M.] Vet Adm Greater Los Angeles Healthcare Syst, North Hills, CA 91343 USA.
[Maidment, Nigel; Lam, Hoa A.; Siegel, Jerome M.] Univ Calif Los Angeles, Dept Psychiat, Los Angeles, CA 90095 USA.
[Siegel, Jerome M.] Univ Calif Los Angeles, Brain Res Inst, Los Angeles, CA 90095 USA.
RP Siegel, JM (reprint author), Vet Adm Greater Los Angeles Healthcare Syst, North Hills, CA 91343 USA.
EM jsiegel@ucla.edu
FU National Institutes of Health [NS14610, MH64109]; Medical Research
Service of the Department of Veterans Affairs
FX Supported by National Institutes of Health Grants NS14610 and MH64109,
and the Medical Research Service of the Department of Veterans Affairs.
NR 43
TC 12
Z9 13
U1 1
U2 9
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 APR 27
PY 2011
VL 31
IS 17
BP 6305
EP 6310
DI 10.1523/JNEUROSCI.0365-11.2011
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA 755MB
UT WOS:000289934600006
PM 21525270
ER
PT J
AU Morikawa, T
Kuchiba, A
Yamauchi, M
Meyerhardt, JA
Shima, K
Nosho, K
Chan, AT
Giovannucci, E
Fuchs, CS
Ogino, S
AF Morikawa, Teppei
Kuchiba, Aya
Yamauchi, Mai
Meyerhardt, Jeffrey A.
Shima, Kaori
Nosho, Katsuhiko
Chan, Andrew T.
Giovannucci, Edward
Fuchs, Charles S.
Ogino, Shuji
TI Association of CTNNB1 (beta-Catenin) Alterations, Body Mass Index, and
Physical Activity With Survival in Patients With Colorectal Cancer
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID ISLAND METHYLATOR PHENOTYPE; MOLECULAR PATHOLOGICAL EPIDEMIOLOGY;
COLON-CANCER; MICROSATELLITE INSTABILITY; E-CADHERIN;
PROGNOSTIC-SIGNIFICANCE; ACTIVITY QUESTIONNAIRE; NUCLEAR ACCUMULATION;
PIK3CA MUTATION; RECTAL-CANCER
AB Context Alterations of the WNT signaling pathway and cadherin-associated protein beta 1 (CTNNB1 or beta-catenin) have been implicated in colorectal carcinogenesis and metabolic diseases.
Objective To test the hypothesis that CTNNB1 activation in colorectal cancer modifies prognostic associations of body mass index (BMI) and level of postdiagnosis physical activity.
Design, Setting, and Patients Two US prospective cohort studies (Nurses' Health Study and the Health Professionals Follow-up Study) were used to evaluate CTNNB1 localization by immunohistochemistry in 955 patients with stage I, II, III, or IV colon and rectal cancer from 1980 through 2004. A Cox proportional hazards model was used to compute the hazard ratio (HR) for mortality, adjusting for clinical and tumor features, including microsatellite instability, CpG island methylator phenotype, level of long interspersed nucleotide element 1 methylation, mutations in KRAS, BRAF, or PIK3CA, and tumor protein p53.
Main Outcome Measures Colorectal cancer-specific mortality and overall mortality through June 30, 2009.
Results In obese patients (BMI >= 30), positive status for nuclear CTNNB1 was associated with significantly better colorectal cancer-specific survival (adjusted HR, 0.24 [95% confidence interval {CI}, 0.12-0.49], P<.001 for interaction; 5-year survival: 0.85 for patients with positive nuclear CTNNB1 status vs 0.78 for those with negative status) and overall survival (adjusted HR, 0.56 [95% CI, 0.35-0.90], P=.03 for interaction; 5-year survival: 0.77 for patients with positive nuclear CTNNB1 status vs 0.74 for those with negative status), while CTNNB1 status was not associated with prognosis among nonobese patients (BMI <30). Among patients with negative status for nuclear CTNNB1 and cancer in stages I, II, or III, postdiagnosis physical activity was associated with better colorectal cancer-specific survival (adjusted HR, 0.33 [95% CI, 0.13-0.81], P=.05 for interaction; 5-year survival: 0.97 for >= 18 vs 0.89 for <18 metabolic equivalent task hours/week), while postdiagnosis physical activity was not associated with colorectal cancer-specific survival among patients with positive status for nuclear CTNNB1 (adjusted HR, 1.07 [95% CI, 0.50-2.30]).
Conclusions Among obese patients only, activation of CTNNB1 was associated with better colorectal cancer-specific survival and overall survival. Postdiagnosis physical activity was associated with better colorectal cancer-specific survival only among patients with negative status for nuclear CTNNB1. These molecular pathological epidemiology findings suggest that the effects of alterations in the WNT-CTNNB1 pathway on outcome are modified by BMI and physical activity. JAMA. 2011;305(16):1685-1694 www.jama.com
C1 [Ogino, Shuji] Harvard Univ, Sch Med, Brigham & Womens Hosp,Dept Med Oncol, Dana Farber Canc Inst,Ctr Mol Oncol Pathol, Boston, MA 02215 USA.
[Chan, Andrew T.; Giovannucci, Edward; Fuchs, Charles S.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Channing Lab,Dept Med, Boston, MA 02215 USA.
[Ogino, Shuji] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Pathol, Boston, MA 02215 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.
[Chan, Andrew T.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
RP Ogino, S (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp,Dept Med Oncol, Dana Farber Canc Inst,Ctr Mol Oncol Pathol, 450 Brookline Ave,Room JF-215C, Boston, MA 02215 USA.
EM shuji_ogino@dfci.harvard.edu
FU US National Institute of Health [P01CA87969, P01CA55075, P50CA127003,
K07CA122826, R01CA151993, R01CA137178]; Bennett Family Fund;
Entertainment Industry Foundation through the National Colorectal Cancer
Research Alliance; Japan Society for Promotion of Science
FX This work was supported by US National Institute of Health grants
P01CA87969, P01CA55075, P50CA127003, K07CA122826, R01CA151993, and
R01CA137178 and by grants from the Bennett Family Fund and the
Entertainment Industry Foundation through the National Colorectal Cancer
Research Alliance. Dr Morikawa was supported by a fellowship grant from
the Japan Society for Promotion of Science. Dr Chan is a Damon Runyon
Clinical Investigator.
NR 58
TC 91
Z9 93
U1 0
U2 5
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD APR 27
PY 2011
VL 305
IS 16
BP 1685
EP 1694
DI 10.1001/jama.2011.513
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 754XG
UT WOS:000289890500022
PM 21521850
ER
PT J
AU Peterson, PN
Shetterly, SM
Clarke, CL
Bekelman, DB
Chan, PS
Allen, LA
Matlock, DD
Magid, DJ
Masoudi, FA
AF Peterson, Pamela N.
Shetterly, Susan M.
Clarke, Christina L.
Bekelman, David B.
Chan, Paul S.
Allen, Larry A.
Matlock, Daniel D.
Magid, David J.
Masoudi, Frederick A.
TI Health Literacy and Outcomes Among Patients With Heart Failure
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID LIMITED LITERACY; CONTROLLED-TRIAL; HOSPITAL ADMISSION; IDENTIFY
PATIENTS; SKILLS; RISK; POPULATION; QUESTIONS; ENROLLEES; MORTALITY
AB Context Little is known about the effects of low health literacy among patients with heart failure, a condition that requires self-management and frequent interactions with the health care system.
Objective To evaluate the association between low health literacy and all-cause mortality and hospitalization among outpatients with heart failure.
Design, Setting, and Patients Retrospective cohort study conducted at Kaiser Permanente Colorado, an integrated managed care organization. Outpatients with heart failure were identified between January 2001 and May 2008, were surveyed by mail, and underwent follow-up for a median of 1.2 years. Health literacy was assessed using 3 established screening questions and categorized as adequate or low. Responders were excluded if they did not complete at least 1 health literacy question or if they did not have at least 1 year of enrollment prior to the survey date.
Main Outcome Measures All-cause mortality and all-cause hospitalization.
Results Of the 2156 patients surveyed, 1547 responded (72% response rate). Of 1494 included responders, 262 (17.5%) had low health literacy. Patients with low health literacy were older, of lower socioeconomic status, less likely to have at least a high school education, and had higher rates of coexisting illnesses. In multivariable Cox regression, low health literacy was independently associated with higher mortality (unadjusted rate, 17.6% vs 6.3%; adjusted hazard ratio, 1.97 [95% confidence interval, 1.3-2.97]; P=.001) but not hospitalization (unadjusted rate, 30.5% vs 23.2%; adjusted hazard ratio, 1.05 [95% confidence interval, 0.8-1.37]; P=.73).
Conclusion Among patients with heart failure in an integrated managed care organization, low health literacy was significantly associated with higher all-cause mortality. JAMA. 2011;305(16):1695-1701 www.jama.com
C1 [Peterson, Pamela N.] Denver Hlth Med Ctr, Div Cardiol, Denver, CO 80204 USA.
[Peterson, Pamela N.; Shetterly, Susan M.; Clarke, Christina L.; Magid, David J.; Masoudi, Frederick A.] Kaiser Permanente Colorado Inst Hlth Res, Denver, CO USA.
[Peterson, Pamela N.; Bekelman, David B.; Allen, Larry A.; Matlock, Daniel D.; Magid, David J.; Masoudi, Frederick A.] Univ Colorado Denver, Aurora, CO USA.
[Bekelman, David B.] Denver VA Med Ctr, Denver, CO USA.
[Chan, Paul S.] St Lukes Mid Amer Heart Inst, Kansas City, MO USA.
[Chan, Paul S.] Univ Missouri, Kansas City, MO 64110 USA.
RP Peterson, PN (reprint author), Denver Hlth Med Ctr, Div Cardiol, Mail Code 0960,777 Bannock St, Denver, CO 80204 USA.
EM pamela.peterson@ucdenver.edu
FU American Heart Association [067001N]; National Heart, Lung, and Blood
Institute [K23HL102224]
FX Dr Peterson is supported by American Heart Association Pharmaceutical
Roundtable grant 067001N. Dr Chan is supported by a Career Development
Grant Award (K23HL102224) from the National Heart, Lung, and Blood
Institute. Dr Allen is supported by an American Heart Association
Scientist Development Award.
NR 32
TC 121
Z9 123
U1 5
U2 16
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 APR 27
PY 2011
VL 305
IS 16
BP 1695
EP 1701
DI 10.1001/jama.2011.512
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA 754XG
UT WOS:000289890500023
PM 21521851
ER
PT J
AU Gheorghiade, M
Braunwald, E
AF Gheorghiade, Mihai
Braunwald, Eugene
TI A Proposed Model for Initial Assessment and Management of Acute Heart
Failure Syndromes
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
ID OUTCOMES; ASSOCIATION; CARDIOLOGY; SOCIETY; LUNG
C1 [Gheorghiade, Mihai] Northwestern Univ, Feinberg Sch Med, Ctr Cardiovasc Innovat, Dept Med, Chicago, IL 60611 USA.
[Braunwald, Eugene] Harvard Univ, Brigham & Womens Hosp, Div Cardiovasc Med, Sch Med,Dept Med,TIMI Study Grp, Boston, MA 02115 USA.
RP Gheorghiade, M (reprint author), Northwestern Univ, Feinberg Sch Med, Ctr Cardiovasc Innovat, Dept Med, 645 N Michigan Ave,Ste 1006, Chicago, IL 60611 USA.
EM m-gheorghiade@northwestern.edu
NR 10
TC 28
Z9 30
U1 0
U2 0
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 APR 27
PY 2011
VL 305
IS 16
BP 1702
EP 1703
DI 10.1001/jama.2011.515
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 754XG
UT WOS:000289890500024
PM 21521852
ER
PT J
AU Singh, N
AF Singh, Nina
TI Unraveling the Biologic Basis of Late-Onset Cytomegalovirus Disease in
High-Risk Organ Transplant Recipients
SO TRANSPLANTATION
LA English
DT Editorial Material
ID T-CELL RECONSTITUTION; PREEMPTIVE THERAPY; PROPHYLAXIS; CMV;
VALGANCICLOVIR; IMMUNITY; CD4(+)
C1 [Singh, Nina] VA Pittsburgh Healthcare Syst, Dept Med, Div Infect Dis, Pittsburgh, PA 15240 USA.
[Singh, Nina] Univ Pittsburgh, Pittsburgh, PA USA.
RP Singh, N (reprint author), VA Pittsburgh Healthcare Syst, Dept Med, Div Infect Dis, Univ Dr C, Pittsburgh, PA 15240 USA.
EM nis5@pitt.edu
NR 13
TC 5
Z9 5
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0041-1337
J9 TRANSPLANTATION
JI Transplantation
PD APR 27
PY 2011
VL 91
IS 8
BP 825
EP 826
DI 10.1097/TP.0b013e3182126eb9
PG 2
WC Immunology; Surgery; Transplantation
SC Immunology; Surgery; Transplantation
GA 746VX
UT WOS:000289277000004
PM 21372754
ER
PT J
AU Russell, PS
Chase, CM
Madsen, JC
Hirohashi, T
Cornell, LD
Sproule, TJ
Colvin, RB
Roopenian, DC
AF Russell, Paul S.
Chase, Catharine M.
Madsen, Joren C.
Hirohashi, Tsutomu
Cornell, Lynn D.
Sproule, Thomas J.
Colvin, Robert B.
Roopenian, Derry C.
TI Coronary Artery Disease From Isolated Non-H2-Determined
Incompatibilities in Transplanted Mouse Hearts
SO TRANSPLANTATION
LA English
DT Article
DE Coronary artery disease; Non-H2-determined incompatibilities; Heart
transplant
ID MINOR HISTOCOMPATIBILITY ANTIGEN; T-CELLS; NKG2D RECEPTOR; H-ANTIGEN;
H60; MICE; ALLOGRAFTS; EXPRESSION; REJECTION; LIGANDS
AB Background. Most studies of vascular disease in transplanted organs have used combinations involving disparities determined by genes of the major histocompatibility complex (MHC). This report describes examples of coronary vascular disease occurring in transplanted mouse hearts involving isolated, non-H2-determined incompatibilities.
Methods. Mice, incompatible in respect of HY, H4, or H60, were selected. For H60, the incompatibility depended on breeding congenic pairs or the introduction of H60 by transgenic methods because the latter method results in more widespread expression. Transplant survival was determined, and the appearance and prevalence of coronary artery vasculopathy (CAV) was established by appropriate histologic methods.
Results. Advanced changes of CAV were found at 56 days in transplants involving incompatibilities confined to HY or H4. In both combinations, skin grafts were also rejected. H60 incompatibility does not result in skin graft rejection and only a minority of heart transplants shows evidence of CAV. If heart transplants are preceded by skin grafts bearing both H60 and HY incompatibilities to promote "help" in generating immunity, H60 incompatible hearts develop advanced CAV. Heart transplants in all non-MHC categories ostensibly survive in excellent condition throughout this period despite their CAV.
Conclusions. CAV can develop as a consequence of non-MHC incompatibilities alone and even when antigens are sparsely expressed on cardiac tissue. Presensitization leads to much more severe vascular disease. Human leukocyte antigen compatible kidney transplants may also develop vascular disease and patients manifesting reactivity to MHC antigens should also be more prone to develop vascular disease because of undetectable non-MHC incompatibilities.
C1 [Russell, Paul S.; Chase, Catharine M.; Madsen, Joren C.; Hirohashi, Tsutomu] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Cornell, Lynn D.] Mayo Clin, Dept Pathol, Rochester, MN USA.
[Sproule, Thomas J.; Roopenian, Derry C.] Jackson Lab, Bar Harbor, ME 04609 USA.
[Colvin, Robert B.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
RP Russell, PS (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Surg, 55 Fruit St, Boston, MA 02114 USA.
EM psrussell@partners.org
FU National Institutes of Health [HL071932, AI28802]; ROTRF [313867044,
980940345]
FX This work was supported by grants from the National Institutes of
Health, HL071932 (J.C.M.) and AI28802 (D.C.R.), and by ROTRF research
grants 313867044 (R.B.C.) and 980940345 (J.C.M.).
NR 35
TC 18
Z9 18
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0041-1337
J9 TRANSPLANTATION
JI Transplantation
PD APR 27
PY 2011
VL 91
IS 8
BP 847
EP 852
DI 10.1097/TP.0b013e3182122f82
PG 6
WC Immunology; Surgery; Transplantation
SC Immunology; Surgery; Transplantation
GA 746VX
UT WOS:000289277000008
PM 21378606
ER
PT J
AU Rittling, SR
AF Rittling, Susan R.
TI Osteopontin in macrophage function
SO EXPERT REVIEWS IN MOLECULAR MEDICINE
LA English
DT Review
ID MONOCYTE CHEMOATTRACTANT PROTEIN-1; MICE LACKING OSTEOPONTIN;
INTEGRIN-BINDING LIGAND; BLOOD MONONUCLEAR-CELLS; MURINE MACROPHAGES;
DEFICIENT MICE; NITRIC-OXIDE; IN-VIVO; INTERSTITIAL FIBROSIS; TRANSGENIC
MICE
AB The secreted phosphorylated protein osteopontin (OPN) is expressed in a variety of tissues and bodily fluids, and is associated with pathologies including tissue injury, infection, autoimmune disease and cancer. Macrophages are ubiquitous, heterogeneous cells that mediate aspects of cell and tissue damage in all these pathologies. Here, the role of OPN in macrophage function is reviewed. OPN is expressed in macrophage cells in multiple pathologies, and the regulation of its expression in these cells has been described in vitro. The protein has been implicated in multiple functions of macrophages, including cytokine expression, expression of inducible nitric oxide synthase, phagocytosis and migration. Indeed, the role of OPN in cells of the macrophage lineage might underlie its physiological role in many pathologies. However, there are numerous instances where the published literature is inconsistent, especially in terms of OPN function in vitro. Although the heterogeneity of OPN and its receptors, or of macrophages themselves, might underlie some of these inconsistencies, it is important to understand the role of OPN in macrophage biology in order to exploit its function therapeutically.
C1 Forsyth Inst, Cambridge, MA 02142 USA.
RP Rittling, SR (reprint author), Forsyth Inst, 245 1st St, Cambridge, MA 02142 USA.
EM srittling@forsyth.org
NR 158
TC 39
Z9 42
U1 1
U2 9
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1462-3994
J9 EXPERT REV MOL MED
JI Expert Rev. Mol. Med.
PD APR 26
PY 2011
VL 13
AR e15
DI 10.1017/S1462399411001839
PG 21
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental
SC Biochemistry & Molecular Biology; Research & Experimental Medicine
GA 754MJ
UT WOS:000289858500001
PM 21545755
ER
PT J
AU Khatana, SAM
Kane, J
Taveira, TH
Bauer, MS
Wu, WC
AF Khatana, Sameed Ahmed M.
Kane, Joshua
Taveira, Tracey H.
Bauer, Mark S.
Wu, Wen-Chih
TI Monitoring and Prevalence Rates of Metabolic Syndrome in Military
Veterans with Serious Mental Illness
SO PLOS ONE
LA English
DT Article
ID 2ND-GENERATION ANTIPSYCHOTIC-DRUGS; CATIE SCHIZOPHRENIA TRIAL; BIPOLAR
DISORDER; CARDIOVASCULAR RISK; BASE-LINE; LIFE-STYLE; HEALTH; GLUCOSE;
OUTPATIENTS; AFFAIRS
AB Background: Cardiovascular disease is the leading cause of mortality among patients with serious mental illness (SMI) and the prevalence of metabolic syndrome-a constellation of cardiovascular risk factors-is significantly higher in these patients than in the general population. Metabolic monitoring among patients using second generation antipsychotics (SGAs)-a risk factor for metabolic syndrome-has been shown to be inadequate despite the release of several guidelines. However, patients with SMI have several factors independent of medication use that predispose them to a higher prevalence of metabolic syndrome. Our study therefore examines monitoring and prevalence of metabolic syndrome in patients with SMI, including those not using SGAs.
Methods and Findings: We retrospectively identified all patients treated at a Veterans Affairs Medical Center with diagnoses of schizophrenia, schizoaffective disorder or bipolar disorder during 2005-2006 and obtained demographic and clinical data. Incomplete monitoring of metabolic syndrome was defined as being unable to determine the status of at least one of the syndrome components. Of the 1,401 patients included (bipolar disorder: 822; schizophrenia: 222; and schizoaffective disorder: 357), 21.4% were incompletely monitored. Only 54.8% of patients who were not prescribed SGAs and did not have previous diagnoses of hypertension or hypercholesterolemia were monitored for all metabolic syndrome components compared to 92.4% of patients who had all three of these characteristics. Among patients monitored for metabolic syndrome completely, age-adjusted prevalence of the syndrome was 48.4%, with no significant difference between the three psychiatric groups.
Conclusions: Only one half of patients with SMI not using SGAs or previously diagnosed with hypertension and hypercholesterolemia were completely monitored for metabolic syndrome components compared to greater than 90% of those with these characteristics. With the high prevalence of metabolic syndrome seen in this population, there appears to be a need to intensify efforts to reduce this monitoring gap.
C1 [Khatana, Sameed Ahmed M.; Taveira, Tracey H.; Wu, Wen-Chih] Providence Vet Affairs Med Ctr, Res Enhancement Award Program, Providence, RI USA.
[Khatana, Sameed Ahmed M.] Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
[Kane, Joshua] Butler Hosp, Providence, RI 02906 USA.
[Taveira, Tracey H.] Univ Rhode Isl, Coll Pharm, Kingston, RI 02881 USA.
[Taveira, Tracey H.; Wu, Wen-Chih] Brown Univ, Dept Med, Providence Vet Affairs Med Ctr, Warren Alpert Med Sch, Providence, RI 02912 USA.
[Bauer, Mark S.] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
[Bauer, Mark S.] VA Boston Healthcare Syst, Boston, MA USA.
RP Khatana, SAM (reprint author), Providence Vet Affairs Med Ctr, Res Enhancement Award Program, Providence, RI USA.
EM skhatana@gmail.com
FU VA Health Services Research & Development Grant [REA-08-263]
FX The study was funded by VA Health Services Research & Development Grant
# REA-08-263. The funders had no role in study design, data collection
and analysis, decision to publish, or preparation of the manuscript.
NR 57
TC 18
Z9 18
U1 1
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 APR 26
PY 2011
VL 6
IS 4
AR e19298
DI 10.1371/journal.pone.0019298
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 756NE
UT WOS:000290018400045
PM 21541294
ER
PT J
AU Nicolaou, KC
Sanchini, S
Sarlah, D
Lu, G
Wu, TR
Nomura, DK
Cravatt, BF
Cubitt, B
de la Torre, JC
Hessell, AJ
Burton, DR
AF Nicolaou, K. C.
Sanchini, Silvano
Sarlah, David
Lu, Gang
Wu, T. Robert
Nomura, Daniel K.
Cravatt, Benjamin F.
Cubitt, Beatrice
de la Torre, Juan C.
Hessell, Ann J.
Burton, Dennis R.
TI Design, synthesis, and biological evaluation of a biyouyanagin compound
library
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE [2+2] photocycloaddition; anti-inflammatory agents; antiviral agents
ID HYPERICUM-CHINENSE; NATURAL-PRODUCTS; ORGANIC-SYNTHESIS; REVISED
STRUCTURE; ANALOGS THEREOF; CLINICAL-TRIALS; DRUG DISCOVERY;
SPIRO-LACTONES; INFLAMMATION; MOLECULES
AB Modern drug discovery efforts rely, to a large extent, on lead compounds from two classes of small organic molecules; namely, natural products (i.e., secondary metabolites) and designed compounds (i.e., synthetic molecules). In this article, we demonstrate how these two domains of lead compounds can be merged through total synthesis and molecular design of analogs patterned after the targeted natural products, whose promising biological properties provide the motivation. Specifically, the present study targeted the naturally occurring biyouyanagins A and B and their analogs through modular chemical synthesis and led to the discovery of small organic molecules possessing anti-HIV and anti-arenavirus properties.
C1 [Nicolaou, K. C.; Sanchini, Silvano; Sarlah, David; Lu, Gang; Wu, T. Robert] Scripps Res Inst, Dept Chem, La Jolla, CA 92037 USA.
[Nicolaou, K. C.; Sanchini, Silvano; Sarlah, David; Lu, Gang; Wu, T. Robert; Nomura, Daniel K.; Cravatt, Benjamin F.] Scripps Res Inst, Skaggs Inst Chem Biol, La Jolla, CA 92037 USA.
[Nicolaou, K. C.] Univ Calif, Dept Chem & Biochem, La Jolla, CA 92093 USA.
[Nomura, Daniel K.; Cravatt, Benjamin F.] Scripps Res Inst, Dept Physiol Chem, La Jolla, CA 92037 USA.
[Cubitt, Beatrice; de la Torre, Juan C.; Hessell, Ann J.; Burton, Dennis R.] Scripps Res Inst, Dept Immunol & Microbiol Sci, La Jolla, CA 92037 USA.
[Burton, Dennis R.] Scripps Res Inst, Int AIDS Vaccine Initiat Neutralising Antibody Ct, La Jolla, CA 92037 USA.
[Burton, Dennis R.] Massachusetts Gen Hosp, Ragon Inst, Massachusetts Inst Technol & Harvard, Boston, MA 02114 USA.
RP Nicolaou, KC (reprint author), Scripps Res Inst, Dept Chem, 10550 N Torrey Pines Rd, La Jolla, CA 92037 USA.
EM kcn@scripps.edu
OI Sarlah, David/0000-0002-8736-8953
FU National Institutes of Health (USA); Skaggs Institute for Chemical
Biology; Universita degli Studi di Urbino "Carlo Bo"; Japan Society for
the Promotion of Science; Natural Sciences and Engineering Research
Council of Canada; National Institute on Drug Abuse [K99DA030908]
FX We thank Dr. Dee-Hua Huang and Dr. Laura Pasternack for NMR
spectroscopic assistance; Dr. Gary Siuzdak and Dr. Raj Chadha for mass
spectrometric and X-ray crystallographic assistance, respectively; and
Eric Rogers for performing the neutralization assays. Financial support
for this work was provided by the National Institutes of Health (USA),
The Skaggs Institute for Chemical Biology, the Universita degli Studi di
Urbino "Carlo Bo" (graduate fellowship to S.S.), the Japan Society for
the Promotion of Science (postdoctoral fellowship to G.L.), the Natural
Sciences and Engineering Research Council of Canada (postdoctoral
fellowship to T.R.W.), and the National Institute on Drug Abuse (award
K99DA030908 to D.K.N.).
NR 37
TC 24
Z9 24
U1 3
U2 21
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 APR 26
PY 2011
VL 108
IS 17
BP 6715
EP 6720
DI 10.1073/pnas.1015258108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 754WM
UT WOS:000289888500011
PM 21245351
ER
PT J
AU Ermann, J
Garrett, WS
Kuchroo, J
Rourida, K
Glickman, JN
Bleich, A
Glimcher, LH
AF Ermann, Joerg
Garrett, Wendy S.
Kuchroo, Juhi
Rourida, Khadija
Glickman, Jonathan N.
Bleich, Andre
Glimcher, Laurie H.
TI Severity of innate immune-mediated colitis is controlled by the cytokine
deficiency-induced colitis susceptibility-1 (Cdcs1) locus
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID INFLAMMATORY-BOWEL-DISEASE; QUANTITATIVE TRAIT LOCUS; T-BET DEFICIENCY;
IL-10-DEFICIENT MICE; GUT MICROBIOTA; GENETICS; NUMBER; CELLS
AB Genetic modifier loci influence the phenotypic expression of many Mendelian traits; insight into disease pathogenesis gained from their identification in animal disease models may impact the treatment of human multigenic disorders. We previously described an innate immune-driven model of spontaneous ulcerative colitis in T-bet(-/-). Rag2(-/-) double-deficient mice that resembles human ulcerative colitis. On a BALB/c background, this disease is highly penetrant and results in the development of colorectal cancer. However, we observed that colitis in T-bet(-/-). Rag2(-/-) mice on a Cn57BL/6 background was significantly less severe. Quantitative trait locus analysis using an N2 backcross strategy revealed a single major quantitative trait locus on chromosome 3 that mapped to the Cdcs1 ( cytokine deficiency-induced colitis susceptibility-1) locus previously identified in the Il10(-/-) and Gnai2(-/-) colitis models. Congenic introduction of the susceptible Cdcs1 interval from C3H/He into the C57BL/6 background restored colitis severity. Bone marrow reconstitution experiments further mapped the effect of host genetics on disease severity to the hematopoietic compartment. There were distinct differences in the expression of several Cdcs1 genes in bone marrow-derived dendritic cells from Cdcs1 congenic mice. We conclude that the Cdcs1 locus controls colitis severity in Tbet(-/-). Rag2(-/-) mice through innate immune cells.
C1 [Ermann, Joerg; Garrett, Wendy S.; Kuchroo, Juhi; Rourida, Khadija; Glimcher, Laurie H.] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
[Ermann, Joerg; Garrett, Wendy S.; Glimcher, Laurie H.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Garrett, Wendy S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Ermann, Joerg; Glimcher, Laurie H.] Brigham & Womens Hosp, Div Rheumatol Immunol & Allergy, Boston, MA 02115 USA.
[Glickman, Jonathan N.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Bleich, Andre] Hannover Med Sch, Inst Lab Anim Sci, D-30625 Hannover, Germany.
[Glickman, Jonathan N.] Caris Diagnost, Newton, MA 02464 USA.
[Glimcher, Laurie H.] Ragon Inst Massachusetts Gen Hosp Masschusetts In, Charlestown, MA 02129 USA.
RP Glimcher, LH (reprint author), Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, 665 Huntington Ave, Boston, MA 02115 USA.
EM lglimche@hsph.harvard.edu
FU National Institutes of Health [CA112663, 1P50CA127003-2, K08AI078942];
Danone Research; Harvard Digestive Diseases Center (National Institutes
of Health) [P30 DK34845]; Clinical Immunology Society/Talecris
FX We thank Jacobo Ramirez for excellent animal care, Kirsten Sigrist for
help with generating Cdcs1 congenic animals, and Dorothy Zhang for
preparing histology slides; and Edward Leiter at The Jackson Laboratory
for help with designing the quantitative trait locus study and critical
reading of the manuscript. This work was supported by National
Institutes of Health Grants CA112663 (to L. H. G.), 1P50CA127003-2 and
K08AI078942 (to W. S. G.), a grant from Danone Research (to L. H. G.), a
Harvard Digestive Diseases Center (National Institutes of Health Grant
P30 DK34845) pilot award (to J.E.), and a Clinical Immunology
Society/Talecris fellowship (to J.E.).
NR 17
TC 15
Z9 15
U1 0
U2 2
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 APR 26
PY 2011
VL 108
IS 17
BP 7137
EP 7141
DI 10.1073/pnas.1104234108
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 754WM
UT WOS:000289888500085
PM 21482794
ER
PT J
AU Butt, AA
Chang, CC
Kuller, L
Goetz, MB
Leaf, D
Rimland, D
Gibert, CL
Oursler, KK
Rodriguez-Barradas, MC
Lim, J
Kazis, LE
Gottlieb, S
Justice, AC
Freiberg, MS
AF Butt, Adeel A.
Chang, Chung-Chou
Kuller, Lewis
Goetz, Matthew Bidwell
Leaf, David
Rimland, David
Gibert, Cynthia L.
Oursler, Krisann K.
Rodriguez-Barradas, Maria C.
Lim, Joseph
Kazis, Lewis E.
Gottlieb, Stephen
Justice, Amy C.
Freiberg, Matthew S.
TI Risk of Heart Failure With Human Immunodeficiency Virus in the Absence
of Prior Diagnosis of Coronary Heart Disease
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Article
ID HIV-INFECTED PATIENTS; LEFT-VENTRICULAR MASS; HEPATITIS-C VIRUS;
MYOCARDIAL-INFARCTION; ANTIRETROVIRAL TREATMENT; CARDIOVASCULAR-DISEASE;
UNINFECTED VETERANS; ALCOHOL-ABUSE; CARDIOMYOPATHY; DYSFUNCTION
AB Background: Whether human immunodeficiency virus (HIV) infection is a risk factor for heart failure (HF) is not clear. The presence of coronary heart disease and alcohol consumption in this population may confound this association.
Methods: To determine whether HIV infection is a risk factor for incident HF, we conducted a population-based, retrospective cohort study of HIV-infected and HIV-uninfected veterans enrolled in the Veterans Aging Cohort Study Virtual Cohort (VACS-VC) and the 1999 Large Health Study of Veteran Enrollees (LHS) from January 1, 2000, to July 31, 2007.
Results: There were 8486 participants (28.2% HIV-infected) enrolled in the VACS-VC who also participated in the 1999 LHS. During the median 7.3 years of follow-up, 286 incident HF events occurred. Age-and race/ethnicity-adjusted HF rates among HIV-infected and HIV-uninfected veterans were 7.12 (95% confidence interval [CI], 6.90-7.34) and 4.82 (95% CI, 4.72-4.91) per 1000 person-years, respectively. Compared with HIV-uninfected veterans, those who were HIV infected had an increased risk of HF (adjusted hazard ratio [HR], 1.81; 95% CI, 1.39-2.36). This association persisted among veterans who did not have a coronary heart disease event or a diagnosis related to alcohol abuse or dependence before the incident HF event (adjusted HR, 1.96; 95% CI, 1.29-2.98). Compared with HIV-uninfected veterans, those who were HIV infected with a baseline Human immunodeficiency virus 1 (HIV-1) RNA level of 500 or more copies/mL had a higher risk of HF (adjusted HR, 2.28; 95% CI, 1.57-3.32), while those with baseline and a recent HIV-1 RNA level less than 500 copies/mL did not (adjusted HR, 1.10; 95% CI, 0.64-1.89; P <.001 for comparison between high and low HIV-1 RNA groups).
Conclusions: Our data suggest that HIV infection is a risk factor for HF. Ongoing viral replication is associated with a higher risk of developing HF.
C1 [Butt, Adeel A.; Chang, Chung-Chou; Freiberg, Matthew S.] Univ Pittsburgh, Sch Med, Dept Med, Pittsburgh, PA 15213 USA.
[Butt, Adeel A.] Vet Affairs VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Goetz, Matthew Bidwell; Leaf, David] VA Greater Angeles Healthcare Syst, Los Angeles, CA USA.
[Goetz, Matthew Bidwell; Leaf, David] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Rimland, David] VA Med Ctr, Atlanta, GA USA.
[Rimland, David] Emory Univ, Sch Med, Atlanta, GA USA.
[Gibert, Cynthia L.] VA Med Ctr, Washington, DC USA.
[Gibert, Cynthia L.] George Washington Univ, Washington, DC USA.
[Oursler, Krisann K.; Gottlieb, Stephen] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Oursler, Krisann K.] VA Maryland Healthcare Syst, Baltimore, MD USA.
[Rodriguez-Barradas, Maria C.] Michael E DeBakey VA Med Ctr, Houston, TX USA.
[Rodriguez-Barradas, Maria C.] Baylor Coll Med, Houston, TX 77030 USA.
[Lim, Joseph; Justice, Amy C.] Yale Univ, Sch Med & Publ Hlth, New Haven, CT USA.
[Gottlieb, Stephen] Baltimore VA Med Ctr, Baltimore, MD USA.
[Justice, Amy C.] VA Connecticut Healthcare Syst, West Haven, CT USA.
[Kuller, Lewis] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
[Kazis, Lewis E.] Boston Univ, Sch Publ Hlth, Ctr Assessment Pharmaceut Practices, Dept Hlth Policy & Management, Boston, MA USA.
RP Butt, AA (reprint author), Univ Pittsburgh, Sch Med, Dept Med, 3601 5th Ave,Ste 3A, Pittsburgh, PA 15213 USA.
EM aabutt@pitt.edu
OI Goetz, Matthew/0000-0003-4542-992X
FU National Institute on Alcohol Abuse and Alcoholism and Veterans Health
Administration Public Health Strategic Health Core Group [U10 AA 13566];
National Heart, Lung, and Blood Institute [HL095136-03]; National
Institute on Aging [AG024896]
FX Funding for the Veterans Aging Cohort Study was provided by grant U10 AA
13566 from the National Institute on Alcohol Abuse and Alcoholism and
Veterans Health Administration Public Health Strategic Health Core
Group, grant HL095136-03 from the National Heart, Lung, and Blood
Institute (Dr Freiberg), and grant AG024896 from the National Institute
on Aging (Dr Oursler).
NR 37
TC 56
Z9 56
U1 1
U2 3
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 APR 25
PY 2011
VL 171
IS 8
BP 737
EP 743
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA 754KK
UT WOS:000289853300004
PM 21518940
ER
PT J
AU Yeh, GY
McCarthy, EP
Wayne, PM
Stevenson, LW
Wood, MJ
Forman, D
Davis, RB
Phillips, RS
AF Yeh, Gloria Y.
McCarthy, Ellen P.
Wayne, Peter M.
Stevenson, Lynne W.
Wood, Malissa J.
Forman, Daniel
Davis, Roger B.
Phillips, Russell S.
TI Tai Chi Exercise in Patients With Chronic Heart Failure A Randomized
Clinical Trial
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Article
ID QUALITY-OF-LIFE; CARDIORESPIRATORY FUNCTION; RHEUMATOID-ARTHRITIS; OLDER
ADULTS; CARDIAC RESYNCHRONIZATION; CHUAN PRACTITIONERS; FUNCTIONAL
STATUS; AEROBIC EXERCISE; 6-MINUTE WALK; BALANCE
AB Background: Preliminary evidence suggests that meditative exercise may have benefits for patients with chronic systolic heart failure (HF); this has not been rigorously tested in a large clinical sample. We sought to investigate whether tai chi, as an adjunct to standard care, improves functional capacity and quality of life in patients with HF.
Methods: A single-blind, multisite, parallel-group, randomized controlled trial evaluated 100 outpatients with systolic HF (New York Heart Association class I-III, left ventricular ejection fraction <= 40%) who were recruited between May 1, 2005, and September 30, 2008. A group-based 12-week tai chi exercise program (n= 50) or time-matched education (n= 50, control group) was conducted. Outcome measures included exercise capacity (6-minute walk test and peak oxygen uptake) and disease-specific quality of life (Minnesota Living With Heart Failure Questionnaire).
Results: Mean (SD) age of patients was 67(11) years; baseline values were left ventricular ejection fraction, 29% (8%) and peak oxygen uptake, 13.5 mL/kg/min; the me-dian New York Heart Association class of HF was class II. At completion of the study, there were no significant differences in change in 6-minute walk distance and peak oxygen uptake (median change [first quartile, third quartile], 35 [-2, 51] vs 2 [-7, 54] meters, P=.95; and 1.1 [-1.1, 1.5] vs -0.5 [-1.2, 1.8] mL/kg/min, P=.81) when comparing tai chi and control groups; however, patients in the tai chi group had greater improvements in quality of life (Minnesota Living With Heart Failure Questionnaire, -19 [-23, -3] vs 1 [-16, 3], P=.02). Improvements with tai chi were also seen in exercise self-efficacy (Cardiac Exercise Self-efficacy Instrument, 0.1 [0.1, 0.6] vs -0.3 [-0.5, 0.2], P <.001) and mood (Profile of Mood States total mood disturbance, -6 [-17, 1] vs -1 [-13, 10], P=.01).
Conclusion: Tai chi exercise may improve quality of life, mood, and exercise self-efficacy in patients with HF.
C1 [Yeh, Gloria Y.; McCarthy, Ellen P.; Wayne, Peter M.; Davis, Roger B.; Phillips, Russell S.] Beth Israel Deaconess Med Ctr, Div Gen Med & Primary Care, Dept Med, Brookline, MA 02446 USA.
[Yeh, Gloria Y.; Wayne, Peter M.; Davis, Roger B.; Phillips, Russell S.] Harvard Univ, Sch Med, Div Res & Educ Complementary & Integrat Med Thera, Boston, MA USA.
[Stevenson, Lynne W.; Forman, Daniel] Brigham & Womens Hosp, Dept Med, Div Cardiovasc, Boston, MA 02115 USA.
[Wood, Malissa J.] Massachusetts Gen Hosp, Dept Med, Div Cardiol, Boston, MA 02114 USA.
RP Yeh, GY (reprint author), Beth Israel Deaconess Med Ctr, Div Gen Med & Primary Care, Dept Med, 1309 Beacon St,2nd Floor, Brookline, MA 02446 USA.
EM gyeh@bidmc.harvard.edu
FU National Center for Complementary and Alternative Medicine [R01
AT002454]; Beth Israel Deaconess Medical Center General Clinical
Research Center, National Institutes of Health (NIH) [RR 01032]; NIH
National Center for Complementary and Alternative Medicine (NCCAM) [K23
AT002624, U19 AT002022]
FX This study was supported by the R01 AT002454 award from the National
Center for Complementary and Alternative Medicine (Dr Phillips) and in
part by grant RR 01032 from the Beth Israel Deaconess Medical Center
General Clinical Research Center from the National Institutes of Health
(NIH). Dr Yeh was supported by the career-investigator award K23
AT002624 from the NIH National Center for Complementary and Alternative
Medicine (NCCAM). Dr Wayne was supported by Center grant U19 AT002022
from the NIH NCCAM.
NR 72
TC 67
Z9 72
U1 8
U2 23
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 APR 25
PY 2011
VL 171
IS 8
BP 750
EP 757
PG 8
WC Medicine, General & Internal
SC General & Internal Medicine
GA 754KK
UT WOS:000289853300006
PM 21518942
ER
PT J
AU Teerlink, JR
AF Teerlink, John R.
TI Mind or Body Evaluating Mind-Body Therapy Efficacy in Heart Failure
Trials
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Editorial Material
C1 [Teerlink, John R.] San Francisco VA Med Ctr, Cardiol Sect, San Francisco, CA 94121 USA.
[Teerlink, John R.] Univ Calif San Francisco, Sch Med, San Francisco, CA USA.
RP Teerlink, JR (reprint author), San Francisco VA Med Ctr, Cardiol Sect, 4150 Clement St, San Francisco, CA 94121 USA.
EM john.teerlink@ucsf.edu
RI Teerlink, John/D-2986-2012
NR 10
TC 0
Z9 0
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 APR 25
PY 2011
VL 171
IS 8
BP 758
EP 759
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 754KK
UT WOS:000289853300007
PM 21518943
ER
PT J
AU Simon, JA
AF Simon, Joel A.
TI Smoking Cessation Interventions: A Primer for Physicians
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Editorial Material
ID TREATING TOBACCO DEPENDENCE; CIGARETTE-SMOKING; UNITED-STATES; BUPROPION
C1 [Simon, Joel A.] Univ Calif San Francisco, Sch Med, San Francisco VA Med Ctr, Gen Internal Med Sect, San Francisco, CA USA.
RP Simon, JA (reprint author), San Francisco VA Med Ctr, Gen Internal Med Sect 111A1, 4150 Clement St, San Francisco, CA 94121 USA.
NR 16
TC 4
Z9 4
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 APR 25
PY 2011
VL 171
IS 8
BP 777
EP 778
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA 754KK
UT WOS:000289853300011
PM 21518947
ER
PT J
AU Trautner, BW
Kelly, PA
Petersen, N
Hysong, S
Kell, H
Liao, KS
Patterson, JE
Naik, AD
AF Trautner, Barbara W.
Kelly, P. Adam
Petersen, Nancy
Hysong, Sylvia
Kell, Harrison
Liao, Kershena S.
Patterson, Jan E.
Naik, Aanand D.
TI A hospital-site controlled intervention using audit and feedback to
implement guidelines concerning inappropriate treatment of
catheter-associated asymptomatic bacteriuria
SO IMPLEMENTATION SCIENCE
LA English
DT Article
ID URINARY-TRACT-INFECTION; CLINICAL-PRACTICE GUIDELINES; INTENSIVE-CARE
UNITS; NOSOCOMIAL INFECTIONS; DISEASES-SOCIETY; ADULTS; IMPACT;
PHYSICIANS; DIAGNOSIS; FRAMEWORK
AB Background: Catheter-associated urinary tract infection (CAUTI) is one of the most common hospital-acquired infections. However, many cases treated as hospital-acquired CAUTI are actually asymptomatic bacteriuria (ABU). Evidence-based guidelines recommend that providers neither screen for nor treat ABU in most catheterized patients, but there is a significant gap between these guidelines and clinical practice. Our objectives are (1) to evaluate the effectiveness of an audit and feedback intervention for increasing guideline-concordant care concerning catheter-associated ABU and (2) to measure improvements in healthcare providers' knowledge of and attitudes toward the practice guidelines associated with the intervention.
Methods/Design: The study uses a controlled pre/post design to test an intervention using audit and feedback of healthcare providers to improve their compliance with ABU guidelines. The intervention and the control sites are two VA hospitals. For objective 1 we will review medical records to measure the clinical outcomes of inappropriate screening for and treatment of catheter-associated ABU. For objective 2 we will survey providers' knowledge and attitudes. Three phases of our protocol are proposed: the first 12-month phase will involve observation of the baseline incidence of inappropriate screening for and treatment of ABU at both sites. This surveillance for clinical outcomes will continue at both sites throughout the study. Phase 2 consists of 12 months of individualized audit and feedback at the intervention site and guidelines distribution at both sites. The third phase, also over 12 months, will provide unit-level feedback at the intervention site to assess sustainability. Healthcare providers at the intervention site during phase 2 and at both sites during phase 3 will complete pre/post surveys of awareness and familiarity (knowledge), as well as of acceptance and outcome expectancy (attitudes) regarding the relevant practice guidelines.
Discussion: Our proposal to bring clinical practice in line with published guidelines has significant potential to decrease overdiagnosis of CAUTI and associated inappropriate antibiotic use. Our study will also provide information about how to maximize effectiveness of audit and feedback to achieve guideline adherence in the inpatient setting.
C1 [Trautner, Barbara W.; Kelly, P. Adam; Petersen, Nancy; Hysong, Sylvia; Kell, Harrison; Naik, Aanand D.] Michael E DeBakey VA Med Ctr, Houston Hlth Serv Res & Dev Ctr Excellence, Houston, TX 77030 USA.
[Trautner, Barbara W.; Petersen, Nancy; Hysong, Sylvia; Liao, Kershena S.; Naik, Aanand D.] Baylor Coll Med, Houston, TX 77030 USA.
[Kelly, P. Adam] SE Louisiana Vet Hlth Care Syst, Res Serv, New Orleans, LA USA.
[Kelly, P. Adam] Tulane Univ, Sch Med, New Orleans, LA 70112 USA.
[Patterson, Jan E.] S Texas Vet Healthcare Syst, Med Serv, San Antonio, TX USA.
RP Trautner, BW (reprint author), Michael E DeBakey VA Med Ctr, Houston Hlth Serv Res & Dev Ctr Excellence, Houston, TX 77030 USA.
EM trautner@bcm.edu
RI Hysong, Sylvia/B-8420-2008
OI Hysong, Sylvia/0000-0002-9063-5207
FU VA HSRD [IIR 09-104]; VA HSR&D Center of Excellence [HFP90-020]; VA
HSR&D Career Development Award [07-018-1]
FX Our project is funded by VA HSR&D IIR 09-104 and partly supported by the
VA HSR&D Center of Excellence (HFP90-020). BWT has a VA Career
Development Award from Rehabilitation Research & Development (B4623).
ADN receives additional support from the National Institute on Aging
(K23AG027144) and a Clinical Scientist Development Award from the Doris
Duke Charitable Foundation. SH receives support from a VA HSR&D Career
Development Award (07-018-1).
NR 39
TC 13
Z9 13
U1 0
U2 8
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1748-5908
J9 IMPLEMENT SCI
JI Implement. Sci.
PD APR 22
PY 2011
VL 6
AR 41
DI 10.1186/1748-5908-6-41
PG 11
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 773LW
UT WOS:000291309800001
PM 21513539
ER
PT J
AU Teng, YQ
Kanasaki, K
Bardeesy, N
Sugimoto, H
Kalluri, R
AF Teng, Yingqi
Kanasaki, Keizo
Bardeesy, Nabeel
Sugimoto, Hikaru
Kalluri, Raghu
TI Deletion of Smad4 in fibroblasts leads to defective chondrocyte
maturation and cartilage production in a TGF beta type II receptor
independent manner
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Smad4; BMP-5; Cartilage; Chondrocyte; Fsp1/S100A4
ID SYNOVIAL FIBROBLASTS; GROWTH-PLATE; PROLIFERATION; EXPRESSION; SKELETAL;
MEDIATOR; S100A4; MARKER
AB The transforming growth factor beta (TGF beta) superfamily growth factors play vital roles during the development, homeostasis, and pathogenesis of multi-cellular organisms. Smad4 serves as an exclusive co-activating smad that elicits most of the transcription responses invoked by the TGF beta superfamily members. We used Cre recombinase driven by the Fsp1/S100A4 promoter to delete the Smad4 gene in fibroblasts. We show that Fsp1/S100A4 is expressed in the elastic and fibrocartilage, and demonstrate that the fsp1-Cre; Smad4 flox/flox mutants have normal body size, but exhibit a short ear phenotype due to the deletion of the Smad4 gene in the ear chondrocytes. In contrast, TGF beta type II receptor deletion using Fsp1-cre does not lead to this phenotype, supporting the notion that non-TGF beta mediated signaling via Smad4 is essential for proper formation of ear cartilage during development. Smad4 deficiency in Fsp1(+) fibroblasts leads to defective chondrocyte maturation and cartilage production, likely due to a deficiency in bone morphogenic protein 5 (BMP-5) mediated signaling via Smad4. Our results emphasize the importance of BMP signaling pathways in the maturation and function of certain lineages of chondrocytes and offer an insight into the heterogeneity of the chondrocyte population in the body. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Teng, Yingqi; Kanasaki, Keizo; Sugimoto, Hikaru; Kalluri, Raghu] Harvard Univ, Sch Med, Div Matrix Biol, Beth Israel Deaconess Med Ctr,Dept Med, Boston, MA 02215 USA.
[Bardeesy, Nabeel] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Massachusetts Gen Hosp Canc Ctr, Boston, MA 02215 USA.
[Kalluri, Raghu] Harvard Mit Div Hlth Sci & Technol, Boston, MA USA.
[Kalluri, Raghu] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02215 USA.
RP Kalluri, R (reprint author), Harvard Univ, Sch Med, Div Matrix Biol, Beth Israel Deaconess Med Ctr,Dept Med, Boston, MA 02215 USA.
EM rkalluri@bidmc.harvard.edu
RI Kalluri, Raghu/E-2677-2015
OI Kalluri, Raghu/0000-0002-2190-547X
FU BIDMC Department of Medicine; NIH [DK 55001, DK 62987, DK 13193, DK
61688]
FX We wish to thank Lauren Orefice for her technical assistance provide to
the authors during the course of this study. This work was primarily
supported by the BIDMC Department of Medicine research funds to the
Division of Matrix Biology, and partially supported by NIH Grants DK
55001, DK 62987, DK 13193 and DK 61688. We also thank Dr. Michael Duncan
for his useful discussion.
NR 16
TC 4
Z9 5
U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD APR 22
PY 2011
VL 407
IS 4
BP 633
EP 639
DI 10.1016/j.bbrc.2011.02.142
PG 7
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 759KI
UT WOS:000290240500002
PM 21376704
ER
PT J
AU Tao, HY
Jin, QH
Koo, DI
Liao, XB
Englund, NP
Wang, Y
Ramamurthy, A
Schultz, PG
Dorsch, M
Kelleher, J
Wu, X
AF Tao, Haiyan
Jin, Qihui
Koo, Dong-In
Liao, Xuebin
Englund, Nathan P.
Wang, Yan
Ramamurthy, Arun
Schultz, Peter G.
Dorsch, Marion
Kelleher, Joseph
Wu, Xu
TI Small Molecule Antagonists in Distinct Binding Modes Inhibit
Drug-Resistant Mutant of Smoothened
SO CHEMISTRY & BIOLOGY
LA English
DT Article
ID HEDGEHOG SIGNALING PATHWAY; BASAL-CELL CARCINOMA; CANCER;
MEDULLOBLASTOMA; CYCLOPAMINE; ACTIVATION
AB Several small molecule antagonists for Smoothened (Smo) have been developed, and achieved promising preclinical efficacy in cancers that are dependent on Hedgehog (Hh) signaling. However, in a recent clinical study, a drug-resistant D473H SMO mutant was identified that is thought to be responsible for cancer relapse in a patient with medulloblastoma. Here, we report two Smo antagonists that bind to distinct sites, as compared to known antagonists and agonists, and inhibit both wild-type and mutant Smo. These findings provide an insight of the ligand-binding sites of Smo and a basis for the development of potential therapeutics for tumors with drug-resistant Smo mutations.
C1 [Tao, Haiyan; Jin, Qihui; Liao, Xuebin; Englund, Nathan P.; Wang, Yan; Wu, Xu] Novartis Res Fdn, Genom Inst, San Diego, CA 92121 USA.
[Koo, Dong-In; Schultz, Peter G.] Scripps Res Inst, Dept Chem, La Jolla, CA 92037 USA.
[Ramamurthy, Arun; Dorsch, Marion; Kelleher, Joseph] Novartis Inst Biomed Res, Cambridge, MA 02139 USA.
[Wu, Xu] Massachusetts Gen Hosp East, Cutaneous Biol Res Ctr, Charlestown, MA 02129 USA.
[Wu, Xu] Harvard Univ, Sch Med, Charlestown, MA 02129 USA.
RP Wu, X (reprint author), Novartis Res Fdn, Genom Inst, San Diego, CA 92121 USA.
EM xwu@cbrc2.mgh.harvard.edu
FU Novartis Research Foundation
FX We thank Dr. Jun Liu for constructs and helpful discussions; Reem Javed,
Richard Soden, Lindsey Aimone, Anlai Wang, and Kathy Hsiao for technical
support; Christopher Trussell for cell sorting; Dr. James K. Chen for
providing mouse SmoM2 construct, and Drs. Silvia Buonamici, Shifeng Pan,
Stefan Peukert, Matthew Tremblay, Charles Cho, and Luke Lairson for
critical comments of the manuscript. This work is supported by the
Novartis Research Foundation (X.W.); H.T., Q.J., X.L., N.P.E., Y.W.,
A.R., M.D., J.K., and X.W. are employees of Novartis. H.T., D.-I.K.,
N.P.E., Y.W., A.R., M.D., and J.K. performed biological experiments.
H.T., X.L., and Q.J. synthesized and characterized compounds. H.T.,
P.G.S., and X.W. analyzed data. H.T. and X.W. conceptualized the project
and wrote the manuscript, and all authors read and edited the
manuscript.
NR 23
TC 29
Z9 30
U1 2
U2 7
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-5521
J9 CHEM BIOL
JI Chem. Biol.
PD APR 22
PY 2011
VL 18
IS 4
BP 432
EP 437
DI 10.1016/j.chembiol.2011.01.018
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 759KL
UT WOS:000290240900008
PM 21513879
ER
PT J
AU Bandukwala, HS
Wu, YQ
Feuerer, M
Chen, YH
Barboza, B
Ghosh, S
Stroud, JC
Benoist, C
Mathis, D
Rao, A
Chen, L
AF Bandukwala, Hozefa S.
Wu, Yongqing
Feuerer, Markus
Chen, Yongheng
Barboza, Bianca
Ghosh, Srimoyee
Stroud, James C.
Benoist, Christophe
Mathis, Diane
Rao, Anjana
Chen, Lin
TI Structure of a Domain-Swapped FOXP3 Dimer on DNA and Its Function in
Regulatory T Cells
SO IMMUNITY
LA English
DT Article
ID TRANSCRIPTION FACTOR FOXP3; TUMOR-SUPPRESSOR P53; IMMUNE DYSREGULATION;
CRYSTAL-STRUCTURE; TARGET GENES; ENTEROPATHY; NFAT; IPEX;
POLYENDOCRINOPATHY; MUTATIONS
AB The transcription factor FOXP3 is essential for the suppressive function of regulatory T cells that are required for maintaining self-tolerance. We have solved the crystal structure of the FOXP3 forkhead domain as a ternary complex with the DNA-binding domain of the transcription factor NFAT1 and a DNA oligonucleotide from the interleukin-2 promoter. A striking feature of this structure is that FOXP3 forms a domain-swapped dimer that bridges two molecules of DNA. Structure-guided or autoimmune disease (IPEX)-associated mutations in the domain-swap interface diminished dimer formation by the FOXP3 forkhead domain without compromising FOXP3 DNA binding. These mutations also eliminated T cell-suppressive activity conferred by FOXP3, both in vitro and in a murine model of autoimmune diabetes in vivo. We conclude that FOXP3-mediated suppressor function requires dimerization through the forkhead domain and that mutations in the dimer interface can lead to the systemic autoimmunity observed in IPEX patients.
C1 [Bandukwala, Hozefa S.; Barboza, Bianca; Ghosh, Srimoyee; Rao, Anjana] Childrens Hosp, Program Cellular & Mol Med, Boston, MA 02115 USA.
[Wu, Yongqing; Chen, Yongheng; Stroud, James C.; Chen, Lin] Univ So Calif, Norris Comprehens Canc Ctr, Dept Chem, Dept Biol Sci, Los Angeles, CA 90089 USA.
[Bandukwala, Hozefa S.; Feuerer, Markus; Ghosh, Srimoyee; Benoist, Christophe; Mathis, Diane; Rao, Anjana] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Bandukwala, Hozefa S.; Barboza, Bianca; Ghosh, Srimoyee; Rao, Anjana] Childrens Hosp, Immune Dis Inst, Boston, MA 02115 USA.
[Bandukwala, Hozefa S.] Childrens Hosp, Dept Pediat, Boston, MA 02115 USA.
RP Rao, A (reprint author), La Jolla Inst Allergy & Immunol, La Jolla, CA 92037 USA.
EM arao@liai.org; linchen@usc.edu
RI Stroud, James/B-3230-2012
OI Stroud, James/0000-0003-0850-4812
FU NIH [AI48213, AI44432, CA42471, AI40127, RO1 GM077320, GM064642, T32];
Juvenile Diabetes Research Foundation [17-2010-421, 16-2007-427]; Lady
Tata Memorial Trust; GlaxoSmithKline-Immune Disease Institute Alliance
FX We thank M.K. Levings and A.N. McMurchy for discussions and for sharing
their findings regarding the IPEX mutations investigated in this study,
the USC NanoBiophysics Core facility for the MALS study, ALS BCSB staff
members C. Ralston, P. Zwart, and K. Royal for help with data
collection, and N. Neamati for help with FRET studies. This work was
supported by NIH grants AI48213, AI44432, CA42471, and AI40127 and
Juvenile Diabetes Research Foundation grants 17-2010-421 and 16-2007-427
(to A.R.) and NIH grants RO1 GM077320 and GM064642 (to L.C.). H.S.B. was
supported by a postdoctoral fellowship from the Lady Tata Memorial Trust
and currently by a postdoctoral fellowship from the
GlaxoSmithKline-Immune Disease Institute Alliance. S.G. is supported by
an NIH postdoctoral training grant (T32).
NR 48
TC 48
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U1 1
U2 12
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
J9 IMMUNITY
JI Immunity
PD APR 22
PY 2011
VL 34
IS 4
BP 479
EP 491
DI 10.1016/j.immuni.2011.02.017
PG 13
WC Immunology
SC Immunology
GA 761AQ
UT WOS:000290367300008
PM 21458306
ER
PT J
AU Smith, BA
Goldberg, NRS
Meshul, CK
AF Smith, Beth A.
Goldberg, Natalie R. S.
Meshul, Charles K.
TI Effects of treadmill exercise on behavioral recovery and neural changes
in the substantia nigra and striatum of the
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned mouse
SO BRAIN RESEARCH
LA English
DT Article
DE Tyrosine hydroxylase; Dopamine; Dopamine transporter; MPTP; Parkinson's
disease; Exercise
ID PARKINSONS-DISEASE; NEUROCHEMICAL DEFICITS; MOTOR INCOORDINATION;
CELL-PROLIFERATION; PHYSICAL-ACTIVITY; BASAL GANGLIA; MODEL; DOPAMINE;
MPTP; MICE
AB Our goal was to extend our understanding of the neural changes behind motor recovery with treadmill exercise in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mouse. We determined the extent of dopamine (DA) terminal changes using Western immunoblotting [striatal dopamine transporter (DAT) and tyrosine hydroxylase (TH)] and alterations in the mean number of DA cells/section by immunohistochemistry and Nissl staining [TH-labeled cells and thionin-stained cells in the substantia nigra pars compacta (SN-PC)]. We measured recovery of gait performance and amount of spontaneous physical activity using the parallel rod activity chamber (PRAC). We hypothesized that the decrease in TH-labeled neurons in the SN-PC due to MPTP will be partially reversed by treadmill exercise, leading to recovery of motor behavior as measured by the PRAC. Following MPTP or vehicle administration, mice ran on the treadmill for 1h/day at 18 cm/s, 5 days/week. Results showed that treadmill exercise improves gait performance and increases physical activity while promoting increased protein expression of striatal DAT and TH. Exercise was effective for all mice; however, effects of early treadmill-based intervention appear to have an additional and unique benefit in mice who received MPTP. We are the first to show that, even following a nearly 50% decrease in the mean number of TH-labeled neurons/section in the SN-PC following MPTP, treadmill exercise leads to an increase of neurons in the SN-PC and improved motor behavior. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Smith, Beth A.] Oregon Hlth & Sci Univ, Dept Neurol, Balance Disorders Lab, Beaverton, OR 97006 USA.
[Smith, Beth A.] Oregon Hlth & Sci Univ, Dept Behav Neurosci, Balance Disorders Lab, Beaverton, OR 97006 USA.
[Goldberg, Natalie R. S.; Meshul, Charles K.] Oregon Hlth & Sci Univ, Dept Behav Neurosci & Pathol, Portland, OR 97239 USA.
[Goldberg, Natalie R. S.; Meshul, Charles K.] Portland VA Med Ctr, Electron Microscopy Facil, Portland, OR 97239 USA.
RP Smith, BA (reprint author), Oregon Hlth & Sci Univ, Dept Neurol, Balance Disorders Lab, West Campus,505 NW 185th Ave, Beaverton, OR 97006 USA.
EM smitbeth@ohsu.edu; natalie.r.sashkin@gmail.com; meshulc@ohsu.edu
RI Smith, Beth/D-2914-2014
OI Smith, Beth/0000-0003-2531-5394
FU NIA [2T32AG023477-06]; Department of Veterans Affairs
FX Beth A. Smith is currently supported on NIA 2T32AG023477-06 (H.
Urbanski, PI). This work was further supported by the Department of
Veterans Affairs Merit Review Program (to Charles K. Meshul). The
authors have no conflicts of interest to disclose. The funding sources
provided funds only and did not have any role in the research.
NR 57
TC 25
Z9 25
U1 0
U2 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD APR 22
PY 2011
VL 1386
BP 70
EP 80
DI 10.1016/j.brainres.2011.02.003
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 755TD
UT WOS:000289958700008
PM 21315689
ER
PT J
AU Huang, KHG
Goedhals, D
Carlson, JM
Brockman, MA
Mishra, S
Brumme, ZL
Hickling, S
Tang, CSW
Miura, T
Seebregts, C
Heckerman, D
Ndung'u, T
Walker, B
Klenerman, P
Steyn, D
Goulder, P
Phillips, R
van Vuuren, C
Frater, J
AF Huang, Kuan-Hsiang Gary
Goedhals, Dominique
Carlson, Jonathan M.
Brockman, Mark A.
Mishra, Swati
Brumme, Zabrina L.
Hickling, Stephen
Tang, Christopher S. W.
Miura, Toshiyuki
Seebregts, Chris
Heckerman, David
Ndung'u, Thumbi
Walker, Bruce
Klenerman, Paul
Steyn, Dewald
Goulder, Philip
Phillips, Rodney
van Vuuren, Cloete
Frater, John
CA Bloemfontein-Oxford Collaborative
TI Progression to AIDS in South Africa Is Associated with both Reverting
and Compensatory Viral Mutations
SO PLOS ONE
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; T-CELL RESPONSES; IMMUNE ESCAPE; HIV-1
GAG; CLASS-I; RESISTANCE MUTATIONS; REPLICATION CAPACITY; LYMPHOCYTE
RESPONSE; MAJOR DETERMINANTS; SET-POINT
AB We lack the understanding of why HIV-infected individuals in South Africa progress to AIDS. We hypothesised that in end-stage disease there is a shifting dynamic between T cell imposed immunity and viral immune escape, which, through both compensatory and reverting viral mutations, results in increased viral fitness, elevated plasma viral loads and disease progression. We explored how T cell responses, viral adaptation and viral fitness inter-relate in South African cohorts recruited from Bloemfontein, the Free State (n = 278) and Durban, KwaZulu-Natal (n = 775). Immune responses were measured by gamma-interferon ELISPOT assays. HLA-associated viral polymorphisms were determined using phylogenetically corrected techniques, and viral replication capacity (VRC) was measured by comparing the growth rate of gag-protease recombinant viruses against recombinant NL4-3 viruses. We report that in advanced disease (CD4 counts <100 cells/mu l), T cell responses narrow, with a relative decline in Gag-directed responses (p<0.0001). This is associated with preserved selection pressure at specific viral amino acids (e. g., the T242N polymorphism within the HLA-B*57/5801 restricted TW10 epitope), but with reversion at other sites (e.g., the T186S polymorphism within the HLA-B*8101 restricted TL9 epitope), most notably in Gag and suggestive of "immune relaxation''. The median VRC from patients with CD4 counts <100 cells/mu l was higher than from patients with CD4 counts >= 500 cells/mu l (91.15% versus 85.19%, p = 0.0004), potentially explaining the rise in viral load associated with disease progression. Mutations at HIV Gag T186S and T242N reduced VRC, however, in advanced disease only the T242N mutants demonstrated increasing VRC, and were associated with compensatory mutations (p = 0.013). These data provide novel insights into the mechanisms of HIV disease progression in South Africa. Restoration of fitness correlates with loss of viral control in late disease, with evidence for both preserved and relaxed selection pressure across the HIV genome. Interventions that maintain viral fitness costs could potentially slow progression.
C1 [Huang, Kuan-Hsiang Gary; Mishra, Swati; Hickling, Stephen; Tang, Christopher S. W.; Klenerman, Paul; Phillips, Rodney; Frater, John] Univ Oxford, Nuffield Dept Clin Med, Oxford, England.
[Goedhals, Dominique; Steyn, Dewald; van Vuuren, Cloete] Univ Free State, Bloemfontein, South Africa.
[Goedhals, Dominique] NHLS, Johannesburg, South Africa.
[Carlson, Jonathan M.; Heckerman, David] Microsoft Res, ESci Grp, Los Angeles, CA USA.
[Brockman, Mark A.; Brumme, Zabrina L.] Simon Fraser Univ, Burnaby, BC V5A 1S6, Canada.
[Brockman, Mark A.; Brumme, Zabrina L.] British Columbia Ctr Excellence HIV AIDS, Vancouver, BC, Canada.
[Brockman, Mark A.; Brumme, Zabrina L.; Miura, Toshiyuki] Harvard Univ, Ragon Inst, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Brockman, Mark A.; Brumme, Zabrina L.; Miura, Toshiyuki; Walker, Bruce] MIT, Boston, MA USA.
[Miura, Toshiyuki] Univ Tokyo, Inst Med Sci, Tokyo, Japan.
[Seebregts, Chris] MRC, Biomed Informat Res Div, Cape Town, South Africa.
[Ndung'u, Thumbi; Walker, Bruce] Univ KwaZulu Natal, HIV Pathogenesis Programme, Doris Duke Med Res Inst, Durban, South Africa.
[Walker, Bruce] Harvard Univ, Div AIDS, Boston, MA 02115 USA.
[Goulder, Philip] Univ Oxford, Dept Paediat, Oxford, England.
[Huang, Kuan-Hsiang Gary; Phillips, Rodney] James Martin 21st Century Sch, Oxford, England.
[Klenerman, Paul; Phillips, Rodney; Frater, John] Oxford NIHR Biomed Res Ctr, Oxford, England.
RP Huang, KHG (reprint author), Univ Oxford, Nuffield Dept Clin Med, Oxford, England.
EM john.frater@ndm.ox.ac.uk
OI Ndung'u, Thumbi/0000-0003-2962-3992; Brockman, Mark/0000-0001-6432-1426
FU James Martin 21st Century School; Medical Research Council; Wellcome
Trust; NIHR Biomedical Research Centre; Canadian Institutes for Health
Research (CIHR); International Development Research Centre (IDRC),
Canada
FX K-HGH is supported by the James Martin 21st Century School. JF is funded
by the Medical Research Council. RP, PG and PK are supported by the
Wellcome Trust. JF and PK are funded by NIHR Biomedical Research Centre
Programme. ZLB is funded by the Canadian Institutes for Health Research
(CIHR). The collection and analysis of 43 Free State sequences was
funded by a grant from the ACACIA and Connectivity Africa programmes of
the International Development Research Centre (IDRC), Canada. The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 41
TC 36
Z9 36
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 22
PY 2011
VL 6
IS 4
AR e19018
DI 10.1371/journal.pone.0019018
PG 20
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 756MO
UT WOS:000290015800032
PM 21544209
ER
PT J
AU Moldovan, GL
D'Andrea, AD
AF Moldovan, George-Lucian
D'Andrea, Alan D.
TI DNA Damage Discrimination at Stalled Replication Forks by the Rad5
Homologs HLTF and SHPRH
SO MOLECULAR CELL
LA English
DT Editorial Material
ID CELL NUCLEAR ANTIGEN; TRANSLESION SYNTHESIS; GENOMIC INSTABILITY;
UBIQUITIN; PCNA; POLYUBIQUITINATION; LIGASE; REPAIR; YEAST
AB In this issue of Molecular Cell, Lin et al. (2011) describe how HLTF and SHPRH, the human homologs of yeast Rad5, can discriminate between MMS-induced versus UV-induced DNA damage. The results have important implications for the suppression of damage-specific mutagenesis and for the maintenance of genomic stability.
C1 [Moldovan, George-Lucian; D'Andrea, Alan D.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA.
RP D'Andrea, AD (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Radiat Oncol, 44 Binney St, Boston, MA 02115 USA.
EM alan_dandrea@dfci.harvard.edu
OI George-Lucian, Moldovan/0000-0003-3825-149X
FU NHLBI NIH HHS [R37 HL052725]; NIDDK NIH HHS [R01 DK043889]
NR 10
TC 3
Z9 3
U1 0
U2 2
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1097-2765
J9 MOL CELL
JI Mol. Cell
PD APR 22
PY 2011
VL 42
IS 2
BP 141
EP 143
DI 10.1016/j.molcel.2011.03.018
PG 3
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 754RF
UT WOS:000289873700002
PM 21504827
ER
PT J
AU Tao, RY
Wei, D
Gao, HL
Liu, YL
DePinho, RA
Dong, XC
AF Tao, Rongya
Wei, Dan
Gao, Hanlin
Liu, Yunlong
DePinho, Ronald A.
Dong, X. Charlie
TI Hepatic FoxOs Regulate Lipid Metabolism via Modulation of Expression of
the Nicotinamide Phosphoribosyltransferase Gene
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID FATTY-ACID OXIDATION; TRANSCRIPTION FACTOR FOXO1; ACTIVATED
PROTEIN-KINASE; FORKHEAD BOX O1; INSULIN ACTION; MITOCHONDRIAL-FUNCTION;
DEPENDENT REGULATION; BIOSYNTHETIC ENZYME; HISTONE DEACETYLASE; LYSINE
ACETYLATION
AB FoxO transcription factors have been implicated in lipid metabolism; however, the underlying mechanisms are not well understood. Here, in an effort to elucidate such mechanisms, we examined the phenotypic consequences of liver-specific deletion of three members of the FoxO family: FoxO1, FoxO3, and FoxO4. These liver-specific triply null mice, designated LTKO, exhibited elevated triglycerides in the liver on regular chow diet. More remarkably, LTKO mice developed severe hepatic steatosis following placement on a high fat diet. Further analyses revealed that hepatic NAD(+) levels and Sirt1 activity were decreased in the liver of the LTKO mice relative to controls. At the mechanistic level, expression profile analyses showed that LTKO livers had significantly down-regulated expression of the nicotinamide phosphoribosyltransferase (Nampt) gene encoding the rate-limiting enzyme in the salvage pathway of NAD(+) biosynthesis. Luciferase reporter assays and chromatin immunoprecipitation analyses demonstrated that Nampt is a transcriptional target gene of FoxOs. Significantly, overexpression of Nampt gene reduced, whereas knockdown increased, hepatic triglyceride levels in vitro and in vivo. Thus, FoxOs control the Nampt gene expression and the NAD(+) signaling in the regulation of hepatic triglyceride homeostasis.
C1 [Tao, Rongya; Wei, Dan; Dong, X. Charlie] Indiana Univ Sch Med, Ctr Med Genom, Dept Biochem & Mol Biol, Ctr Computat Biol & Bioinformat, Indianapolis, IN 46202 USA.
[Liu, Yunlong] Indiana Univ Sch Med, Ctr Med Genom, Dept Med & Mol Genet, Ctr Computat Biol & Bioinformat, Indianapolis, IN 46202 USA.
[Gao, Hanlin] City Hope Natl Med Ctr, Beckman Res Inst, Dept Canc Biol, Duarte, CA 91010 USA.
[DePinho, Ronald A.] Dana Farber Canc Inst, Belfer Inst Appl Canc Sci, Boston, MA 02115 USA.
[DePinho, Ronald A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[DePinho, Ronald A.] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[DePinho, Ronald A.] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
RP Dong, XC (reprint author), Indiana Univ Sch Med, Ctr Med Genom, Dept Biochem & Mol Biol, Ctr Computat Biol & Bioinformat, 635 Barnhill Dr,MS1021D, Indianapolis, IN 46202 USA.
EM xcdong@iupui.edu
RI tao, rongya/B-8042-2014
OI tao, rongya/0000-0002-3316-5587
FU NIDDK [R00DK077505]
FX This work was supported, in whole or in part, by National Institutes of
Health Grant R00DK077505 from the NIDDK.
NR 90
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Z9 56
U1 2
U2 10
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 APR 22
PY 2011
VL 286
IS 16
BP 14681
EP 14690
DI 10.1074/jbc.M110.201061
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 750NW
UT WOS:000289556200087
PM 21388966
ER
PT J
AU Haberer, JE
Cook, A
Walker, AS
Ngambi, M
Ferrier, A
Mulenga, V
Kityo, C
Thomason, M
Kabamba, D
Chintu, C
Gibb, DM
Bangsberg, DR
AF Haberer, Jessica E.
Cook, Adrian
Walker, A. Sarah
Ngambi, Marjorie
Ferrier, Alex
Mulenga, Veronica
Kityo, Cissy
Thomason, Margaret
Kabamba, Desiree
Chintu, Chifumbe
Gibb, Diana M.
Bangsberg, David R.
TI Excellent Adherence to Antiretrovirals in HIV plus Zambian Children Is
Compromised by Disrupted Routine, HIV Nondisclosure, and Paradoxical
Income Effects
SO PLOS ONE
LA English
DT Article
ID THERAPY ADHERENCE; IMMUNOLOGICAL OUTCOMES; MEDICATION ADHERENCE; VIRAL
SUPPRESSION; INFECTED CHILDREN; TRIAL; DISCLOSURE; HISTORY; AFRICA
AB Introduction: A better understanding of pediatric antiretroviral therapy (ART) adherence in sub-Saharan Africa is necessary to develop interventions to sustain high levels of adherence.
Methodology/Principal Findings: Adherence among 96 HIV-infected Zambian children (median age 6, interquartile range [IQR] 2,9) initiating fixed-dose combination ART was measured prospectively (median 23 months; IQR 20,26) with caregiver report, clinic and unannounced home-based pill counts, and medication event monitoring systems (MEMS). HIV-1 RNA was determined at 48 weeks. Child and caregiver characteristics, socio-demographic status, and treatment-related factors were assessed as predictors of adherence. Median adherence was 97.4% (IQR 96.1,98.4%) by visual analog scale, 94.8% (IQR 86,100%) by caregiver-reported last missed dose, 96.9% (IQR 94.5,98.2%) by clinic pill count, 93.4% (IQR 90.2,96.7%) by unannounced home-based pill count, and 94.8% (IQR 87.8,97.7%) by MEMS. At 48 weeks, 72.6% of children had HIV-1 RNA < 50 copies/ml. Agreement among adherence measures was poor; only MEMS was significantly associated with viral suppression (p = 0.013). Predictors of poor adherence included changing residence, school attendance, lack of HIV disclosure to children aged nine to 15 years, and increasing household income.
Conclusions/Significance: Adherence among children taking fixed-dose combination ART in sub-Saharan Africa is high and sustained over two years. However, certain groups are at risk for treatment failure, including children with disrupted routines, no knowledge of their HIV diagnosis among older children, and relatively high household income, possibly reflecting greater social support in the setting of greater poverty.
C1 [Haberer, Jessica E.; Bangsberg, David R.] Massachusetts Gen Hosp, Ctr Global Hlth, Boston, MA 02114 USA.
[Cook, Adrian; Walker, A. Sarah; Ferrier, Alex; Thomason, Margaret; Gibb, Diana M.] MRC, Clin Trials Unit, London, England.
[Ngambi, Marjorie; Mulenga, Veronica; Kabamba, Desiree; Chintu, Chifumbe] Univ Teaching Hosp, Lusaka, Zambia.
[Kityo, Cissy] Joint Clin Res Ctr, Kampala, Uganda.
RP Haberer, JE (reprint author), Massachusetts Gen Hosp, Ctr Global Hlth, Boston, MA 02114 USA.
EM jhaberer@partners.org
FU European and Developing Countries Clinical Trials Partnership (EDCTP)
[EDCTP 2004.01.H.d2.33011]; US National Institute of Mental Health
[K23-87228, K24-87227]; Mark and Lisa Schwartz Foundation
FX CHAPAS-1 is funded by the European and Developing Countries Clinical
Trials Partnership (EDCTP 2004.01.H.d2.33011). Cipla Ltd donated the
first-line drugs. Drs. Haberer and Bangsberg are supported by the US
National Institute of Mental Health (K23-87228 and K24-87227,
respectively) and the Mark and Lisa Schwartz Foundation. The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 32
TC 39
Z9 39
U1 1
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 21
PY 2011
VL 6
IS 4
AR e18505
DI 10.1371/journal.pone.0018505
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 756ME
UT WOS:000290014500006
PM 21533031
ER
PT J
AU de Jong, JLO
Burns, CE
Chen, AT
Pugach, E
Mayhall, EA
Smith, ACH
Feldman, HA
Zhou, Y
Zon, LI
AF de Jong, Jill L. O.
Burns, Caroline Erter
Chen, Aye T.
Pugach, Emily
Mayhall, Elizabeth A.
Smith, Alexandra C. H.
Feldman, Henry A.
Zhou, Yi
Zon, Leonard I.
TI Characterization of immune-matched hematopoietic transplantation in
zebrafish
SO BLOOD
LA English
DT Article
ID STEM-CELL ASSAYS; MHC CLASS-I; MUTATIONS; MUTANTS; LINEAGE; SYSTEM; VIVO
AB Evaluating hematopoietic stem cell (HSC) function in vivo requires a long-term transplantation assay. Although zebrafish are a powerful model for discovering the genetics of hematopoiesis, hematopoietic transplantation approaches have been underdeveloped. Here we established a long-term reconstitution assay in adult zebrafish. Primary and secondary recipients showed multilineage engraftment at 3 months after transplantation. Limiting dilution data suggest that at least 1 in 65 000 zebrafish marrow cells contain re-populating activity, consistent with mammalian HSC frequencies. We defined zebrafish haplotypes at the proposed major histocompatibility complex locus on chromosome 19 and tested functional significance through hematopoietic transplantation. Matching donors and recipients dramatically increased engraftment and percentage donor chimerism compared with unmatched fish. These data constitute the first functional test of zebrafish histocompatibility genes, enabling the development of matched hematopoietic transplantations. This lays the foundation for competitive transplantation experiments with mutant zebrafish HSCs and chemicals to test for effects on engraftment, thereby providing a model for human hematopoietic diseases and treatments not previously available. (Blood. 2011;117(16):4234-4242)
C1 [de Jong, Jill L. O.; Burns, Caroline Erter; Chen, Aye T.; Pugach, Emily; Mayhall, Elizabeth A.; Smith, Alexandra C. H.; Zhou, Yi; Zon, Leonard I.] Harvard Univ, Sch Med, Childrens Hosp Boston, Div Hematol Oncol,Harvard Stem Cell Inst, Boston, MA 02115 USA.
[de Jong, Jill L. O.; Burns, Caroline Erter; Chen, Aye T.; Pugach, Emily; Mayhall, Elizabeth A.; Smith, Alexandra C. H.; Zhou, Yi; Zon, Leonard I.] Harvard Univ, Sch Med, Stem Cell Program, Harvard Stem Cell Inst, Boston, MA 02115 USA.
[de Jong, Jill L. O.; Burns, Caroline Erter; Chen, Aye T.; Pugach, Emily; Mayhall, Elizabeth A.; Smith, Alexandra C. H.; Zhou, Yi; Zon, Leonard I.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Harvard Stem Cell Inst,Howard Hughes Med Inst, Boston, MA 02115 USA.
[Feldman, Henry A.] Childrens Hosp Boston, Clin Res Program, Boston, MA USA.
RP Zon, LI (reprint author), Harvard Univ, Sch Med, Childrens Hosp Boston, Div Hematol Oncol,Harvard Stem Cell Inst, 1 Blackfan Cir,Karp Bldg,7th Fl, Boston, MA 02115 USA.
EM zon@enders.tch.harvard.edu
FU National Institute of Diabetes and Digestive and Kidney Diseases
[1K01DK067179, 5K08DK074595]; Harvard Clinical and Translational Science
Center (Catalyst; National Institutes of Health) [UL1 RR-025758]; Howard
Hughes Medical Institute; National Institutes of Health (National Heart,
Lung, and Blood Institute) [5R01HL48801-13]
FX This work was supported by the National Institute of Diabetes and
Digestive and Kidney Diseases (Career Development Award 1K01DK067179, C.
E. B.; and Career Development Award 5K08DK074595, J.L. O.d.J.). H. A. F.
was supported by the Harvard Clinical and Translational Science Center
(Catalyst; National Institutes of Health UL1 RR-025758). L.I.Z. is
supported by Howard Hughes Medical Institute and the National Institutes
of Health (National Heart, Lung, and Blood Institute grant
5R01HL48801-13).
NR 25
TC 20
Z9 20
U1 0
U2 3
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 APR 21
PY 2011
VL 117
IS 16
BP 4234
EP 4242
DI 10.1182/blood-2010-09-307488
PG 9
WC Hematology
SC Hematology
GA 753VK
UT WOS:000289807600013
PM 21346254
ER
PT J
AU Ouyang, J
Juszczynski, P
Rodig, SJ
Green, MR
O'Donnell, E
Currie, T
Armant, M
Takeyama, K
Monti, S
Rabinovich, GA
Ritz, J
Kutok, JL
Shipp, MA
AF Ouyang, Jing
Juszczynski, Przemyslaw
Rodig, Scott J.
Green, Michael R.
O'Donnell, Evan
Currie, Treeve
Armant, Myriam
Takeyama, Kunihiko
Monti, Stefano
Rabinovich, Gabriel A.
Ritz, Jerome
Kutok, Jeffery L.
Shipp, Margaret A.
TI Viral induction and targeted inhibition of galectin-1 in EBV+
posttransplant lymphoproliferative disorders
SO BLOOD
LA English
DT Article
ID EPSTEIN-BARR-VIRUS; LATENT MEMBRANE PROTEIN-1; B-CELL-LYMPHOMA;
NF-KAPPA-B; HODGKIN LYMPHOMA; C-JUN; GLYCAN INTERACTIONS; CLASSICAL
HODGKIN; IMMUNE PRIVILEGE; STERNBERG CELLS
AB Posttransplant lymphoproliferative disorders (PTLDs) are potentially fatal, EBV-driven B-cell malignancies that develop in immunocompromised solid organ or hematopoietic stem cell recipients. In PTLD, the expression of EBV proteins, including latent membrane protein 1 (LMP1) and LMP2A, viral immune evasion strategies, and impaired host immune surveillance foster the proliferation of EBV-transformed B cells. Current PTLD treatment strategies include reduction of immunosuppression, which increases the risk of graft rejection, anti-CD20 treatment, combination chemotherapy, and administration of EBV-specific cytotoxic T cells. In the present study, we report that EBV-transformed lymphoblastoid B-cell lines (LCLs) and primary PTLDs over-express galectin-1 (Gal1), a carbohydrate-binding lectin that induces tolerogenic dendritic cells and triggers the selective apoptosis of CD4(+) Th1 and Th17 cells and cytotoxic T cells. In transcriptional reporter assays, LMP2A and LMP1 each increased Gal1-driven luciferase expression, and the combination of LMP2A and LMP1 was additive. In addition, small interfering RNA (siRNA)-mediated depletion of LMP2A decreased Gal1 protein abundance in EBV-transformed LCLs. Gal1 expression in LCLs was dependent on both activating protein 1 (AP-1) and PI3K. Anewly developed neutralizing Gal1 mAb selectively inhibited Gal1-mediated apoptosis of EBV-specific CD8(+) T cells. Given the tolerogenic and immunosuppressive function of Gal1, antibody-mediated Gal1 neutralization may represent a novel immunotherapeutic strategy for PTLD and other Gal1-expressing tumors. (Blood. 2011;117(16):4315-4322)
C1 [Ouyang, Jing; Juszczynski, Przemyslaw; Green, Michael R.; O'Donnell, Evan; Takeyama, Kunihiko; Ritz, Jerome; Shipp, Margaret A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
[Rodig, Scott J.; Currie, Treeve; Kutok, Jeffery L.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Armant, Myriam] Harvard Univ, Sch Med, Ctr Human Cell Therapy, Immune Dis Inst, Boston, MA USA.
[Monti, Stefano] Broad Inst, Cambridge, MA USA.
[Rabinovich, Gabriel A.] Consejo Nacl Invest Cient & Tecn, Inst Biol & Med Expt, Lab Inmunopatol, Buenos Aires, DF, Argentina.
RP Shipp, MA (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 450 Brookline Ave, Boston, MA 02215 USA.
EM margaret_shipp@dfci.harvard.edu
RI Selerski, Marcin/A-7594-2012; Green, Michael/F-3482-2013;
OI Green, Michael/0000-0001-6309-9472; Monti, Stefano/0000-0002-9376-0660;
Ritz, Jerome/0000-0001-5526-4669
FU Leukemia & Lymphoma Society; Miller Family Research Fund
FX This work was supported by funding from the Leukemia & Lymphoma Society
and from the Miller Family Research Fund.
NR 41
TC 24
Z9 24
U1 0
U2 11
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 APR 21
PY 2011
VL 117
IS 16
BP 4315
EP 4322
DI 10.1182/blood-2010-11-320481
PG 8
WC Hematology
SC Hematology
GA 753VK
UT WOS:000289807600021
PM 21300977
ER
PT J
AU Fearing, MK
Israel, EJ
Sahai, I
Rapalino, O
Lisovsky, M
AF Fearing, Marsha Kay
Israel, Esther J.
Sahai, Inderneel
Rapalino, Otto
Lisovsky, Mikhail
TI Case 12-2011: A 9-Month-Old Boy with Acute Liver Failure Microvesicular
hepatic steatosis due to CACT deficiency
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID SJOGREN-LARSSON-SYNDROME; MAGNETIC-RESONANCE SPECTROSCOPY;
ZELLWEGER-SYNDROME; MR SPECTROSCOPY; MYELINATION; DISORDERS; DIAGNOSIS;
DISEASE; BRAIN; DEATH
C1 [Fearing, Marsha Kay; Israel, Esther J.; Sahai, Inderneel] Massachusetts Gen Hosp, Serv Pediat, Boston, MA 02114 USA.
[Rapalino, Otto] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Fearing, Marsha Kay; Israel, Esther J.; Sahai, Inderneel] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
[Rapalino, Otto] Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02115 USA.
[Lisovsky, Mikhail] Dartmouth Hitchcock Med Ctr, Dept Pathol, Lebanon, NH 03766 USA.
[Lisovsky, Mikhail] Dartmouth Coll, Hitchcock Med Ctr, Dartmouth Med Sch, Dept Pathol, Hanover, NH 03756 USA.
RP Fearing, MK (reprint author), Massachusetts Gen Hosp, Serv Pediat, Boston, MA 02114 USA.
NR 42
TC 2
Z9 2
U1 0
U2 2
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD APR 21
PY 2011
VL 364
IS 16
BP 1545
EP 1556
PG 12
WC Medicine, General & Internal
SC General & Internal Medicine
GA 752VH
UT WOS:000289722700014
PM 21506744
ER
PT J
AU Frakt, A
Carroll, AE
Pollack, HA
Reinhardt, U
AF Frakt, Austin
Carroll, Aaron E.
Pollack, Harold A.
Reinhardt, Uwe
TI Our Flawed but Beneficial Medicaid Program
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
ID MORTALITY
C1 [Frakt, Austin] VA Boston Healthcare Syst, Hlth Care Financing & Econ, Boston, MA USA.
[Frakt, Austin] Boston Univ, Boston, MA 02215 USA.
[Carroll, Aaron E.] Indiana Univ, Sch Med, Ctr Hlth Policy & Professionalism Res, Indianapolis, IN USA.
[Pollack, Harold A.] Univ Chicago, Sch Social Serv Adm, Chicago, IL 60637 USA.
[Reinhardt, Uwe] Princeton Univ, Woodrow Wilson Sch Publ & Int Affairs, Princeton, NJ 08544 USA.
RP Frakt, A (reprint author), VA Boston Healthcare Syst, Hlth Care Financing & Econ, Boston, MA USA.
RI Pollack, Harold/A-1166-2007
NR 5
TC 11
Z9 11
U1 0
U2 2
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD APR 21
PY 2011
VL 364
IS 16
DI 10.1056/NEJMp1103168
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 752VH
UT WOS:000289722700004
PM 21470001
ER
PT J
AU Depauw, N
Seco, J
AF Depauw, Nicolas
Seco, Joao
TI Sensitivity study of proton radiography and comparison with kV and MV
x-ray imaging using GEANT4 Monte Carlo simulations
SO PHYSICS IN MEDICINE AND BIOLOGY
LA English
DT Article
ID MULTIPLE COULOMB SCATTERING; COMPUTED-TOMOGRAPHY; THERAPY; RESOLUTION;
TOOLKIT; DENSITY
AB The imaging sensitivity of proton radiography has been studied and compared with kV and MV x-ray imaging using Monte Carlo simulations. A phantom was specifically modeled using 21 different material inserts with densities ranging from 0.001 to 1.92 g cm(-3). These simulations were run using the MGH double scattered proton beam, scanned pencil proton beams from 200 to 490 MeV, as well as pure 50 keV, 100 keV, 1MeV and 2MeV gamma x-ray beams. In order to compare the physics implied in both proton and photon radiography without being biased by the current state of the art in detector technology, the detectors were considered perfect. Along with spatial resolution, the contrast-to-noise ratio was evaluated and compared for each material. These analyses were performed using radiographic images that took into account the following: only primary protons, both primary and secondary protons, and both contributions while performing angular and energetic cuts. Additionally, tissue-to-tissue contrasts in an actual lung cancer patient case were studied for simulated proton radiographs and compared against the original kV x-ray image which corresponds to the current patient set-up image in the proton clinic. This study highlights the poorer spatial resolution of protons versus x-rays for radiographic imaging purposes, and the excellent density resolution of proton radiography. Contrasts around the tumor are higher using protons in a lung cancer patient case. The high-density resolution of proton radiography is of great importance for specific tumor diagnostics, such as in lung cancer, where x-ray radiography operates poorly. Furthermore, the use of daily proton radiography prior to proton therapy would ameliorate patient set-up while reducing the absorbed dose delivered through imaging.
C1 [Depauw, Nicolas; Seco, Joao] Massachusetts Gen Hosp, Dept Radiat Oncol, Francis H Burr Proton Therapy Ctr, Boston, MA 02114 USA.
RP Depauw, N (reprint author), Massachusetts Gen Hosp, Dept Radiat Oncol, Francis H Burr Proton Therapy Ctr, Boston, MA 02114 USA.
EM ndepauw@partners.org
RI Seco, Joao/J-4451-2012
NR 20
TC 23
Z9 23
U1 0
U2 4
PU IOP PUBLISHING LTD
PI BRISTOL
PA DIRAC HOUSE, TEMPLE BACK, BRISTOL BS1 6BE, ENGLAND
SN 0031-9155
J9 PHYS MED BIOL
JI Phys. Med. Biol.
PD APR 21
PY 2011
VL 56
IS 8
BP 2407
EP 2421
DI 10.1088/0031-9155/56/8/006
PG 15
WC Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging
SC Engineering; Radiology, Nuclear Medicine & Medical Imaging
GA 749PL
UT WOS:000289480700007
PM 21427482
ER
PT J
AU Trott, CM
Wayth, RB
Macquart, JPR
Tingay, SJ
AF Trott, Cathryn M.
Wayth, Randall B.
Macquart, Jean-Pierre R.
Tingay, Steven J.
TI SOURCE DETECTION IN INTERFEROMETRIC VISIBILITY DATA. I. FUNDAMENTAL
ESTIMATION LIMITS
SO ASTROPHYSICAL JOURNAL
LA English
DT Article
DE methods: statistical; radio continuum: general; techniques:
interferometric
ID ARRAY; CALIBRATION; SKY; PRECISION; CATALOG
AB Transient radio signals of astrophysical origin present an avenue for studying the dynamic universe. With the next generation of radio interferometers being planned and built, there is great potential for detecting and studying large samples of radio transients. Currently used image-based techniques for detecting radio sources have not been demonstrated to be optimal, and there is a need for development of more sophisticated algorithms and methodology for comparing different detection techniques. A visibility-space detector benefits from our good understanding of visibility-space noise properties and does not suffer from the image artifacts and need for deconvolution in image-space detectors. In this paper, we propose a method for designing optimal source detectors using visibility data, building on statistical decision theory. The approach is substantially different to conventional radio astronomy source detection. Optimal detection requires an accurate model for the data, and we present a realistic model for the likelihood function of radio interferometric data, including the effects of calibration, signal confusion, and atmospheric phase fluctuations. As part of this process, we derive fundamental limits on the calibration of an interferometric array, including the case where many relatively weak "in-beam" calibrators are used. These limits are then applied, along with a model for atmospheric phase fluctuations, to determine the limits on measuring source position, flux density, and spectral index, in the general case. We then present an optimal visibility-space detector using realistic models for an interferometer.
C1 [Trott, Cathryn M.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Trott, Cathryn M.; Wayth, Randall B.; Macquart, Jean-Pierre R.; Tingay, Steven J.] Curtin Univ Technol, Int Ctr Radio Astron Res, Bentley, WA 6102, Australia.
RP Trott, CM (reprint author), Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
EM ctrott@pet.mgh.harvard.edu
RI Wayth, Randall/B-2444-2013; Trott, Cathryn/B-5325-2013; Tingay,
Steven/B-5271-2013; Macquart, Jean-Pierre/B-5306-2013
OI Wayth, Randall/0000-0002-6995-4131; Trott, Cathryn/0000-0001-6324-1766;
NR 24
TC 12
Z9 12
U1 0
U2 5
PU IOP PUBLISHING LTD
PI BRISTOL
PA DIRAC HOUSE, TEMPLE BACK, BRISTOL BS1 6BE, ENGLAND
SN 0004-637X
J9 ASTROPHYS J
JI Astrophys. J.
PD APR 20
PY 2011
VL 731
IS 2
AR 81
DI 10.1088/0004-637X/731/2/81
PG 14
WC Astronomy & Astrophysics
SC Astronomy & Astrophysics
GA 753MM
UT WOS:000289779600004
ER
PT J
AU Nguyen, PL
Gu, XM
Lipsitz, SR
Choueiri, TK
Choi, WW
Lei, Y
Hoffman, KE
Hu, JC
AF Nguyen, Paul L.
Gu, Xiangmei
Lipsitz, Stuart R.
Choueiri, Toni K.
Choi, Wesley W.
Lei, Yin
Hoffman, Karen E.
Hu, Jim C.
TI Cost Implications of the Rapid Adoption of Newer Technologies for
Treating Prostate Cancer
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID MODULATED RADIATION-THERAPY; SEER-MEDICARE DATA; PROTON-BEAM; TRENDS
AB Purpose
Intensity-modulated radiation therapy (IMRT) and laparoscopic or robotic minimally invasive radical prostatectomy (MIRP) are costlier alternatives to three-dimensional conformal radiation therapy (3D-CRT) and open radical prostatectomy for treating prostate cancer. We assessed temporal trends in their utilization and their impact on national health care spending.
Methods
Using Surveillance, Epidemiology, and End Results-Medicare linked data, we determined treatment patterns for 45,636 men age >= 65 years who received definitive surgery or radiation for localized prostate cancer diagnosed from 2002 to 2005. Costs attributable to prostate cancer care were the difference in Medicare payments in the year after versus the year before diagnosis.
Results
Patients received surgery (26%), external RT (38%), or brachytherapy with or without RT (36%). Among surgical patients, MIRP utilization increased substantially (1.5% among 2002 diagnoses v 28.7% among 2005 diagnoses, P < .001). For RT, IMRT utilization increased substantially (28.7% v 81.7%; P < .001) and for men receiving brachytherapy, supplemental IMRT increased significantly (8.5% v 31.1%; P < .001). The mean incremental cost of IMRT versus 3D-CRT was $10,986 (in 2008 dollars); of brachytherapy plus IMRT versus brachytherapy plus 3D-CRT was $10,789; of MIRP versus open RP was $293. Extrapolating these figures to the total US population results in excess spending of $282 million for IMRT, $59 million for brachytherapy plus IMRT, and $4 million for MIRP, compared to less costly alternatives for men diagnosed in 2005.
Conclusion
Costlier prostate cancer therapies were rapidly and widely adopted, resulting in additional national spending of more than $350 million among men diagnosed in 2005 and suggesting the need for comparative effectiveness research to weigh their costs against their benefits.
C1 [Nguyen, Paul L.] Brigham & Womens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
Brigham & Womens Hosp, Ctr Surg & Publ Hlth, Boston, MA 02115 USA.
Dana Farber Canc Inst, Lank Ctr Genitourinary Oncol, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Boston, MA USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
RP Nguyen, PL (reprint author), Brigham & Womens Hosp, Dana Farber Canc Inst, 75 Francis St, Boston, MA 02115 USA.
EM pnguyen@LROC.harvard.edu
FU Department of Defense [W81XWH-081-0283]; Joint Center for Radiation
Therapy foundation; Robert and Kathy Salipante Minimally Invasive
Urologic Oncology Fellowship
FX Supported by Department of Defense Physician Training Award
W81XWH-081-0283 (J.C.H.), a Joint Center for Radiation Therapy
foundation grant (P.L.N.), and a Robert and Kathy Salipante Minimally
Invasive Urologic Oncology Fellowship (W.W.C.).
NR 22
TC 169
Z9 170
U1 1
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 APR 20
PY 2011
VL 29
IS 12
BP 1517
EP 1524
DI 10.1200/JCO.2010.31.1217
PG 8
WC Oncology
SC Oncology
GA 752SO
UT WOS:000289714600021
PM 21402604
ER
PT J
AU Hahn, NM
Stadler, WM
Zon, RT
Waterhouse, D
Picus, J
Nattam, S
Johnson, CS
Perkins, SM
Waddell, MJ
Sweeney, CJ
AF Hahn, Noah M.
Stadler, Walter M.
Zon, Robin T.
Waterhouse, David
Picus, Joel
Nattam, Sreenivasa
Johnson, Cynthia S.
Perkins, Susan M.
Waddell, Mary Jane
Sweeney, Christopher J.
TI Phase II Trial of Cisplatin, Gemcitabine, and Bevacizumab As First-Line
Therapy for Metastatic Urothelial Carcinoma: Hoosier Oncology Group GU
04-75
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID TRANSITIONAL-CELL CARCINOMA; LONG-TERM-SURVIVAL; BLADDER-CANCER; TUMOR
ANGIOGENESIS; COLORECTAL-CANCER; PLUS GEMCITABINE; BREAST-CANCER;
GROWTH-FACTOR; LUNG-CANCER; PACLITAXEL
AB Purpose
Novel approaches are needed for patients with metastatic urothelial cancer (UC). This trial assessed the efficacy and toxicity of bevacizumab in combination with cisplatin and gemcitabine (CGB) as first-line treatment for patients with metastatic UC.
Patients and Methods Chemotherapy-naive patients with metastatic or unresectable UC received cisplatin 70 mg/m(2) on day 1, gemcitabine 1,000 to 1,250 mg/m(2) on days 1 and 8, and bevacizumab 15 mg/kg on day 1, every 21 days.
Results
Forty-three patients with performance status of 0 (n = 26) or 1 (n = 17) and median age of 66 years were evaluable for toxicity and response. Grade 3 to 4 hematologic toxicity included neutropenia (35%), thrombocytopenia (12%), anemia (12%), and neutropenic fever (2%). Grade 3 to 5 nonhematologic toxicity included deep vein thrombosis/pulmonary embolism (21%), hemorrhage (7%), cardiac (7%), hypertension (5%), and proteinuria (2%). Three treatment-related deaths (CNS hemorrhage, sudden cardiac death, and aortic dissection) were observed. Best response by Response Evaluation Criteria in Solid Tumors was complete response in eight patients (19%) and partial response in 23 patients (53%), for an overall response rate of 72%. Stable disease lasting >= 12 weeks occurred in four patients (9%), and progressive disease occurred in six patients (14%). With a median follow-up of 27.2 months (range, 3.5 to 40.9 months), median progression-free survival (PFS) was 8.2 months (95% CI, 6.8 to 10.3 months) with a median overall survival (OS) time of 19.1 months (95% CI, 12.4 to 22.7 months). The study-defined goal of 50% improvement in PFS was not met.
Conclusion
CGB demonstrates promising OS and antiangiogenic treatment-related toxicities in the phase II setting of metastatic UC. The full risk/benefit profile of CGB in patients with metastatic UC will be determined by an ongoing phase III intergroup trial.
C1 [Hahn, Noah M.] Indiana Univ Melvin & Bren Simon Canc Ctr, Indianapolis, IN 46202 USA.
Indiana Univ Sch Med, Indianapolis, IN USA.
No Indiana Canc Res Consortium, South Bend, IN USA.
Ft Wayne Oncol & Hematol, Ft Wayne, IN USA.
Univ Chicago, Chicago, IL 60637 USA.
Oncol & Hematol Care, Cincinnati, OH USA.
Washington Univ, Sch Med, Barnes Jewish Hosp, Siteman Canc Ctr, St Louis, MO USA.
Washington Univ, St Louis, MO USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Hahn, NM (reprint author), Indiana Univ Melvin & Bren Simon Canc Ctr, Indiana Canc Pavil Room RT445,535 Barnhill Dr, Indianapolis, IN 46202 USA.
EM nhahn@iupui.edu
FU Genentech, South San Francisco, CA
FX Supported by investigator-initiated funds from Genentech, South San
Francisco, CA.
NR 49
TC 99
Z9 100
U1 0
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 APR 20
PY 2011
VL 29
IS 12
BP 1525
EP 1530
DI 10.1200/JCO.2010.31.6067
PG 6
WC Oncology
SC Oncology
GA 752SO
UT WOS:000289714600022
PM 21422406
ER
PT J
AU Ho, TH
Barbera, L
Saskin, R
Lu, H
Neville, BA
Earle, CC
AF Ho, Thi H.
Barbera, Lisa
Saskin, Refik
Lu, Hong
Neville, Bridget A.
Earle, Craig C.
TI Trends in the Aggressiveness of End-of-Life Cancer Care in the Universal
Health Care System of Ontario, Canada
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID ADMINISTRATIVE DATABASES; LUNG-CANCER; QUALITY; INDICATORS; POPULATION;
CONTINUITY
AB Purpose
To describe trends in the aggressiveness of end-of-life (EOL) cancer care in a universal health care system in Ontario, Canada, between 1993 and 2004, and to compare with findings reported in the United States.
Methods
A population-based, retrospective, cohort study that used administrative data linked to registry data. Aggressiveness of EOL care was defined as the occurrence of at least one of the following indicators: last dose of chemotherapy received within 14 days of death; more than one emergency department (ED) visit within 30 days of death; more than one hospitalization within 30 days of death; or at least one intensive care unit (ICU) admission within 30 days of death.
Results
Among 227,161 patients, 22.4% experienced at least one incident of potentially aggressive EOL cancer care. Multivariable analyses showed that with each successive year, patients were significantly more likely to encounter some aggressive intervention (odds ratio, 1.01; 95% CI, 1.01 to 1.02). Multiple emergency department (ED) visits, ICU admissions, and chemotherapy use increased significantly over time, whereas multiple hospital admissions declined (P < .05). Patients were more likely to receive aggressive EOL care if they were men, were younger, lived in rural regions, had a higher level of comorbidity, or had breast, lung, or hematologic malignancies. Chemotherapy and ICU utilization were lower in Ontario than in the United States.
Conclusion
Aggressiveness of cancer care near the EOL is increasing over time in Ontario, Canada, although overall rates were lower than in the United States. Health system characteristics and patient or physician cultural factors may play a role in the observed differences. J Clin Oncol 29:1587-1591. (C) 2011 by American Society of Clinical Oncology
C1 [Earle, Craig C.] Sunnybrook Hlth Sci Ctr, Inst Clin Evaluat Sci, Toronto, ON M4N 3M5, Canada.
Ontario Inst Canc Res, Toronto, ON, Canada.
Odette Canc Ctr, Toronto, ON, Canada.
Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Earle, CC (reprint author), Sunnybrook Hlth Sci Ctr, Inst Clin Evaluat Sci, 2075 Bayview Ave,Room G-106, Toronto, ON M4N 3M5, Canada.
EM craig.earle@ices.on.ca
FU Government of Ontario; Ontario Ministry of Health and Long-Term Care;
National Cancer Institute [CA 91753-02]
FX Supported by the Ontario Institute for Cancer Research through funding
provided by the Government of Ontario and by the Institute for Clinical
Evaluative Sciences, which is funded by an annual grant from the Ontario
Ministry of Health and Long-Term Care; and by Grant No. CA 91753-02 from
the National Cancer Institute.
NR 26
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Z9 128
U1 1
U2 11
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 APR 20
PY 2011
VL 29
IS 12
BP 1587
EP 1591
DI 10.1200/JCO.2010.31.9897
PG 5
WC Oncology
SC Oncology
GA 752SO
UT WOS:000289714600030
PM 21402603
ER
PT J
AU Ng, K
Sargent, DJ
Goldberg, RM
Meyerhardt, JA
Green, EM
Pitot, HC
Hollis, BW
Pollak, MN
Fuchs, CS
AF Ng, Kimmie
Sargent, Daniel J.
Goldberg, Richard M.
Meyerhardt, Jeffrey A.
Green, Erin M.
Pitot, Henry C.
Hollis, Bruce W.
Pollak, Michael N.
Fuchs, Charles S.
TI Vitamin D Status in Patients With Stage IV Colorectal Cancer: Findings
From Intergroup Trial N9741
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID COLON-CANCER; CARCINOMA-CELLS; BREAST-CANCER; ANALOG EB1089; B
RADIATION; GROWTH; D-3; 1,25-DIHYDROXYVITAMIN-D3; SUPPLEMENTATION;
CARCINOGENESIS
AB Purpose
Previous studies have suggested that higher plasma 25-hydroxyvitamin D(3) [25(OH) D] levels are associated with decreased colorectal cancer risk and improved survival, but the prevalence of vitamin D deficiency in advanced colorectal cancer and its influence on outcomes are unknown.
Patients and Methods
We prospectively measured plasma 25(OH) D levels in 515 patients with stage IV colorectal cancer participating in a randomized trial of chemotherapy. Vitamin D deficiency was defined as 25(OH) D lower than 20 ng/mL, insufficiency as 20 to 29 ng/mL, and sufficiency as >= 30 ng/mL. We examined the association between baseline 25(OH) D level and selected patient characteristics. Cox proportional hazards models were used to calculate hazard ratios (HR) for death, disease progression, and tumor response, adjusted for prognostic factors.
Results
Among 515 eligible patients, 50% of the study population was vitamin D deficient, and 82% were vitamin D insufficient. Plasma 25(OH) D levels were lower in black patients compared to white patients and patients of other race (median, 10.7 v 21.1 v 19.3 ng/mL, respectively; P < .001), and females compared to males (median, 18.3 v 21.7 ng/mL, respectively; P = .0005). Baseline plasma 25(OH) D levels were not associated with patient outcome, although given the distribution of plasma levels in this cohort, statistical power for survival analyses were limited.
Conclusion
Vitamin D deficiency is highly prevalent among patients with stage IV colorectal cancer receiving first-line chemotherapy, particularly in black and female patients. J Clin Oncol 29:1599-1606. (C) 2011 by American Society of Clinical Oncology
C1 [Ng, Kimmie] Dana Farber Canc Inst, Boston, MA 02115 USA.
Brigham & Womens Hosp, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Boston, MA USA.
N Cent Canc Treatment Grp, Rochester, MN USA.
Mayo Clin, Rochester, MN USA.
Univ N Carolina, Chapel Hill, NC USA.
Med Univ S Carolina, Charleston, SC 29425 USA.
McGill Univ, Jewish Gen Hosp, Montreal, PQ H3T 1E2, Canada.
RP Ng, K (reprint author), Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA.
EM kng4@partners.org
RI Pollak, Michael/G-9094-2011; Goldberg , Richard/M-1311-2013;
OI Pollak, Michael/0000-0003-3047-0604; Sargent, Daniel/0000-0002-2684-4741
FU National Cancer Institute, National Institutes of Health [CA25224,
CA32102, CA38926, CA21115, P50CA127003, T32CA009001-34]; American
Society of Clinical Oncology; Charles A. King Trust; Bank of America;
Pharmacia Corporation (now Pfizer Oncology); Sanofi-Aventis
FX Supported by Grants No. CA25224, CA32102, CA38926, CA21115, P50CA127003,
and T32CA009001-34 (K.N.) from the National Cancer Institute, National
Institutes of Health; by an American Society of Clinical Oncology Young
Investigator Award (K.N.); by The Charles A. King Trust Postdoctoral
Fellowship Award, Bank of America, Co-Trustee (K.N.); as well as by
Pharmacia Corporation (now Pfizer Oncology) and Sanofi-Aventis. The
contents of this article are solely the responsibility of the authors
and do not necessarily represent the official views of the National
Cancer Institute or the National Institutes of Health, American Society
of Clinical Oncology (ASCO), or The ASCO Foundation.
NR 41
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Z9 34
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 APR 20
PY 2011
VL 29
IS 12
BP 1599
EP 1606
DI 10.1200/JCO.2010.31.7255
PG 8
WC Oncology
SC Oncology
GA 752SO
UT WOS:000289714600032
PM 21422438
ER
PT J
AU Seibler, P
Graziotto, J
Jeong, H
Simunovic, F
Klein, C
Krainc, D
AF Seibler, Philip
Graziotto, John
Jeong, Hyun
Simunovic, Filip
Klein, Christine
Krainc, Dimitri
TI Mitochondrial Parkin Recruitment Is Impaired in Neurons Derived from
Mutant PINK1 Induced Pluripotent Stem Cells
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID HUMAN FIBROBLASTS; DEFINED FACTORS; DISEASE; MUTATIONS; PGC-1-ALPHA;
PATIENT; NEURODEGENERATION; PATHOGENESIS; DYSFUNCTION; BIOGENESIS
AB Genetic Parkinson disease (PD) has been associated with mutations in PINK1, a gene encoding a mitochondrial kinase implicated in the regulation of mitochondrial degradation. While the studies so far examined PINK1 function in non-neuronal systems or through PINK1 knockdown approaches, there is an imperative to examine the role of endogenous PINK1 in appropriate human-derived and biologically relevant cell models. Here we report the generation of induced pluripotent stem (iPS) cells from skin fibroblasts taken from three PD patients with nonsense (c.1366C>T; p.Q456X) or missense (c.509T>G; p.V170G) mutations in the PINK1 gene. These cells were differentiated into dopaminergic neurons that upon mitochondrial depolarization showed impaired recruitment of lentivirally expressed Parkin to mitochondria, increased mitochondrial copy number, and upregulation of PGC-1 alpha, an important regulator of mitochondrial biogenesis. Importantly, these alterations were corrected by lentiviral expression of wild-type PINK1 in mutant iPS cell-derived PINK1 neurons. In conclusion, our studies suggest that fibroblasts from genetic PD can be reprogrammed and differentiated into neurons. These neurons exhibit distinct phenotypes that should be amenable to further mechanistic studies in this relevant biological context.
C1 [Seibler, Philip; Graziotto, John; Jeong, Hyun; Simunovic, Filip; Krainc, Dimitri] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol,MassGen Inst Neurodegenerat Dis, Charlestown, MA 02129 USA.
[Seibler, Philip; Klein, Christine] Univ Lubeck, Dept Neurol, Sect Clin & Mol Neurogenet, D-23562 Lubeck, Germany.
[Simunovic, Filip] Mediterranean Inst Life Sci, Split 21000, Croatia.
RP Krainc, D (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol,MassGen Inst Neurodegenerat Dis, 114 16th St,Room 2008, Charlestown, MA 02129 USA.
EM krainc@helix.mgh.harvard.edu
FU German Academic Exchange Service; Fritz Thyssen Foundation; Volkswagen
Foundation; Hermann and Lilly Schilling Foundation; [R01NS051303]
FX This work was supported by R01NS051303 (D. K.), the German Academic
Exchange Service (P. S.), and the Fritz Thyssen Foundation (C. K.). C.
K. is a recipient of a career development award from the Volkswagen
Foundation and from the Hermann and Lilly Schilling Foundation. We thank
George Daley (Children's Hospital, Boston, MA) for providing retroviral
reprogramming constructs, Laurence Daheron (Massachusetts General
Hospital, Boston, MA) for helpful discussions and experimental advice,
and Stuart Chambers and Lorenz Studer (Sloan-Kettering Institute, New
York, NY) for helpful technical advice.
NR 41
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Z9 179
U1 2
U2 18
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 APR 20
PY 2011
VL 31
IS 16
BP 5970
EP 5976
DI 10.1523/JNEUROSCI.4441-10.2011
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 753JV
UT WOS:000289769400011
PM 21508222
ER
PT J
AU Peralta, CA
Shlipak, MG
Judd, S
Cushman, M
McClellan, W
Zakai, NA
Safford, MM
Zhang, XA
Muntner, P
Warnock, D
AF Peralta, Carmen A.
Shlipak, Michael G.
Judd, Suzanne
Cushman, Mary
McClellan, William
Zakai, Neil A.
Safford, Monika M.
Zhang, Xiao
Muntner, Paul
Warnock, David
TI Detection of Chronic Kidney Disease With Creatinine, Cystatin C, and
Urine Albumin-to-Creatinine Ratio and Association With Progression to
End-Stage Renal Disease and Mortality
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID GLOMERULAR-FILTRATION-RATE; RACIAL-DIFFERENCES; CARDIOVASCULAR EVENTS;
ELDERLY PERSONS; STROKE REGARDS; US ADULTS; ALL-CAUSE; REASONS;
POPULATION; RISK
AB Context A triple-marker approach for chronic kidney disease (CKD) evaluation has not been well studied.
Objective To evaluate whether combining creatinine, cystatin C, and urine albumin-to-creatinine ratio (ACR) would improve identification of risks associated with CKD compared with creatinine alone.
Design, Setting, and Participants Prospective cohort study involving 26 643 US adults enrolled in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study from January 2003 to June 2010. Participants were categorized into 8 groups defined by estimated glomerular filtration rate (GFR) determined by creatinine and by cystatin C of either <60 or >= 60 mL/min/1.73 m(2) and ACR of either <30 or >= 30 mg/g.
Main Outcome Measures All-cause mortality and incident end-stage renal disease with median follow-up of 4.6 years.
Results Participants had a mean age of 65 years, 40% were black, and 54% were women. Of 26 643 participants, 1940 died and 177 developed end-stage renal disease. Among participants without CKD defined by creatinine, 24% did not have CKD by either ACR or cystatin C. Compared with those with CKD defined by creatinine alone, the hazard ratio for death in multivariable-adjusted models was 3.3 (95% confidence interval [CI], 2.0-5.6) for participants with CKD defined by creatinine and ACR; 3.2 (95% CI, 2.2-4.7) for those with CKD defined by creatinine and cystatin C, and 5.6 (95% CI, 3.9-8.2) for those with CKD defined by all biomarkers. Among participants without CKD defined by creatinine, 3863 (16%) had CKD detected by ACR or cystatin C. Compared with participants who did not have CKD by any measure, the HRs for mortality were 1.7 (95% CI, 1.4-1.9) for participants with CKD defined by ACR alone, 2.2 (95% CI, 1.9-2.7) for participants with CKD defined by cystatin C alone, and 3.0 (95% CI, 2.4-3.7) for participants with CKD defined by both measures. Risk of incident end-stage renal disease was higher among those with CKD defined by all markers (34.1 per 1000 person-years; 95% CI, 28.7-40.5 vs 0.33 per 1000 person-years; 95% CI, 0.05-2.3) for those with CKD defined by creatinine alone. The second highest end-stage renal disease rate was among persons missed by the creatinine measure but detected by both ACR and cystatin C (rate per 1000 person-years, 6.4; 95% CI, 3.6-11.3). Net reclassification improvement for death was 13.3% (P<.001) and for end-stage renal disease was 6.4% (P<.001) after adding estimated GFR cystatin C in fully adjusted models with estimated GFR creatinine and ACR.
Conclusion Adding cystatin C to the combination of creatinine and ACR measures improved the predictive accuracy for all-cause mortality and end-stage renal disease.
C1 [Peralta, Carmen A.; Shlipak, Michael G.] San Francisco VA Med Ctr, Dept Med, San Francisco, CA USA.
[Peralta, Carmen A.; Shlipak, Michael G.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Judd, Suzanne; Zhang, Xiao] Univ Alabama Birmingham, Sch Publ Hlth, Dept Biostat, Birmingham, AL USA.
[Muntner, Paul] Univ Alabama Birmingham, Sch Publ Hlth, Dept Epidemiol, Birmingham, AL USA.
[Safford, Monika M.; Warnock, David] Univ Alabama Birmingham, Dept Med, Birmingham, AL USA.
[Cushman, Mary; Zakai, Neil A.] Univ Vermont, Dept Med, Burlington, VT 05405 USA.
[Cushman, Mary; Zakai, Neil A.] Univ Vermont, Dept Pathol, Burlington, VT 05405 USA.
[McClellan, William] Emory Univ, Dept Med, Atlanta, GA 30322 USA.
RP Peralta, CA (reprint author), 4150 Clement St,111A1, San Francisco, CA 94121 USA.
EM carmenalicia.peralta@ucsf.edu
FU Amgen; National Institute of Neurological Disorders and Stroke, National
Institutes of Health, Department of Health and Human Services [U01
NS041588]; Amgen Corp.; National Institutes of Diabetes and Digestive
and Kidney Diseases [1K23SK082793-01]; Robert Wood Johnson Harold Amos
award; American Heart Association [0640012N]; [R01AG034853];
[R01DK066488]; [R01HL085757]; [R01DK078124]; [R21HL091217]
FX All authors have completed and submitted the ICMJE Form for Disclosure
of Potential Conflicts of Interest. Dr Warnock reported that he is a
consultant for Amgen Corp and has received research support from Amgen.
Dr Cushman reported receiving research support from Amgen. Dr McClellen
reported receiving research support from Amgen. Otherwise, no other
conflicts of interest were reported.; This research project is supported
by cooperative agreement U01 NS041588 from the National Institute of
Neurological Disorders and Stroke, National Institutes of Health,
Department of Health and Human Services. Additional funding was provided
by an investigator-initiated grant-in-aid from Amgen Corp. Dr Peralta is
funded by the National Institutes of Diabetes and Digestive and Kidney
Diseases grant 1K23SK082793-01 and a Robert Wood Johnson Harold Amos
award. Dr Shlipak is funded by grants R01AG034853 (PI), R01DK066488
(PI), R01HL085757 (Co-Investigator), R01DK078124 (Co-Investigator), and
R21HL091217 (Co-Investigator) and by an American Heart Association
Established Investigator Award (0640012N; PI)
NR 32
TC 192
Z9 200
U1 3
U2 17
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 APR 20
PY 2011
VL 305
IS 15
BP 1545
EP 1552
DI 10.1001/jama.2011.468
PG 8
WC Medicine, General & Internal
SC General & Internal Medicine
GA 752HU
UT WOS:000289683000023
PM 21482744
ER
PT J
AU Gellad, WF
Good, CB
AF Gellad, Walid F.
Good, C. Bernie
TI Angiotensin receptor blockers (ARBs)
SO CANADIAN MEDICAL ASSOCIATION JOURNAL
LA English
DT Letter
C1 [Gellad, Walid F.] Univ Pittsburgh, VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA 15260 USA.
[Good, C. Bernie] Univ Pittsburgh, Sch Med, VA Pittsburgh Hlth Care Syst, Pittsburgh, PA USA.
RP Gellad, WF (reprint author), Univ Pittsburgh, VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA 15260 USA.
NR 2
TC 0
Z9 0
U1 0
U2 1
PU CMA-CANADIAN MEDICAL ASSOC
PI OTTAWA
PA 1867 ALTA VISTA DR, OTTAWA, ONTARIO K1G 3Y6, CANADA
SN 0820-3946
J9 CAN MED ASSOC J
JI Can. Med. Assoc. J.
PD APR 19
PY 2011
VL 183
IS 7
BP 826
EP 826
DI 10.1503/cmaj.111-2036
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 748YD
UT WOS:000289428200041
PM 21502367
ER
PT J
AU Catanzaro, JM
Guerriero, JL
Liu, JX
Ullman, E
Sheshadri, N
Chen, JJ
Zong, WX
AF Catanzaro, Joseph M.
Guerriero, Jennifer L.
Liu, Jingxuan
Ullman, Erica
Sheshadri, Namratha
Chen, John J.
Zong, Wei-Xing
TI Elevated Expression of Squamous Cell Carcinoma Antigen (SCCA) Is
Associated with Human Breast Carcinoma
SO PLOS ONE
LA English
DT Article
ID MONOCLONAL-ANTIBODIES; TREATMENT RESPONSE; CERVICAL-CANCER; LUNG-CANCER;
SENSITIVITY; ORIGIN; LINES
AB Squamous cell carcinoma antigen (SCCA) belongs to the serine protease inhibitor (Serpin) family of proteins. Elevated expression of SCCA has been used as a biomarker for aggressive squamous cell carcinoma (SCC) in cancers of the cervix, lung, head and neck, and liver. However, SCCA expression in breast cancer has not been investigated. Immunohistochemical analysis of SCCA expression was performed on tissue microarrays containing breast tumor tissues (n = 1,360) and normal breast epithelium (n = 124). SCCA expression was scored on a tiered scale (0-3) independently by two evaluators blind to the patient's clinical status. SCCA expression was observed in Grade I (0.3%), Grade II (2.5%), and Grade III (9.4%) breast cancers (p < 0.0001). Comparing tissues categorized into the three non-metastatic TNM stages, I-III, SCCA positivity was seen in 2.4% of Stage I cancers, 3.1% of Stage II cancers, and 8.6% of Stage III breast cancers (p = 0.0005). No positive staining was observed in normal/non-neoplastic breast tissue (0 out of 124). SCCA expression also correlated to estrogen receptor/progesterone receptor (ER/PR) double-negative tumors (p = 0.0009). Compared to SCCA-negative patients, SCCA-positive patients had both a worse overall survival and recurrence-free survival (p < 0.0001 and p < 0.0001, respectively). This study shows that SCCA is associated with both advanced stage and high grade human breast carcinoma, and suggests the necessity to further explore the role of SCCA in breast cancer development and treatment.
C1 [Catanzaro, Joseph M.; Guerriero, Jennifer L.; Ullman, Erica; Sheshadri, Namratha; Zong, Wei-Xing] SUNY Stony Brook, Dept Mol Genet & Microbiol, Stony Brook, NY 11794 USA.
[Liu, Jingxuan] SUNY Stony Brook, Dept Pathol, Stony Brook, NY 11794 USA.
[Chen, John J.] SUNY Stony Brook, Dept Preventat Med, Stony Brook, NY 11794 USA.
RP Catanzaro, JM (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
EM wzong@notes.cc.sunysb.edu
FU National Institutes of Health (NIH) [T32GM00796247, NIH T32CA009176, NIH
CA098092, NIH CA129536, Susan Komen KG081538]; Carol Baldwin Breast
Cancer Research Foundation
FX This work was supported by National Institutes of Health (NIH)
T32GM00796247, NIH T32CA009176, NIH CA098092, NIH CA129536, Susan Komen
KG081538, and the Carol Baldwin Breast Cancer Research Foundation. The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 26
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Z9 26
U1 0
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 19
PY 2011
VL 6
IS 4
AR e19096
DI 10.1371/journal.pone.0019096
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 752EC
UT WOS:000289671100050
PM 21526154
ER
PT J
AU Jo, H
Lo, PK
Li, YT
Loison, F
Green, S
Wang, J
Silberstein, LE
Ye, KQ
Chen, HX
Luo, HBR
AF Jo, Hakryul
Lo, Pang-Kuo
Li, Yitang
Loison, Fabien
Green, Sarah
Wang, Jake
Silberstein, Leslie E.
Ye, Keqiang
Chen, Hexin
Luo, Hongbo R.
TI Deactivation of Akt by a small molecule inhibitor targeting pleckstrin
homology domain and facilitating Akt ubiquitination
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE chemical screening; cell death
ID CANCER; PI3K; DISCOVERY; 3-KINASES; PATHWAY; CELLS; PTEN
AB The phosphatidylinositol-3,4,5-triphosphate (PIP3) binding function of pleckstrin homology (PH) domain is essential for the activation of oncogenic Akt/PKB kinase. Following the PIP3-mediated activation at the membrane, the activated Akt is subjected to other regulatory events, including ubiquitination-mediated deactivation. Here, by identifying and characterizing an allosteric inhibitor, SC66, we show that the facilitated ubiquitination effectively terminates Akt signaling. Mechanistically, SC66 manifests a dual inhibitory activity that directly interferes with the PH domain binding to PIP3 and facilitates Akt ubiquitination. A known PH domain-dependent allosteric inhibitor, which stabilizes Akt, prevents the SC66-induced Akt ubiquitination. A cancer-relevant Akt1 (e17k) mutant is unstable, making it intrinsically sensitive to functional inhibition by SC66 in cellular contexts in which the PI3K inhibition has little inhibitory effect. As a result of its dual inhibitory activity, SC66 manifests a more effective growth suppression of transformed cells that contain a high level of Akt signaling, compared with other inhibitors of PIP3/Akt pathway. Finally, we show the anticancer activity of SC66 by using a soft agar assay as well as a mouse xenograft tumor model. In conclusion, in this study, we not only identify a dual-function Akt inhibitor, but also demonstrate that Akt ubiquitination could be chemically exploited to effectively facilitate its deactivation, thus identifying an avenue for pharmacological intervention in Akt signaling.
C1 [Lo, Pang-Kuo; Chen, Hexin] Univ S Carolina, Dept Biol Sci, Columbia, SC 29208 USA.
[Jo, Hakryul; Li, Yitang; Loison, Fabien; Green, Sarah; Wang, Jake; Silberstein, Leslie E.; Luo, Hongbo R.] Harvard Univ, Sch Med, Dept Pathol, Dana Farber Harvard Canc Ctr, Boston, MA 02115 USA.
[Ye, Keqiang] Emory Univ, Dept Pathol & Lab Med, Atlanta, GA 30322 USA.
RP Chen, HX (reprint author), Univ S Carolina, Dept Biol Sci, Columbia, SC 29208 USA.
EM hchen@biol.sc.edu; hongbo.luo@childrens.harvard.edu
RI Loison, Fabien/G-3385-2014
OI Loison, Fabien/0000-0002-6678-1730
FU National Institutes of Health (NIH) [HL066987, HL085100, AI076471,
HL092020, GM076084]; American Cancer Society
FX The authors thank all members of the H.R.L. laboratory. The screening
was performed in the Institute of Chemistry and Cell Biology-Longwood
Screening Facility. This study was supported by National Institutes of
Health (NIH) Training Grant HL066987 (to H.J.); NIH Grants HL085100,
AI076471, HL092020, and GM076084 (to H.L.); and Research Scholar grants
from the American Cancer Society (to H.L. and H.C.).
NR 30
TC 28
Z9 28
U1 0
U2 9
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 APR 19
PY 2011
VL 108
IS 16
BP 6486
EP 6491
DI 10.1073/pnas.1019062108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 752GV
UT WOS:000289680400035
PM 21464312
ER
PT J
AU Cannon, CP
Rich, JD
Murphy, SA
Braunwald, E
AF Cannon, Christopher P.
Rich, Jonathan D.
Murphy, Sabina A.
Braunwald, Eugene
TI Previous Aspirin Use in Acute Coronary Syndromes More Than a Marker?
Reply
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Letter
ID OUTCOMES; BENEFIT
C1 [Cannon, Christopher P.] Brigham & Womens Hosp, TIMI Study Grp, Boston, MA 02115 USA.
RP Cannon, CP (reprint author), Brigham & Womens Hosp, TIMI Study Grp, 75 Francis St, Boston, MA 02115 USA.
EM cpcannon@partners.org
NR 4
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 0735-1097
EI 1558-3597
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 19
PY 2011
VL 57
IS 16
BP 1715
EP 1716
DI 10.1016/j.jacc.2011.01.014
PG 2
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 749JH
UT WOS:000289460800017
ER
PT J
AU Yasuda, T
Kometani, K
Takahashi, N
Imai, Y
Aiba, Y
Kurosaki, T
AF Yasuda, Tomoharu
Kometani, Kohei
Takahashi, Noriko
Imai, Yuuki
Aiba, Yuichi
Kurosaki, Tomohiro
TI ERKs Induce Expression of the Transcriptional Repressor Blimp-1 and
Subsequent Plasma Cell Differentiation
SO SCIENCE SIGNALING
LA English
DT Article
ID MEMORY B-CELLS; ACTIVATED PROTEIN-KINASE; MAP KINASE; GERMINAL-CENTERS;
T-LYMPHOCYTES; TERMINAL DIFFERENTIATION; IMMUNOGLOBULIN-G; RECEPTOR;
STAT3; AUTOIMMUNITY
AB In immune cells, the positive role of the extracellular signal-regulated kinase (ERK) signaling pathway in cell cycle progression and survival is well established; however, it is unclear whether ERK signaling plays a role in cell differentiation. Here, we report that ERKs are essential for the differentiation of B cells into antibody-producing plasma cells and that ERKs induce the expression of Prdm1, which encodes Blimp-1, a transcriptional repressor and "master regulator" of plasma cell differentiation. Transgenic mice with conditional deletion of both ERK1 and ERK2 in germinal center (GC) B cells lacked plasma cells differentiated after GC formation, and memory B cells from these mice failed to differentiate into plasma cells. In addition, ERK1- and ERK2-deficient B cells exhibited impaired Prdm1 expression upon stimulation with antibody against CD40 in the presence of interleukin-4; conversely, enforced expression of Prdm1 in ERK1- and ERK2-deficient B cells restored the generation of plasma cells. Thus, our study suggests that cytokines stimulate ERKs to induce the production of Blimp-1 and that ERKs thereby contribute to the process of cellular differentiation.
C1 [Yasuda, Tomoharu; Kometani, Kohei; Takahashi, Noriko; Aiba, Yuichi; Kurosaki, Tomohiro] RIKEN, Lab Lymphocyte Differentiat, Res Ctr Allergy & Immunol, Kanagawa 2300045, Japan.
[Imai, Yuuki] Dana Farber Canc Inst, Div Mol & Cellular Oncol, Dept Med Oncol, Boston, MA 02115 USA.
[Imai, Yuuki] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Kurosaki, Tomohiro] Osaka Univ, Lab Lymphocyte Differentiat, WPI Immunol Frontier Res Ctr, Osaka 5650871, Japan.
RP Kurosaki, T (reprint author), RIKEN, Lab Lymphocyte Differentiat, Res Ctr Allergy & Immunol, Kanagawa 2300045, Japan.
EM kurosaki@rcai.riken.jp
RI Kurosaki, Tomohiro/D-1306-2009
OI Kurosaki, Tomohiro/0000-0002-6352-304X
FU Ministry of Education, Culture, Sports, Science and Technology of Japan;
Japan Science and Technology Agency, Core Research for Evolutional
Science and Technology
FX This work was supported by grants to T.Y. and T.K. from the Ministry of
Education, Culture, Sports, Science and Technology of Japan and by a
grant to T.K. from Japan Science and Technology Agency, Core Research
for Evolutional Science and Technology.
NR 53
TC 28
Z9 29
U1 0
U2 0
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1945-0877
J9 SCI SIGNAL
JI Sci. Signal.
PD APR 19
PY 2011
VL 4
IS 169
AR ra25
DI 10.1126/scisignal.2001592
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 752GW
UT WOS:000289680600004
PM 21505187
ER
PT J
AU Chen, GD
Fachin, F
Fernandez-Suarez, M
Wardle, BL
Toner, M
AF Chen, Grace D.
Fachin, Fabio
Fernandez-Suarez, Marta
Wardle, Brian L.
Toner, Mehmet
TI Nanoporous Elements in Microfluidics for Multiscale Manipulation of
Bioparticles
SO SMALL
LA English
DT Article
ID CARBON NANOTUBES; PARTICLE SEPARATION; CHIP; MICROCHIP; MEMBRANES;
DEVICE; CELLS; FLOW; ELECTROPHORESIS; FLUORESCENCE
AB Solid materials, such as silicon, glass, and polymers, dominate as structural elements in microsystems including microfluidics. Porous elements have been limited to membranes sandwiched between microchannel layers or polymer monoliths. This paper reports the use of micropatterned carbon-nanotube forests confined inside microfluidic channels for mechanically and/or chemically capturing particles ranging over three orders of magnitude in size. Nanoparticles below the internanotube spacing (80 nm) of the forest can penetrate inside the forest and interact with the large surface area created by individual nanotubes. For larger particles (> 80 nm), the ultrahigh porosity of the nanotube elements reduces the fluid boundary layer and enhances particle-structure interactions on the outer surface of the patterned nanoporous elements. Specific biomolecular recognition is demonstrated using cells (approximate to 10 mu m), bacteria (approximate to 1 mu m), and viral-sized particles (approximate to 40 nm) using both effects. This technology can provide unprecedented control of bioseparation processes to access bioparticles of interest, opening new pathways for both research and point-of-care diagnostics.
C1 [Chen, Grace D.; Fernandez-Suarez, Marta; Toner, Mehmet] Massachusetts Gen Hosp, BioMEMS Resource Ctr, Charlestown, MA 02139 USA.
[Fachin, Fabio; Wardle, Brian L.] MIT, Dept Aeronaut & Astronaut, Cambridge, MA 02139 USA.
RP Toner, M (reprint author), Massachusetts Gen Hosp, BioMEMS Resource Ctr, 114 16th St, Charlestown, MA 02139 USA.
EM mehmet_toner@hms.harvard.edu
FU National Institute of Biomedical Imaging and Bioengineering (BioMEMS
Resource Center) [P41 EB002503]; U.S. Department of State's Fulbright
Science and Technology
FX We thank Octavio Hurtado (MGH) and Namiko Yamamoto (MIT) for technical
support with nano- and microfabrication procedures. This work was
supported by the National Institute of Biomedical Imaging and
Bioengineering under Grant P41 EB002503 (BioMEMS Resource Center) and
U.S. Department of State's Fulbright Science and Technology Award.
NR 41
TC 33
Z9 34
U1 2
U2 37
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1613-6810
J9 SMALL
JI Small
PD APR 18
PY 2011
VL 7
IS 8
BP 1061
EP 1067
DI 10.1002/smll.201002076
PG 7
WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience &
Nanotechnology; Materials Science, Multidisciplinary; Physics, Applied;
Physics, Condensed Matter
SC Chemistry; Science & Technology - Other Topics; Materials Science;
Physics
GA 756FL
UT WOS:000289997000011
PM 21413145
ER
PT J
AU Bowers, WJ
Breakefield, XO
Sena-Esteves, M
AF Bowers, William J.
Breakefield, Xandra O.
Sena-Esteves, Miguel
TI Genetic therapy for the nervous system
SO HUMAN MOLECULAR GENETICS
LA English
DT Review
ID AMYOTROPHIC-LATERAL-SCLEROSIS; SPINAL MUSCULAR-ATROPHY; NEURONAL
CEROID-LIPOFUSCINOSIS; PLURIPOTENT STEM-CELLS; SINGLE-CHAIN ANTIBODY;
BLOOD-BRAIN-BARRIER; MUCOPOLYSACCHARIDOSIS-VII MICE; CONVECTION-ENHANCED
DELIVERY; ADENOASSOCIATED VIRUS TYPE-2; AMINO-ACID DECARBOXYLASE
AB Genetic therapy is undergoing a renaissance with expansion of viral and synthetic vectors, use of oligonucleotides (RNA and DNA) and sequence-targeted regulatory molecules, as well as genetically modified cells, including induced pluripotent stem cells from the patients themselves. Several clinical trials for neurologic syndromes appear quite promising. This review covers genetic strategies to ameliorate neurologic syndromes of different etiologies, including lysosomal storage diseases, Alzheimer's disease and other amyloidopathies, Parkinson's disease, spinal muscular atrophy, amyotrophic lateral sclerosis and brain tumors. This field has been propelled by genetic technologies, including identifying disease genes and disruptive mutations, design of genomic interacting elements to regulate transcription and splicing of specific precursor mRNAs and use of novel non-coding regulatory RNAs. These versatile new tools for manipulation of genetic elements provide the ability to tailor the mode of genetic intervention to specific aspects of a disease state.
C1 [Bowers, William J.] Univ Rochester, Dept Neurol, Ctr Neural Dev & Dis, Sch Med & Dent, Rochester, NY 14642 USA.
[Breakefield, Xandra O.] Massachusetts Gen Hosp, Ctr Neurosci, Boston, MA 02114 USA.
[Breakefield, Xandra O.] Massachusetts Gen Hosp, Mol Neurogenet Unit, Dept Neurol, Boston, MA 02114 USA.
[Breakefield, Xandra O.] Massachusetts Gen Hosp, Ctr Mol Imaging Res, Dept Radiol, Boston, MA 02114 USA.
[Breakefield, Xandra O.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Sena-Esteves, Miguel] Univ Massachusetts, Sch Med, Dept Neurol, Gene Therapy Ctr,Interdisciplinary Grad Program, Worcester, MA 01605 USA.
RP Breakefield, XO (reprint author), Massachusetts Gen Hosp East, Mol Neurogenet Unit, 13th St,Bldg 149, Charlestown, MA 02129 USA.
EM breakefield@hms.harvard.edu
FU NIH/NCI [CA069246]; NIH/NINDS [NS242791, R01NS066310, U01NS064096]; NIH
[R01-AG026328]; NIH/NICHHD [R01HD060576]
FX Support for X.O.B. comes from NIH/NCI CA069246 and NIH/NINDS NS242791,
for W.J.B. from NIH R01-AG026328 and for M.S.-E. from NIH/NINDS
R01NS066310, U01NS064096 and NIH/NICHHD R01HD060576.
NR 188
TC 35
Z9 36
U1 2
U2 18
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD APR 15
PY 2011
VL 20
SI 1
BP R28
EP R41
DI 10.1093/hmg/ddr110
PG 14
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 763VG
UT WOS:000290587200006
PM 21429918
ER
PT J
AU Nihal, M
Stutz, N
Schmit, T
Ahmad, N
Wood, GS
AF Nihal, Minakshi
Stutz, Nathalie
Schmit, Travis
Ahmad, Nihal
Wood, Gary S.
TI Polo-like kinase 1 (Plk1) is expressed by cutaneous T-cell lymphomas
(CTCLs) and its downregulation promotes cell cycle arrest and apoptosis
SO CELL CYCLE
LA English
DT Article
DE CTCL; Plk1; cell cycle; apoptosis
ID SMALL-MOLECULE INHIBITOR; COMMON CLONAL ORIGIN; CANCER-CELLS;
POLO-LIKE-KINASE-1; CYTOKINESIS; SURVIVIN; MITOSIS; TRANSFORMATION;
INDUCTION; DEPLETION
AB Polo-like kinases are serine/threonine kinases crucial for mitosis and DNA integrity. Plk1, the most well studied member of this family, is upregulated in several cancers, as well as in dividing cells with peak expression during G(2)/M phase. Recently, employing lesional skin from patients with cutaneous T-cell lymphoma (CTCL), we showed that Plk1 was increased mainly in advanced lesions. In this study, employing western blot and quantitative RT-PCR analyses, we demonstrated that Plk1 was overexpressed in multiple CTCL cell lines (HH, Hut78, MyLa, SeAx and SZ4). Further, a genetic knockdown (by short hairpin RNA) or enzyme activity inhibition (via a small molecule inhibitor, GW843682X) was found to result in a decrease in cell growth, viability and proliferation. Plk1 inhibition in CTCL cells also resulted in: (1) increased G(2)/M phase cell cycle arrest, (2) alteration in key mitotic proteins, (3) apoptosis and (4) multiple mitotic errors. Given our findings, clinical trials of Plk1 inhibitors in CTCL may be a promising area for further translational investigation. We speculate that overexpression of Plk1 may prove to be relevant to the progression and prognosis of CTCL through its direct impact on the regulation of tumor cell proliferation and indirect influence on the acquisition of somatic mutations by proliferating tumor cells.
C1 [Wood, Gary S.] William S Middleton Mem Vet Adm Med Ctr, Madison, WI USA.
[Nihal, Minakshi; Stutz, Nathalie; Ahmad, Nihal; Wood, Gary S.] Dept Dermatol, Madison, WI USA.
[Schmit, Travis] Univ Wisconsin, Dept Pediat, Madison, WI USA.
[Nihal, Minakshi; Ahmad, Nihal; Wood, Gary S.] Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI USA.
[Nihal, Minakshi; Ahmad, Nihal; Wood, Gary S.] Paul P Carbone Comprehens Canc Ctr, Madison, WI USA.
RP Wood, GS (reprint author), William S Middleton Mem Vet Adm Med Ctr, Madison, WI USA.
EM gwood@dermatology.wisc.edu
FU Department of Veterans Affairs, Office of Research and Development,
Biomedical Laboratory Research and Development Service
FX This material is based on work supported by the Department of Veterans
Affairs, Office of Research and Development, Biomedical Laboratory
Research and Development Service. The contents do not represent the
views of the Deptartment of Veterans Affairs or the U.S. Government.
NR 47
TC 17
Z9 19
U1 0
U2 4
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4101
J9 CELL CYCLE
JI Cell Cycle
PD APR 15
PY 2011
VL 10
IS 8
BP 1303
EP 1311
DI 10.4161/cc.10.8.15353
PG 9
WC Cell Biology
SC Cell Biology
GA 758EV
UT WOS:000290145100026
PM 21436619
ER
PT J
AU Mathews, R
Peterson, ED
Chen, AY
Wang, TY
Chin, CT
Fonarow, GC
Cannon, CP
Rumsfeld, JS
Roe, MT
Alexander, KP
AF Mathews, Robin
Peterson, Eric D.
Chen, Anita Y.
Wang, Tracy Y.
Chin, Chee Tang
Fonarow, Gregg C.
Cannon, Christopher P.
Rumsfeld, John S.
Roe, Matthew T.
Alexander, Karen P.
TI In-Hospital Major Bleeding During ST-Elevation and Non ST-Elevation
Myocardial Infarction Care: Derivation and Validation of a Model from
the ACTION Registry (R)-GWTG (TM)
SO AMERICAN JOURNAL OF CARDIOLOGY
LA English
DT Article
ID ACUTE CORONARY SYNDROMES; QUALITY IMPROVEMENT; CLINICAL-OUTCOMES; RISK
SCORE; IMPACT; INTERVENTION; REGISTRY; CRUSADE
AB Bleeding, a common complication of acute myocardial infarction (AMI) treatment, is associated with worse outcomes. A contemporary model for major bleeding associated with AMI treatment can stratify patients at elevated risk for bleeding and is needed to risk-adjust AMI practice and outcomes. Using the Acute Coronary Treatment and Intervention Outcomes Network Registry Get With the Guidelines (ACTION Registry GWTG) database, an in-hospital major bleeding risk model was developed in a population of patients with ST-segment elevation myocardial infarction and non ST-segment elevation myocardial infarction. The model used only baseline variables and was developed (n = 72,313) and validated (n = 17,960) in patients with AMI (at 251 United States centers from January 2007 to December 2008). The 12 most statistically and clinically significant variables were incorporated into the final regression model. The calibration plots are shown, and the model discrimination is demonstrated in derivation and validation cohorts, as well as across key subgroups. The rate of major bleeding in the overall population was 10.8%. The 12 factors associated with major bleeding in the model were heart rate, baseline hemoglobin, female gender, baseline serum creatinine, age, electro-cardiographic changes, heart failure or shock, diabetes, peripheral artery disease, body weight, systolic blood pressure, and home warfarin use. The risk model discriminated well in the derivation (C-statistic = 0.73) and validation (C-statistic = 0.71) cohorts. A risk score for major bleeding corresponded well with observed bleeding: very low risk (3.9%), low risk (7.3%), moderate risk (16.1%), high risk (29.0%), and very high risk (39.8%). In conclusion, the ACTION Registry GWTG in-hospital major bleeding model stratifies risk for major bleeding using variables at presentation and enables risk-adjusted bleeding outcomes for quality improvement initiatives and clinical decision making. (C) 2011 Elsevier Inc. All rights reserved. (Am J Cardiol 2011;107:1136-1143)
C1 [Mathews, Robin; Peterson, Eric D.; Chen, Anita Y.; Wang, Tracy Y.; Chin, Chee Tang; Roe, Matthew T.; Alexander, Karen P.] Duke Univ, Med Ctr, Duke Clin Res Inst, Durham, NC 27706 USA.
[Chin, Chee Tang] Natl Heart Ctr Singapore, Singapore, Singapore.
[Fonarow, Gregg C.] Univ Calif Los Angeles, Med Ctr, Dept Med, Los Angeles, CA 90024 USA.
[Cannon, Christopher P.] Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA.
[Rumsfeld, John S.] Denver Vet Affairs Med Ctr, Denver, CO USA.
RP Alexander, KP (reprint author), Duke Univ, Med Ctr, Duke Clin Res Inst, Durham, NC 27706 USA.
EM karen.alexander@duke.edu
FU Bristol-Myers Squibb (New York, New York)/Sanofi Pharmaceuticals (St.
Louis, Missouri); Agency for Healthcare Research and Quality, Rockville,
Maryland [U18HS016964]
FX The Acute Coronary Treatment and Intervention Outcomes Network Registry
Get With the Guidelines (ACTION Registry-GWTG) is an initiative of the
American College of Cardiology Foundation, Washington, District of
Columbia, and the American Heart Association, Dallas, Texas, with
partnering support from Society of Chest Pain Centers, Dublin, Ohio, the
Society of Hospital Medicine, Philadelphia, Pennsylvania, and the
American College of Emergency Physicians, Irving, Texas. The registry is
sponsored by Bristol-Myers Squibb (New York, New York)/Sanofi
Pharmaceuticals (St. Louis, Missouri). This project received
infrastructure support from the Agency for Healthcare Research and
Quality, Rockville, Maryland, under grant U18HS016964. The content is
solely the responsibility of the investigators and does not necessarily
represent the official views of the Agency for Healthcare Research and
Quality. The funding source had no role in the design or implementation
of the study or in the decision to seek publication.
NR 14
TC 64
Z9 65
U1 0
U2 2
PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
PI BRIDGEWATER
PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA
SN 0002-9149
J9 AM J CARDIOL
JI Am. J. Cardiol.
PD APR 15
PY 2011
VL 107
IS 8
BP 1136
EP 1143
DI 10.1016/j.amjcard.2010.12.009
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 752OQ
UT WOS:000289702400006
PM 21324428
ER
PT J
AU Rahilly-Tierney, CR
Spiro, A
Vokonas, P
Gaziano, JM
AF Rahilly-Tierney, Catherine R.
Spiro, Avron, III
Vokonas, Pantel
Gaziano, J. Michael
TI Relation Between High-Density Lipoprotein Cholesterol and Survival to
Age 85 Years in Men (from the VA Normative Aging Study)
SO AMERICAN JOURNAL OF CARDIOLOGY
LA English
DT Article
ID CORONARY-HEART-DISEASE; EXCEPTIONAL LONGEVITY; TRIGLYCERIDES
AB No previous researchers have sought to determine whether high-density lipoprotein (HDL) cholesterol levels are associated with survival to 85 years of age in a prospective cohort of aging men. We selected 652 men (mean age 65 years) enrolled in the VA Normative Aging Study who had >= 1 HDL cholesterol level documented during the study and who were old enough on the date of HDL cholesterol measurement to reach 85 years of age by the end of follow-up (July 1, 2008). We categorized initial HDL cholesterol into <40 mg/dl (reference group), 40 to 49 mg/dl or >= 50 mg/dl. Information on co-morbidities, lifestyle factors, measured lipid parameters, and medications were collected during triennial visits. We used proportional hazards to determine hazard ratios (HRs) for mortality before age 85 years for each category of initial HDL cholesterol compared to the reference adjusting for co-morbidities, calculated low-density lipoprotein cholesterol, medications, smoking, body mass index, and alcohol consumption. Treating HDL cholesterol as a continuous predictor, we also determined the HR for each 10-mg/dl increment in HDL cholesterol. Fully adjusted HR (95% confidence interval) for survival to 85 years of age for participants with an initial HDL cholesterol level >= 50 mg/dl compared to the reference was 0.72 (0.53 to 0.98). Each 10-mg/dl increment in HDL cholesterol was associated with a 14% (HR 0.86, 0.78 to 0.96) decrease in risk of mortality before 85 years of age. In conclusion, after adjusting for other factors associated with longevity, higher HDL cholesterol levels were significantly associated with survival to 85 years of age. Published by Elsevier Inc. (Am J Cardiol 2011;107:1173-1177)
C1 [Rahilly-Tierney, Catherine R.; Spiro, Avron, III; Vokonas, Pantel; Gaziano, J. Michael] Boston VA Healthcare Syst, MAVERIC, Boston, MA USA.
[Rahilly-Tierney, Catherine R.; Gaziano, J. Michael] Brigham & Womens Hosp, Div Aging, Boston, MA 02115 USA.
[Rahilly-Tierney, Catherine R.; Gaziano, J. Michael] Harvard Univ, Sch Med, Boston, MA USA.
[Spiro, Avron, III; Vokonas, Pantel] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Spiro, Avron, III; Vokonas, Pantel] VA Normat Aging Study, Boston, MA USA.
[Vokonas, Pantel] Boston Univ, Sch Med, Boston, MA 02118 USA.
RP Rahilly-Tierney, CR (reprint author), Boston VA Healthcare Syst, MAVERIC, Boston, MA USA.
EM Catherine.Rahilly@va.gov
OI Spiro III, Avron/0000-0003-4080-8621
FU Cooperative Studies Program/ERIC; United States Department of Veterans
Affairs, Massachusetts Veterans Epidemiology Research and Information
Center (MAVERIC); VA Merit Review
FX The VA Normative Aging Study is supported by the Cooperative Studies
Program/ERIC, United States Department of Veterans Affairs, and is a
research component of the Massachusetts Veterans Epidemiology Research
and Information Center (MAVERIC). This research was also supported by a
VA Merit Review and a VA Research Career Scientist award to Dr. Spiro.
NR 13
TC 15
Z9 15
U1 0
U2 2
PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
PI BRIDGEWATER
PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA
SN 0002-9149
J9 AM J CARDIOL
JI Am. J. Cardiol.
PD APR 15
PY 2011
VL 107
IS 8
BP 1173
EP 1177
DI 10.1016/j.amjcard.2010.12.015
PG 5
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 752OQ
UT WOS:000289702400012
PM 21296318
ER
PT J
AU Lopez, CA
Daaboul, GG
Vedula, RS
Ozkumur, E
Bergstein, DA
Geisbert, TW
Fawcett, HE
Goldberg, BB
Connor, JH
Unlu, MS
AF Lopez, Carlos A.
Daaboul, George G.
Vedula, Rahul S.
Oezkumur, Emre
Bergstein, David A.
Geisbert, Thomas W.
Fawcett, Helen E.
Goldberg, Bennett B.
Connor, John H.
Uenlue, M. Selim
TI Label-free, multiplexed virus detection using spectral reflectance
imaging
SO BIOSENSORS & BIOELECTRONICS
LA English
DT Article
DE Virus detection; Label-free; Interferometry; Biosensor; High-throughput;
Microarray; Quantitative sensing
ID VESICULAR STOMATITIS-VIRUS; MICROARRAY APPLICATIONS;
ELECTRON-MICROSCOPY; INFLUENZA-VIRUS; MOUTH-DISEASE; BIOSENSORS;
DIAGNOSIS; DNA; FUTURE; AGENTS
AB We demonstrate detection of whole viruses and viral proteins with a new label-free platform based on spectral reflectance imaging. The Interferometric Reflectance Imaging Sensor (IRIS) has been shown to be capable of sensitive protein and DNA detection in a real time and high-throughput format. Vesicular stomatitis virus (VSV) was used as the target for detection as it is well-characterized for protein composition and can be modified to express viral coat proteins from other dangerous, highly pathogenic agents for surrogate detection while remaining a biosafety level 2 agent. We demonstrate specific detection of intact VSV virions achieved with surface-immobilized antibodies acting as capture probes which is confirmed using fluorescence imaging. The limit of detection is confirmed down to 3.5 x 10(5) plaque-forming units/mL (PFUs/mL). To increase specificity in a clinical scenario, both the external glycoprotein and internal viral proteins were simultaneously detected with the same antibody arrays with detergent-disrupted purified VSV and infected cell lysate solutions. Our results show sensitive and specific virus detection with a simple surface chemistry and minimal sample preparation on a quantitative label-free interferometric platform. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Lopez, Carlos A.; Vedula, Rahul S.; Goldberg, Bennett B.; Uenlue, M. Selim] Boston Univ, Dept Elect & Comp Engn, Boston, MA 02215 USA.
[Daaboul, George G.; Goldberg, Bennett B.; Uenlue, M. Selim] Boston Univ, Dept Biomed Engn, Boston, MA 02215 USA.
[Oezkumur, Emre] Harvard Univ, Massachusetts Gen Hosp, Ctr Canc, Ctr Engn Med, Boston, MA 02114 USA.
[Bergstein, David A.] Zoiray Technol Inc, Boston, MA USA.
[Geisbert, Thomas W.] Univ Texas Galveston, Med Branch, Galveston Natl Lab, Galveston, TX 77550 USA.
[Geisbert, Thomas W.] Univ Texas Galveston, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77550 USA.
[Fawcett, Helen E.; Connor, John H.] Boston Univ, Photon Ctr, Boston, MA 02215 USA.
[Geisbert, Thomas W.; Connor, John H.] Boston Univ, Sch Med, Dept Microbiol, Boston, MA 02118 USA.
[Goldberg, Bennett B.; Uenlue, M. Selim] Boston Univ, Dept Phys, Boston, MA 02215 USA.
RP Unlu, MS (reprint author), Boston Univ, Dept Elect & Comp Engn, Boston, MA 02215 USA.
EM selim@bu.edu
RI Unlu, Selim/B-4244-2013;
OI Connor, John/0000-0002-8867-7256
FU US Army Research Laboratories (ARL) [W911NF-06-2-0040]; National
Institutes of Health (NIH) [R21 GM074872-01A1]
FX We would like to thank Marcella Chiari and members of the Institute of
Molecular Recognition, National Research Council of Italy, for the kind
use of the copolymeric surface chemistry employed in these studies.
Funding for this research was generously provided by the US Army
Research Laboratories (ARL) grant W911NF-06-2-0040 and the National
Institutes of Health (NIH) grant R21 GM074872-01A1.
NR 33
TC 24
Z9 25
U1 0
U2 37
PU ELSEVIER ADVANCED TECHNOLOGY
PI OXFORD
PA OXFORD FULFILLMENT CENTRE THE BOULEVARD, LANGFORD LANE, KIDLINGTON,
OXFORD OX5 1GB, OXON, ENGLAND
SN 0956-5663
J9 BIOSENS BIOELECTRON
JI Biosens. Bioelectron.
PD APR 15
PY 2011
VL 26
IS 8
BP 3432
EP 3437
DI 10.1016/j.bios.2011.01.019
PG 6
WC Biophysics; Biotechnology & Applied Microbiology; Chemistry, Analytical;
Electrochemistry; Nanoscience & Nanotechnology
SC Biophysics; Biotechnology & Applied Microbiology; Chemistry;
Electrochemistry; Science & Technology - Other Topics
GA 754OE
UT WOS:000289863900007
PM 21342761
ER
PT J
AU Campuzano, S
Kuralay, F
Lobo-Castanon, MJ
Bartosik, M
Vyavahare, K
Palecek, E
Haake, DA
Wang, J
AF Campuzano, Susana
Kuralay, Filiz
Lobo-Castanon, M. Jesus
Bartosik, Martin
Vyavahare, Kedar
Palecek, Emil
Haake, David A.
Wang, Joseph
TI Ternary monolayers as DNA recognition interfaces for direct and
sensitive electrochemical detection in untreated clinical samples
SO BIOSENSORS & BIOELECTRONICS
LA English
DT Article
DE Dithiols; Self-assembled monolayer; Clinical samples; Electrochemical
detection; Hybridization; DNA
ID SELF-ASSEMBLED MONOLAYERS; IMPEDANCE SPECTROSCOPY; GOLD; HYBRIDIZATION;
ELECTRODES; IMMOBILIZATION; BIOSENSORS; SURFACES; AU(111); DEVICES
AB Detection of specific DNA sequences in clinical samples is a key goal of studies on DNA biosensors and gene chips. Herein we present a highly sensitive electrochemical genosensor for direct measurements of specific DNA sequences in undiluted and untreated human serum and urine samples. Such genosensing relies on a new ternary interface involving hexanedithiol (HDT) co-immobilized with the thiolated capture probe (SHCP) on gold surfaces, followed by the incorporation of 6-mercapto-1-hexanol (MCH) as diluent. The performance of ternary monolayers prepared with linear dithiols of different lengths was systematically examined, compared and characterized by cyclic voltammetry and electrochemical impedance spectroscopy, with HDT exhibiting the most favorable analytical performance. The new SHCP/HDT + MCH monolayer led to a 80-fold improvement in the signal-to-noise ratio (S/N) for 1 nM target DNA in undiluted human serum over the common SHCP+MCH binary alkanethiol interface, and allowed the direct quantification of the target DNA down to 7 pM (28 amol) and 17 pM (68 amol) in undiluted/untreated serum and urine, respectively. It also displayed attractive antifouling properties, as indicated from the favorable S/N obtained after a prolonged exposure (24 h) to untreated biological matrices. These attractive features of the SHCP/HDT + MCH sensor interface indicate considerable promise for a wide range of clinical applications. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Campuzano, Susana; Kuralay, Filiz; Lobo-Castanon, M. Jesus; Vyavahare, Kedar; Wang, Joseph] Univ Calif San Diego, Dept Nanoengn, La Jolla, CA 92093 USA.
[Bartosik, Martin; Palecek, Emil] Acad Sci Czech Republic, Inst Biophys, CS-61265 Brno, Czech Republic.
[Haake, David A.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90095 USA.
[Haake, David A.] Vet Affairs Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA.
RP Wang, J (reprint author), Univ Calif San Diego, Dept Nanoengn, La Jolla, CA 92093 USA.
EM josephwang@ucsd.edu
RI Campuzano Ruiz, Susana/C-6448-2011; Bartosik, Martin/B-5648-2011; Lobo
Castanon, Maria Jesus/E-8757-2011; Palecek, Emil/C-1075-2013; Wang,
Joseph/C-6175-2011
OI Lobo Castanon, Maria Jesus/0000-0002-2964-9490; Palecek,
Emil/0000-0003-2561-8336;
FU National Institutes of Health [U01 AI075565]; Programa Becas Complutense
del Amo; University of Oviedo; Spanish Ministerio de Ciencia e
Innovacion [PR 2009-0430]; Scientific and Technical Council of Turkey
(TUBITAK)
FX Financial support from the National Institutes of Health (Award U01
AI075565) is gratefully acknowledged. SC, MJLC and FK acknowledge
fellowships from Programa Becas Complutense del Amo (2010-2011),
University of Oviedo and Spanish Ministerio de Ciencia e Innovacion (PR
2009-0430), and The Scientific and Technical Council of Turkey
(TUBITAK), respectively. EP and MB thank the Czech-Republic Ministry of
Education, Youth and Sports (ME09038).
NR 26
TC 54
Z9 55
U1 5
U2 43
PU ELSEVIER ADVANCED TECHNOLOGY
PI OXFORD
PA OXFORD FULFILLMENT CENTRE THE BOULEVARD, LANGFORD LANE, KIDLINGTON,
OXFORD OX5 1GB, OXON, ENGLAND
SN 0956-5663
J9 BIOSENS BIOELECTRON
JI Biosens. Bioelectron.
PD APR 15
PY 2011
VL 26
IS 8
BP 3577
EP 3583
DI 10.1016/j.bios.2011.02.004
PG 7
WC Biophysics; Biotechnology & Applied Microbiology; Chemistry, Analytical;
Electrochemistry; Nanoscience & Nanotechnology
SC Biophysics; Biotechnology & Applied Microbiology; Chemistry;
Electrochemistry; Science & Technology - Other Topics
GA 754OE
UT WOS:000289863900030
PM 21377347
ER
PT J
AU Jenkins, RW
Clarke, CJ
Canals, D
Snider, AJ
Gault, CR
Heffernan-Stroud, L
Wu, BX
Simbari, F
Roddy, P
Kitatani, K
Obeid, LM
Hannun, YA
AF Jenkins, Russell W.
Clarke, Christopher J.
Canals, Daniel
Snider, Ashley J.
Gault, Christopher R.
Heffernan-Stroud, Linda
Wu, Bill X.
Simbari, Fabio
Roddy, Patrick
Kitatani, Kazuyuki
Obeid, Lina M.
Hannun, Yusuf A.
TI Regulation of CC Ligand 5/RANTES by Acid Sphingomyelinase and Acid
Ceramidase
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID NIEMANN-PICK-DISEASE; DELTA-MEDIATED PHOSPHORYLATION; RANTES CHEMOKINE
GENE; LUNG EPITHELIAL-CELLS; SMOOTH-MUSCLE-CELLS; BETA-GLUCOSIDASE 1;
SECRETORY SPHINGOMYELINASE; SPHINGOSINE 1-PHOSPHATE; TNF-ALPHA;
LYSOSOMAL SPHINGOMYELINASE
AB Acid sphingomyelinase (aSMase) generates the bioactive lipid ceramide (Cer) from hydrolysis of sphingomyelin (SM). However, its precise roles in regulating specific sphingolipid-mediated biological processes remain ill defined. Interestingly, the aSMase gene gives rise to two distinct enzymes, lysosomal sphingomyelinase (L-SMase) and secretory sphingomyelinase (S-SMase) via alternative trafficking of a shared protein precursor. Previously, our laboratory identified Ser(508) as a crucial residue for the constitutive and regulated secretion of S-SMase in response to inflammatory cytokines, and demonstrated a role for S-SMase in formation of select cellular Cer species (Jenkins, R. W., Canals, D., Idkowiak-Baldys, J., Simbari, F., Roddy, P., Perry, D. M., Kitatani, K., Luberto, C., and Hannun, Y. A. (2010) J. Biol. Chem. 285, 35706-35718). In the present study using a chemokine/cytokine screen, we identified the chemokine CCL5 (formerly known as RANTES) as a candidate-specific downstream target for aSMase. Regulation of CCL5 by aSMase was subsequently validated using both loss-of-function and gain-of-function models indicating that aSMase is both necessary and sufficient for CCL5 production. Interestingly, cells deficient in acid ceramidase (aCDase) also exhibited defects in CCL5 induction, whereas cells deficient in sphingosine kinase- 1 and -2 exhibited higher levels of CCL5, suggesting that sphingosine and not sphingosine 1-phosphate (S1P) is responsible for the positive signal to CCL5. Consistent with this, co-expression of aSMase and aCDase was sufficient to strongly induce CCL5. Taken together, these data identify a novel role for aSMase (particularly S-SMase) in chemokine elaboration by pro-inflammatory cytokines and highlight a novel and shared function for aSMase and aCDase.
C1 [Jenkins, Russell W.; Clarke, Christopher J.; Canals, Daniel; Wu, Bill X.; Roddy, Patrick; Kitatani, Kazuyuki; Hannun, Yusuf A.] Med Univ S Carolina, Dept Biochem & Mol Biol, Charleston, SC 29425 USA.
[Snider, Ashley J.; Gault, Christopher R.; Heffernan-Stroud, Linda; Obeid, Lina M.] Med Univ S Carolina, Dept Med, Charleston, SC 29425 USA.
[Snider, Ashley J.; Gault, Christopher R.; Heffernan-Stroud, Linda; Obeid, Lina M.] Ralph H Johnson Vet Affairs Hosp, Charleston, SC 29401 USA.
[Simbari, Fabio] CSIC, Inst Adv Chem Catalonia, Dept Biomed Chem, ES-08034 Barcelona, Spain.
[Kitatani, Kazuyuki] Tottori Univ Hosp, Dept Clin Lab, Yonago, Tottori 6838504, Japan.
RP Hannun, YA (reprint author), 173 Ashley Ave,POB 250509, Charleston, SC 29425 USA.
EM hannun@musc.edu
OI Canals, Daniel/0000-0002-9293-5123; Kitatani,
Kazuyuki/0000-0002-8516-6135; obeid, lina/0000-0002-0734-0847
FU National Institutes of Health [P01 CA097132]; NCI; MSTP Training
[GM08716, GM062887]; NIGMS [CA097132]; American Heart Association [AHA
081509E]; Medical University of South Carolina Hollings Cancer Center
Abney Foundation; Ministerio de Educacion y Ciencia (Spain)
[AP2006-02190]; Japan Society for the Promotion of Science [21890144]
FX This work was supported, in whole or in part, by National Institutes of
Health Grant P01 CA097132 (to Y. A. H.) from the NCI, MSTP Training
Grant GM08716 (to R. W. J.), Grant GM062887 from the NIGMS (to L. M.
O.), Grant CA097132 from the NCI (to L M. O.), American Heart
Association Pre-doctoral Fellowship AHA 081509E (to R. W. J.), a Medical
University of South Carolina Hollings Cancer Center Abney Foundation
Scholarship (to R. W. J.), Ministerio de Educacion y Ciencia (Spain)
Predoctoral Fellowship AP2006-02190 (to F. S.), and the Japan Society
for the Promotion of Science Grant-in-aid for Young Scientists
(Start-up) 21890144 (to K. K.).
NR 93
TC 18
Z9 18
U1 0
U2 4
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 APR 15
PY 2011
VL 286
IS 15
BP 13292
EP 13303
DI 10.1074/jbc.M110.163378
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 746XH
UT WOS:000289282200050
PM 21335555
ER
PT J
AU Ogata, N
Shinoda, Y
Wettschureck, N
Offermanns, S
Takeda, S
Nakamura, K
Segre, GV
Chung, U
Kawaguchi, H
AF Ogata, Naoshi
Shinoda, Yusuke
Wettschureck, Nina
Offermanns, Stefan
Takeda, Shu
Nakamura, Kozo
Segre, Gino V.
Chung, Ung-il
Kawaguchi, Hiroshi
TI G alpha(q) Signal in Osteoblasts Is Inhibitory to the Osteoanabolic
Action of Parathyroid Hormone
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID GROWTH-FACTOR-I; G-PROTEINS; BONE; RECEPTOR; CELLS; EXPRESSION; PTH;
DIFFERENTIATION; ACTIVATION; MICE
AB This study examined the role of the G alpha(q) signal constituted by G alpha(q) and G alpha(11) (encoded by Gn alpha(q) and Gn alpha(11), respectively), a major intracellular pathway of parathyroid hormone (PTH), in the PTH osteoanabolic action by the gain- and loss-of-function analyses. Transgenic mice with osteoblast-specific overexpression of the constitutively active Gn alpha(q) gene under the control of 2.3-kb type I collagen alpha 1 chain (Col1a1) promoter exhibited osteopenia with decreased bone formation parameters and did not respond to the daily PTH treatment. We then established osteoblast-specific Gn alpha(q) and Gn alpha(11) double-knock-out (cDKO) mice by crossing the 2.3-kb Col1a1 promoter-Cre recombinase transgenic mice and those with Gn alpha(q) gene flanked with loxP and global ablation of Gn alpha(11) (Col1a1-Cre(+/-);Gn alpha(fl/fl)(q);Gna(11)(-/-)) and found that the cDKO and single knock-out litterrnates of Gn alpha(q) or Gn alpha(11) exhibited normal bone volume and turnover under physiological conditions. With a daily injection of PTH, however, the cDKO mice, but not the single knock-out mice, showed higher bone volume and turnover than the wild-type littermates. Cultures of primary osteoblasts derived from cDKO and wild-type littermates confirmed enhancement of the PTH osteoanabolic action by the G alpha(q) signal deficiency in a cell-autonomous mechanism, in association with the membrane translocation of protein kinase C delta. This enhancement was reproduced by oyerexpression of regulator of G protein signaling-2, a G alpha(q) signal inhibitor, in osteoblastic MC3T3-E1 cells. Hence, the G alpha(q) signal plays an inhibitory role in the PTH osteoanabolic action, suggesting that its suppression may lead to a novel treatment in combination with PTH against osteoporosis.
C1 [Kawaguchi, Hiroshi] Univ Tokyo, Fac Med, Dept Sensory & Motor Syst Med, Tokyo 1138655, Japan.
[Ogata, Naoshi] Univ Tokyo, Dept Bone & Cartilage Regenerat Med, Tokyo 1138655, Japan.
[Chung, Ung-il] Univ Tokyo, Ctr Dis Biol & Integrat Med, Tokyo 1138655, Japan.
[Wettschureck, Nina; Offermanns, Stefan] Max Planck Inst Heart & Lung Res, Dept Pharmacol, D-61231 Bad Nauheim, Germany.
[Takeda, Shu] Keio Univ, Sch Med, Dept Endocrinol & Metab, Tokyo 1608582, Japan.
[Segre, Gino V.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
RP Kawaguchi, H (reprint author), Univ Tokyo, Fac Med, Dept Sensory & Motor Syst Med, 7-3-1 Bunkyo, Tokyo 1138655, Japan.
EM kawaguchi-ort@h.u-tokyo.ac.jp
RI takeda, shu/B-5195-2012
FU Japanese Ministry of Education,Culture, Sports, Science, and Technology
[21390416, 22659267, 22390286]
FX This work was supported by Grants-in-aid for Scientific Research
21390416, 22659267, and 22390286 from the Japanese Ministry of
Education,Culture, Sports, Science, and Technology.
NR 45
TC 9
Z9 11
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 APR 15
PY 2011
VL 286
IS 15
BP 13733
EP 13740
DI 10.1074/jbc.M110.200196
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 746XH
UT WOS:000289282200091
PM 21345793
ER
PT J
AU Mar, JC
Wells, CA
Quackenbush, J
AF Mar, Jessica C.
Wells, Christine A.
Quackenbush, John
TI Defining an informativeness metric for clustering gene expression data
SO BIOINFORMATICS
LA English
DT Article
ID DATA SET; VALIDATION; MODEL; NUMBER
AB Motivation: Unsupervised 'cluster' analysis is an invaluable tool for exploratory microarray data analysis, as it organizes the data into groups of genes or samples in which the elements share common patterns. Once the data are clustered, finding the optimal number of informative subgroups within a dataset is a problem that, while important for understanding the underlying phenotypes, is one for which there is no robust, widely accepted solution.
Results: To address this problem we developed an 'informativeness metric' based on a simple analysis of variance statistic that identifies the number of clusters which best separate phenotypic groups. The performance of the informativeness metric has been tested on both experimental and simulated datasets, and we contrast these results with those obtained using alternative methods such as the gap statistic.
C1 [Mar, Jessica C.; Quackenbush, John] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Mar, Jessica C.; Quackenbush, John] Dana Farber Canc Inst, Det Biostat & Computat Biol, Boston, MA 02115 USA.
[Wells, Christine A.] Griffith Univ, Natl Ctr Adult Stem Cell Res, Eskitis Inst Cell & Mol Therapies, Brisbane, Qld 4111, Australia.
[Quackenbush, John] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
RP Mar, JC (reprint author), Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
EM jess@jimmy.harvard.edu; johnq@jimmy.harvard.edu
RI Wells, Christine/A-5071-2010
OI Wells, Christine/0000-0003-3133-3628
FU Australian Research Council [LX0882502]; National Health and Medical
Research Council, Australia [481945]; US National Institute for Human
Genome Research [P50 HG004233]; US National Library of Medicine [R01
LM010129]
FX Australian Research Council International linkage project (LX0882502 to
C.A.W.). C.A.W. is supported by a CDA fellowship (481945) from the
National Health and Medical Research Council, Australia. J.Q. and J.C.M.
were supported by a grant from the US National Institute for Human
Genome Research (P50 HG004233); J.Q. was also supported by a grant from
the US National Library of Medicine (R01 LM010129).
NR 16
TC 28
Z9 28
U1 2
U2 6
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1367-4803
EI 1460-2059
J9 BIOINFORMATICS
JI Bioinformatics
PD APR 15
PY 2011
VL 27
IS 8
BP 1094
EP 1100
DI 10.1093/bioinformatics/btr074
PG 7
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Computer Science, Interdisciplinary Applications; Mathematical &
Computational Biology; Statistics & Probability
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Computer Science; Mathematical & Computational Biology; Mathematics
GA 747DX
UT WOS:000289301600007
PM 21330289
ER
PT J
AU Rahman, SMJ
Gonzalez, AL
Li, M
Seeley, EH
Zimmerman, LJ
Zhang, XQJ
Manier, ML
Olson, SJ
Shah, RN
Miller, AN
Putnam, JB
Miller, YE
Franklin, WA
Blot, WJ
Carbone, DP
Shyr, Y
Caprioli, RM
Massion, PP
AF Rahman, S. M. Jamshedur
Gonzalez, Adriana L.
Li, Ming
Seeley, Erin H.
Zimmerman, Lisa J.
Zhang, Xueqiong J.
Manier, M. Lisa
Olson, Sandra J.
Shah, Ronak N.
Miller, Alison N.
Putnam, Joe B.
Miller, York E.
Franklin, Wilbur A.
Blot, William J.
Carbone, David P.
Shyr, Yu
Caprioli, Richard M.
Massion, Pierre P.
TI Lung Cancer Diagnosis from Proteomic Analysis of Preinvasive Lesions
SO CANCER RESEARCH
LA English
DT Article
ID MIGRATION INHIBITORY FACTOR; IMAGING MASS-SPECTROMETRY; WHITE-LIGHT
BRONCHOSCOPY; SQUAMOUS-CELL CARCINOMA; AUTOFLUORESCENCE BRONCHOSCOPY;
PRECANCEROUS LESIONS; PROTEIN EXPRESSION; METASTASIS; INTEROBSERVER;
ANGIOGENESIS
AB Early detection may help improve survival from lung cancer. In this study, our goal was to derive and validate a signature from the proteomic analysis of bronchial lesions that could predict the diagnosis of lung cancer. Using previously published studies of bronchial tissues, we selected a signature of nine matrix-assisted laser desorption ionization mass spectrometry (MALDI MS) mass-to-charge ratio features to build a prediction model diagnostic of lung cancer. The model was based on MALDI MS signal intensity (MALDI score) from bronchial tissue specimens from our 2005 published cohort of 51 patients. The performance of the prediction model in identifying lung cancer was tested in an independent cohort of bronchial specimens from 60 patients. The probability of having lung cancer based on the proteomic analysis of the bronchial specimens was characterized by an area under the receiver operating characteristic curve of 0.77 (95% CI 0.66-0.88) in this validation cohort. Eight of the nine features were identified and validated by Western blotting and immunohistochemistry. These results show that proteomic analysis of endobronchial lesions may facilitate the diagnosis of lung cancer and the monitoring of high-risk individuals for lung cancer in surveillance and chemoprevention trials. Cancer Res; 71(8); 3009-17. (C)2011 AACR.
C1 [Massion, Pierre P.] Vanderbilt Univ, Div Allergy Pulm & Crit Care Med, Dept Med, Vanderbilt Ingram Canc Ctr,Med Ctr,Sch Med, Nashville, TN 37232 USA.
[Gonzalez, Adriana L.; Olson, Sandra J.] Vanderbilt Univ, Dept Pathol, Vanderbilt Ingram Canc Ctr, Sch Med, Nashville, TN 37232 USA.
[Seeley, Erin H.; Manier, M. Lisa; Carbone, David P.; Caprioli, Richard M.] Vanderbilt Univ, Mass Spectrometry Res Ctr, Vanderbilt Ingram Canc Ctr, Sch Med, Nashville, TN 37232 USA.
[Seeley, Erin H.; Zimmerman, Lisa J.; Manier, M. Lisa; Carbone, David P.; Caprioli, Richard M.] Vanderbilt Univ, Dept Biochem, Vanderbilt Ingram Canc Ctr, Sch Med, Nashville, TN 37232 USA.
[Zhang, Xueqiong J.; Shyr, Yu] Vanderbilt Univ, Div Canc Biostat, Vanderbilt Ingram Canc Ctr, Sch Med,Dept Biostat, Nashville, TN 37232 USA.
[Carbone, David P.] Vanderbilt Univ, Div Hematol & Oncol, Vanderbilt Ingram Canc Ctr, Sch Med,Dept Med, Nashville, TN 37232 USA.
[Putnam, Joe B.] Vanderbilt Univ, Dept Thorac Surg, Vanderbilt Ingram Canc Ctr, Sch Med, Nashville, TN 37232 USA.
[Blot, William J.] Vanderbilt Univ, Div Epidemiol, Vanderbilt Ingram Canc Ctr, Sch Med,Dept Med, Nashville, TN 37232 USA.
[Miller, Alison N.; Massion, Pierre P.] Vet Affairs Med Ctr, Nashville, TN 37212 USA.
[Miller, York E.] Univ Colorado, Dept Med, Div Pulm, Denver Vet Affairs Med Ctr, Denver, CO USA.
[Franklin, Wilbur A.] Univ Colorado, Dept Pathol, Denver, CO 80202 USA.
RP Massion, PP (reprint author), Vanderbilt Univ, Div Allergy Pulm & Crit Care Med, Dept Med, Vanderbilt Ingram Canc Ctr,Med Ctr,Sch Med, 640 PRB, Nashville, TN 37232 USA.
EM pierre.massion@vanderbilt.edu
FU National Institute of Health [CA102353, P50 CA 90949, P50 CA58187];
Vanderbilt-Ingram Cancer Center [P30 CA68485]; Department of Defense
[W81XWH-05-1-0179]; NIH/NIGMS [5R01-GM58008]
FX This work was supported by the National Institute of Health (CA102353 to
P. P. Massion, the Lung SPORE P50 CA 90949 to D. P. Carbone, and the
Lung SPORE P50 CA58187 to Y.E. Miller and W. A. Franklin),
Vanderbilt-Ingram Cancer Center Core Support Grant (P30 CA68485 to P. P.
Massion and R. M. Caprioli), Department of Defense (W81XWH-05-1-0179 to
R. M. Caprioli) and NIH/NIGMS (5R01-GM58008 to R. M. Caprioli).
NR 42
TC 31
Z9 33
U1 1
U2 10
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
IS 8
BP 3009
EP 3017
DI 10.1158/0008-5472.CAN-10-2510
PG 9
WC Oncology
SC Oncology
GA 749YL
UT WOS:000289507800021
PM 21487035
ER
PT J
AU Duda, DG
Kozin, SV
Kirkpatrick, ND
Xu, L
Fukumura, D
Jain, RK
AF Duda, Dan G.
Kozin, Sergey V.
Kirkpatrick, Nathaniel D.
Xu, Lei
Fukumura, Dai
Jain, Rakesh K.
TI CXCL12 (SDF1 alpha)-CXCR4/CXCR7 Pathway Inhibition: An Emerging
Sensitizer for Anticancer Therapies?
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID GROWTH IN-VIVO; CXCR4 ANTAGONIST CTCE-9908; BREAST-CANCER METASTASIS;
TUMOR-GROWTH; KINASE INHIBITOR; PROGENITOR CELLS; TGF-BETA; RECEPTOR;
ANGIOGENESIS; VEGF
AB Addition of multiple molecularly targeted agents to the existing armamentarium of chemotherapeutics and radiotherapies represents a significant advance in the management of several advanced cancers. In certain tumor types with no efficacious therapy options, these agents have become the first line of therapy, for example, sorafenib in advanced hepatocellular carcinoma or bevacizumab in recurrent glioblastoma. Unfortunately, in many cases, the survival benefits are modest, lasting only weeks to a few months. Moreover, they may not show benefit in patients with localized disease (i.e., in the adjuvant setting). Recent studies have provided increasing evidence that activation of the chemokine CXCL12 (SDF1 alpha) pathway is a potential mechanism of tumor resistance to both conventional therapies and biological agents via multiple complementary actions: (i) by directly promoting cancer cell survival, invasion, and the cancer stem and/or tumor-initiating cell phenotype; (ii) by recruiting "distal stroma" (i.e., myeloid bone marrow-derived cells) to indirectly facilitate tumor recurrence and metastasis; and (iii) by promoting angiogenesis directly or in a paracrine manner. Here, we discuss recent preclinical and clinical data that support the potential use of anti-CXCL12 agents (e.g., AMD3100, NOX-A12, or CCX2066) as sensitizers to currently available therapies by targeting the CXCL12/CXCR4 and CXCL12/CXCR7 pathways. Clin Cancer Res; 17(8); 2074-80. (C) 2011 AACR.
C1 [Duda, Dan G.; Kozin, Sergey V.; Kirkpatrick, Nathaniel D.; Xu, Lei; Fukumura, Dai; Jain, Rakesh K.] Massachusetts Gen Hosp, Steele Lab, Boston, MA 02114 USA.
[Duda, Dan G.; Kozin, Sergey V.; Kirkpatrick, Nathaniel D.; Xu, Lei; Fukumura, Dai; Jain, Rakesh K.] Harvard Univ, Sch Med, Boston, MA USA.
RP Duda, DG (reprint author), Massachusetts Gen Hosp, Steele Lab, Cox 734,100 Blossom St, Boston, MA 02114 USA.
EM duda@steele.mgh.harvard.edu; jain@steele.mgh.harvard.edu
FU Dyax; AstraZeneca; MedImmune; NIH [P01-CA080124, R01-CA115767,
R01-CA085140, R01-CA126642, T32-CA073479, R21-CA139168, R01-CA096915];
Federal Share/NCI Proton Beam Program Income, Department of Defense
[W81XWH-10-1-0016]; American Cancer Society [RSG-11-073-01-TBG];
National Foundation for Cancer Research
FX R.K. Jain: commercial research grant, Dyax, AstraZeneca, and MedImmune;
consultant and/or advisory board, AstraZeneca, Dyax, Astellas-Fibrogen,
Regeneron, SynDevRx, Genzyme, Morphosys, and Noxxon Pharma; speaker
honorarium, Genzyme; stock ownership, SynDevRx. D.G. Duda, S.V. Kozin,
N.D. Kirkpatrick, L. Xu, and D. Fukumura disclosed no potential
conflicts of interest.; NIH grants P01-CA080124, R01-CA115767,
R01-CA085140, R01-CA126642, T32-CA073479, R21-CA139168, R01-CA096915,
and Federal Share/NCI Proton Beam Program Income, Department of Defense
Award W81XWH-10-1-0016, American Cancer Society Grant RSG-11-073-01-TBG,
and a National Foundation for Cancer Research Grant.
NR 89
TC 176
Z9 186
U1 2
U2 34
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD APR 15
PY 2011
VL 17
IS 8
BP 2074
EP 2080
DI 10.1158/1078-0432.CCR-10-2636
PG 7
WC Oncology
SC Oncology
GA 750NP
UT WOS:000289555500002
PM 21349998
ER
PT J
AU Shaw, AT
Solomon, B
AF Shaw, Alice T.
Solomon, Benjamin
TI Targeting Anaplastic Lymphoma Kinase in Lung Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID EML4-ALK FUSION GENE; ALK; ADENOCARCINOMA; IDENTIFICATION; TRANSCRIPTS;
INHIBITION; MUTATIONS; FEATURES; NPM
AB Several decades of cancer research have revealed a pivotal role for tyrosine kinases as key regulators of signaling pathways, controlling cell growth and differentiation. Deregulation of tyrosine kinase-mediated signaling occurs frequently in cancer and is believed to drive the initiation and progression of disease. Chromosomal rearrangements involving the tyrosine kinase anaplastic lymphoma kinase (ALK) occur in a variety of human malignancies including non-small cell lung cancer (NSCLC), anaplastic large cell lymphomas, and inflammatory myofibroblastic tumors. The aberrant activation of ALK signaling leads to "oncogene addiction" and marked sensitivity to ALK inhibitors such as crizotinib (PF-02341066). This review focuses on ALK rearrangements in NSCLC, starting with the discovery of the EML4-ALK fusion oncogene, and culminating in the recent validation of ALK as a therapeutic target in patients with ALK-rearranged NSCLC. Current efforts seek to expand the role of ALK kinase inhibition in lung and other cancers and to address the molecular basis for the development of resistance. Clin Cancer Res; 17(8); 2081-6. (C) 2011 AACR.
C1 [Shaw, Alice T.] Massachusetts Gen Hosp, Ctr Canc, Thorac Oncol Ctr, Boston, MA 02114 USA.
[Shaw, Alice T.] MIT, Koch Inst Integrat Canc Res, Cambridge, MA 02139 USA.
[Solomon, Benjamin] Peter MacCallum Canc Ctr, Dept Haematol & Med Oncol, Melbourne, Vic, Australia.
RP Shaw, AT (reprint author), Massachusetts Gen Hosp, Ctr Canc, Thorac Oncol Ctr, Profess Off Bldg 222, Boston, MA 02114 USA.
EM ashaw1@partners.org
FU Novartis; AstraZeneca; Pfizer
FX A.T. Shaw, commercial research support, Novartis, AstraZeneca;
consultant, Pfizer, Millennium Pharmaceuticals. B. Solomon, commercial
research support, consultant, Pfizer.
NR 36
TC 117
Z9 126
U1 4
U2 19
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD APR 15
PY 2011
VL 17
IS 8
BP 2081
EP 2086
DI 10.1158/1078-0432.CCR-10-1591
PG 6
WC Oncology
SC Oncology
GA 750NP
UT WOS:000289555500003
PM 21288922
ER
PT J
AU Takezawa, K
Okamoto, I
Nishio, K
Janne, PA
Nakagawa, K
AF Takezawa, Ken
Okamoto, Isamu
Nishio, Kazuto
Jaenne, Pasi A.
Nakagawa, Kazuhiko
TI Role of ERK-BIM and STAT3-Survivin Signaling Pathways in ALK
Inhibitor-Induced Apoptosis in EML4-ALK-Positive Lung Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID LARGE-CELL LYMPHOMA; EML4-ALK FUSION GENE; NPM-ALK; MEDIATED
LYMPHOMAGENESIS; KINASE INHIBITORS; EGFR MUTATIONS; CYCLE ARREST; STAT3;
IDENTIFICATION; GEFITINIB
AB Purpose: EML4-ALK (echinoderm microtubule-associated protein-like 4 anaplastic lymphoma kinase) was recently identified as a transforming fusion gene in non-small cell lung cancer. The purpose of the present study was to characterize the mechanism of malignant transformation by EML4-ALK.
Experimental Design: We established NIH 3T3 cells that stably express variant 1 or 3 of EML4-ALK and examined the signaling molecules that function downstream of EML4-ALK.
Results: Forced expression of EML4-ALK induced marked activation of extracellular signal-regulated kinase (ERK) and STAT3, but not that of AKT. Inhibition of ERK or STAT3 signaling resulted in substantial attenuation of the proliferation of cells expressing either variant of EML4-ALK, suggesting that these signaling pathways function downstream of EML4-ALK in lung cancer cells. The specific ALK inhibitor TAE684 induced apoptosis that was accompanied both by upregulation of BIM, a proapoptotic member of the Bcl-2 family, and by downregulation of survivin, a member of the inhibitor of apoptosis protein (IAP) family, in EML4-ALK-expressing NIH 3T3 cells as well as in H3122 human lung cancer cells harboring endogenous EML4-ALK. Depletion of BIM and overexpression of survivin each inhibited TAE684-induced apoptosis, suggesting that both upregulation of BIM and downregulation of survivin contribute to TAE684-induced apoptosis in EML4-ALK-positive lung cancer cells. Furthermore, BIM and survivin expression was found to be independently regulated by ERK and STAT3 signaling pathways, respectively.
Conclusions: ALK inhibitor-induced apoptosis is mediated both by BIM upregulation resulting from inhibition of ERK signaling as well as by survivin downregulation resulting from inhibition of STAT3 signaling in EML4-ALK-positive lung cancer cells. Clin Cancer Res; 17(8); 2140-8. (C) 2011 AACR.
C1 [Takezawa, Ken; Okamoto, Isamu; Nakagawa, Kazuhiko] Kinki Univ, Fac Med, Dept Med Oncol, Osaka 5898511, Japan.
[Nishio, Kazuto] Kinki Univ, Fac Med, Dept Genome Biol, Osaka 5898511, Japan.
[Jaenne, Pasi A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Jaenne, Pasi A.] Dana Farber Canc Inst, Lowe Ctr Thorac Oncol, Boston, MA 02115 USA.
RP Okamoto, I (reprint author), Kinki Univ, Fac Med, Dept Med Oncol, 377-2 Ohno Higashi, Osaka 5898511, Japan.
EM chi-okamoto@dotd.med.kindai.ac.jp
NR 40
TC 66
Z9 73
U1 2
U2 12
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD APR 15
PY 2011
VL 17
IS 8
BP 2140
EP 2148
DI 10.1158/1078-0432.CCR-10-2798
PG 9
WC Oncology
SC Oncology
GA 750NP
UT WOS:000289555500009
PM 21415216
ER
PT J
AU Muldoon, LL
Lewin, SJ
Dosa, E
Kraemer, DF
Pagel, MA
Doolittle, ND
Neuwelt, EA
AF Muldoon, Leslie L.
Lewin, Seth J.
Dosa, Edit
Kraemer, Dale F.
Pagel, Michael A.
Doolittle, Nancy D.
Neuwelt, Edward A.
TI Imaging and Therapy with Rituximab Anti-CD20 Immunotherapy in an Animal
Model of Central Nervous System Lymphoma
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID PRIMARY CNS LYMPHOMA; BLOOD-BRAIN-BARRIER; HIGH-DOSE METHOTREXATE;
NON-HODGKINS-LYMPHOMA; TERM-FOLLOW-UP; TUMOR XENOGRAFT; RAT MODEL;
PHASE-II; NUDE RAT; CHEMOTHERAPY
AB Purpose: To evaluate the effect of rituximab monoclonal antibody (mAb) on MRI tumor volumetrics and efficacy in a rat model of central nervous system (CNS) lymphoma when delivery to the brain was optimized with osmotic blood-brain barrier disruption (BBBD).
Experimental Design: Female nude rats with intracerebral MC116 human B-cell lymphoma xenografts underwent baseline MRI and were randomized into 5 groups (n = 6 per group): (i) BBBD saline control; (ii) methotrexate with BBBD; (iii) rituximab with BBBD; (iv) rituximab and methotrexate with BBBD; and (v) intravenous rituximab. Tumor volumes were assessed by MRI at 1 week, and rats were followed for survival.
Results: BBBD increased delivery of yttrium-90-radiolabeled mAb in the model of CNS lymphoma. Control rats showed 201 +/- 102% increase in tumor volume on MRI 1 week after entering the study and median 14-day survival (range: 6-33). Tumor growth on MRI was slowed in the methotrexate treatment group, but survival time (median: 7 days; range: 5-12) was not different from controls. Among 17 evaluable rats treated with rituximab, 10 showed decreased tumor volume on MRI. All rituximab groups had increased survival compared with control, with a combined median of 43 days (range: 20-60, P < 0.001). There were no differences by route of delivery or combination with methotrexate.
Conclusions: Rituximab was effective at decreasing tumor volume and improving survival in a model of CNS lymphoma and was not affected by combination with methotrexate or by BBBD. We suggest that rituximab warrants further study in human primary CNS lymphoma. Clin Cancer Res; 17(8); 2207-15. (C) 2011 AACR.
C1 [Muldoon, Leslie L.; Lewin, Seth J.; Dosa, Edit; Doolittle, Nancy D.; Neuwelt, Edward A.] Oregon Hlth & Sci Univ, Dept Neurol, Portland, OR 97239 USA.
[Muldoon, Leslie L.] Oregon Hlth & Sci Univ, Dept Cell & Dev Biol, Portland, OR 97239 USA.
[Neuwelt, Edward A.] Oregon Hlth & Sci Univ, Dept Neurosurg, Portland, OR 97239 USA.
[Kraemer, Dale F.] Oregon Hlth & Sci Univ, Dept Publ Hlth & Prevent Med, Portland, OR 97239 USA.
[Kraemer, Dale F.] Oregon Hlth & Sci Univ, Dept Med Informat & Clin Epidemiol, Portland, OR 97239 USA.
[Kraemer, Dale F.] Oregon State Univ, Dept Pharm Practice, Portland, OR USA.
[Pagel, Michael A.; Neuwelt, Edward A.] Portland VA Med Ctr, Portland, OR USA.
RP Neuwelt, EA (reprint author), Oregon Hlth & Sci Univ, Dept Neurol, 3181 SW Sam Jackson Pk Rd,L603, Portland, OR 97239 USA.
EM neuwelte@ohsu.edu
FU Veterans Administration Merit Review Grant; NIH [NS053468, CA137488,
NS44687]
FX This study was supported by a Veterans Administration Merit Review Grant
and by NIH grants NS053468, CA137488, and NS44687 to E.A. Neuwelt.
NR 38
TC 13
Z9 15
U1 0
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD APR 15
PY 2011
VL 17
IS 8
BP 2207
EP 2215
DI 10.1158/1078-0432.CCR-10-2923
PG 9
WC Oncology
SC Oncology
GA 750NP
UT WOS:000289555500015
PM 21385922
ER
PT J
AU Ishii, Y
Papa, L
Bahadur, U
Yue, ZY
Aguirre-Ghiso, J
Shioda, T
Waxman, S
Germain, D
AF Ishii, Yuki
Papa, Luena
Bahadur, Urvashi
Yue, Zhenyu
Aguirre-Ghiso, Julio
Shioda, Toshi
Waxman, Samuel
Germain, Doris
TI Bortezomib Enhances the Efficacy of Fulvestrant by Amplifying the
Aggregation of the Estrogen Receptor, Which Leads to a Proapoptotic
Unfolded Protein Response
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID BREAST-CANCER CELLS; FACTOR-KAPPA-B; PROTEASOME; RESISTANCE; ALPHA;
ACTIVATION; MYELOMA; LIGAND; INDEPENDENCE; ICI-182,780
AB Purpose: Fulvestrant is known to promote the degradation of the estrogen receptor (ER) in the nucleus. However, fulvestrant also promotes the aggregation of the newly synthesized ER in the cytoplasm. Accumulation of protein aggregates leads to cell death but this effect is limited as a result of their elimination by the proteasome. We tested whether combining fulvestrant with the proteasome inhibitor, bortezomib, could enhance the accumulation of ER aggregates and cause apoptotic cell death.
Experimental Design: The rate of aggregation of the ER was monitored in ER+ breast cancer cells lines, T47D, ZR-75.1, BT474, MDA-MB-361, MCF-7, fulvestrant resistance MCF-7, and tamoxifen-resistant T47D-cyclin D1 cells. Activation of the unfolded protein response, apoptosis, and metabolic rate were also monitored in these cell lines following treatment with fulvestrant, bortezomib, or bortezomib in combination with fulvestrant.
Results: We found that bortezomib enhances the fulvestrant-mediated aggregation of the ER in the cytoplasm without blocking the degradation of the ER in the nucleus. Further, these aggregates activate a sustained unfolded protein response leading to apoptotic cell death. Further, we show that the combination induced tumor regression in a breast cancer mouse model of tamoxifen resistance.
Conclusions: Adding bortezomib to fulvestrant enhances its efficacy by taking advantage of the unique ability of fulvestrant to promote cytoplasmic aggregates of the ER. As this effect of fulvestrant is independent of the transcriptional activity of the ER, these results suggest that this novel combination may be effective in breast cancers that are ER+ but estrogen independent. Clin Cancer Res; 17(8); 2292-300. (C) 2011 AACR.
C1 [Germain, Doris] Mt Sinai Sch Med, Dept Med, Div Hematol Oncol, Tisch Canc Inst, New York, NY 10029 USA.
[Yue, Zhenyu] Mt Sinai Sch Med, Dept Neurol & Neurosci, New York, NY 10029 USA.
[Shioda, Toshi] Massachusetts Gen Hosp, Ctr Canc, Ctr Canc Res, Charlestown, MA USA.
[Shioda, Toshi] Harvard Univ, Sch Med, Charlestown, MA USA.
RP Germain, D (reprint author), Mt Sinai Sch Med, Dept Med, Div Hematol Oncol, Tisch Canc Inst, 1 Gustave L Levy Pl,Box 1079, New York, NY 10029 USA.
EM doris.germain@mssm.edu
OI Aguirre-Ghiso, Julio/0000-0002-6694-6507
FU Samuel Waxman Cancer Research Foundation; Chemotherapy Foundation;
NIH/National Cancer Institute [T32 CA78207]
FX This work was supported by a grant from the Samuel Waxman Cancer
Research Foundation and from the Chemotherapy Foundation to D. Germain.
L. Papa is supported by NIH/National Cancer Institute training Grant T32
CA78207.
NR 27
TC 17
Z9 17
U1 1
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD APR 15
PY 2011
VL 17
IS 8
BP 2292
EP 2300
DI 10.1158/1078-0432.CCR-10-1745
PG 9
WC Oncology
SC Oncology
GA 750NP
UT WOS:000289555500023
PM 21292820
ER
PT J
AU Mendez, E
Lohavanichbutr, P
Fan, WH
Houck, JR
Rue, TC
Doody, DR
Futran, ND
Upton, MP
Yueh, B
Zhao, LP
Schwartz, SM
Chen, C
AF Mendez, Eduardo
Lohavanichbutr, Pawadee
Fan, Wenhong
Houck, John R.
Rue, Tessa C.
Doody, David R.
Futran, Neal D.
Upton, Melissa P.
Yueh, Bevan
Zhao, Lue Ping
Schwartz, Stephen M.
Chen, Chu
TI Can a Metastatic Gene Expression Profile Outperform Tumor Size as a
Predictor of Occult Lymph Node Metastasis in Oral Cancer Patients?
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID SQUAMOUS-CELL-CARCINOMA; EXTRACAPSULAR SPREAD; CAVITY; HEAD
AB Purpose: To determine the differential gene expression between oral squamous cell carcinoma (OSCC) with and without metastasis to cervical lymph nodes and to assess prediction of nodal metastasis by using molecular features.
Experimental Design: We used Affymetrix U133 2.0 plus arrays to compare the tumor genome-wide gene expression of 73 node-positive OSCCs with 40 node-negative OSCCs (>= 18 months). Multivariate linear regression was used to estimate the association between gene expression and nodal metastasis. Stepwise logistic regression and receiver operating characteristics (ROC) analysis were used to generate predictive models and to compare these with models by using tumor size alone.
Results: We identified five genes differentially expressed between node-positive and node-negative OSCCs after adjusting for tumor size and human papillomavirus status: REEP1, RNF145, CTONG2002744, MYO5A, and FBXO32. Stepwise regression identified a four-gene model (MYO5A, RFN145, FBXO32, and CTONG2002744) as the most predictive of nodal metastasis. A leave-one-out ROC analysis revealed that our model had a higher area under the curve (AUC) for identifying occult nodal metastasis compared with that of a model by tumor size alone (respective AUC: 0.85 and 0.61; P = 0.011). A model combining tumor size and gene expression did not further improve the prediction of occult metastasis. Independent validation using 31 metastatic and 13 nonmetastatic cases revealed a significant underexpression of CTONG2002744 (P = 0.0004).
Conclusions: These results suggest that our gene expression markers of OSCC metastasis hold promise for improving current clinical practice. Confirmation by others and functional studies of CTONG2002744 is warranted. Clin Cancer Res; 17(8); 2466-73. (C) 2011 AACR.
C1 [Mendez, Eduardo; Lohavanichbutr, Pawadee; Houck, John R.; Doody, David R.; Schwartz, Stephen M.; Chen, Chu] Fred Hutchinson Canc Res Ctr, Program Epidemiol, Seattle, WA 98109 USA.
[Fan, Wenhong; Zhao, Lue Ping] Fred Hutchinson Canc Res Ctr, Program Biostat & Biomath, Seattle, WA 98109 USA.
[Yueh, Bevan] Univ Minnesota, Dept Otolaryngol Head & Neck Surg, Minneapolis, MN USA.
[Mendez, Eduardo; Futran, Neal D.; Chen, Chu] Univ Washington, Dept Otolaryngol Head & Neck Surg, Seattle, WA 98195 USA.
[Rue, Tessa C.; Zhao, Lue Ping] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Upton, Melissa P.] Univ Washington, Dept Pathol, Seattle, WA 98195 USA.
[Schwartz, Stephen M.; Chen, Chu] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Mendez, Eduardo] VA Puget Sound Hlth Care Syst, Surg & Perioperat Care Serv, Seattle, WA USA.
RP Chen, C (reprint author), Fred Hutchinson Canc Res Ctr, Program Epidemiol, 1100 Fairview Ave N,M-5C800,POB 19024, Seattle, WA 98109 USA.
EM cchen@fhcrc.org
OI Yueh, Bevan/0000-0003-1380-1053
FU National Cancer Institute, NIH, Bethesda, MD; National Center for
Research Resources (NCRR) [1K1L2RR025015-01]; Robert Wood Johnson
Foundation; Fred Hutchinson Cancer Research Center
FX This study was supported by grant R01CA095419 from the National Cancer
Institute, NIH, Bethesda, MD; grant 1K1L2RR025015-01 from the National
Center for Research Resources (NCRR); the Harold Amos Medical Faculty
Development Program from the Robert Wood Johnson Foundation; funds from
the Fred Hutchinson Cancer Research Center; and resources from and use
of facilities at the VA Puget Sound Health Care System, University of
Washington Medical Center and Harborview Medical Center, Seattle, WA.
NR 22
TC 11
Z9 11
U1 2
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD APR 15
PY 2011
VL 17
IS 8
BP 2466
EP 2473
DI 10.1158/1078-0432.CCR-10-0175
PG 8
WC Oncology
SC Oncology
GA 750NP
UT WOS:000289555500041
PM 21300763
ER
PT J
AU Anglesio, MS
George, J
Kulbe, H
Friedlander, M
Rischin, D
Lemech, C
Power, J
Coward, J
Cowin, PA
House, CM
Chakravarty, P
Gorringe, KL
Campbell, IG
Okamoto, A
Birrer, MJ
Huntsman, DG
de Fazio, A
Kalloger, SE
Balkwill, F
Gilks, CB
Bowtell, DD
AF Anglesio, Michael S.
George, Joshy
Kulbe, Hagen
Friedlander, Michael
Rischin, Danny
Lemech, Charlotte
Power, Jeremy
Coward, Jermaine
Cowin, Prue A.
House, Colin M.
Chakravarty, Probir
Gorringe, Kylie L.
Campbell, Ian G.
Okamoto, Aikou
Birrer, Michael J.
Huntsman, David G.
de Fazio, Anna
Kalloger, Steve E.
Balkwill, Frances
Gilks, C. Blake
Bowtell, David D.
CA Australian Ovarian Canc Study Grp
TI IL6-STAT3-HIF Signaling and Therapeutic Response to the Angiogenesis
Inhibitor Sunitinib in Ovarian Clear Cell Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID HORMONE-RELATED PROTEIN; RECURRENT EPITHELIAL OVARIAN;
NECROSIS-FACTOR-ALPHA; GENE-EXPRESSION; PHASE-II; SEROUS CARCINOMA;
POOR-PROGNOSIS; FALLOPIAN-TUBE; ENDOMETRIOSIS; INTERLEUKIN-6
AB Purpose: Ovarian clear cell adenocarcinoma (OCCA) is an uncommon histotype that is generally refractory to platinum-based chemotherapy. We analyze here the most comprehensive gene expression and copy number data sets, to date, to identify potential therapeutic targets of OCCA.
Experimental Design: Gene expression and DNA copy number were carried out using primary human OCCA tumor samples, and findings were confirmed by immunohistochemistry on tissue microarrays. Circulating interleukin (IL) 6 levels were measured in serum from patients with OCCA or high-grade serous cancers and related to progression-free and overall survival. Two patients were treated with sunitinib, and their therapeutic responses were measured clinically and by positron emission tomography.
Results: We find specific overexpression of the IL6-STAT3-HIF (interleukin 6-signal transducer and activator of transcription 3-hypoxia induced factor) pathway in OCCA tumors compared with high-grade serous cancers. Expression of PTHLH and high levels of circulating IL6 in OCCA patients may explain the frequent occurrence of hypercalcemia of malignancy and thromboembolic events in OCCA. We describe amplification of several receptor tyrosine kinases, most notably MET, suggesting other potential therapeutic targets. We report sustained clinical and functional imaging responses in two OCCA patients with chemotherapy-resistant disease who were treated with sunitinib, thus showing significant parallels with renal clear cell cancer.
Conclusions: Our findings highlight important therapeutic targets in OCCA, suggest that more extensive clinical trials with sunitinib in OCCA are warranted, and provide significant impetus to the growing realization that OCCA is molecularly and clinically distinct to other forms of ovarian cancer. Clin Cancer Res; 17(8); 2538-48. (C) 2011 AACR.
C1 [Anglesio, Michael S.; George, Joshy; Rischin, Danny; Power, Jeremy; Cowin, Prue A.; House, Colin M.; Gorringe, Kylie L.; Campbell, Ian G.; Bowtell, David D.] Peter MacCallum Canc Ctr, Melbourne, Vic 8006, Australia.
[George, Joshy; Bowtell, David D.] Univ Melbourne, Dept Biochem & Mol Biol, Parkville, Vic 3052, Australia.
[Friedlander, Michael; Lemech, Charlotte] Royal Hosp Women, Dept Med Oncol, Sydney, NSW, Australia.
[de Fazio, Anna] Univ Sydney, Westmead Millennium Inst, Westmead Hosp, Westmead Inst Canc Res, Sydney, NSW 2006, Australia.
[Anglesio, Michael S.; Huntsman, David G.; Gilks, C. Blake] Univ British Columbia, Dept Pathol, Vancouver, BC, Canada.
[Kalloger, Steve E.; Gilks, C. Blake] Prostate Res Ctr, Genet Pathol Evaluat Ctr, Vancouver, BC, Canada.
[Kalloger, Steve E.; Gilks, C. Blake] Vancouver Gen Hosp, Dept Pathol, Vancouver, BC V5Z 1M9, Canada.
[Kulbe, Hagen; Coward, Jermaine; Chakravarty, Probir] Queen Mary Univ London, Barts Canc Inst, Ctr Canc & Inflammat, London, England.
[Okamoto, Aikou] Jikei Univ, Dept Obstet & Gynecol, Sch Med, Tokyo, Japan.
[Okamoto, Aikou] Jikei Univ, Dept Gene Therapy, Sch Med, Inst DNA Med, Tokyo, Japan.
[Birrer, Michael J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Bowtell, DD (reprint author), Peter MacCallum Canc Ctr, Locked Bag 1 Abeckett St, Melbourne, Vic 8006, Australia.
EM d.bowtell@petermac.org
RI Coward, Jermaine/C-1779-2012; friedlander, michael/G-3490-2013; deFazio,
Anna/D-3939-2013; campbell, Ian/F-6006-2011; Coward,
Jermaine/F-2903-2016; Bowtell, David/H-1007-2016;
OI friedlander, michael/0000-0002-6488-0604; deFazio,
Anna/0000-0003-0057-4744; Coward, Jermaine/0000-0002-2309-9379; Bowtell,
David/0000-0001-9089-7525; Lemech, Charlotte/0000-0002-5399-9431;
Anglesio, Michael/0000-0003-1639-5003; Balkwill,
Frances/0000-0002-5587-9759
FU Victorian Life Sciences Computation Initiative; initiative of the
Victorian Government; U.S. Army Medical Research and Materiel Command
[DAMD17-01-1-0729]; Cancer Council Tasmania; Cancer Foundation of
Western Australia; National Health and Medical Research Council of
Australia
FX This research was supported by a Victorian Life Sciences Computation
Initiative grant on its Peak Computing Facility at the University of
Melbourne, an initiative of the Victorian Government. AOCS was supported
by the U.S. Army Medical Research and Materiel Command under
DAMD17-01-1-0729, The Cancer Council Tasmania, The Cancer Foundation of
Western Australia, and the National Health and Medical Research Council
of Australia.
NR 57
TC 99
Z9 103
U1 2
U2 21
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD APR 15
PY 2011
VL 17
IS 8
BP 2538
EP 2548
DI 10.1158/1078-0432.CCR-10-3314
PG 11
WC Oncology
SC Oncology
GA 750NP
UT WOS:000289555500049
PM 21343371
ER
PT J
AU Litovchick, L
Florens, LA
Swanson, SK
Washburn, MP
DeCaprio, JA
AF Litovchick, Larisa
Florens, Laurence A.
Swanson, Selene K.
Washburn, Michael P.
DeCaprio, James A.
TI DYRK1A protein kinase promotes quiescence and senescence through DREAM
complex assembly
SO GENES & DEVELOPMENT
LA English
DT Article
DE retinoblastoma-like protein p130; growth arrest; cell cycle; Down
syndrome; phosphorylation; cellular senescence
ID CELL-CYCLE CONTROL; DOWN-SYNDROME; IN-VIVO; IDENTIFICATION TECHNOLOGY;
CAENORHABDITIS-ELEGANS; REPRESSOR COMPLEX; TUMOR-SUPPRESSOR; B-MYB;
DROSOPHILA; E2F
AB In the absence of growth signals, cells exit the cell cycle and enter into G0 or quiescence. Alternatively, cells enter senescence in response to inappropriate growth signals such as oncogene expression. The molecular mechanisms required for cell cycle exit into quiescence or senescence are poorly understood. The DREAM (DP, RB [retinoblastoma], E2F, and MuvB) complex represses cell cycle-dependent genes during quiescence. DREAM contains p130, E2F4, DP1, and a stable core complex of five MuvB-like proteins: LIN9, LIN37, LIN52, LIN54, and RBBP4. In mammalian cells, the MuvB core dissociates from p130 upon entry into the cell cycle and binds to BMYB during S phase to activate the transcription of genes expressed late in the cell cycle. We used mass spectroscopic analysis to identify phosphorylation sites that regulate the switch of the MuvB core from BMYB to DREAM. Here we report that DYRK1A can specifically phosphorylate LIN52 on serine residue 28, and that this phosphorylation is required for DREAM assembly. Inhibiting DYRK1A activity or point mutation of LIN52 disrupts DREAM assembly and reduces the ability of cells to enter quiescence or undergo Ras-induced senescence. These data reveal an important role for DYRK1A in the regulation of DREAM activity and entry into quiescence.
C1 [Litovchick, Larisa; DeCaprio, James A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
[Litovchick, Larisa; DeCaprio, James A.] Harvard Univ, Brigham & Womens Hosp, Dept Med, Sch Med, Boston, MA 02115 USA.
[Florens, Laurence A.; Swanson, Selene K.; Washburn, Michael P.] Stowers Inst Biomed Res, Kansas City, MO 64110 USA.
[Washburn, Michael P.] Univ Kansas, Med Ctr, Dept Pathol & Lab Med, Kansas City, KS 66160 USA.
[DeCaprio, James A.] Dana Farber Canc Inst, Belfer Inst Appl Canc Sci, Boston, MA 02215 USA.
RP DeCaprio, JA (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
EM james_decaprio@dfci.harvard.edu
OI Florens, Laurence/0000-0002-9310-6650; Washburn,
Michael/0000-0001-7568-2585
FU Public Health Service [P01CA050661, RO1CA93804, R01CA63113]; DOD
[W81XWH-08-1-0048]
FX We are grateful to M. Padi for help with bioinformatics analysis, and to
R. Toddings and Y. Skversky for technical assistance. We thank Eric
McIntush (Bethyl Laboratories) for antibodies, and N. Dyson and W. G.
Kaelin Jr. for helpful suggestions. This work was supported in part by
Public Health Service grants P01CA050661, RO1CA93804, and R01CA63113 to
J.A.D., and by the DOD New Investigator Award W81XWH-08-1-0048 to L.L.
NR 58
TC 75
Z9 76
U1 2
U2 5
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 0890-9369
EI 1549-5477
J9 GENE DEV
JI Genes Dev.
PD APR 15
PY 2011
VL 25
IS 8
BP 801
EP 813
DI 10.1101/gad.2034211
PG 13
WC Cell Biology; Developmental Biology; Genetics & Heredity
SC Cell Biology; Developmental Biology; Genetics & Heredity
GA 750PD
UT WOS:000289559600004
PM 21498570
ER
PT J
AU Tschop, K
Conery, AR
Litovchick, L
DeCaprio, JA
Settleman, J
Harlow, E
Dyson, N
AF Tschoep, Katrin
Conery, Andrew R.
Litovchick, Larisa
DeCaprio, James A.
Settleman, Jeffrey
Harlow, Ed
Dyson, Nicholas
TI A kinase shRNA screen links LATS2 and the pRB tumor suppressor
SO GENES & DEVELOPMENT
LA English
DT Article
DE retinoblastoma tumor suppressor; LATS2; HIPPO pathway; DREAM complex;
senescence; G1 arrest
ID CELL-CYCLE EXIT; ONCOGENE-INDUCED SENESCENCE; RETINOBLASTOMA PROTEIN;
HETEROCHROMATIN FOCI; HIPPO PATHWAY; PREMATURE SENESCENCE;
PROSTATE-CANCER; PROMOTER HYPERMETHYLATION; MOLECULAR DISSECTION;
CONTACT INHIBITION
AB pRB-mediated inhibition of cell proliferation is a complex process that depends on the action of many proteins. However, little is known about the specific pathways that cooperate with the Retinoblastoma protein (pRB) and the variables that influence pRB's ability to arrest tumor cells. Here we describe two shRNA screens that identify kinases that are important for pRB to suppress cell proliferation and pRB-mediated induction of senescence markers. The results reveal an unexpected effect of LATS2, a component of the Hippo pathway, on pRB-induced phenotypes. Partial knockdown of LATS2 strongly suppresses some pRB-induced senescence markers. Further analysis shows that LATS2 cooperates with pRB to promote the silencing of E2F target genes, and that reduced levels of LATS2 lead to defects in the assembly of DREAM (DP, RB [retinoblastoma], E2F, and MuvB) repressor complexes at E2F-regulated promoters. Kinase assays show that LATS2 can phosphorylate DYRK1A, and that it enhances the ability of DYRK1A to phosphorylate the DREAM subunit LIN52. Intriguingly, the LATS2 locus is physically linked with RB1 on 13q, and this region frequently displays loss of heterozygosity in human cancers. Our results reveal a functional connection between the pRB and Hippo tumor suppressor pathways, and suggest that low levels of LATS2 may undermine the ability of pRB to induce a permanent cell cycle arrest in tumor cells.
C1 [Tschoep, Katrin; Settleman, Jeffrey; Dyson, Nicholas] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA 02129 USA.
[Conery, Andrew R.; Harlow, Ed] Harvard Univ, Dept Biol Chem & Mol Pharmacol, Sch Med, Boston, MA 02115 USA.
[Litovchick, Larisa; DeCaprio, James A.] Dana Farber Canc Inst, Boston, MA 02215 USA.
RP Dyson, N (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA 02129 USA.
EM dyson@helix.mgh.harvard.edu
FU NIH [GM81607, CA64402]; German Research Foundation (DFG) [TS 235/1-1];
ACS [PF-07-030-01-CCG]
FX We thank Jianmin Zhang for the pWPI-YAP(S127A) expression vector, and
Anurag Singh for providing the pWPI-H-Ras12V expression vector. We also
thank Endre Anderssen for advice and help with statistical data
analysis, and Patricia Greninger for assistance with the microarray gene
expression analysis. We are also very grateful to W. Endege and members
of the Dyson and Harlow laboratories for helpful discussions and
technical assistance and reading of the manuscript. We especially thank
Peter Adams and Phil Hinds for valuable advice and critical reading of
the manuscript. This work was supported by NIH grants GM81607 and
CA64402 (to N.D). K. T. was supported by the German Research Foundation
(DFG) post-doctoral research fellowship TS 235/1-1. A. R. C. was
supported by ACS post-doctoral fellowship number PF-07-030-01-CCG. N.D.
is the MGH Cancer Center Saltonstall Foundation Scholar.
NR 91
TC 55
Z9 57
U1 1
U2 9
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 0890-9369
EI 1549-5477
J9 GENE DEV
JI Genes Dev.
PD APR 15
PY 2011
VL 25
IS 8
BP 814
EP 830
DI 10.1101/gad.2000211
PG 17
WC Cell Biology; Developmental Biology; Genetics & Heredity
SC Cell Biology; Developmental Biology; Genetics & Heredity
GA 750PD
UT WOS:000289559600005
PM 21498571
ER
PT J
AU Healy, BC
Engler, D
Gholipour, T
Weiner, H
Bakshi, R
Chitnis, T
AF Healy, Brian C.
Engler, David
Gholipour, Taha
Weiner, Howard
Bakshi, Rohit
Chitnis, Tanuja
TI Accounting for disease modifying therapy in models of clinical
progression in multiple sclerosis
SO JOURNAL OF THE NEUROLOGICAL SCIENCES
LA English
DT Article
DE Disease modifying therapy; Disease progression; Longitudinal analysis;
Multiple sclerosis; Statistical modeling
ID NATURAL-HISTORY; LONGITUDINAL DATA; DISABILITY; MS; TRIALS
AB Identifying predictors of clinical progression in patients with relapsing-remitting multiple sclerosis (RRMS) is complicated in the era of disease modifying therapy (DMT) because patients follow many different DMT regimens. To investigate predictors of progression in a treated RRMS sample, a cohort of RRMS patients was prospectively followed in the Comprehensive Longitudinal Investigation of Multiple Sclerosis at the Brigham and Women's Hospital (CLIMB). Enrollment criteria were exposure to either interferon-beta (IFN-beta, n = 164) or glatiramer acetate (GA, n = 114) for at least 6 months prior to study entry. Baseline demographic and clinical features were used as candidate predictors of longitudinal clinical change on the Expanded Disability Status Scale (EDSS). We compared three approaches to account for DMT effects in statistical modeling. In all approaches, we analyzed all patients together and stratified based on baseline DMT. Model 1 used all available longitudinal EDSS scores, even those after on-study DMT changes. Model 2 used only clinical observations prior to changing DMT. Model 3 used causal statistical models to identify predictors of clinical change. When all patients were considered using Model 1, patients with a motor symptom as the first relapse had significantly larger change in EDSS scores during follow-up (p = 0.04); none of the other clinical or demographic variables significantly predicted change. In Models 2 and 3, results were generally unchanged. DMT modeling choice had a modest impact on the variables classified as predictors of EDSS score change. Importantly, however, interpretation of these predictors is dependent upon modeling choice. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Healy, Brian C.; Gholipour, Taha; Weiner, Howard; Bakshi, Rohit; Chitnis, Tanuja] Harvard Univ, Partners MS Ctr, Sch Med, Brigham & Womens Hosp,Dept Neurol, Brookline, MA 02115 USA.
[Healy, Brian C.] Massachusetts Gen Hosp, Ctr Biostat, Boston, MA 02114 USA.
[Engler, David] Brigham Young Univ, Dept Stat, Provo, UT 84602 USA.
RP Healy, BC (reprint author), Harvard Univ, Partners MS Ctr, Sch Med, Brigham & Womens Hosp,Dept Neurol, 6th Floor,1 Brookline Pl, Brookline, MA 02115 USA.
EM bchealy@partners.org
FU Merck-Serono
FX All authors had nothing to disclose related to this work. The CLIMB
study is sponsored in part by Merck-Serono.
NR 18
TC 4
Z9 4
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0022-510X
EI 1878-5883
J9 J NEUROL SCI
JI J. Neurol. Sci.
PD APR 15
PY 2011
VL 303
IS 1-2
BP 109
EP 113
DI 10.1016/j.jns.2010.12.024
PG 5
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 747SO
UT WOS:000289339900018
PM 21251671
ER
PT J
AU Berkey, CS
Willett, WC
Frazier, AL
Rosner, B
Tamimi, RM
Colditz, GA
AF Berkey, Catherine S.
Willett, Walter C.
Frazier, A. Lindsay
Rosner, Bernard
Tamimi, Rulla M.
Colditz, Graham A.
TI Prospective Study of Growth and Development in Older Girls and Risk of
Benign Breast Disease in Young Women
SO CANCER
LA English
DT Article
DE adolescents; preteens; age at menarche; height; weight; BMI; height
growth spurt; peak growth velocity; BBD; breast cancer
ID BODY-MASS INDEX; NURSES HEALTH; EARLY-LIFE; MILK CONSUMPTION; CANCER
RISK; PROSPECTIVE COHORT; AMERICAN WOMEN; HEIGHT GROWTH; CHILDHOOD;
ADOLESCENCE
AB BACKGROUND: In adult women with retrospective data, childhood adiposity, pubertal growth and development were associated with benign breast disease (BBD) and/or breast cancer. The authors prospectively evaluated these childhood/adolescent characteristics and BBD risk. METHODS: The Growing Up Today Study (GUTS) included females, aged 9-15 years in 1996, who completed annual questionnaires through 2001, then 2003, 2005, and 2007. Participants annually/biennially provided information on menarche, height, and weight, from which the authors derived body mass index (BMI in kg/m(2)). Peak height growth velocity (PHV in cm/year) was estimated from longitudinal data. On 2005-2007 surveys, 6899 females (18-27 years of age) reported whether a healthcare provider ever diagnosed BBD (n = 147), and whether it was confirmed by biopsy (n = 67). Logistic models investigated risk factors adjusted for age, alcohol, pregnancy, and maternal history. RESULTS: More childhood adiposity (odds ratio [OR], 0.91/[kg/m(2)]; P = .04) and shorter adult height (OR, 0.93/inch shorter; P = .07) were associated with lower risk of biopsy-confirmed BBD. Girls with most rapid height growth were at increased risk (OR, 2.12; P = .09) relative to those with the slowest growth. Age at menarche was not associated (OR, 1.11/year; P = .32) nor was adult BMI (adjusted for childhood BMI: OR, 1.01/[kg/m(2)]; P = .98); larger BMI increases (childhood to adulthood) were not protective (OR + 1.04/[kg/m(2)]; P = .37). Among girls with maternal breast cancer, those with more rapid growth had higher risk (OR, 1.47/[cm/year]; P = .02). All estimates were age-adjusted. CONCLUSIONS: Increased BBD risk (likely evolving to elevated breast cancer risk) was observed in thinner girls, girls with the most rapid growth, and taller women. Contrary to expectations, later menarche age was not protective against BBD, consistent with studies that found BBD patients are not protected against breast cancer by later menarche. Cancer 2011;117:1612-20. (C) 2011 American Cancer Society.
C1 [Berkey, Catherine S.; Frazier, A. Lindsay; Rosner, Bernard; Tamimi, Rulla M.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA.
[Berkey, Catherine S.; Frazier, A. Lindsay; Rosner, Bernard; Tamimi, Rulla M.] Harvard Univ, Sch Med, Boston, MA USA.
[Willett, Walter C.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Willett, Walter C.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Frazier, A. Lindsay] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Colditz, Graham A.] Washington Univ, Sch Med, Alvin J Siteman Canc Ctr, St Louis, MO USA.
RP Berkey, CS (reprint author), Brigham & Womens Hosp, Dept Med, Channing Lab, 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 Breast Cancer Research Foundation (New York, NY); National Institutes of
Health (Bethesda, Md) [DK46834]; American Institute for Cancer Research;
American Cancer Society
FX This study was supported by a grant from The Breast Cancer Research
Foundation (New York, NY) and by DK46834 from the National Institutes of
Health (Bethesda, Md). Dr. Frazier was supported by an award from the
American Institute for Cancer Research. Dr. Colditz was supported, in
part, by an American Cancer Society Clinical Research Professorship.
NR 37
TC 15
Z9 15
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 APR 15
PY 2011
VL 117
IS 8
BP 1612
EP 1620
DI 10.1002/cncr.25692
PG 9
WC Oncology
SC Oncology
GA 746AM
UT WOS:000289213300009
PM 21328325
ER
PT J
AU Hirata, H
Hinoda, Y
Majid, S
Chen, Y
Zaman, MS
Ueno, K
Nakajima, K
Tabatabai, ZL
Ishii, N
Dahiya, R
AF Hirata, Hiroshi
Hinoda, Yuji
Majid, Shahana
Chen, Yi
Zaman, Mohd S.
Ueno, Koji
Nakajima, Koichi
Tabatabai, Z. Laura
Ishii, Nobuhisa
Dahiya, Rajvir
TI DICKKOPF-4 Activates the Noncanonical c-Jun-NH2 Kinase Signaling Pathway
While Inhibiting the Wnt-Canonical Pathway in Human Renal Cell Carcinoma
SO CANCER
LA English
DT Article
DE real-time reverse transcriptase-polymerase chain reaction; 3-(4,
5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-
tetrazolium assay; colony-formation assay; fluorescence-activated cell
sorting; invasion assay; wound-healing assay; in vivo study; T-cell
factor/lymphoid enhancer factor reporter assay; noncanonical pathway;
canonical pathway
ID CANCER CELLS; COLORECTAL-CANCER; ANTAGONIST GENE; BREAST-CANCER; FAMILY
GENES; BETA-CATENIN; APOPTOSIS; JNK; EXPRESSION; REIC/DKK-3
AB BACKGROUND: To the authors' knowledge, the functional significance of the Wnt antagonist dickkopf homolog 4 (DKK4) has not been investigated previously in renal cancer. METHODS: The authors initially observed that the expression of DKK4 was significantly higher in renal cancer tissues compared with adjacent normal kidney tissues. To assess the function of DKK4, stable DKK4-transfected cells were established, and functional analyses were performed, including a T-cell factor/lymphoid enhancer factor (TCF/LEF) reporter assay and tests for cell viability, colony formation, apoptosis, cell cycle, invasive capability, wound-healing capability, and in vivo tumor growth. RESULTS: The relative TCF/LEF activity was significantly lower in DKK4-transfected cells compared with empty vector, and nuclear beta-catenin expression was decreased in DKK4 transfectants. In addition, expression levels of the beta-catenin downstream effector proteins cyclin D1 and c-Myc were decreased in DKK4 transfectants. However, greater invasiveness and migration were observed in stably transfected DKK4 cells. Increased growth of DKK4-transfected tumors also was observed in nude mice. Members of the Wnt noncanonical/c-Jun-NH2 kinase (JNK) signaling pathway also were effected, such as c-Jun, which had significantly increased expression and phosphorylation in DKK4-stable transfectants, and matrix metalloproteinase-2, which had significantly increased expression in DKK4-stable transfectants. CONCLUSIONS: This is the first study to indicate that DKK4 expression is increased in renal cancer tissues and that DKK4 activates the noncanonical JNK signaling pathway while inhibiting the Wnt-canonical pathway. Cancer 2011;117:1649-60. (C) 2010 American Cancer Society.
C1 [Hirata, Hiroshi; Majid, Shahana; Chen, Yi; Zaman, Mohd S.; Ueno, Koji; Dahiya, Rajvir] San Francisco VA Med Ctr, Dept Urol, San Francisco, CA USA.
[Hirata, Hiroshi; Majid, Shahana; Chen, Yi; Zaman, Mohd S.; Ueno, Koji; Tabatabai, Z. Laura; Dahiya, Rajvir] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Hinoda, Yuji] Yamaguchi Univ, Grad Sch Med, Dept Oncol & Lab Med, Yamaguchi, Japan.
[Nakajima, Koichi; Ishii, Nobuhisa] Toho Univ, Fac Med, Dept Urol, Tokyo, Japan.
[Tabatabai, Z. Laura] San Francisco VA Med Ctr, Dept Pathol, San Francisco, CA USA.
RP Dahiya, R (reprint author), Vet Affairs Med Ctr, Urol Res Ctr 112F, 4150 Clement St, San Francisco, CA 94121 USA.
EM rdahiya@urology.ucsf.edu
RI Chen, Yi /J-4807-2012
FU National Institutes of Health [RO1CA130860, RO1CA111470, T32-DK07790];
Veterans Affairs Research Enhancement Award Program (REAP); Merit Review
grants; Yamada Science Foundation
FX This study was supported by grants RO1CA130860, RO1CA111470, T32-DK07790
from the National Institutes of Health; by the Veterans Affairs Research
Enhancement Award Program (REAP); by Merit Review grants, and by the
Yamada Science Foundation.
NR 35
TC 17
Z9 18
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 APR 15
PY 2011
VL 117
IS 8
BP 1649
EP 1660
DI 10.1002/cncr.25666
PG 12
WC Oncology
SC Oncology
GA 746AM
UT WOS:000289213300013
PM 21472712
ER
PT J
AU Sui, J
Sheehan, J
Hwang, WC
Bankston, LA
Burchett, SK
Huang, CY
Liddington, RC
Beigel, JH
Marasco, WA
AF Sui, Jianhua
Sheehan, Jared
Hwang, William C.
Bankston, Laurie A.
Burchett, Sandra K.
Huang, Chiung-Yu
Liddington, Robert C.
Beigel, John H.
Marasco, Wayne A.
TI Wide Prevalence of Heterosubtypic Broadly Neutralizing Human
Anti-Influenza A Antibodies
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID INFLUENZA-A VIRUS; UNIVERSAL ANTIBODIES; AVIAN INFLUENZA; FUSION
PEPTIDE; HEMAGGLUTININ; INFECTION; SUBTYPES; VACCINE; PROTECTION;
INDUCTION
AB Background. Lack of life-long immunity against influenza viruses represents a major global health care problem with profound medical and economic consequences. A greater understanding of the broad-spectrum "heterosubtypic'' neutralizing human antibody (BnAb) response to influenza should bring us closer toward a universal influenza vaccine.
Methods. Serum samples obtained from 77 volunteers in an H5N1 vaccine study were analyzed for cross-reactive antibodies (Abs) against both subtype hemagglutinins (HAs) and a highly conserved pocket on the HA stem of Group 1 viruses. Cross-reactive Abs in commercial intravenous immunoglobulin were affinity purified using H5-coupled beads followed by step-wise monoclonal antibody competition or acid elution. Enzyme-linked immunosorbent assays were used to quantify cross-binding, and neutralization activity was determined with HA-pseudotyped viruses.
Results. Prevaccination serum samples have detectable levels of heterosubtypic HA binding activity to both Group 1 and 2 influenza A viruses, including subtypes H5 and H7, respectively, to which study subjects had not been vaccinated. Two different populations of Broadly neutralizing Abs (BnAbs) were purified from intravenous immunoglobulin by H5 beads: similar to 0.01% of total immunoglobulin G can bind to HAs from both Group 1 and 2 and neutralize H1N1 and H5N1 viruses; similar to 0.001% is F10-like Abs directed against the HA stem pocket on Group 1 viruses.
Conclusion. These data-to our knowledge, for the first time-quantitatively show the presence, albeit at low levels, of two populations of heterosubtypic BnAbs against influenza A in human serum. These observations warrant further investigation to determine their origin, host polymorphism(s) that may affect their expression levels and how to boost these BnAb responses by vaccination to reach sustainable protective levels.
C1 [Sui, Jianhua; Sheehan, Jared; Marasco, Wayne A.] Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA.
[Sui, Jianhua; Marasco, Wayne A.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Burchett, Sandra K.] Childrens Hosp, Div Infect Dis, Boston, MA 02115 USA.
[Hwang, William C.; Bankston, Laurie A.; Burchett, Sandra K.; Liddington, Robert C.] Sanford Burnham Med Res Inst, Infect & Inflammatory Dis Ctr, La Jolla, CA USA.
[Huang, Chiung-Yu] NIAID, NIH, Bethesda, MD 20892 USA.
[Beigel, John H.] SAIC Frederick Inc, NIAID, NCI, Lab Immunoregulat,Div Intramural Res, Frederick, MD USA.
RP Marasco, WA (reprint author), Dana Farber Canc Inst, Dept Canc Immunol & AIDS, 44 Binney St,JFB 824, Boston, MA 02115 USA.
EM wayne_marasco@dfci.harvard.edu
OI SUI, JIANHUA/0000-0002-1272-9662
FU National Institute of Allergy and Infectious Diseases, National
Institute of Health [U01-AI074518]; National Cancer Institute, National
Institute of Health [HHSN261200800001E]; National Institutes of Health
(NIH)
FX This project has been funded in whole or in part with federal funds from
the National Institute of Allergy and Infectious Diseases, National
Institute of Health (U01-AI074518); and the National Cancer Institute,
National Institute of Health (HHSN261200800001E). 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 US
Government.; J. Sui and W.A.M. have received a share of patent royalties
paid to their institution from Genentech/Roche for the licensed patent
that covers antibodies such as the F10 that was used in the study. R.L.
and L.B. have received grant support, travel/meeting expenses, and
institutional support for writing assistance, medicines, equipment, or
administrative support from the National Institutes of Health (NIH).
W.C.H. and J. Sheehan have received support from the NIH through their
institutions. All other authors: no conflicts.
NR 24
TC 56
Z9 57
U1 1
U2 8
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 APR 15
PY 2011
VL 52
IS 8
BP 1003
EP 1009
DI 10.1093/cid/cir121
PG 7
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 747DI
UT WOS:000289300100008
PM 21460314
ER
PT J
AU Cadena, J
Tierney, CJ
Restrepo, MI
AF Cadena, Jose
Tierney, Carrie J.
Restrepo, Marcos I.
TI Preventing Ventilator Associated Pneumonia: Looking Beyond the Bundles
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Letter
ID PROGRAM; IMPACT
C1 [Cadena, Jose; Restrepo, Marcos I.] Univ Texas Hlth Sci Ctr San Antonio, Dept Med, San Antonio, TX 78229 USA.
[Cadena, Jose] S Texas Vet Hlth Care Syst, Dept Med, San Antonio, TX USA.
[Restrepo, Marcos I.] VERDICT Res Ctr, Dept Pulm & Crit Care Med, San Antonio, TX USA.
RP Cadena, J (reprint author), 7703 Floyd Curl Dr MC 7881, San Antonio, TX 78229 USA.
EM cadenazuluag@uthscsa.e-du
RI Restrepo, Marcos/H-4442-2014
FU NHLBI NIH HHS [K23HL096054, K23 HL096054]
NR 9
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD APR 15
PY 2011
VL 52
IS 8
BP 1083
EP 1084
DI 10.1093/cid/cir127
PG 2
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 747DI
UT WOS:000289300100026
PM 21460331
ER
PT J
AU Klawiter, EC
Schmidt, RE
Trinkaus, K
Liang, HF
Budde, MD
Naismith, RT
Song, SK
Cross, AH
Benzinger, TL
AF Klawiter, Eric C.
Schmidt, Robert E.
Trinkaus, Kathryn
Liang, Hsiao-Fang
Budde, Matthew D.
Naismith, Robert T.
Song, Sheng-Kwei
Cross, Anne H.
Benzinger, Tammie L.
TI Radial diffusivity predicts demyelination in ex vivo multiple sclerosis
spinal cords
SO NEUROIMAGE
LA English
DT Article
DE Multiple sclerosis; Diffusion tensor imaging; Postmortum; Spinal cord
ID AXONAL DAMAGE; MAGNETIC-RESONANCE; WHITE-MATTER; MS PATIENTS; TENSOR;
LESIONS; MRI; BRAIN; ABNORMALITIES; ENCEPHALOMYELITIS
AB Objective: Correlation of diffusion tensor imaging (DTI) with histochemical staining for demyelination and axonal damage in multiple sclerosis (MS) ex vivo human cervical spinal cords.
Background: In MS, demyelination, axonal degeneration, and inflammation contribute to disease pathogenesis to variable degrees. Based upon in vivo animal studies with acute injury and histopathologic correlation, we hypothesized that DTI can differentiate between axonal and myelin pathologies within humans.
Methods: DTI was performed at 4.7 Ton 9 MS and 5 normal control fixed cervical spinal cord blocks following autopsy. Sections were then stained for Luxol fast blue (LFB), Bielschowsky silver, and hematoxylin and eosin (H&E). Regions of interest (ROIs) were graded semi-quantitatively as normal myelination, mild (<50%) demyelination. or moderate-severe (>50%) demyelination. Corresponding axonal counts were manually determined on Bielschowsky silver. ROIs were mapped to co-registered DTI parameter slices. DTI parameters evaluated included standard quantitative assessments of apparent diffusion coefficient (ADC), relative anisotropy (RA), axial diffusivity and radial diffusivity. Statistical correlations were made between histochemical gradings and DTI parameters using linear mixed models.
Results: Within ROIs in MS subjects, increased radial diffusivity distinguished worsening seventies of demyelination. Relative anisotropy was decreased in the setting of moderate-severe demyelination compared to normal areas and areas of mild demyelination. Radial diffusivity, ADC, and RA became increasingly altered within quartiles of worsening axonal counts. Axial diffusivity did not correlate with axonal density (p=0.091).
Conclusions: Increased radial diffusivity can serve as a surrogate for demyelination. However, radial diffusivity was also altered with axon injury, suggesting that this measure is not pathologically specific within chronic human MS tissue. We propose that radial diffusivity can serve as a marker of overall tissue integrity within chronic MS lesions. This study provides pathologic foundation for on-going in vivo DTI studies in MS. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Klawiter, Eric C.; Naismith, Robert T.; Cross, Anne H.] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA.
[Schmidt, Robert E.] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA.
[Trinkaus, Kathryn] Washington Univ, Sch Med, Div Biostat, St Louis, MO 63110 USA.
[Liang, Hsiao-Fang; Budde, Matthew D.; Song, Sheng-Kwei; Benzinger, Tammie L.] Washington Univ, Sch Med, Biomed MR Lab, Dept Radiol, St Louis, MO 63110 USA.
RP Klawiter, EC (reprint author), Massachusetts Gen Hosp, 15 Parkman St,WAC 835, Boston, MA 02446 USA.
EM eklawiter@partners.org
FU NIH [R01 NS054194, P01 NS059560, R01 DK19645, K23NS052430-01A1,
UL1RR024992]; National MS Society [CA1012, RG 3670A3/2]; American
Academy of Neurology Foundation; Manny and Rosalyn Rosenthal-Dr. John L
Trotter Chair in Neuroimmunology of Barnes-Jewish Hospital Foundation;
Bracco/American Roentgen Ray Society
FX NIH funding included R01 NS054194 (S.K.S.), P01 NS059560 (A.H.C.), R01
DK19645 (R.E.S.), K23NS052430-01A1 (R.T.N.) and UL1RR024992 (E.C.K.).
National MS Society funding included CA1012 (A.H.C.) and RG 3670A3/2
(S.K.S.). E.C.K. was supported by an American Academy of Neurology
Foundation Clinical Research Training Fellowship. A.H.C. was supported
in part by the Manny and Rosalyn Rosenthal-Dr. John L Trotter Chair in
Neuroimmunology of Barnes-Jewish Hospital Foundation. T.B. was supported
by a Bracco/American Roentgen Ray Society Scholar Award.
NR 36
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PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD APR 15
PY 2011
VL 55
IS 4
BP 1454
EP 1460
DI 10.1016/j.neuroimage.2011.01.007
PG 7
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 741DO
UT WOS:000288843500007
PM 21238597
ER
PT J
AU Qin, HX
Zheng, XJ
Zhong, XF
Shetty, AK
Elias, PM
Bollag, WB
AF Qin, Haixia
Zheng, Xiangjian
Zhong, Xiaofeng
Shetty, Anita K.
Elias, Peter M.
Bollag, Wendy B.
TI Aquaporin-3 in keratinocytes and skin: Its role and interaction with
phospholipase D2
SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
LA English
DT Review
ID CALCIUM-SENSING RECEPTOR; STRATUM-CORNEUM HYDRATION; MURINE EPIDERMAL
DIFFERENTIATION; ALTERNATIVELY SPLICED FORM; WATER CHANNEL AQUAPORIN-3;
EXTRACELLULAR CALCIUM; PERMEABILITY BARRIER;
ULTRASTRUCTURAL-LOCALIZATION; XENOPUS OOCYTES; POTENTIAL ROLE
AB Aquaporin 3 (AQP3) is an aquaglyceroporin that transports water and glycerol and is expressed in the epidermis, among other epithelial tissues. We have recently shown that there is an association between this glycerol channel and phospholipase D2 (PLD2) in caveolin-rich membrane microdomains. While PLD2 is able to hydrolyze membrane phospholipids to generate phosphatidic acid, this enzyme also catalyzes, in the presence of primary alcohols, a transphosphatidylation reaction to produce a phosphatidylalcohol. We have proposed that AQP3 associated with PLD2 provides the physiological primary alcohol glycerol to PLD2 for use in the transphosphatidylation reaction to generate phosphatidylglycerol (PG). Further, we have proposed that PG functions as a signaling molecule to mediate early epidermal keratinocyte differentiation, and manipulation of this signaling module inhibits keratinocyte proliferation and enhances differentiation. In contrast, other investigators have suggested a proliferative role for AQP3 in keratinocytes. In addition, AQP3 knockout mice exhibit an epidermal phenotype, characterized by dry skin, decreased elasticity and delayed barrier repair and wound healing, which can be corrected by glycerol but not other humectants. AQP3 levels have also been found to be altered in human skin diseases. In this article the evidence supporting a role for AQP3 in the epidermis will be discussed. Published by Elsevier Inc.
C1 [Bollag, Wendy B.] Georgia Hlth Sci Univ, Med Coll Georgia, Dept Physiol, Augusta, GA 30912 USA.
[Bollag, Wendy B.] Charlie Norwood VA Med Ctr, Augusta, GA 30904 USA.
[Qin, Haixia; Zheng, Xiangjian; Zhong, Xiaofeng; Shetty, Anita K.; Bollag, Wendy B.] Georgia Hlth Sci Univ, Med Coll Georgia, Inst Mol Med & Genet, Augusta, GA 30912 USA.
[Elias, Peter M.] San Francisco VA Med Ctr, San Francisco, CA 94121 USA.
[Elias, Peter M.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RP Bollag, WB (reprint author), Georgia Hlth Sci Univ, Med Coll Georgia, Dept Physiol, 1120 15th St, Augusta, GA 30912 USA.
EM wbollag@georgiahealth.edu
FU Veterans' Administration; National Institutes of Health/National
Institute of Arthritis, Musculoskeletal and Skin Diseases [AR45212]
FX This project was supported by a Merit Award from the Veterans'
Administration and a grant from the National Institutes of
Health/National Institute of Arthritis, Musculoskeletal and Skin
Diseases #AR45212.
NR 68
TC 14
Z9 15
U1 0
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-9861
J9 ARCH BIOCHEM BIOPHYS
JI Arch. Biochem. Biophys.
PD APR 15
PY 2011
VL 508
IS 2
SI SI
BP 138
EP 143
DI 10.1016/j.abb.2011.01.014
PG 6
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 740DO
UT WOS:000288772000003
PM 21276418
ER
PT J
AU Katiyar, SK
AF Katiyar, Santosh K.
TI Green tea prevents non-melanoma skin cancer by enhancing DNA repair
SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
LA English
DT Review
DE Chemoprevention; Contact hypersensitivity; Cyclobutane pyrimidine
dimers; Green tea polyphenols; Nucleotide excision repair; Non-melanoma
skin cancer; Ultraviolet radiation
ID RADIATION-INDUCED IMMUNOSUPPRESSION; ULTRAVIOLET-RADIATION; CONTACT
HYPERSENSITIVITY; PYRIMIDINE DIMERS; MOUSE SKIN; XERODERMA-PIGMENTOSUM;
TOPICAL APPLICATION; HYDROPHILIC CREAM; HAIRLESS MICE; RISK-FACTOR
AB Excessive exposure of the skin to solar ultraviolet (UV) radiation is one of the major factors for the development of skin cancers, including non-melanoma. For the last several centuries the consumption of dietary phytochemicals has been linked to numerous health benefits including the photoprotection of the skin. Green tea has been consumed as a popular beverage world-wide and skin photoprotection by green tea polyphenols (GTPs) has been widely investigated. In this article, we have discussed the recent investigations and mechanistic studies which define the potential efficacy of GTPs on the prevention of non-melanoma skin cancer. UV-induced DNA damage, particularly the formation of cyclobutane pyrimidine dimers, has been implicated in immunosuppression and initiation of skin cancer. Topical application or oral administration of green tea through drinking water of mice prevents UVB-induced skin tumor development, and this prevention is mediated, at least in part, through rapid repair of DNA. The DNA repair by GTPs is mediated through the induction of interleukin (IL)-12 which has been shown to have DNA repair ability. The new mechanistic investigations support and explain the anti-photocarcinogenic activity, in particular anti-non-melanoma skin cancer, of green tea and explain the benefits of green tea for human health. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Katiyar, Santosh K.] Univ Alabama, Dept Dermatol, Ctr Comprehens Canc, Birmingham, AL 35294 USA.
[Katiyar, Santosh K.] Univ Alabama, Dept Dermatol, Nutr Obes Res Ctr, Birmingham, AL 35294 USA.
[Katiyar, Santosh K.] Birmingham Vet Affairs Med Ctr, Birmingham, AL 35294 USA.
RP Katiyar, SK (reprint author), Univ Alabama, Dept Dermatol, Ctr Comprehens Canc, 1670 Univ Blvd,Volker Hall 557, Birmingham, AL 35294 USA.
EM skatiyar@uab.edu
FU National Institutes of Health [CA104428, CA140832, AT002536]; Veteran
Affairs Merit Review Award
FX The work reported from Dr. Katiyar's laboratory was supported by the
funds from National Institutes of Health (CA104428, CA140832, and
AT002536) and Veteran Affairs Merit Review Award. The content of this
article does not necessarily reflect the views or policies of the
funding agencies. Grateful thanks to all of the past and present members
of my research group for their outstanding contributions.
NR 67
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PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-9861
J9 ARCH BIOCHEM BIOPHYS
JI Arch. Biochem. Biophys.
PD APR 15
PY 2011
VL 508
IS 2
SI SI
BP 152
EP 158
DI 10.1016/j.abb.2010.11.015
PG 7
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 740DO
UT WOS:000288772000005
PM 21094124
ER
PT J
AU Athar, M
Walsh, SB
Kopelovich, L
Elmets, CA
AF Athar, Mohammad
Walsh, Stephanie B.
Kopelovich, Levy
Elmets, Craig A.
TI Pathogenesis of nonmelanoma skin cancers in organ transplant recipients
SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
LA English
DT Review
DE Immunosuppression; Skin cancer; Organ transplant recepients;
Pathogenesis; Prevention
ID ULTRAVIOLET-RADIATION; CYCLOSPORINE-A; IMMUNOSUPPRESSIVE THERAPY;
ORNITHINE-DECARBOXYLASE; MEDICAL PROGRESS; CELL CARCINOMA; INDUCED
TUMORS; HAIRLESS MICE; CHEMOPREVENTION; CARCINOGENESIS
AB Nonmelanoma skin cancer (NMSC) is the most common human cancer, with an incidence of more than 1.2 million per year in the USA. The risk for the development of NMSCs increases by approximately 10-250 fold in chronically immune suppressed organ transplant recipients (OTRs). Solar UVB is the most common etiologic factor in the development of this neoplasm, both in immune competent and immune suppressed populations. This review provides a description of NMSC in OTRs. It also provides an account of the various immunologic and non-immune-dependent mechanisms involved in the pathogenesis and progression of NMSCs in OTRs. Finally, this review addresses possible strategies for the prevention of this cancer, particularly focusing on the aspects that may be incorporated to prevent negative effects of chemopreventive chemicals on graft survival. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Athar, Mohammad; Walsh, Stephanie B.; Elmets, Craig A.] Univ Alabama, Dept Dermatol, Birmingham, AL 35294 USA.
[Athar, Mohammad; Walsh, Stephanie B.; Elmets, Craig A.] Univ Alabama, Skin Dis Res Ctr, Birmingham, AL 35294 USA.
[Kopelovich, Levy] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
[Elmets, Craig A.] Birmingham VA Med Ctr, Birmingham, AL USA.
RP Athar, M (reprint author), Univ Alabama, Dept Dermatol, Volker Hall,Room 509,1530 3rd Ave S, Birmingham, AL 35294 USA.
EM mathar@uab.edu
FU NIH [R01 ES015323, N01-CN-43300, P30 AR050948, R21 ES017494, T32
AR053458]
FX This work was supported in part by NIH grants R01 ES015323 (to MA),
N01-CN-43300 (to MA), P30 AR050948, R21 ES017494 (to MA), and T32
AR053458 (SBW).
NR 53
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PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-9861
J9 ARCH BIOCHEM BIOPHYS
JI Arch. Biochem. Biophys.
PD APR 15
PY 2011
VL 508
IS 2
SI SI
BP 159
EP 163
DI 10.1016/j.abb.2011.01.004
PG 5
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 740DO
UT WOS:000288772000006
PM 21232524
ER
PT J
AU Siegle, GJ
Steinhauer, SR
Friedman, ES
Thompson, WS
Thase, ME
AF Siegle, Greg J.
Steinhauer, Stuart R.
Friedman, Edward S.
Thompson, Wesley S.
Thase, Michael E.
TI Remission Prognosis for Cognitive Therapy for Recurrent Depression Using
the Pupil: Utility and Neural Correlates
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Affect; cognitive therapy; depression; emotion; psychophysiology;
psychotherapy; pupilometry; remission
ID EMOTIONAL INFORMATION; UNIPOLAR DEPRESSION; BEHAVIORAL THERAPY; MAJOR
DEPRESSION; RESPONSES; INVENTORY; FMRI; RUMINATION; SEVERITY; DILATION
AB Background: Although up to 60% of people with major depressive disorder respond to cognitive therapy (CT) in controlled trials, clinicians do not routinely use standardized assessments to inform which patients should receive this treatment. Inexpensive, noninvasive prognostic indicators could aid in matching patients with appropriate treatments. Pupillary response to emotional information is an excellent candidate, reflecting limbic reactivity and executive control. This study examined 1) whether pretreatment assessment of pupillary responses to negative information were associated with remission in CT and 2) their associated brain mechanisms.
Methods: We examined whether pretreatment pupillary responses to emotional stimuli were prognostic for remission in an inception cohort of 32 unipolar depressed adults to 16 to 20 sessions of CT. Twenty patients were then assessed on the same task using functional magnetic resonance imaging. Pupillary responses were assessed in 51 never-depressed controls for reference.
Results: Remission was associated with either low initial severity or the combination of higher initial severity and low sustained pupillary responses to negative words (87% correct classification of remitters and nonremitters, 93% sensitivity, 80% specificity; 88% correct classification of high-severity participants, p < .01, 90% sensitivity, 92% specificity). Increased pupillary responses were associated with increased activity in dorsolateral prefrontal regions associated with executive control and emotion regulation.
Conclusions: For patients with higher severity, disruptions of executive control mechanisms responsible for initiating emotion regulation, which are indexed by low sustained pupil responses and targeted in therapy, maybe key to remitting in this intervention. These mechanisms can be measured using inexpensive noninvasive psychophysiological assessments.
C1 [Siegle, Greg J.; Steinhauer, Stuart R.; Friedman, Edward S.; Thase, Michael E.] Western Psychiat Inst & Clin, Dept Psychiat, Pittsburgh, PA 15213 USA.
[Siegle, Greg J.; Steinhauer, Stuart R.; Friedman, Edward S.; Thase, Michael E.] Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
[Steinhauer, Stuart R.] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Thompson, Wesley S.] Univ Calif San Diego, Dept Psychiat, San Diego, CA 92103 USA.
[Thase, Michael E.] Univ Penn, Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA.
[Thase, Michael E.] Philadelphia Vet Affairs Med Ctr, Philadelphia, PA USA.
RP Siegle, GJ (reprint author), Western Psychiat Inst & Clin, Dept Psychiat, 3811 OHara St, Pittsburgh, PA 15213 USA.
EM gsiegle@pitt.edu
FU National Institute of Mental Health [MH082998, MH064159, MH60473,
MH55762, MH58397, MH58356]; National Alliance for Research on
Schizophrenia and Depression; Veteran's Administration; Veteran's
Research Foundation; Agency for Healthcare Research and Quality; Eli
Lilly and Co.; GlaxoSmithKline; National Institute of Mental Health;
Sepracor, Inc.; American Psychiatric Publishing, Inc.; Guilford
Publications; Herald House; Oxford University Press; W.W. Norton and
Company, Inc.; Aspect Medical Systems; Indevus; AstraZeneca;
Bristol-Myers Squibb; Sanofi-Aventis; Wyeth-Ayerst; Cyberonics;
Novartis; North Star/St. Jude Medical; Medtronics; Respironics; Springer
FX This work was supported by National Institute of Mental Health Grant
Nos. MH082998, MH064159, MH60473, MH55762, MH58397, and MH58356;
National Alliance for Research on Schizophrenia and Depression, the
Veteran's Administration, and the Veteran's Research Foundation. The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the article. This material is the
result of work supported with resources and the use of facilities at the
Pittsburgh VA Healthcare System, Highland Drive Division. We thank Roma
Konecky, Lisa Farace, Agnes Haggerty, Mauri Cesare, Mandy Collier, Kelly
Magee, and the staff of the Mood Disorders Treatment and Research
Program at Western Psychiatric Institute and Clinic. Pupillary response
data from a subset of the participants in the current study, on
different tasks, has been published in other articles (19,23,34,36) but
not with regard to therapeutic change. Data on a subset of these
participants who were assessed with functional magnetic resonance
imaging following their pupil dilation assessment has also been
published (6,19,28), as have relationships of rumination to therapeutic
response in a superset of these participants (5). The data presented in
those publications do not overlap with this article. Portions of this
article were presented at the meeting of the Association for Behavioral
and Cognitive Therapies (2008), Orlando, Florida.; Greg Siegle is a
consultant for Trial IQ. Michael Thase reported having served as an
adviser/consultant for AstraZeneca; Bristol-Myers Squibb Company; Dey
Pharma LP; Eli Lilly and Co.; Forest Laboratories; Gerson Lehman Group;
GlaxoSmithKline; Guidepoint Global; H. Lundbeck A/S; MedAvante, Inc.;
Merck and Co., Inc.; Neuronetics, Inc.; Novartis; Otsuka; Ortho-McNeil
Pharmaceuticals; Pamlab, LLC; Pfizer (formerly Wyeth Ayerst
Pharmaceuticals); Schering-Plough (formerly Organon, Inc.); Shire US,
Inc.; Supernus Pharmaceuticals; Takeda (Lundbeck); and Transcept
Pharmaceuticals. Dr. Thase has been a member of the Speakers Bureaus for
AstraZeneca; Bristol-Myers Squibb Company; Eli Lilly and Co.; Merck and
Co., Inc.; and Pfizer (formerly Wyeth Ayerst Pharmaceuticals). He
receives grant funding from the Agency for Healthcare Research and
Quality, Eli Lilly and Co., GlaxoSmithKline, National Institute of
Mental Health, and Sepracor, Inc. Dr. Thase has equity holdings in
MedAvante, Inc. and receives royalty income from American Psychiatric
Publishing, Inc., Guilford Publications, Herald House, Oxford University
Press, and W.W. Norton and Company, Inc. His wife is employed as the
group scientific director for Embryon (Formerly Advogent; Embryon does
business with Bristol-Myers Squibb and Pfizer/Wyeth). Dr. Friedman has
obtained grant/research support from Aspect Medical Systems, Indevus,
AstraZeneca, Bristol-Myers Squibb, Sanofi-Aventis, Wyeth-Ayerst,
Cyberonics, Novartis, North Star/St. Jude Medical, Medtronics,
Respironics, National Institute of Mental Health, and Agency for
Healthcare Research and Quality. Dr. Friedman also has received other
financial or material support (expert testimony, patents, royalties)
from Springer. The work was conducted at the University of Pittsburgh
School of Medicine and VA Pittsburgh Healthcare System. All other
authors reported no biomedical financial interests or potential
conflicts of interest.
NR 38
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PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD APR 15
PY 2011
VL 69
IS 8
BP 726
EP 733
DI 10.1016/j.biopsych.2010.12.041
PG 8
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 741GS
UT WOS:000288852800009
PM 21447417
ER
PT J
AU Akavia, UD
Litvin, O
Sanchez-Garcia, F
Kotliar, HCD
Kim, J
Garraway, LA
Pe'er, D
AF Akavia, Uri David
Litvin, Oren
Sanchez-Garcia, Felix
Kotliar, Helen C. Dylan
Kim, Jessica
Garraway, Levi A.
Pe'er, Dana
TI A systems approach to understanding tumor specific drug response
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Akavia, Uri David; Litvin, Oren; Sanchez-Garcia, Felix; Kotliar, Helen C. Dylan; Pe'er, Dana] Columbia Univ, New York, NY USA.
[Kim, Jessica; Garraway, Levi A.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol,Broad Inst Harvard & MIT, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA SY17-02
DI 10.1158/1538-7445.AM2011-SY17-02
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701306067
ER
PT J
AU Akhavanfard, S
Rivera, MN
Dias-Santagata, DC
Vargas, SO
Pomeroy, S
Haber, DA
Iafrate, AJ
AF Akhavanfard, Sara
Rivera, Miguel N.
Dias-Santagata, Dora C.
Vargas, Sara O.
Pomeroy, Scott
Haber, Daniel A.
Iafrate, A. John
TI The tumor suppressor WTX is inactivated in a subset of pediatric tumors
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Akhavanfard, Sara; Rivera, Miguel N.; Dias-Santagata, Dora C.; Haber, Daniel A.; Iafrate, A. John] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Vargas, Sara O.; Pomeroy, Scott] Boston Childrens Hosp, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 4349
DI 10.1158/1538-7445.AM2011-4349
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701405262
ER
PT J
AU Anderson, KS
Wong, J
D'Souza, G
Riemer, AB
Lorch, J
Haddad, R
Pai, S
Longtine, J
Bryan, J
McClean, M
Labaer, J
Kelsey, K
Posner, MR
AF Anderson, Karen S.
Wong, Jessica
D'Souza, Gypsyamber
Riemer, Angelika B.
Lorch, Jochen
Haddad, Robert
Pai, Sarah
Longtine, Janina
Bryan, Janine
McClean, Michael
Labaer, Joshua
Kelsey, Karl
Posner, Marshall R.
TI Serum antibodies to the HPV16 proteome as biomarkers for head and neck
cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Anderson, Karen S.; Wong, Jessica; Riemer, Angelika B.; Lorch, Jochen; Haddad, Robert] Dana Farber Canc Inst, Boston, MA 02115 USA.
[D'Souza, Gypsyamber; Pai, Sarah] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
[Longtine, Janina] Brigham Amd Womens Hosp, Boston, MA USA.
[Bryan, Janine] Merck & Co Inc, West Point, PA USA.
[McClean, Michael] Boston Univ, Schoool Publ Hlth, Boston, MA 02215 USA.
[Labaer, Joshua] Arizona State Univ, Biodesign Inst, Tempe, AZ USA.
[Kelsey, Karl] Brown Univ, Sch Med, Providence, RI 02912 USA.
[Posner, Marshall R.] Mt Sinai Sch Med, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 902
DI 10.1158/1538-7445.AM2011-902
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701400231
ER
PT J
AU Asara, JM
Cantley, LC
Engelman, JA
AF Asara, John M.
Cantley, Lewis C.
Engelman, Jeffrey A.
TI A targeted approach to identify activators of class IA
phosphoinositide-3-kinase in cancers using tandem mass spectrometry
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Asara, John M.; Cantley, Lewis C.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Engelman, Jeffrey A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 5121
DI 10.1158/1538-7445.AM2011-5121
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701305272
ER
PT J
AU Bao, Y
Nimptsch, K
Chan, AT
Ng, K
Meyerhardt, JA
Willett, WC
Giovannucci, E
Fuchs, CS
AF Bao, Ying
Nimptsch, Katharina
Chan, Andrew T.
Ng, Kimmie
Meyerhardt, Jeffrey A.
Willett, Walter C.
Giovannucci, Edward
Fuchs, Charles S.
TI Reported behavior of eating anything at anytime and risk of colorectal
cancer in women
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Bao, Ying] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Nimptsch, Katharina; Willett, Walter C.; Giovannucci, Edward] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Chan, Andrew T.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Ng, Kimmie; Meyerhardt, Jeffrey A.; Fuchs, Charles S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 1903
DI 10.1158/1538-7445.AM2011-1903
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701406088
ER
PT J
AU Barretina, J
Stransky, N
Caponigro, G
Kim, S
Margolin, A
Venkhatesan, K
Kryukov, G
Berger, M
Monahan, J
Morais, P
Meltzer, J
Mahan, S
Sonkin, D
Raman, P
Jones, M
Meyer, V
Wilson, C
Thibault, J
Murray, L
Callahan, A
Che, J
Shipway, A
Li, NX
Engels, I
Su, A
Pinchback, R
Nedzel, J
Liefeld, T
Niu, LL
Hatton, C
Palescandolo, E
Gupta, S
Onofrio, R
Sougnez, C
MacConaill, L
Winckler, W
Reich, M
Mesirov, J
Ardlie, K
Getz, G
Morrissey, M
Warmuth, M
Meyerson, M
Finan, P
Golub, T
Weber, B
Harris, J
Sellers, W
Schlegel, R
Garraway, L
AF Barretina, Jordi
Stransky, Nicolas
Caponigro, Giordano
Kim, Sungjoon
Margolin, Adam
Venkhatesan, Kavitha
Kryukov, Gregory
Berger, Michael
Monahan, John
Morais, Paula
Meltzer, Jodi
Mahan, Scott
Sonkin, Dmitriy
Raman, Pichai
Jones, Michael
Meyer, Vic
Wilson, Christopher
Thibault, Joseph
Murray, Lauren
Callahan, Adam
Che, John
Shipway, Aaron
Li, Nanxin
Engels, Ingo
Su, Andrew
Pinchback, Reid
Nedzel, Jared
Liefeld, Ted
Niu, Lili
Hatton, Charles
Palescandolo, Emanuele
Gupta, Supriya
Onofrio, Robert
Sougnez, Carrie
MacConaill, Laura
Winckler, Wendy
Reich, Michael
Mesirov, Jill
Ardlie, Kristin
Getz, Gad
Morrissey, Michael
Warmuth, Markus
Meyerson, Matthew
Finan, Peter
Golub, Todd
Weber, Barbara
Harris, Jennifer
Sellers, William
Schlegel, Robert
Garraway, Levi
TI Integrative analysis of the Cancer Cell Line Encyclopedia reveals
genetic and transcriptional predictors of compound sensitivity
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Barretina, Jordi; Stransky, Nicolas; Margolin, Adam; Kryukov, Gregory; Berger, Michael; Morais, Paula; Mahan, Scott; Murray, Lauren; Callahan, Adam; Pinchback, Reid; Nedzel, Jared; Liefeld, Ted; Gupta, Supriya; Onofrio, Robert; Sougnez, Carrie; Winckler, Wendy; Reich, Michael; Mesirov, Jill; Ardlie, Kristin; Getz, Gad; Meyerson, Matthew; Golub, Todd; Garraway, Levi] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Caponigro, Giordano; Venkhatesan, Kavitha; Monahan, John; Meltzer, Jodi; Sonkin, Dmitriy; Raman, Pichai; Jones, Michael; Meyer, Vic; Wilson, Christopher; Morrissey, Michael; Warmuth, Markus; Finan, Peter; Weber, Barbara; Sellers, William; Schlegel, Robert] Novartis Inst Biomed Res, Cambridge, MA USA.
[Kim, Sungjoon; Thibault, Joseph; Che, John; Shipway, Aaron; Li, Nanxin; Engels, Ingo; Su, Andrew; Harris, Jennifer] Novartis Res Fdn, Genom Inst, San Diego, CA USA.
[Niu, Lili; Hatton, Charles; Palescandolo, Emanuele; MacConaill, Laura] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 5455
DI 10.1158/1538-7445.AM2011-5455
PG 1
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701300326
ER
PT J
AU Bendell, J
LoRusso, P
Kwak, E
Pandya, S
Musib, L
Jones, C
De Crespigny, A
Belvin, M
McKenzie, M
Gates, MR
Chan, I
Shapiro, G
AF Bendell, Johanna
LoRusso, Patricia
Kwak, Eunice
Pandya, Susan
Musib, Luna
Jones, Cheryl
De Crespigny, Alex
Belvin, Marcia
McKenzie, Meghan
Gates, Mary R.
Chan, Iris
Shapiro, Geoffrey
TI Clinical combination of the MEK inhibitor GDC-0973 and the PI3K
inhibitor GDC-0941: A first-in-human phase Ib study in patients with
advanced solid tumors
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Bendell, Johanna] Sarah Cannon Res Inst, Nashville, TN USA.
[LoRusso, Patricia] Karmanos Canc Inst, Detriot, MI USA.
[Kwak, Eunice] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Pandya, Susan] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Musib, Luna; Jones, Cheryl; De Crespigny, Alex; Belvin, Marcia; McKenzie, Meghan; Gates, Mary R.; Chan, Iris] Genentech Inc, San Francisco, CA 94080 USA.
[Shapiro, Geoffrey] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-89
DI 10.1158/1538-7445.AM2011-LB-89
PG 2
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701404354
ER
PT J
AU Berger, MF
Lawrence, MS
Demichelis, F
Drier, Y
Cibulskis, K
Sivachenko, AY
Sboner, A
Esgueva, R
Pflueger, D
Sougnez, C
Onofrio, R
Carter, SL
Park, K
Habegger, L
Ambrogio, L
Fennell, T
Parking, M
Saksena, G
Voet, D
Ramose, AH
Pugh, TJ
Wilkinson, J
Fisher, S
Winckler, W
Mahan, S
Ardlie, K
Baldwin, J
Simons, JW
Kitabayashi, N
MacDonald, TY
Kantoff, PW
Chin, L
Gabriel, SB
Gerstein, MB
Golub, TR
Meyerson, M
Tewari, A
Lander, ES
Getz, G
Rubin, MA
Garraway, LA
AF Berger, Michael F.
Lawrence, Michael S.
Demichelis, Francesca
Drier, Yotam
Cibulskis, Kristian
Sivachenko, Andrey Y.
Sboner, Andrea
Esgueva, Raquel
Pflueger, Dorothee
Sougnez, Carrie
Onofrio, Robert
Carter, Scott L.
Park, Kyung
Habegger, Lukas
Ambrogio, Lauren
Fennell, Timothy
Parking, Melissa
Saksena, Gordon
Voet, Douglas
Ramose, Alex H.
Pugh, Trevor J.
Wilkinson, Jane
Fisher, Sheila
Winckler, Wendy
Mahan, Scott
Ardlie, Kristin
Baldwin, Jennifer
Simons, Jonathan W.
Kitabayashi, Naoki
MacDonald, Theresa Y.
Kantoff, Philip W.
Chin, Lynda
Gabriel, Stacey B.
Gerstein, Mark B.
Golub, Todd R.
Meyerson, Matthew
Tewari, Ashutosh
Lander, Eric S.
Getz, Gad
Rubin, Mark A.
Garraway, Levi A.
TI Characterization of complex chromosomal aberrations in prostate cancer
from whole genome sequencing
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Berger, Michael F.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Lawrence, Michael S.; Cibulskis, Kristian; Sivachenko, Andrey Y.; Sougnez, Carrie; Onofrio, Robert; Carter, Scott L.; Ambrogio, Lauren; Fennell, Timothy; Parking, Melissa; Saksena, Gordon; Voet, Douglas; Ramose, Alex H.; Pugh, Trevor J.; Wilkinson, Jane; Fisher, Sheila; Winckler, Wendy; Mahan, Scott; Ardlie, Kristin; Baldwin, Jennifer; Gabriel, Stacey B.; Golub, Todd R.; Lander, Eric S.; Getz, Gad] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Demichelis, Francesca; Esgueva, Raquel; Pflueger, Dorothee; Park, Kyung; Kitabayashi, Naoki; MacDonald, Theresa Y.; Tewari, Ashutosh; Rubin, Mark A.] Weill Cornell Med Coll, New York, NY USA.
[Drier, Yotam] Weitzmann Inst, Rehovot, Israel.
[Sboner, Andrea; Habegger, Lukas; Gerstein, Mark B.] Yale Univ, New Haven, CT USA.
[Simons, Jonathan W.] Prostate Canc Fdn, Santa Monica, CA USA.
[Kantoff, Philip W.; Chin, Lynda; Meyerson, Matthew; Garraway, Levi A.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 3925
DI 10.1158/1538-7445.AM2011-3925
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701403247
ER
PT J
AU Bitler, BG
Nicodemus, JP
Li, H
Cai, Q
Soring, K
Birrer, MJ
Connolly, DC
Godwin, AK
Cairns, P
Wu, H
Zhang, RG
AF Bitler, Benjamin G.
Nicodemus, Jasmine P.
Li, Hua
Cai, Qi
Soring, Keri
Birrer, Michael J.
Connolly, Denise C.
Godwin, Andrew K.
Cairns, Paul
Wu, Hong
Zhang, Rugang
TI Wnt5a-dependent induction of senescence suppresses epithelial ovarian
cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Bitler, Benjamin G.; Nicodemus, Jasmine P.; Li, Hua; Cai, Qi; Soring, Keri; Connolly, Denise C.; Godwin, Andrew K.; Cairns, Paul; Wu, Hong; Zhang, Rugang] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[Birrer, Michael J.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 1230
DI 10.1158/1538-7445.AM2011-1230
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701401473
ER
PT J
AU Blackburn, JS
Liu, S
Langenau, DM
AF Blackburn, Jessica S.
Liu, Sali
Langenau, David M.
TI Notch expression expands the pre-malignant pool of T-cell acute
lymphoblastic leukemia clones without affecting self-renewal
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Blackburn, Jessica S.; Liu, Sali; Langenau, David M.] Massachusetts Gen Hosp, Charlestown, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 4293
DI 10.1158/1538-7445.AM2011-4293
PG 1
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701301301
ER
PT J
AU Braun, CR
Mintseris, J
Gavathiotis, E
Bird, GH
Gygi, SP
Walensky, LD
AF Braun, Craig R.
Mintseris, Julian
Gavathiotis, Evripidis
Bird, Gregory H.
Gygi, Steven P.
Walensky, Loren D.
TI Photoreactive stapled peptides to capture cancer proteins and define
their sites of interaction
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Braun, Craig R.; Gavathiotis, Evripidis; Bird, Gregory H.; Walensky, Loren D.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Mintseris, Julian; Gygi, Steven P.] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 4871
DI 10.1158/1538-7445.AM2011-4871
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701403451
ER
PT J
AU Braun, CR
Mintseris, J
Gavathiotis, E
Bird, GH
Gygi, SP
Walensky, LD
AF Braun, Craig R.
Mintseris, Julian
Gavathiotis, Evripidis
Bird, Gregory H.
Gygi, Steven P.
Walensky, Loren D.
TI Photo reactive stapled peptides for target discovery in cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Braun, Craig R.; Gavathiotis, Evripidis; Bird, Gregory H.; Walensky, Loren D.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Mintseris, Julian; Gygi, Steven P.] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-241
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701306024
ER
PT J
AU Braun, CR
Mintseris, J
Gavathiotis, E
Bird, GH
Gygi, SP
Walensky, LD
AF Braun, Craig R.
Mintseris, Julian
Gavathiotis, Evripidis
Bird, Gregory H.
Gygi, Steven P.
Walensky, Loren D.
TI Photoreactive stapled peptides for target discovery in cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Braun, Craig R.; Gavathiotis, Evripidis; Bird, Gregory H.; Walensky, Loren D.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Mintseris, Julian; Gygi, Steven P.] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-241
DI 10.1158/1538-7445.AM2011-LB-241
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701305385
ER
PT J
AU Cato, L
Brown, M
AF Cato, Laura
Brown, Myles
TI Identification of the role of linker histone H1 in estrogen receptor
binding and activity
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Cato, Laura; Brown, Myles] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 260
DI 10.1158/1538-7445.AM2011-260
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701402191
ER
PT J
AU Cerchia, L
Esposito, CL
Catuogno, S
Iaboni, M
Draetta, G
Condorelli, G
de Franciscis, V
AF Cerchia, Laura
Esposito, Carla Lucia
Catuogno, Silvia
Iaboni, Margherita
Draetta, Giulio
Condorelli, Gerolama
de Franciscis, Vittorio
TI Specific targeting of cancer cells with RNA aptamers
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Cerchia, Laura; Esposito, Carla Lucia; Catuogno, Silvia; de Franciscis, Vittorio] CNR, IEOS, I-80125 Naples, Italy.
[Iaboni, Margherita; Condorelli, Gerolama] Univ Naples Federico II, DBPCM, Naples, Italy.
[Draetta, Giulio] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 626
DI 10.1158/1538-7445.AM2011-626
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701401023
ER
PT J
AU Chandarlapaty, S
Sawai, A
Rodrik-Outmezguine, V
Scaltriti, M
Serra, V
Baselga, J
Rosen, N
AF Chandarlapaty, Sarat
Sawai, Ayana
Rodrik-Outmezguine, Vanessa
Scaltriti, Maurizio
Serra, Violeta
Baselga, Jose
Rosen, Neal
TI Inhibition of PI3K-AKT signaling causes a FOXO-dependent induction of
receptor tyrosine kinase expression and phosphorylation in cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Chandarlapaty, Sarat; Sawai, Ayana; Rodrik-Outmezguine, Vanessa; Rosen, Neal] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Scaltriti, Maurizio; Baselga, Jose] Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
[Serra, Violeta] Vall dHebron Hosp, Barcelona, Spain.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 4690
DI 10.1158/1538-7445.AM2011-4690
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701305174
ER
PT J
AU Chang, I
Liu, J
Majid, S
Saini, S
Zaman, MS
Chen, Y
Singh, K
Shahryari, V
Sandhu, H
Yamamura, S
Dahiya, AV
Deng, GR
Tanaka, Y
AF Chang, Inik
Liu, Jan
Majid, Shahana
Saini, Sharanjot
Zaman, Mohd S.
Chen, Yi
Singh, Kamaldeep
Shahryari, Varahram
Sandhu, Herman
Yamamura, Soichiro
Dahiya, Angela V.
Deng, Guoren
Tanaka, Yuichiro
TI Protective effect of catechol-O-methyltransferase in human renal cell
carcinogenesis
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Chang, Inik; Liu, Jan; Majid, Shahana; Saini, Sharanjot; Zaman, Mohd S.; Chen, Yi; Singh, Kamaldeep; Shahryari, Varahram; Sandhu, Herman; Yamamura, Soichiro; Dahiya, Angela V.; Deng, Guoren; Tanaka, Yuichiro] San Francisco VA Med Ctr, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 1343
DI 10.1158/1538-7445.AM2011-1343
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701304257
ER
PT J
AU Chatziapostolou, M
Iliopoulos, D
AF Chatziapostolou, Maria
Iliopoulos, Dimitrios
TI Epigenetic-microRNA networks in colon cancer stem cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Chatziapostolou, Maria; Iliopoulos, Dimitrios] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 972
DI 10.1158/1538-7445.AM2011-972
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701303306
ER
PT J
AU Chen, J
Contino, G
Gurumurthy, S
Bardeesy, N
AF Chen, Jeff
Contino, Gianmarco
Gurumurthy, Sushma
Bardeesy, Nabeel
TI Effects of KRASG12D and P53 oncogenes on pancreatic cellular plasticity
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Chen, Jeff] Univ Calif Davis, Davis, CA 95616 USA.
[Contino, Gianmarco; Gurumurthy, Sushma; Bardeesy, Nabeel] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2462
DI 10.1158/1538-7445.AM2011-2462
PG 1
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701301361
ER
PT J
AU Chen, YA
Chen, ZH
Tsai, YY
Qu, XT
Iversen, E
Barnholtz-Sloan, J
Fridley, BL
Permuth-Wey, J
Risch, H
Cunningham, JM
Vierkant, RA
Fenstermacher, D
Sutphen, R
Phelan, CM
Monteiro, AN
Birrer, MJ
Cramer, DW
Narod, SA
McLaughlin, J
Schildkraut, JM
Goode, EL
Sellers, TA
AF Chen, Yian A.
Chen, Zhihua
Tsai, Ya-Yu
Qu, Xiaotao
Iversen, Edwin
Barnholtz-Sloan, Jill
Fridley, Brooke L.
Permuth-Wey, Jenny
Risch, Harvey
Cunningham, Julie M.
Vierkant, Robert A.
Fenstermacher, David
Sutphen, Rebecca
Phelan, Catherine M.
Monteiro, Alvaro N.
Birrer, Michael J.
Cramer, Daniel W.
Narod, Steven A.
McLaughlin, John
Schildkraut, Joellen M.
Goode, Ellen L.
Sellers, Thomas A.
TI Pathway and gene set analyses for epithelial ovarian cancer (EOC)
genome-wide association study (GWAS)
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Chen, Yian A.; Chen, Zhihua; Tsai, Ya-Yu; Qu, Xiaotao; Permuth-Wey, Jenny; Fenstermacher, David; Phelan, Catherine M.; Monteiro, Alvaro N.; Sellers, Thomas A.] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Iversen, Edwin; Schildkraut, Joellen M.] Duke Univ, Durham, NC USA.
[Barnholtz-Sloan, Jill] Case Comprehens Canc Ctr, Cleveland, OH USA.
[Fridley, Brooke L.; Cunningham, Julie M.; Vierkant, Robert A.; Goode, Ellen L.] Mayo Clin, Coll Med, Rochester, MN USA.
[Risch, Harvey] Yale Univ, New Haven, CT USA.
[Sutphen, Rebecca] Univ S Florida, Tampa, FL USA.
[Birrer, Michael J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Cramer, Daniel W.] Harvard Univ, Sch Med, Boston, MA USA.
[Narod, Steven A.] Ctr Res Womens Hlth, Toronto, ON, Canada.
[McLaughlin, John] Canc Care Ontario, Toronto, ON, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 4729
DI 10.1158/1538-7445.AM2011-4729
PG 2
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701400248
ER
PT J
AU Cheng, YK
Beroukhim, R
Levine, RL
Mellinghoff, IK
Holland, EC
Michor, F
AF Cheng, Yu-Kang
Beroukhim, Rameen
Levine, Ross L.
Mellinghoff, Ingo K.
Holland, Eric C.
Michor, Franziska
TI A mathematical methodology for determining the temporal order of pathway
alterations in cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Cheng, Yu-Kang; Beroukhim, Rameen; Michor, Franziska] DFCI, Boston, MA USA.
[Levine, Ross L.; Mellinghoff, Ingo K.; Holland, Eric C.] MSKCC, New York, NY USA.
NR 4
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-26
DI 10.1158/1538-7445.AM2011-LB-26
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701305421
ER
PT J
AU Cheung, LWT
Hennessy, BT
Li, J
Yu, SX
Myers, AP
Djordjevic, B
Lu, YL
Stemke-Hale, K
Zhang, F
Ju, ZL
Cantley, LC
Scherer, SE
Liang, H
Lu, KH
Russell, BR
Mills, GB
AF Cheung, Lydia Wai Ting
Hennessy, Bryan T.
Li, Jie
Yu, Shuangxing
Myers, Andrea P.
Djordjevic, Bojana
Lu, Yiling
Stemke-Hale, Katherine
Zhang, Fan
Ju, Zhenlin
Cantley, Lewis C.
Scherer, Steve E.
Liang, Han
Lu, Karen H.
Russell, Broaddus R.
Mills, Gordon B.
TI Mutation and functional analysis of PIK3CA and PIK3R1 in endometrial
cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Cheung, Lydia Wai Ting; Li, Jie; Yu, Shuangxing; Djordjevic, Bojana; Lu, Yiling; Stemke-Hale, Katherine; Zhang, Fan; Ju, Zhenlin; Liang, Han; Lu, Karen H.; Russell, Broaddus R.; Mills, Gordon B.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Hennessy, Bryan T.] Beaumont Hosp, Dublin 9, Ireland.
[Hennessy, Bryan T.] Royal Coll Surg, Dublin, Ireland.
[Myers, Andrea P.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Cantley, Lewis C.] Harvard Univ, Sch Med, Boston, MA USA.
[Scherer, Steve E.] Baylor Coll Med, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-247
DI 10.1158/1538-7445.AM2011-LB-247
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701302438
ER
PT J
AU Cho, YJ
Tamayo, P
Tsherniak, A
Meyerson, M
Mesirov, JP
Pomeroy, SL
AF Cho, Yoon-Jae
Tamayo, Pablo
Tsherniak, Aviad
Meyerson, Matthew
Mesirov, Jill P.
Pomeroy, Scott L.
TI Molecular classification and risk-stratification in medulloblastoma
using an integrative genomic approach
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Cho, Yoon-Jae; Pomeroy, Scott L.] Childrens Hosp, Boston, MA 02115 USA.
[Tamayo, Pablo; Tsherniak, Aviad; Mesirov, Jill P.] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Meyerson, Matthew] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 4760
DI 10.1158/1538-7445.AM2011-4760
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701303282
ER
PT J
AU Chun, E
Lee, MS
Asomaning, K
Wain, JC
Heist, R
Su, L
Christiani, DC
AF Chun, EunMi
Lee, Mi-Sun
Asomaning, Kofi
Wain, John C.
Heist, Rebecca
Su, Li
Christiani, David C.
TI Aspirin, NSAIDs, statins and risk of lung cancer: Gene by drug
interaction
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Chun, EunMi; Lee, Mi-Sun; Asomaning, Kofi; Su, Li; Christiani, David C.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Environm & Occupat Med & Epidemiol Program, Boston, MA 02115 USA.
[Wain, John C.; Heist, Rebecca] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Wain, John C.; Heist, Rebecca] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 284
DI 10.1158/1538-7445.AM2011-284
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701304470
ER
PT J
AU Coticchia, CM
Curatolo, AS
Zurakowski, D
Matulonis, UA
Moses, MA
AF Coticchia, Christine M.
Curatolo, Adam S.
Zurakowski, David
Matulonis, Ursula A.
Moses, Marsha A.
TI Urinary MMP-2 and MMP-9 predict the presence of ovarian cancer in women
with normal CA125 levels
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Coticchia, Christine M.; Curatolo, Adam S.; Zurakowski, David; Moses, Marsha A.] Childrens Hosp Boston, Boston, MA USA.
[Coticchia, Christine M.; Zurakowski, David; Matulonis, Ursula A.; Moses, Marsha A.] Harvard Univ, Sch Med, Boston, MA USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2818
DI 10.1158/1538-7445.AM2011-2818
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701404363
ER
PT J
AU Denlinger, CS
Keedy, VL
Cleary, JM
Kubasek, W
Onsum, M
Moulis, S
Garcia, G
Schoeberl, B
MacBeath, G
Nering, R
Murray, J
Moyo, V
Wong, KK
Shapiro, G
AF Denlinger, Crystal S.
Keedy, Vicki L.
Cleary, James M.
Kubasek, William
Onsum, Matthew
Moulis, Sharon
Garcia, Gabriela
Schoeberl, Birgit
MacBeath, Gavin
Nering, Rachel
Murray, James
Moyo, Victor
Wong, Kwok-Kin
Shapiro, Geoffrey
TI Phase I dose escalation study of MM-121, a fully human monoclonal
antibody to ErbB3, in patients with advanced solid tumors
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Denlinger, Crystal S.] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[Keedy, Vicki L.] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[Cleary, James M.; Wong, Kwok-Kin; Shapiro, Geoffrey] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Kubasek, William; Onsum, Matthew; Moulis, Sharon; Garcia, Gabriela; Schoeberl, Birgit; MacBeath, Gavin; Nering, Rachel; Murray, James; Moyo, Victor] Merrimack Pharmaceut, Cambridge, MA USA.
OI wong, kwok kin/0000-0001-6323-235X
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-410
DI 10.1158/1538-7445.AM2011-LB-410
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701404445
ER
PT J
AU Du, JY
He, F
Julian, BN
Mani, DR
Kung, A
Golub, T
AF Du, Jinyan
He, Frank
Julian, Bina
Mani, D. R.
Kung, Andrew
Golub, Todd
TI Systematic understanding of tyrosine kinase activation pattern in human
cancers
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Du, Jinyan; He, Frank; Julian, Bina; Mani, D. R.; Golub, Todd] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Kung, Andrew] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-330
DI 10.1158/1538-7445.AM2011-LB-330
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701306009
ER
PT J
AU Duan, ZF
Choy, E
Harmon, D
Liu, XZ
Mankin, H
Hornicek, F
AF Duan, Zhenfeng
Choy, Edwin
Harmon, David
Liu, Xianzhe
Mankin, Henry
Hornicek, Francis
TI Synthesis and evaluation of NSC23925 isomers to reverse multidrug
resistance in cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Duan, Zhenfeng; Choy, Edwin; Harmon, David; Liu, Xianzhe; Mankin, Henry; Hornicek, Francis] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 1732
DI 10.1158/1538-7445.AM2011-1732
PG 1
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701300080
ER
PT J
AU Ebi, H
Corcoran, RB
Singh, A
Chen, Z
Song, Y
Lifshits, E
Ryan, DP
Meyerhardt, JA
Benes, C
Settleman, J
Cantley, LC
Wong, KK
Engelman, JA
AF Ebi, Hiromichi
Corcoran, Ryan B.
Singh, Anurag
Chen, Zhao
Song, Youngchul
Lifshits, Eugene
Ryan, David P.
Meyerhardt, Jeffrey A.
Benes, Cyril
Settleman, Jeffrey
Cantley, Lewis C.
Wong, Kwok-Kin
Engelman, Jeffrey A.
TI Receptor tyrosine kinases, not KRAS, activate PI3K in KRAS mutant
colorectal cancers
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Ebi, Hiromichi; Corcoran, Ryan B.; Singh, Anurag; Song, Youngchul; Lifshits, Eugene; Ryan, David P.; Benes, Cyril; Settleman, Jeffrey; Engelman, Jeffrey A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Chen, Zhao; Meyerhardt, Jeffrey A.; Wong, Kwok-Kin] Dana Faber Canc Inst, Boston, MA USA.
[Cantley, Lewis C.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
OI wong, kwok kin/0000-0001-6323-235X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 956
DI 10.1158/1538-7445.AM2011-956
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701400265
ER
PT J
AU Ercan, D
Zhou, WJ
Yanagita, M
Capelletti, M
Rogers, A
Xiao, Y
Gray, NS
Janne, PA
AF Ercan, Dalia
Zhou, Wenjun
Yanagita, Masahiko
Capelletti, Marzia
Rogers, Andrew
Xiao, Yun
Gray, Nathanael S.
Janne, Pasi A.
TI Amplification of ERK2 mediates resistance to the novel irreversible EGFR
inhibitor WZ4002
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Ercan, Dalia; Zhou, Wenjun; Yanagita, Masahiko; Capelletti, Marzia; Rogers, Andrew; Xiao, Yun; Gray, Nathanael S.; Janne, Pasi A.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 4736
DI 10.1158/1538-7445.AM2011-4736
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701400255
ER
PT J
AU Fernandez, CA
Millholland, JM
Zwarthoff, EC
Loughlin, KR
Feldman, A
Karnes, RJ
Shuber, AP
AF Fernandez, Cecilia A.
Millholland, John M.
Zwarthoff, Ellen C.
Loughlin, Kevin R.
Feldman, Adam
Karnes, R. Jeffrey
Shuber, Anthony P.
TI Development of a non-invasive, multi-analyte assay for the triage of
patients presenting with hematuria
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Fernandez, Cecilia A.; Millholland, John M.; Shuber, Anthony P.] Predict Biosci, Lexington, MA USA.
[Zwarthoff, Ellen C.] Erasmus MC, Rotterdam, Netherlands.
[Loughlin, Kevin R.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Feldman, Adam] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Karnes, R. Jeffrey] Mayo Clin, Rochester, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-313
DI 10.1158/1538-7445.AM2011-LB-313
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701405416
ER
PT J
AU Fotoyati, A
Abu-Ali, S
Wang, PS
Deleyrolle, L
Lee, C
Tricott, J
Chen, J
Franciosi, S
Nakamura, Y
Sugita, Y
Uchiumi, T
Kuwano, M
Leavitt, BR
Singh, S
Jury, A
Jones, C
Wakimoto, H
Reynolds, BA
Pallen, CJ
Dunn, SE
AF Fotoyati, Abbas
Abu-Ali, Sam
Wang, Pei-Shan
Deleyrolle, Loic
Lee, Cathy
Tricott, Joanna
Chen, James
Franciosi, Sonia
Nakamura, Yas
Sugita, Yasuo
Uchiumi, Takeshi
Kuwano, Michihiko
Leavitt, Blair R.
Singh, Sheila
Jury, Alexa
Jones, Chris
Wakimoto, Hiroaki
Reynolds, Brent A.
Pallen, Catherine J.
Dunn, Sandra E.
TI Y-box binding protein-1 (YB-1) inhibition triggers differentiation of
normal and cancer stem cells from the brain
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Fotoyati, Abbas; Abu-Ali, Sam; Wang, Pei-Shan; Lee, Cathy; Tricott, Joanna; Chen, James; Pallen, Catherine J.; Dunn, Sandra E.] Univ British Columbia, Vancouver, BC V5Z 1M9, Canada.
[Deleyrolle, Loic; Reynolds, Brent A.] Univ Florida, Gainesville, FL USA.
[Franciosi, Sonia; Leavitt, Blair R.] Ctr Mol Med & Therapy, Vancouver, BC, Canada.
[Nakamura, Yas; Uchiumi, Takeshi] St Marys Hosp, Kurume, Fukuoka, Japan.
[Sugita, Yasuo; Kuwano, Michihiko] Kurume Univ, Kurume, Fukuoka 830, Japan.
[Singh, Sheila] McMaster Univ, Hamilton, ON, Canada.
[Jury, Alexa; Jones, Chris] Imperial Canc Res, Sutton, Surrey, England.
[Wakimoto, Hiroaki] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-101
DI 10.1158/1538-7445.AM2011-LB-101
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701303335
ER
PT J
AU Galimberti, F
Busch, A
Chinyengetere, F
Ma, T
Sekula, D
Memoli, V
Dragnev, K
Liu, F
Andrew, AS
Greninger, P
Robbins, D
Settleman, J
Benes, C
Dmitrovsky, E
AF Galimberti, Fabrizio
Busch, Alex
Chinyengetere, Fadzai
Ma, Tian
Sekula, David
Memoli, Vincent
Dragnev, Konstantin
Liu, Fang
Andrew, Angeline S.
Greninger, Patricia
Robbins, David
Settleman, Jeff
Benes, Cyril
Dmitrovsky, Ethan
TI Gene expression profile predicts response to smoothened inhibitors in
epithelial cancers
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Galimberti, Fabrizio; Busch, Alex; Chinyengetere, Fadzai; Ma, Tian; Sekula, David; Memoli, Vincent; Dragnev, Konstantin; Liu, Fang; Andrew, Angeline S.; Robbins, David; Dmitrovsky, Ethan] Dartmouth Coll, Hitchcock Med Ctr, Dartmouth Med Sch, Hanover, NH 03756 USA.
[Greninger, Patricia; Settleman, Jeff; Benes, Cyril] Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 1615
DI 10.1158/1538-7445.AM2011-1615
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701401027
ER
PT J
AU Ganem, NJ
O'Rourke, KP
Pellman, D
AF Ganem, Neil J.
O'Rourke, Kevin P.
Pellman, David
TI Defining novel pathways that arrest genetically unstable tetraploid
cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Ganem, Neil J.; O'Rourke, Kevin P.; Pellman, David] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2941
DI 10.1158/1538-7445.AM2011-2941
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701402298
ER
PT J
AU Garcia-Garcia, C
Serra, V
Scaltriti, M
Ibrahim, Y
Guzman, M
Jessen, K
Liu, Y
Rommel, C
Tabernero, J
Baselga, J
AF Garcia-Garcia, Celina
Serra, Violeta
Scaltriti, Maurizio
Ibrahim, Yasir
Guzman, Marta
Jessen, Katti
Liu, Yi
Rommel, Christian
Tabernero, Josep
Baselga, Jose
TI Combination of TORC1/2 and MEK kinase inhibitors in colorectal cancer
models
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Garcia-Garcia, Celina; Serra, Violeta; Ibrahim, Yasir; Guzman, Marta] Vall dHebron Inst Oncol, Expt Therapeut Program, Barcelona, Spain.
[Scaltriti, Maurizio; Baselga, Jose] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Jessen, Katti; Liu, Yi; Rommel, Christian] Intellikine, La Jolla, CA USA.
[Tabernero, Josep] Vall dHebron Univ Hosp, Med Oncol Serv, Barcelona, Spain.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 653
DI 10.1158/1538-7445.AM2011-653
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701401348
ER
PT J
AU Gavathiotis, E
Reyna, D
Walensky, L
AF Gavathiotis, Evripidis
Reyna, Denis
Walensky, Loren
TI Small molecule activation of BAX-mediated apoptosis through direct
engagement of the BAX trigger site
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Gavathiotis, Evripidis; Reyna, Denis; Walensky, Loren] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 5476
DI 10.1158/1538-7445.AM2011-5476
PG 1
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701300186
ER
PT J
AU Ge, RB
Wang, ZW
Zeng, Q
Xu, XY
Olumi, A
AF Ge, Rongbin
Wang, Zongwei
Zeng, Qing
Xu, Xiaoyin
Olumi, Aria
TI F-box protein 10, an NF-KB-dependent anti-apoptotic protein, regulates
TRAIL-induced apoptosis through modulating c-Fos/c-FLIP pathway
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Ge, Rongbin; Wang, Zongwei; Olumi, Aria] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Zeng, Qing; Xu, Xiaoyin] Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 4099
DI 10.1158/1538-7445.AM2011-4099
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701402071
ER
PT J
AU George, RE
Luther, W
Ahmad, Z
Cullis, ER
Webber, H
Rodig, S
Pearson, ADJ
Chesler, L
AF George, Rani E.
Luther, William
Ahmad, Zahida
Cullis, Elizabeth R.
Webber, Hannah
Rodig, Scott
Pearson, Andrew D. J.
Chesler, Louis
TI The ALK-F1174L mutation accelerates MYCN-driven tumorigenesis in a
murine transgenic neuroblastoma model
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [George, Rani E.; Luther, William] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Ahmad, Zahida; Cullis, Elizabeth R.; Webber, Hannah; Pearson, Andrew D. J.; Chesler, Louis] Inst Canc Res, Sutton, Surrey, England.
[Rodig, Scott] Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 4757
DI 10.1158/1538-7445.AM2011-4757
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701303279
ER
PT J
AU Hahn, WC
AF Hahn, William C.
TI Functional genomics, transformation, and resistance
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Hahn, William C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA SY25-01
DI 10.1158/1538-7445.AM2011-SY25-01
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701306077
ER
PT J
AU Harris, LN
Sprecher, E
Wei-Gu, L
Lezon-Geyda, K
Sakar, S
Krop, I
Winer, EP
Tuck, DP
AF Harris, Lyndsay N.
Sprecher, Emmett
Wei-Gu, Lisa
Lezon-Geyda, Kimberly
Sakar, Sudipa
Krop, Ian
Winer, Eric P.
Tuck, David P.
TI Dynamic changes in gene expression after one dose of trastuzumab (T)
reveal novel biomarkers of response to combination therapy in HER2
positive early stage breast cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Harris, Lyndsay N.; Sprecher, Emmett; Wei-Gu, Lisa; Lezon-Geyda, Kimberly; Sakar, Sudipa; Tuck, David P.] Yale Univ, New Haven, CT USA.
[Krop, Ian; Winer, Eric P.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 4719
DI 10.1158/1538-7445.AM2011-4719
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701404372
ER
PT J
AU Heishi, T
Tsukada, K
Huang, YH
Kozin, S
Jain, RK
Fukumura, D
AF Heishi, Takahiro
Tsukada, Kosuke
Huang, Yuhui
Kozin, Sergey
Jain, Rakesh K.
Fukumura, Dal
TI Restoration of pen-vascular nitric oxide gradient radio-sensitizes
murine breast cancers via vascular normalization.
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Heishi, Takahiro; Tsukada, Kosuke; Huang, Yuhui; Kozin, Sergey; Jain, Rakesh K.; Fukumura, Dal] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-288
DI 10.1158/1538-7445.AM2011-LB-288
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701303403
ER
PT J
AU Heo, YS
Nagrath, S
Moore, AL
Malinowska, I
Zenali, M
Kwiatkowski, D
Toner, M
AF Heo, Yun Seok
Nagrath, Sunitha
Moore, Alessandra L.
Malinowska, Izabela
Zenali, Mahnaz
Kwiatkowski, David
Toner, Mehmet
TI Universal vitrification of circulating tumor cells (CTCs) by ultra-fast
cooling
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Heo, Yun Seok; Nagrath, Sunitha; Moore, Alessandra L.; Zenali, Mahnaz; Toner, Mehmet] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Engn Med, Boston, MA USA.
[Malinowska, Izabela; Kwiatkowski, David] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 4894
DI 10.1158/1538-7445.AM2011-4894
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701403475
ER
PT J
AU Horst, D
Shivdasani, RA
AF Horst, David
Shivdasani, Ramesh A.
TI Selectively high Wnt pathway activity in subpopulations of colon cancer
cells and its significance for tumor initiation
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Horst, David; Shivdasani, Ramesh A.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 5205
DI 10.1158/1538-7445.AM2011-5205
PG 1
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701300379
ER
PT J
AU Hulleman, E
Cloos, J
Noske, D
Tannous, BA
Vandertop, P
Kaspers, GL
Wurdinger, T
AF Hulleman, Esther
Cloos, Jacqueline
Noske, David
Tannous, Bakhos A.
Vandertop, P.
Kaspers, GertJan L.
Wurdinger, Tom
TI A chemical screen for the identification of novel therapeutics for
pediatric brain tumors
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Hulleman, Esther] Vrije Univ Amsterdam, Med Ctr, Dept Pediat Oncol, Neurooncol Res Grp, Amsterdam, Netherlands.
[Hulleman, Esther] Vrije Univ Amsterdam, Med Ctr, Dept Hematol, Neurooncol Res Grp, Amsterdam, Netherlands.
[Hulleman, Esther; Noske, David; Wurdinger, Tom] Vrije Univ Amsterdam, Med Ctr, Dept Neurosurg, Neurooncol Res Grp, Amsterdam, Netherlands.
[Cloos, Jacqueline] Vrije Univ Amsterdam, Med Ctr, Pediat Oncol Hematol, Amsterdam, Netherlands.
[Tannous, Bakhos A.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Tannous, Bakhos A.] Harvard Univ, Sch Med, Boston, MA USA.
[Vandertop, P.] Vrije Univ Amsterdam, Med Ctr, Dept & Neurosurg, Amsterdam, Netherlands.
[Kaspers, GertJan L.] Vrije Univ Amsterdam, Med Ctr, Dept Pediat Oncol Hematol, Amsterdam, Netherlands.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 3461
DI 10.1158/1538-7445.AM2011-3461
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701301387
ER
PT J
AU Ignatius, MS
Chen, E
Elpek, N
Nielsen, P
Linardic, C
Mempel, T
Langenau, DM
AF Ignatius, Myron S.
Chen, Eleanor
Elpek, Natalie
Nielsen, Petur
Linardic, Corinne
Mempel, Thorsten
Langenau, David M.
TI In vivo imaging identifies that myf5+embryonal
rhabdomyosarcoma-propagating cells are dynamically reorganized during
tumor growth
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Ignatius, Myron S.; Chen, Eleanor; Elpek, Natalie; Nielsen, Petur; Mempel, Thorsten; Langenau, David M.] Massachusetts Gen Hosp, Charlestown, MA USA.
[Linardic, Corinne] Duke Med Ctr, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 481
DI 10.1158/1538-7445.AM2011-481
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701302063
ER
PT J
AU Johnson, BE
AF Johnson, Bruce E.
TI Improving patient outcomes in lung cancer by targeting different driver
mutations
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Johnson, Bruce E.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA PL04-01
DI 10.1158/1538-7445.AM2011-PL04-01
PG 2
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701400241
ER
PT J
AU Johnson, N
Li, YC
Walton, Z
Li, DA
Moreau, L
Rodig, SJ
D'Andrea, AD
Thomas, H
Newell, DR
Curtin, NJ
Wong, KK
Shapiro, GI
AF Johnson, Neil
Li, Yu-Chen
Walton, Zandra
Li, Danan
Moreau, Lisa
Rodig, Scott J.
D'Andrea, Alan D.
Thomas, Huw
Newell, David R.
Curtin, Nicola J.
Wong, Kwok K.
Shapiro, Geoffrey I.
TI Combined cdk1 and PARP inhibition results in tumor regression in a
KrasG12D p53L/L murine lung adenocarcinoma model
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Johnson, Neil; Li, Yu-Chen; Walton, Zandra; Li, Danan; Moreau, Lisa; Rodig, Scott J.; D'Andrea, Alan D.; Wong, Kwok K.; Shapiro, Geoffrey I.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Thomas, Huw; Newell, David R.; Curtin, Nicola J.] Newcastle Univ, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2979
DI 10.1158/1538-7445.AM2011-2979
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701402401
ER
PT J
AU Kang, J
D'Andrea, A
Kozono, D
AF Kang, Josephine
D'Andrea, Alan
Kozono, David
TI Fanconi anemia pathway and DNA repair-based prognostic signatures in
ovarian cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Kang, Josephine] Harvard Radiat Oncol Program, Boston, MA USA.
[D'Andrea, Alan; Kozono, David] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2751
DI 10.1158/1538-7445.AM2011-2751
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701406100
ER
PT J
AU Karst, AM
Leyanon, K
Drapkin, R
AF Karst, Alison M.
Leyanon, Keren
Drapkin, Ronny
TI Transformation of primary human fallopian tube secretory epithelial
cells: A cell of origin for high-grade serous ovarian carcinoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Karst, Alison M.; Leyanon, Keren; Drapkin, Ronny] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 1588
DI 10.1158/1538-7445.AM2011-1588
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701302291
ER
PT J
AU Kashiwagi, S
Righi, E
Yuan, JP
Santosuosso, M
Ingraham, R
Orsulic, S
Birrer, M
Penson, R
Dranoff, G
Poznansky, MC
AF Kashiwagi, Satoshi
Righi, Elda
Yuan, Jianping
Santosuosso, Michael
Ingraham, Rachel
Orsulic, Sandra
Birrer, Michael
Penson, Richard
Dranoff, Glenn
Poznansky, Mark C.
TI Blockade of the CXCL12/CXCR4 axis with AMD3100 induces multimodal
antitumor effects in murine ovarian cancer and prolongs survival
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Kashiwagi, Satoshi; Righi, Elda; Yuan, Jianping; Santosuosso, Michael; Ingraham, Rachel; Birrer, Michael; Penson, Richard; Poznansky, Mark C.] Massachusetts Gen Hosp, Charlestown, MA USA.
[Orsulic, Sandra] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
[Dranoff, Glenn] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-387
DI 10.1158/1538-7445.AM2011-LB-387
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701400316
ER
PT J
AU Kawabata, S
Mercado, J
Hollander, MC
Wilson, W
Regales, L
Pao, W
Janne, PA
Wong, KK
Dennis, PA
AF Kawabata, Shigeru
Mercado, Jose
Hollander, M. Christine
Wilson, Willie
Regales, Lucia
Pao, William
Janne, Pasi A.
Wong, Kwok-Kin
Dennis, Phillip A.
TI Rapamycin prolongs overall survival and progression-free survival in a
mouse model of lung cancer in never smokers resistant to erlotinib
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Kawabata, Shigeru; Mercado, Jose; Hollander, M. Christine; Wilson, Willie; Dennis, Phillip A.] NCI, Med Oncol Branch, CCR, Bethesda, MD 20892 USA.
[Regales, Lucia] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Pao, William] Vanderbilt Univ, Nashville, TN 37235 USA.
[Janne, Pasi A.; Wong, Kwok-Kin] Dana Farber Canc Inst, Boston, MA 02115 USA.
OI wong, kwok kin/0000-0001-6323-235X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2836
DI 10.1158/1538-7445.AM2011-2836
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701302368
ER
PT J
AU Kawabata, S
Hollander, MC
Munasinghe, JP
Mercado, J
Brinster, LR
Butman, JA
Lonser, RR
Regales, L
Pao, W
Janne, PA
Wong, KK
Dennis, PA
AF Kawabata, Shigeru
Hollander, M. Christine
Munasinghe, Jeeva P.
Mercado, Jose
Brinster, Lauren R.
Butman, John A.
Lonser, Russell R.
Regales, Lucia
Pao, William
Janne, Pasi A.
Wong, Kwok-Kin
Dennis, Phillip A.
TI A new mouse model for epithelial ear neoplasms based upon expression of
mutant EGFRL858R/T790M
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Kawabata, Shigeru; Hollander, M. Christine; Mercado, Jose; Dennis, Phillip A.] NCI, Med Oncol Branch, CCR, Bethesda, MD 20892 USA.
[Munasinghe, Jeeva P.] NINDS, MRI Res Facil, Bethesda, MD 20892 USA.
[Brinster, Lauren R.] Div Vet Resources, Bethesda, MD USA.
[Butman, John A.] Ctr Clin, Radiol & Imaging Sci, Bethesda, MD USA.
[Lonser, Russell R.] NINDS, Surg Neurol Branch, Bethesda, MD 20892 USA.
[Regales, Lucia] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Pao, William] Vanderbilt Univ, Nashville, TN 37235 USA.
[Janne, Pasi A.; Wong, Kwok-Kin] Dana Farber Canc Inst, Boston, MA 02115 USA.
OI wong, kwok kin/0000-0001-6323-235X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2417
DI 10.1158/1538-7445.AM2011-2417
PG 1
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701300458
ER
PT J
AU Keith, RL
Blatchford, PJ
Kittelson, JK
Jackson, M
Franklin, WA
Minna, J
Kelly, K
Mao, J
Massion, P
Wilson, DO
Hirsch, FR
Bunn, PA
Geraci, MW
Miller, YE
AF Keith, Robert L.
Blatchford, Patrick J.
Kittelson, John K.
Jackson, Mary
Franklin, Wilbur A.
Minna, John
Kelly, Karen
Mao, Jenny
Massion, Pierre
Wilson, David O.
Hirsch, Fred R.
Bunn, Paul A.
Geraci, Mark W.
Miller, York E.
CA SPORE LCBCC Iloprost Trial
TI Oral iloprost improves endobronchial dysplasia in former smokers
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Keith, Robert L.; Miller, York E.] Denver Vet Affairs Med Ctr, Denver, CO USA.
[Blatchford, Patrick J.; Kittelson, John K.] Univ Colorado Denver, Aurora, CO USA.
[Jackson, Mary; Franklin, Wilbur A.; Kelly, Karen; Hirsch, Fred R.; Bunn, Paul A.; Geraci, Mark W.] Univ Colorado, Ctr Comprehens Canc, Aurora, CO USA.
[Minna, John] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Mao, Jenny] Univ Calif Los Angeles, Los Angeles, CA USA.
[Massion, Pierre] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
[Wilson, David O.] Univ Pittsburgh, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-90
DI 10.1158/1538-7445.AM2011-LB-90
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701404355
ER
PT J
AU Kim, HG
Mandinova, A
Hwang, SY
Schreiber, SL
Lee, SW
AF Kim, Hyung-Gu
Mandinova, Anna
Hwang, So Young
Schreiber, Stuart L.
Lee, Sam W.
TI DDR1 receptor kinase pathway as an emerging target in cancer
therapeutics
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Kim, Hyung-Gu; Mandinova, Anna; Hwang, So Young; Lee, Sam W.] Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA USA.
[Kim, Hyung-Gu; Mandinova, Anna; Hwang, So Young; Lee, Sam W.] Harvard Univ, Sch Med, Charlestown, MA USA.
[Schreiber, Stuart L.] Broad Inst Harvard & Massachusetts Inst Technol, Cambridge, MA USA.
NR 0
TC 0
Z9 1
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2313
DI 10.1158/1538-7445.AM2011-2313
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701304362
ER
PT J
AU Kim, YJ
Zhang, AY
Karl, D
Eisenger, K
Simon, MC
Yoon, SS
AF Kim, Yeo-Jung
Zhang, Alexia Y.
Karl, Daniel
Eisenger, Karin
Simon, M. Celeste
Yoon, Sam S.
TI Metronomic doxorubicin blocks hypoxia inducible factor-mediated
responses to hypoxia in sarcomas and augments the effects of anti-VEGF
therapy
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Kim, Yeo-Jung; Eisenger, Karin; Simon, M. Celeste] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Zhang, Alexia Y.; Karl, Daniel; Yoon, Sam S.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2851
DI 10.1158/1538-7445.AM2011-2851
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701303264
ER
PT J
AU Knutson, CG
Raczynski, AR
Zeng, Y
Iffrig, EM
Wishnok, JS
Korzenik, JR
Tannenbaum, SR
AF Knutson, Charles G.
Raczynski, Arek R.
Zeng, Yu
Iffrig, Elizabeth M.
Wishnok, John S.
Korzenik, Joshua R.
Tannenbaum, Steven R.
TI Discovery and application of a biomarker cassette to inflammatory bowel
disease
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Knutson, Charles G.; Raczynski, Arek R.; Zeng, Yu; Iffrig, Elizabeth M.; Wishnok, John S.; Tannenbaum, Steven R.] MIT, Cambridge, MA 02139 USA.
[Korzenik, Joshua R.] Massachusetts Gen Hosp, Cambridge, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 5113
DI 10.1158/1538-7445.AM2011-5113
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701305265
ER
PT J
AU Kozono, D
Nitta, M
Ng, K
Zinn, PO
Kushwaha, D
Koay, D
Merzon, D
Zhu, K
Zhu, S
Ligon, K
Chen, C
AF Kozono, David
Nitta, Masayuki
Ng, Kimberly
Zinn, Pascal O.
Kushwaha, Deepa
Koay, Debbie
Merzon, Dmitry
Zhu, Kaya
Zhu, Shan
Ligon, Keith
Chen, Clark
TI c-Myc modulates the dynamic transition between tumor initiating states
in glioblastoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Kozono, David; Nitta, Masayuki; Ng, Kimberly; Zinn, Pascal O.; Kushwaha, Deepa; Koay, Debbie; Merzon, Dmitry; Zhu, Kaya; Zhu, Shan; Ligon, Keith; Chen, Clark] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 3301
DI 10.1158/1538-7445.AM2011-3301
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701304049
ER
PT J
AU Kryukov, GV
Berger, MF
Stransky, N
Barretina, J
Onofrio, R
Caponigro, G
Sougnez, C
Monahan, J
Shefler, E
Venkhatesan, K
Cibulskis, K
Morais, P
Sivachenko, A
Meltzer, J
Lawrence, M
Ramos, A
Getz, G
Thibault, J
Mahan, S
Jones, M
Morrissey, M
Sonkin, D
Ardlie, KG
Golub, T
Weber, B
Warmuth, M
Sellers, W
Harris, J
Schlegel, R
Garraway, LA
AF Kryukov, Gregory V.
Berger, Michael F.
Stransky, Nicolas
Barretina, Jordi
Onofrio, Robert
Caponigro, Giordano
Sougnez, Carrie
Monahan, John
Shefler, Erica
Venkhatesan, Kavitha
Cibulskis, Kristian
Morais, Paula
Sivachenko, Andrey
Meltzer, Jodi
Lawrence, Michael
Ramos, Alex
Getz, Gad
Thibault, Joseph
Mahan, Scott
Jones, Michael
Morrissey, Michael
Sonkin, Dmitry
Ardlie, Kristin G.
Golub, Todd
Weber, Barbara
Warmuth, Markus
Sellers, William
Harris, Jennifer
Schlegel, Robert
Garraway, Levi A.
CA Broads Genome Sequencing Platform
TI Separating the wheat from the chaff: A first look at the Cancer Cell
Lines Encyclopedia sequencing data
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Kryukov, Gregory V.; Berger, Michael F.; Stransky, Nicolas; Barretina, Jordi; Onofrio, Robert; Sougnez, Carrie; Shefler, Erica; Cibulskis, Kristian; Morais, Paula; Sivachenko, Andrey; Lawrence, Michael; Ramos, Alex; Getz, Gad; Mahan, Scott; Ardlie, Kristin G.; Golub, Todd] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Caponigro, Giordano; Monahan, John; Venkhatesan, Kavitha; Meltzer, Jodi; Jones, Michael; Morrissey, Michael; Sonkin, Dmitry; Weber, Barbara; Warmuth, Markus; Sellers, William; Schlegel, Robert] Novartis Inst BioMed Res, Cambridge, MA USA.
[Thibault, Joseph; Harris, Jennifer; Broads Genome Sequencing Platform] Novartis Res Fdn, Genom Inst, San Diego, CA USA.
[Garraway, Levi A.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Garraway, Levi A.] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 923
DI 10.1158/1538-7445.AM2011-923
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701305331
ER
PT J
AU Kuruppu, D
Van Den Berg, N
Mahmood, U
Tanabe, KK
AF Kuruppu, Darshini
Van Den Berg, Nynke
Mahmood, Umar
Tanabe, Kenneth K.
TI Noninvasive reporter gene imaging for optimization of HSV-1 oncolysis in
hepatic metastases
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Kuruppu, Darshini; Van Den Berg, Nynke; Mahmood, Umar; Tanabe, Kenneth K.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 5319
DI 10.1158/1538-7445.AM2011-5319
PG 1
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701301185
ER
PT J
AU Kwong, LN
Jiang, S
Liu, HY
Chin, L
AF Kwong, Lawrence N.
Jiang, Shan
Liu, Huiyun
Chin, Lynda
TI Preclinical therapeutics in genetically engineered mouse models of
inducible NRAS and BRAF mutant melanoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Kwong, Lawrence N.; Jiang, Shan; Liu, Huiyun; Chin, Lynda] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2856
DI 10.1158/1538-7445.AM2011-2856
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701303269
ER
PT J
AU LaBelle, JL
Katz, SG
Bird, GH
Gavathiotis, E
Stewart, ML
Fisher, JK
Godes, M
Walensky, LD
AF LaBelle, James L.
Katz, Samuel G.
Bird, Gregory H.
Gavathiotis, Evripidis
Stewart, Michelle L.
Fisher, Jill K.
Godes, Marina
Walensky, Loren D.
TI Therapeutic reactivation of cell death in refractory hematologic cancers
using a broad spectrum BIM BH3 death helix
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [LaBelle, James L.; Katz, Samuel G.; Bird, Gregory H.; Gavathiotis, Evripidis; Stewart, Michelle L.; Fisher, Jill K.; Godes, Marina; Walensky, Loren D.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 1775
DI 10.1158/1538-7445.AM2011-1775
PG 1
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701300180
ER
PT J
AU Li, Y
Tian, RY
Iglehart, JD
Wang, ZGC
Richardson, AL
AF Li, Yang
Tian, Ruiyang
Iglehart, J. Dirk
Wang, Zhigang C.
Richardson, Andrea L.
TI The amplified cancer gene LAPTM4B plays a critical role in autophagosome
maturation and promotes cancer cell survival during metabolic stress
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Li, Yang; Tian, Ruiyang; Wang, Zhigang C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Iglehart, J. Dirk; Richardson, Andrea L.] Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 3772
DI 10.1158/1538-7445.AM2011-3772
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701400081
ER
PT J
AU Liao, S
Liu, JQ
Jain, RK
Xu, L
AF Liao, Shan
Liu, JieQiong
Jain, Rakesh K.
Xu, Lei
TI TGF-beta blockade controls ascites by preventing abnormalization of
lymphatic vessels in orthotopic human ovarian carcinoma model
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Liao, Shan; Jain, Rakesh K.; Xu, Lei] Massachusetts Gen Hosp, Cambridge, MA USA.
[Liu, JieQiong] Cent S Univ, Xiangya Hosp 2, Changsha, Hunan, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 1579
DI 10.1158/1538-7445.AM2011-1579
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701302283
ER
PT J
AU Lin, WC
Francis, J
Watanabe, H
Yan, Q
Kaelin, WG
Meyerson, M
AF Lin, Wenchu
Francis, Joshua
Watanabe, Hideo
Yan, Qin
Kaelin, William G.
Meyerson, Matthew
TI Inhibition of Men1-deficient tumor growth by inactivation of the Rbp2
histone demethylase
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Lin, Wenchu; Francis, Joshua; Watanabe, Hideo; Kaelin, William G.; Meyerson, Matthew] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Yan, Qin] Yale Univ, Sch Med, New Haven, CT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 62
DI 10.1158/1538-7445.AM2011-62
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701403042
ER
PT J
AU Lipinski, M
Furuya, T
Kim, M
Hoffman, G
Ng, A
Blenis, J
Xavior, R
Yuan, JY
AF Lipinski, Marta
Furuya, Tsuyoshi
Kim, Minsu
Hoffman, Greg
Ng, Aylwin
Blenis, John
Xavior, Ramnik
Yuan, Junying
TI Control of class III PI 3-kinase in autophagy and cancers
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Lipinski, Marta; Furuya, Tsuyoshi; Kim, Minsu; Hoffman, Greg; Blenis, John; Yuan, Junying] Harvard Univ, Sch Med, Boston, MA USA.
[Ng, Aylwin; Xavior, Ramnik] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA SY09-01
DI 10.1158/1538-7445.AM2011-SY09-01
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701306096
ER
PT J
AU Liu, JQ
Liao, S
Diop, B
Chen, W
Goel, S
Huang, YH
Boucher, Y
Jain, RK
Xu, L
AF Liu, Jieqiong
Liao, Shan
Diop, Benjamin
Chen, Wei
Goel, Shom
Huang, Yuhui
Boucher, Yves
Jain, Rakesh K.
Xu, Lei
TI TGF-beta blockade improves the distribution and efficacy of
chemotherapeutic agents in breast carcinoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Liu, Jieqiong] Cent S Univ, Xiangya Hosp 2, Dept Breast Surg, Changsha, Hunan, Peoples R China.
[Liao, Shan; Diop, Benjamin; Chen, Wei; Goel, Shom; Huang, Yuhui; Boucher, Yves; Jain, Rakesh K.; Xu, Lei] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 715
DI 10.1158/1538-7445.AM2011-715
PG 1
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701300008
ER
PT J
AU Liu, QS
Zhou, D
Shiotani, B
Gray, NS
Elledge, SJ
Zou, L
AF Liu, Qingsong
Zhou, Danny
Shiotani, Bunsho
Gray, Nathanael S.
Elledge, Stephen J.
Zou, Lee
TI Discovery and optimization of potent and selective benzonaphthyridinone
analogs as dual mTOR/ATR small molecular inhibitors for treatment of
cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Liu, Qingsong; Gray, Nathanael S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Zhou, Danny; Elledge, Stephen J.] Harvard Univ, Sch Med, Boston, MA USA.
[Shiotani, Bunsho; Zou, Lee] Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 1358
DI 10.1158/1538-7445.AM2011-1358
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701304271
ER
PT J
AU Ma, WX
Gutierrez, A
Goff, D
Geron, I
Sadarangani, A
Shih, A
Recart, AC
Jiang, QF
Wu, JC
Wu, CC
Leu, H
Wall, R
Geyrozaga, R
Diccianni, M
Li, K
VanArsdale, T
Wei, P
Carson, D
Look, AT
Jamieson, C
AF Ma, Wenxue
Gutierrez, Alejandro
Goff, Daniel
Geron, Ifat
Sadarangani, Anil
Shih, Alice
Recart, Angela Court
Jiang, Qingfei
Wu, Jerry C.
Wu, Christina C.
Leu, Heather
Wall, Russell
Geyrozaga, Rhonnie
Diccianni, Mitchell
Li, Kang
VanArsdale, Todd
Wei, Ping
Carson, Dennis
Look, A. Thomas
Jamieson, Catriona
TI A selective Notch1 mAb targets leukemia progenitor cells in T-ALL
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Ma, Wenxue; Goff, Daniel; Geron, Ifat; Sadarangani, Anil; Shih, Alice; Recart, Angela Court; Jiang, Qingfei; Wu, Jerry C.; Wu, Christina C.; Leu, Heather; Wall, Russell; Geyrozaga, Rhonnie; Diccianni, Mitchell; Carson, Dennis; Jamieson, Catriona] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Gutierrez, Alejandro; Look, A. Thomas] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Li, Kang; VanArsdale, Todd; Wei, Ping] Pfizer Inc, La Jolla, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 974
DI 10.1158/1538-7445.AM2011-974
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701303309
ER
PT J
AU Maire, CL
Ramkissoon, SH
Ligon, KL
AF Maire, Cecile L.
Ramkissoon, Shakti H.
Ligon, Keith L.
TI Conditional Pten loss in Olig2 expressing neural stem/progenitor cells
results in massive myelination and disruption of the neuronal
differentiation in the absence of neoplasia
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Maire, Cecile L.; Ramkissoon, Shakti H.; Ligon, Keith L.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 3304
DI 10.1158/1538-7445.AM2011-3304
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701304053
ER
PT J
AU McHenry, KT
Jacobson, E
Donovan, J
Levine, K
Zhang, JX
Fisher, DE
Zawel, L
Porter, D
AF McHenry, Kevin T.
Jacobson, Elena
Donovan, Jerry
Levine, Kymberly
Zhang, Jingxin
Fisher, David E.
Zawel, Leigh
Porter, Dale
TI The Smac mimetic LBW242 induces apoptosis in melanoma in a
TLR-3-dependent and TNFR-independent manner
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [McHenry, Kevin T.; Jacobson, Elena; Donovan, Jerry; Levine, Kymberly; Zhang, Jingxin; Zawel, Leigh; Porter, Dale] Novartis Inst BioMed Res, Cambridge, MA USA.
[Fisher, David E.] Massachusetts Gen Hosp, Charlestown, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-19
DI 10.1158/1538-7445.AM2011-LB-19
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701306013
ER
PT J
AU McKenna, ES
Tamayo, P
Cho, YJ
Mora-Blanco, EL
Sansam, CG
Tillman, EJ
Koellhoffer, EC
Pomeroy, SL
Roberts, CWM
AF McKenna, Elizabeth S.
Tamayo, Pablo
Cho, Yoon-Jae
Mora-Blanco, E. Lorena
Sansam, Courtney G.
Tillman, Erik J.
Koellhoffer, Edward C.
Pomeroy, Scott L.
Roberts, Charles W. M.
TI Epigenetic inactivation of the tumor suppressor BIN1 drives
proliferation of SNF5-deficient tumors
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [McKenna, Elizabeth S.; Mora-Blanco, E. Lorena; Sansam, Courtney G.; Tillman, Erik J.; Koellhoffer, Edward C.; Roberts, Charles W. M.] Harvard Univ, Childrens Hosp Boston, Div Hematol Oncol,Dept Pediat,Med Sch, Dept Pediat Oncol,Dana Farber Canc Inst, Boston, MA 02115 USA.
[Tamayo, Pablo] MIT, Eli & Edythe L Broad Inst, Cambridge, MA 02139 USA.
[Tamayo, Pablo] Harvard Univ, Cambridge, MA 02138 USA.
[Cho, Yoon-Jae; Pomeroy, Scott L.] Childrens Hosp Boston, Dept Neurol, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 66
DI 10.1158/1538-7445.AM2011-66
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701403046
ER
PT J
AU Mine, N
Yamamoto, S
Saito, N
Kufe, DW
VonHoff, DD
Kawabe, T
AF Mine, Naoki
Yamamoto, Sayaka
Saito, Naoya
Kufe, Donald W.
VonHoff, Daniel D.
Kawabe, Takumi
TI CBP501-calmodulin binding contributes to sensitizing tumor cells to CDDP
and BLM
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Mine, Naoki; Yamamoto, Sayaka; Saito, Naoya; Kawabe, Takumi] CANBAS, Numazu, Japan.
[Kufe, Donald W.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[VonHoff, Daniel D.] Translat Genom Res Inst TGen, Phoenix, AZ USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2635
DI 10.1158/1538-7445.AM2011-2635
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701304399
ER
PT J
AU Mita, A
Rodon, J
Dummer, R
Baselga, J
Shou, YP
Feng, WT
Mahalingam, D
Thomas, A
Granvil, C
Amakye, D
Tawbi, H
AF Mita, Alain
Rodon, Jordi
Dummer, Reinhard
Baselga, Jose
Shou, Yaping
Feng, Wentao
Mahalingam, Devalingam
Thomas, Anne
Granvil, Camille
Amakye, Dereck
Tawbi, Hussein
TI A Phase I evaluation of safety, pharmacokinetics (PK) and
pharmacodynamics (PD) of LDE225, a smoothened (Smo) antagonist, in
patients with advanced solid tumors
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Mita, Alain; Mahalingam, Devalingam] UTHSCSA, San Antonio, TX USA.
[Rodon, Jordi] Vall dHebron Inst Oncol, Barcelona, Spain.
[Dummer, Reinhard] Univ Zurich Hosp, CH-8091 Zurich, Switzerland.
[Baselga, Jose] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Shou, Yaping; Amakye, Dereck] Novartis Inst BioMed Res, Cambridge, MA USA.
[Feng, Wentao; Granvil, Camille] Novartis Pharmaceut, Florham Pk, NJ USA.
[Thomas, Anne] Univ Leicester, Leicester, Leics, England.
[Tawbi, Hussein] Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 1288
DI 10.1158/1538-7445.AM2011-1288
PG 2
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701405281
ER
PT J
AU Mortazavi, F
Dubinett, SM
Rettig, MB
AF Mortazavi, Fariborz (Fred)
Dubinett, Steven M.
Rettig, Matthew B.
TI c-Crk proto-oncogene and TGF-beta signaling pathway contribute to
transcriptional repression of p120-catenin in non-small cell lung cancer
cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Mortazavi, Fariborz (Fred); Rettig, Matthew B.] Univ Calif Los Angeles, VA Greater LA Healthcare Syst, Los Angeles, CA USA.
[Dubinett, Steven M.] Univ Calif Los Angeles, Los Angeles, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 1084
DI 10.1158/1538-7445.AM2011-1084
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701402453
ER
PT J
AU Mostoslaysky, R
Sebastian, C
Zhong, L
Giacosa, S
Toiber, D
AF Mostoslaysky, Raul
Sebastian, Carlos
Zhong, Lei
Giacosa, Sofia
Toiber, Deborah
TI The role of the histone deacetylase SIRT6 in glucose homeostasis and
cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Mostoslaysky, Raul; Sebastian, Carlos; Zhong, Lei; Giacosa, Sofia; Toiber, Deborah] Harvard Univ, Massachusetts Gen Hosp, Ctr Canc, Sch Med, Boston, MA 02114 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA SY11-02
DI 10.1158/1538-7445.AM2011-SY11-02
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701302353
ER
PT J
AU Nagrath, S
Moore, AL
Zenali, M
Chekaluk, YI
Peters, EM
Kwiatowski, DJ
Haber, DA
Henske, EP
Toner, M
AF Nagrath, Sunitha
Moore, Alessandra L.
Zenali, Mahnaz
Chekaluk, Yvonne I.
Peters, Elizabeth M.
Kwiatowski, David J.
Haber, Daniel A.
Henske, Elizabeth P.
Toner, Mehmet
TI Novel microfluidic technology and biology based approach for isolation
and characterization of circulating cells from the peripheral blood of
patients with Lymphangioleiomyomatosis
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Nagrath, Sunitha] Univ Michigan, Ann Arbor, MI 48109 USA.
[Moore, Alessandra L.; Zenali, Mahnaz; Haber, Daniel A.; Toner, Mehmet] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Chekaluk, Yvonne I.; Peters, Elizabeth M.; Kwiatowski, David J.; Henske, Elizabeth P.] Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 1571
DI 10.1158/1538-7445.AM2011-1571
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701302276
ER
PT J
AU Nair, VS
Raz, DJ
Ray, RM
Jablons, DM
AF Nair, Viswam S.
Raz, Dan J.
Ray, Roshni M.
Jablons, David M.
TI Augmenting 18F-Fluorodeoxyglucose PET with a gene classifier for outcome
prediction in patients with resected, non-small cell lung cancer: A
pilot study
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Nair, Viswam S.] Stanford, Stanford, CA USA.
[Raz, Dan J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Ray, Roshni M.] UCSF, Hellen Diller Canc Ctr, San Francisco, CA USA.
[Jablons, David M.] Univ Calif San Francisco, Med Ctr, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 3197
DI 10.1158/1538-7445.AM2011-3197
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701405142
ER
PT J
AU Narayanan, R
Levin, BS
Maeder, ML
Joung, JK
Nutt, CL
Louis, DN
AF Narayanan, Radhakrishnan
Levin, Benjamin S.
Maeder, Morgan L.
Joung, J. Keith
Nutt, Catherine L.
Louis, David N.
TI Exploring temozolomide resistance in glioblastoma using a combinatorial
zinc-finger library approach
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Narayanan, Radhakrishnan; Levin, Benjamin S.; Maeder, Morgan L.; Joung, J. Keith; Nutt, Catherine L.; Louis, David N.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 1718
DI 10.1158/1538-7445.AM2011-1718
PG 1
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701300038
ER
PT J
AU Nardi, V
Song, YC
Cosper, AK
Lam, Q
Barria, JAS
Boland, GM
Yeap, B
Bergethon, K
Scialabba, VL
Settleman, J
Ryan, DP
Borger, DR
Hoang, MP
Bhan, AK
Iafrate, AJ
Cusack, JC
Engelman, JA
Dias-Santagata, D
AF Nardi, Valentina
Song, Young Chul
Cosper, Arjola K.
Quynh Lam
Barria, Juan Antonio Santamaria
Boland, Genevieve Marie
Yeap, Beow
Bergethon, Kristin
Scialabba, Vanessa L.
Settleman, Jeffrey
Ryan, David P.
Borger, Darrell R.
Hoang, Mai P.
Bhan, Atul K.
Iafrate, Anthony J.
Cusack, James C.
Engelman, Jeffrey A.
Dias-Santagata, Dora
TI Activation of PI3K in Merkel cell carcinoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Nardi, Valentina; Cosper, Arjola K.; Quynh Lam; Barria, Juan Antonio Santamaria; Boland, Genevieve Marie; Yeap, Beow; Bergethon, Kristin; Scialabba, Vanessa L.; Ryan, David P.; Borger, Darrell R.; Hoang, Mai P.; Bhan, Atul K.; Iafrate, Anthony J.; Cusack, James C.; Dias-Santagata, Dora] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Song, Young Chul; Settleman, Jeffrey; Engelman, Jeffrey A.] Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2210
DI 10.1158/1538-7445.AM2011-2210
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701405162
ER
PT J
AU Neviani, P
Harb, J
Oaks, J
Walker, C
Santhanam, R
Paisie, C
Eiring, A
Zhang, B
Perazzona, B
Ma, Y
Mao, C
Marcucci, G
Holyoake, T
Volinia, S
Cortes, J
Caligiuri, M
Huettner, C
Bittman, R
Chen, CS
Arlinghaus, R
Hokland, P
Roy, DC
Bhatia, R
Perrotti, D
AF Neviani, Paolo
Harb, Jason
Oaks, Joshua
Walker, Christopher
Santhanam, Ramasamy
Paisie, Carolyn
Eiring, Anna
Zhang, Bin
Perazzona, Bastianella
Ma, Y.
Mao, Charlene
Marcucci, Guido
Holyoake, Tessa
Volinia, Stefano
Cortes, Jorge
Caligiuri, Michael
Huettner, Claudia
Bittman, Robert
Chen, Ching-Shih
Arlinghaus, Ralph
Hokland, Peter
Roy, Denis-Claude
Bhatia, Ravi
Perrotti, Danilo
TI BCR-ABL1 kinase activity but not its expression is dispensable for Ph
plus quiescent stem cell survival which depends on the PP2A-controlled
Jak2 activation and is sensitive to FTY720 treatment
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Neviani, Paolo; Harb, Jason; Oaks, Joshua; Walker, Christopher; Santhanam, Ramasamy; Paisie, Carolyn; Eiring, Anna; Ma, Y.; Mao, Charlene; Marcucci, Guido; Caligiuri, Michael; Chen, Ching-Shih; Perrotti, Danilo] Ohio State Univ, Med Ctr, Columbus, OH 43210 USA.
[Zhang, Bin; Bhatia, Ravi] City Hope Natl Med Ctr, Natl Med Ctr, Duarte, CA USA.
[Perazzona, Bastianella; Cortes, Jorge; Arlinghaus, Ralph] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Holyoake, Tessa] Univ Glasgow, Glasgow, Lanark, Scotland.
[Volinia, Stefano] Univ Ferrera, Ferrara, Italy.
[Huettner, Claudia] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Bittman, Robert] CUNY, New York, NY 10021 USA.
[Hokland, Peter] Aarhus Sygehus, Aarhus, Denmark.
[Roy, Denis-Claude] Univ Montreal, Montreal, PQ, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-109
DI 10.1158/1538-7445.AM2011-LB-109
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701303344
ER
PT J
AU Ni, M
Chen, YW
Bailey, ST
Imai, Y
Liu, XS
Brown, M
AF Ni, Min
Chen, Yiwen
Bailey, Shannon T.
Imai, Yuuki
Liu, X. Shirley
Brown, Myles
TI Targeting androgen receptor in estrogen receptor-negative breast cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Ni, Min; Chen, Yiwen; Bailey, Shannon T.; Imai, Yuuki; Liu, X. Shirley; Brown, Myles] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 941
DI 10.1158/1538-7445.AM2011-941
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701406032
ER
PT J
AU Nitsche, CJ
Moore, RM
Maertin, S
Mayerle, J
Lerch, MM
Grippo, P
Gukovskaya, AS
AF Nitsche, Claudia J.
Moore, Ryan M.
Maertin, Sandrina
Mayerle, Julia
Lerch, Markus M.
Grippo, Paul
Gukovskaya, Anna S.
TI Autophagy in pancreatic cancer cells is mediated through a non-canonical
Beclin-1 independent pathway
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Nitsche, Claudia J.; Maertin, Sandrina; Mayerle, Julia; Lerch, Markus M.] Ernst Moritz Arndt Univ Greifswald, Dept Internal Med A, Greifswald, Germany.
[Moore, Ryan M.; Gukovskaya, Anna S.] VA Greater Los Angeles Hlth Care Syst, Los Angeles, CA USA.
[Moore, Ryan M.; Gukovskaya, Anna S.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Grippo, Paul] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 3775
DI 10.1158/1538-7445.AM2011-3775
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701400098
ER
PT J
AU Ojesina, AI
Kostic, A
Pedamallu, CS
Jung, J
Duke, F
Getz, G
Meyerson, M
AF Ojesina, Akinyemi I.
Kostic, Aleksandar
Pedamallu, Chandra Sekhar
Jung, Joonil
Duke, Fujiko
Getz, Gad
Meyerson, Matthew
TI PathSeq: A comprehensive computational tool for pathogen discovery by
deep sequencing of human cancer tissues
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Ojesina, Akinyemi I.; Kostic, Aleksandar; Pedamallu, Chandra Sekhar; Jung, Joonil; Duke, Fujiko; Meyerson, Matthew] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Ojesina, Akinyemi I.; Kostic, Aleksandar; Pedamallu, Chandra Sekhar; Jung, Joonil; Duke, Fujiko; Meyerson, Matthew] Broad Inst, Boston, MA USA.
[Getz, Gad] Broad Inst, Cambridge, MA USA.
OI Ojesina, Akinyemi/0000-0003-0755-3639
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 949
DI 10.1158/1538-7445.AM2011-949
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701406034
ER
PT J
AU Okamoto, W
Okamoto, I
Tanaka, K
Arao, T
Nishio, K
Fukuoka, M
Janne, P
Nakagawa, K
AF Okamoto, Wataru
Okamoto, Isamu
Tanaka, Kaoru
Arao, Tokuzo
Nishio, Kazuto
Fukuoka, Masahiro
Janne, Pasi
Nakagawa, Kazuhiko
TI TAK-701, a humanized monoclonal antibody to HGF, reverses gefitinib
resistance induced by tumor-derived HGF in non-small cell lung cancer
with an EGFR mutation
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Okamoto, Wataru; Okamoto, Isamu; Tanaka, Kaoru; Arao, Tokuzo; Nishio, Kazuto; Nakagawa, Kazuhiko] Kinki Univ, Sch Med, Osaka 589, Japan.
[Fukuoka, Masahiro] Izumi City Hosp, Osaka, Japan.
[Janne, Pasi] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 1731
DI 10.1158/1538-7445.AM2011-1731
PG 1
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701300078
ER
PT J
AU Ou, WB
Fletcher, CDM
Demetri, GD
Fletcher, JA
AF Ou, Wen-Bin
Fletcher, Christopher D. M.
Demetri, George D.
Fletcher, Jonathan A.
TI Protein kinase C theta (PKCO) and c-Jun regulate proliferation through
cyclin Olin KIT-independent gastrointestinal stromal tumors
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Ou, Wen-Bin; Fletcher, Christopher D. M.; Fletcher, Jonathan A.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Demetri, George D.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 952
DI 10.1158/1538-7445.AM2011-952
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701400261
ER
PT J
AU Paccez, JD
Vasquez, G
Tamura, RE
Duncan, K
Vasconcellos, J
Wiesner, T
Libermann, T
Zerbini, LF
AF Paccez, Juliano D.
Vasquez, Gabriela
Tamura, Rodrigo E.
Duncan, Kristal
Vasconcellos, Jaira
Wiesner, Theresa
Libermann, Towia
Zerbini, Luiz F.
TI Receptor tyrosine kinase AXL as a new target for prostate cancer therapy
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Paccez, Juliano D.; Tamura, Rodrigo E.; Duncan, Kristal; Wiesner, Theresa; Zerbini, Luiz F.] ICGEB, Cape Town, South Africa.
[Vasquez, Gabriela; Vasconcellos, Jaira; Libermann, Towia] BIDMC, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 3053
DI 10.1158/1538-7445.AM2011-3053
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701403143
ER
PT J
AU Palanichamy, K
Patel, D
Erkkinen, M
Reardon, Z
Noda, SE
Chakravarti, A
AF Palanichamy, Kamalakannan
Patel, Disha
Erkkinen, Michael
Reardon, Zachary
Noda, Shin-el
Chakravarti, Arnab
TI Aurora B silencing attenuates radiation resistance through PARP and
identification of a missense mutation in aurora B as a determinant of
radiosensitization in gliomas
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Palanichamy, Kamalakannan; Patel, Disha; Noda, Shin-el; Chakravarti, Arnab] Ohio State Univ, Med Ctr, Columbus, OH 43210 USA.
[Erkkinen, Michael; Reardon, Zachary] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2484
DI 10.1158/1538-7445.AM2011-2484
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701302022
ER
PT J
AU Patnaik, A
Courtney, K
Bellinger, G
Lunsford, E
Robichaud, K
Grant, A
Lenkinski, R
Pedrosa, I
Signoretti, S
Wooster, R
Cantley, L
AF Patnaik, Akash
Courtney, Kevin
Bellinger, Gary
Lunsford, Elaine
Robichaud, Kyle
Grant, Aaron
Lenkinski, Robert
Pedrosa, Ivan
Signoretti, Sabina
Wooster, Richard
Cantley, Lewis
TI Targeting the PI3K/mTOR pathway in genetically engineered mouse models
of prostate cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Patnaik, Akash; Cantley, Lewis] Harvard Univ, Sch Med, Beth Israel Deaconess, Boston, MA USA.
[Courtney, Kevin; Signoretti, Sabina] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Bellinger, Gary; Lunsford, Elaine; Robichaud, Kyle; Grant, Aaron; Lenkinski, Robert; Pedrosa, Ivan] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Wooster, Richard] GlaxoSmithKline Inc, Collegeville, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-418
DI 10.1158/1538-7445.AM2011-LB-418
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701404343
ER
PT J
AU Plyler, RJ
Wang, WX
Ghobrial, IM
Roccaro, AM
Korde, N
Zingone, A
Landgren, O
Calvo, KR
AF Plyler, Ryan J.
Wang, Weixin
Ghobrial, Irene M.
Roccaro, Aldo M.
Korde, Neha
Zingone, Adriana
Landgren, Ola
Calvo, Katherine R.
TI Cytokine profiles in bone marrow supernatant and peripheral blood of
patients with multiple myeloma and Waldenstrom's macroglobulinemia
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Plyler, Ryan J.] Georgetown Sch Med, Georgetown, DC USA.
[Wang, Weixin; Calvo, Katherine R.] NIH, Bethesda, MD 20892 USA.
[Ghobrial, Irene M.; Roccaro, Aldo M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Korde, Neha; Zingone, Adriana; Landgren, Ola] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 802
DI 10.1158/1538-7445.AM2011-802
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701302342
ER
PT J
AU Polyak, K
AF Polyak, Kornelia
TI The clinical significance of intratumor diversity in breast cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Polyak, Kornelia] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA PL03-03
DI 10.1158/1538-7445.AM2011-PL03-03
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701303219
ER
PT J
AU Poynter, JN
Christensen, B
Nelson, HH
Amatruda, JF
Frazier, AL
Ross, JA
AF Poynter, Jenny N.
Christensen, Brock
Nelson, Heather H.
Amatruda, James F.
Frazier, A. Lindsay
Ross, Julie A.
TI DNA methylation patterns distinguish histologic subtypes of pediatric
germ cell tumors
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Poynter, Jenny N.; Nelson, Heather H.; Ross, Julie A.] Univ Minnesota, Minneapolis, MN USA.
[Christensen, Brock] Brown Univ, Providence, RI 02912 USA.
[Amatruda, James F.] Univ Texas Southwestern, Dallas, TX USA.
[Frazier, A. Lindsay] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 872
DI 10.1158/1538-7445.AM2011-872
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701405455
ER
PT J
AU Prencipe, M
Madden, S
O'Neill, A
Culhane, A
O'Connor, D
Klocker, H
Gallagher, WM
Watson, W
AF Prencipe, Maria
Madden, Stephen
O'Neill, Amanda
Culhane, Aedin
O'Connor, Darran
Klocker, Helmut
Gallagher, William M.
Watson, William
TI Transcriptomic profiling of castrate resistant prostate cancer cells:
identification of transcription factors associated with androgen
resistance
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Prencipe, Maria; O'Neill, Amanda; O'Connor, Darran; Gallagher, William M.; Watson, William] Univ Coll Dublin, Dublin 2, Ireland.
[Madden, Stephen] Dublin City Univ, Dublin 9, Ireland.
[Culhane, Aedin] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Klocker, Helmut] Med Univ Innsbruck, A-6020 Innsbruck, Austria.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-278
DI 10.1158/1538-7445.AM2011-LB-278
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701305445
ER
PT J
AU Pugh, TJ
Lawrence, M
Sougnez, C
Getz, G
Attiyeh, E
Hogarty, M
Diskin, S
Yaei, M
Diamond, M
Asgharzadeh, S
Sposto, R
Wei, JS
Badgett, T
London, WB
Gastier-Foster, J
Smith, MA
Gerhard, DS
Seeger, R
Khan, J
Meyerson, ML
Maris, JM
AF Pugh, Trevor J.
Lawrence, Michael
Sougnez, Carrie
Getz, Gad
Attiyeh, Edward
Hogarty, Michael
Diskin, Sharon
Yaei, Mosse
Diamond, Maura
Asgharzadeh, Shahab
Sposto, Richard
Wei, Jun S.
Badgett, Thomas
London, Wendy B.
Gastier-Foster, Julie
Smith, Malcolm A.
Gerhard, Daniela S.
Seeger, Robert
Khan, Javed
Meyerson, Matthew L.
Maris, John M.
CA NCI Therapeutically Applicable Res
TI Exome sequencing of 81 neuroblastomas identifies a wide diversity of
somatic mutation
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Pugh, Trevor J.; Lawrence, Michael; Sougnez, Carrie; Getz, Gad; Meyerson, Matthew L.; NCI Therapeutically Applicable Res] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Attiyeh, Edward; Hogarty, Michael; Diskin, Sharon; Yaei, Mosse; Diamond, Maura; Maris, John M.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Asgharzadeh, Shahab; Sposto, Richard; Seeger, Robert] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Wei, Jun S.; Badgett, Thomas; Smith, Malcolm A.; Gerhard, Daniela S.; Khan, Javed] NCI, Bethesda, MD 20892 USA.
[London, Wendy B.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[London, Wendy B.] Childrens Oncol Grp, Stat & Data Ctr, Boston, MA USA.
[Gastier-Foster, Julie] Nationwide Childrens Hosp, Columbus, OH USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 4756
DI 10.1158/1538-7445.AM2011-4756
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701303278
ER
PT J
AU Qi, J
Filippakopoulos, P
McKeown, M
Shaw, KL
Smith, WB
French, CA
Kung, AL
Knapp, S
Bradner, JE
AF Qi, Jun
Filippakopoulos, Panagis
McKeown, Michael
Shaw, Katharin L.
Smith, William B.
French, Christopher A.
Kung, Andrew L.
Knapp, Stefan
Bradner, James E.
TI BET bromodomain inhibitors for cancer therapy
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Qi, Jun; McKeown, Michael; Shaw, Katharin L.; Smith, William B.; Bradner, James E.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Filippakopoulos, Panagis; Knapp, Stefan] Univ Oxford, Oxford, England.
[French, Christopher A.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Kung, Andrew L.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Lurie Family Imaging Ctr, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2318
DI 10.1158/1538-7445.AM2011-2318
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701304366
ER
PT J
AU Qi, L
Xu, CX
Sarosiek, KA
Ligon, AH
Rodig, SJ
Wong, KK
Letai, AG
Shapiro, GI
AF Qi, Li
Xu, Chunxiao
Sarosiek, Kristopher A.
Ligon, Azra H.
Rodig, Scott J.
Wong, Kwok-Kin
Letai, Anthony G.
Shapiro, Geoffrey I.
TI A subset of small cell lung cancer (SCLC) cell lines is Mcl-1-dependent
and responds to cyclin-dependent kinase (cdk)9 inhibition in vitro and
in vivo
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Qi, Li; Xu, Chunxiao; Sarosiek, Kristopher A.; Wong, Kwok-Kin; Letai, Anthony G.; Shapiro, Geoffrey I.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Ligon, Azra H.; Rodig, Scott J.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
OI wong, kwok kin/0000-0001-6323-235X
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-22
DI 10.1158/1538-7445.AM2011-LB-22
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701305410
ER
PT J
AU Raab, MS
Breitkreutz, I
Leber, B
Weitz, L
Hayden, PJ
Larsen, TO
Cllausen, MH
Fruehauf, J
Nissen, F
Mier, W
Haberkorn, U
Podar, K
Ho, AD
Goldschmidt, H
Anderson, KC
Kraemer, A
AF Raab, Marc S.
Breitkreutz, Iris
Leber, Blanka
Weitz, Ludmila
Hayden, Patrick J.
Larsen, Thomas O.
Cllausen, Mads H.
Fruehauf, Johannes
Nissen, Felix
Mier, Walter
Haberkorn, Uwe
Podar, Klaus
Ho, Anthony D.
Goldschmidt, Hartmut
Anderson, Kenneth C.
Kraemer, Alwin
TI Inhibition of centrosomal clustering suppresses tumor growth in vivo
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Raab, Marc S.; Breitkreutz, Iris; Nissen, Felix; Mier, Walter; Haberkorn, Uwe; Ho, Anthony D.; Goldschmidt, Hartmut] Heidelberg Univ, Sch Med, Heidelberg, Germany.
[Leber, Blanka; Weitz, Ludmila; Kraemer, Alwin] German Canc Res Ctr, Heidelberg, Germany.
[Hayden, Patrick J.; Podar, Klaus; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Larsen, Thomas O.; Cllausen, Mads H.] Tech Univ Denmark, Copenhagen, Denmark.
[Fruehauf, Johannes] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 660
DI 10.1158/1538-7445.AM2011-660
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701401403
ER
PT J
AU Rickman, DS
Soong, TTD
Moss, B
Kitabayashi, N
Bunting, K
Naseeruddin, S
Garraway, LA
Berger, MF
Melnick, A
Elemento, O
Rubin, MA
AF Rickman, David S.
Soong, Ta-tsen David
Moss, Benjamin
Kitabayashi, Naoki
Bunting, Karen
Naseeruddin, Saif
Garraway, Levi A.
Berger, Michael F.
Melnick, Ari
Elemento, Olivier
Rubin, Mark A.
TI Oncogene-mediated alterations in chromatin conformation
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Rickman, David S.; Soong, Ta-tsen David; Moss, Benjamin; Kitabayashi, Naoki; Bunting, Karen; Naseeruddin, Saif; Melnick, Ari; Elemento, Olivier; Rubin, Mark A.] Weill Cornell Med Coll, New York, NY USA.
[Garraway, Levi A.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Broad Inst, Boston, MA 02115 USA.
[Berger, Michael F.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-249
DI 10.1158/1538-7445.AM2011-LB-249
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701303162
ER
PT J
AU Sakakibara, K
Saito, N
Sato, T
Suzuki, A
Hasegawa, Y
Friedman, JM
Suganuma, M
Kufe, DW
VanHoff, DD
Iwami, T
Kawabe, T
AF Sakakibara, Keiichi
Saito, Naoya
Sato, Takuji
Suzuki, Atsushi
Hasegawa, Yoko
Friedman, Jonathan M.
Suganuma, Masashi
Kufe, Donald W.
VanHoff, Daniel D.
Iwami, Tadahiko
Kawabe, Takumi
TI CBS9106 is a novel low toxic reversible oral CRM1 inhibitor with CRM1
degrading activity
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Sakakibara, Keiichi; Saito, Naoya; Sato, Takuji; Suzuki, Atsushi; Hasegawa, Yoko; Friedman, Jonathan M.; Suganuma, Masashi; Iwami, Tadahiko; Kawabe, Takumi] CanBas Co Ltd, Numazu, Japan.
[Kufe, Donald W.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[VanHoff, Daniel D.] Translat Genom Res Inst TGen, Phoenix, AZ USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 658
DI 10.1158/1538-7445.AM2011-658
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701401401
ER
PT J
AU Samimi, G
Wong, C
Spong, SM
Birrer, MJ
AF Samimi, Goli
Wong, Carol
Spong, Suzanne M.
Birrer, Michael J.
TI The CTGF antibody FG-3019 blocks CTGF-stimulated migration in ovarian
cancer cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Samimi, Goli] NCI, Bethesda, MD 20892 USA.
[Wong, Carol; Spong, Suzanne M.] FibroGen Inc, San Francisco, CA USA.
[Birrer, Michael J.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 509
DI 10.1158/1538-7445.AM2011-509
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701302124
ER
PT J
AU Sanda, T
Tyner, JW
Gutierrez, A
Ngo, VN
Moriggl, R
Ahn, Y
Glover, J
Chang, BH
Willis, SG
Zhou, WJ
Gray, NS
Staudt, LM
Druker, BJ
Look, AT
AF Sanda, Takaomi
Tyner, Jeffrey W.
Gutierrez, Alejandro
Ngo, Vu N.
Moriggl, Richard
Ahn, Yebin
Glover, Jason
Chang, Bill H.
Willis, Stephanie G.
Zhou, Wenjun
Gray, Nathanael S.
Staudt, Louis M.
Druker, Brian J.
Look, A. Thomas
TI Pathway dependence on the tyrosine kinase TYK2 in T-cell acute
lymphoblastic leukemia
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Sanda, Takaomi; Gutierrez, Alejandro; Ahn, Yebin; Zhou, Wenjun; Gray, Nathanael S.; Look, A. Thomas] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Tyner, Jeffrey W.; Glover, Jason; Chang, Bill H.; Willis, Stephanie G.; Druker, Brian J.] Oregon Hlth & Sci Univ, Knight Canc Inst, Portland, OR 97201 USA.
[Ngo, Vu N.] City Hope Natl Med Ctr, Duarte, CA 91010 USA.
[Moriggl, Richard] Ludwig Boltzmann Inst Canc Res, Vienna, Austria.
[Staudt, Louis M.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2809
DI 10.1158/1538-7445.AM2011-2809
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701304483
ER
PT J
AU Santamaria-Barria, JA
Sloss, CM
Cusack, JC
AF Santamaria-Barria, Juan A.
Sloss, Callum M.
Cusack, James C.
TI HB-EGF expression in gastric cancer promotes chemotherapy resistance and
represents a promising target for molecular therapy and a novel
biomarker of 5-FU resistance
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Santamaria-Barria, Juan A.; Sloss, Callum M.; Cusack, James C.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2129
DI 10.1158/1538-7445.AM2011-2129
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701402139
ER
PT J
AU Sasaki, T
Okuda, K
Zheng, W
Butrynski, J
Capelletti, M
Wang, LP
Gray, N
Wilner, KD
Christensen, JG
Demetri, GD
Shapiro, GI
Rodig, SJ
Eck, MJ
Janne, PA
AF Sasaki, Takaaki
Okuda, Katsuhiro
Zheng, Wei
Butrynski, James
Capelletti, Marzia
Wang, Liping
Gray, Nathanael
Wilner, Keith D.
Christensen, James G.
Demetri, George D.
Shapiro, Geoffrey I.
Rodig, Scott J.
Eck, Michael J.
Janne, Pasi A.
TI Secondary mutations in ALK and resistance to ALK kinase inhibitors
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Sasaki, Takaaki; Okuda, Katsuhiro; Zheng, Wei; Butrynski, James; Capelletti, Marzia; Wang, Liping; Gray, Nathanael; Demetri, George D.; Shapiro, Geoffrey I.; Eck, Michael J.; Janne, Pasi A.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Wilner, Keith D.; Christensen, James G.] Pfizer Global Res & Dev, La Jolla, CA USA.
[Rodig, Scott J.] Brigham & Womens Hosp, Boston, MA 02115 USA.
OI Sasaki, Takaaki/0000-0002-6505-8786
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 1541
DI 10.1158/1538-7445.AM2011-1541
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701302169
ER
PT J
AU Schmitt, AD
Fuchs, BC
McGinn, CM
Goodwin, JM
Tanabe, KK
Lanuti, M
AF Schmitt, Anthony D.
Fuchs, Bryan C.
McGinn, Christopher M.
Goodwin, Jonathan M.
Tanabe, Kenneth K.
Lanuti, Michael
TI Epithelial to mesenchymal transition mediates sensitivity to viral
oncolysis in vitro and in a xenograft flank tumor model of non small
cell lung cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Schmitt, Anthony D.; Fuchs, Bryan C.; Tanabe, Kenneth K.; Lanuti, Michael] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[McGinn, Christopher M.] Cornell Univ, New York, NY 10021 USA.
[Goodwin, Jonathan M.] Scripps Res Inst, La Jolla, CA 92037 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 3366
DI 10.1158/1538-7445.AM2011-3366
PG 1
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701300471
ER
PT J
AU Schwartz, B
Hofer, M
Lemieux, M
Bauer, D
Cameron, M
West, N
Agoston, E
Ince, T
Christie, A
Aster, J
Sallan, S
Kung, A
Bradner, J
French, CA
AF Schwartz, Brian
Hofer, Matthias
Lemieux, Madeleine
Bauer, Daniel
Cameron, Michael
West, Nathan
Agoston, Elin
Ince, Tan
Christie, Amanda
Aster, Jon
Sallan, Stephen
Kung, Andrew
Bradner, James
French, Chris A.
TI Differentiation of NUT midline carcinoma by epigenomic reprogramming
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Schwartz, Brian; Hofer, Matthias; Cameron, Michael; Agoston, Elin; Ince, Tan; Aster, Jon; French, Chris A.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Lemieux, Madeleine; Sallan, Stephen; Kung, Andrew; Bradner, James] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Bauer, Daniel] Childrens Hosp Boston, Boston, MA USA.
[West, Nathan] Harvard Univ, Sch Med, Boston, MA USA.
[Christie, Amanda] Dana Farber Canc Inst, Lurie Family Imaging Ctr, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2575
DI 10.1158/1538-7445.AM2011-2575
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701400394
ER
PT J
AU Shacham, S
Nir, R
Sandanayaka, V
Shechter, S
Williams, J
Damaj, B
Draetta, G
Kauffman, M
AF Shacham, Sharon
Nir, Raphael
Sandanayaka, Vincent
Shechter, Sharon
Williams, Jennifer
Damaj, Bassam
Draetta, Giulio
Kauffman, Michael
TI Discovery of SINE: Selective inhibitors of nuclear export increase
levels of regulatory proteins p53, p21, FOXO and I kappa B leading to
apoptosis of malignant cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Shacham, Sharon; Sandanayaka, Vincent; Shechter, Sharon; Kauffman, Michael] Karyopharm Therapeut, Newton, MA USA.
[Nir, Raphael; Williams, Jennifer] SBH Sci, Natick, MA USA.
[Damaj, Bassam] Bioquant Inc, San Diego, CA USA.
[Draetta, Giulio] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2580
DI 10.1158/1538-7445.AM2011-2580
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701400399
ER
PT J
AU Shimamura, T
Carretero, J
Xu, CX
Capelletti, M
Rikova, K
Gu, TL
Kobayashi, S
Rogers, A
Janne, PA
Wong, KK
Shapiro, GI
AF Shimamura, Takeshi
Carretero, Julian
Xu, Chunxiao
Capelletti, Marzia
Rikova, Klarisa
Gu, Ting-Lei
Kobayashi, Susumu
Rogers, Andrew
Janne, Pasi A.
Wong, Kwok-Kin
Shapiro, Geoffrey I.
TI Chronic inhibition of mutant EGFR in NSCLC leads to EGFR TKI resistance
by TGF-beta 1 mediated epithelial to mesenchymal transition
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Shimamura, Takeshi; Xu, Chunxiao; Capelletti, Marzia; Rogers, Andrew; Janne, Pasi A.; Wong, Kwok-Kin; Shapiro, Geoffrey I.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Carretero, Julian] Univ Valencia, Valencia, Spain.
[Rikova, Klarisa] Cell Signaling Technol, Danvers, MA USA.
[Gu, Ting-Lei] Cell Signaling Technol, Boston, MA USA.
[Kobayashi, Susumu] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
OI wong, kwok kin/0000-0001-6323-235X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-399
DI 10.1158/1538-7445.AM2011-LB-399
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701400320
ER
PT J
AU Smallridge, RC
Copland, JA
Brose, MS
Wadsworth, JT
Houvras, Y
Bible, KC
Shah, MH
Gramza, AW
Klopper, JP
von Roemeling, R
AF Smallridge, Robert C.
Copland, John A.
Brose, Marcia S.
Wadsworth, J. Trad
Houvras, Yariv
Bible, Keith C.
Shah, Manisha H.
Gramza, Ann W.
Klopper, Joshua P.
von Roemeling, Reinhard
TI Phase 1 study of CS-7017, an oral PPAR-gamma agonist, in combination
with paclitaxel in advanced anaplastic thyroid cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Smallridge, Robert C.; Copland, John A.] Mayo Clin, Jacksonville, FL 32224 USA.
[Brose, Marcia S.] Univ Penn, Philadelphia, PA 19104 USA.
[Wadsworth, J. Trad] East Virginia Med Ctr, Norfolk, VA USA.
[Houvras, Yariv] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Bible, Keith C.] Mayo Clin, Rochester, MN USA.
[Shah, Manisha H.] Ohio State Med Ctr, Columbus, OH USA.
[Gramza, Ann W.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Klopper, Joshua P.] Univ Colorado, Aurora, CO USA.
[von Roemeling, Reinhard] Daiichi Sankyo Inc, Edison, NJ USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 1278
DI 10.1158/1538-7445.AM2011-1278
PG 2
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701405270
ER
PT J
AU Song, YR
Zhang, Q
Bash, R
Yin, CY
Yang, CY
Gilbert, D
Wang, S
Bullitt, E
Kafri, T
McCarthy, KD
Louis, DN
Miller, CR
Van Dyke, T
AF Song, Yurong
Zhang, Qian
Bash, Ryan
Yin, Chaoying
Yang, Chunyu
Gilbert, Debra
Wang, Sophie
Bullitt, Elizabeth
Kafri, Tal
McCarthy, Ken D.
Louis, David N.
Miller, C. Ryan
Van Dyke, Terry
TI Delineation of grade-specific molecular drivers in inducible preclinical
mouse models of astrocytoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Song, Yurong; Zhang, Qian; Gilbert, Debra; Wang, Sophie; Van Dyke, Terry] Natl Canc Inst Frederick, Frederick, MD USA.
[Bash, Ryan; Yin, Chaoying; Yang, Chunyu; Bullitt, Elizabeth; Kafri, Tal; McCarthy, Ken D.; Miller, C. Ryan] Univ N Carolina, Chapel Hill, NC USA.
[Louis, David N.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Louis, David N.] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2854
DI 10.1158/1538-7445.AM2011-2854
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701303267
ER
PT J
AU Sridhar, S
Nagesha, D
Tada, D
Kumar, R
Makrigiorgos, GM
Cormack, R
AF Sridhar, Srinivas
Nagesha, Dattatri
Tada, Dayane
Kumar, Rajiv
Makrigiorgos, G. Mike
Cormack, Robert
TI Radio-sensitizer eluting nanoporous coatings on fiducials markers:
Biological in-situ dose-painting for IGRT
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Sridhar, Srinivas; Nagesha, Dattatri; Tada, Dayane; Kumar, Rajiv] Northeastern Univ, Boston, MA 02115 USA.
[Makrigiorgos, G. Mike] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Cormack, Robert] Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2674
DI 10.1158/1538-7445.AM2011-2674
PG 1
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701300309
ER
PT J
AU Stegmaier, K
Crompton, B
Jessneck, J
Ross, K
Gupta, S
Plank, LV
Winckler, W
Tolliday, N
AF Stegmaier, Kimberly
Crompton, Brian
Jessneck, Jonathan
Ross, Kenneth
Gupta, Supriya
Plank, Lynn Ver
Winckler, Wendy
Tolliday, Nicola
TI Modulating transcription factor abnormalities in pediatric cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Stegmaier, Kimberly; Crompton, Brian; Jessneck, Jonathan; Plank, Lynn Ver] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Ross, Kenneth; Gupta, Supriya; Winckler, Wendy; Tolliday, Nicola] Broad Inst, Cambridge, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-240
DI 10.1158/1538-7445.AM2011-LB-240
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701305384
ER
PT J
AU Sun, T
Yang, M
Chen, SY
Balk, S
Pomerantz, M
Brown, M
Kantoff, PW
Lee, GSM
AF Sun, Tong
Yang, Ming
Chen, Shaoyong
Balk, Steven
Pomerantz, Mark
Brown, Myles
Kantoff, Philip W.
Lee, Gwo-Shu Mary
TI MicroRNA signatures of castration resistant human prostate cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Sun, Tong; Yang, Ming; Pomerantz, Mark; Brown, Myles; Kantoff, Philip W.; Lee, Gwo-Shu Mary] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Chen, Shaoyong; Balk, Steven] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 174
DI 10.1158/1538-7445.AM2011-174
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701404099
ER
PT J
AU Tessema, MZ
Yingling, CM
Thomas, CL
Klinge, DM
Bernauer, AM
Stidley, C
Joste, N
Dahlberg, S
Schiller, J
Belinsky, SA
AF Tessema, Mathewos Z.
Yingling, Christin M.
Thomas, Cynthia L.
Klinge, Donna M.
Bernauer, Amanda M.
Stidley, Chris
Joste, Nancy
Dahlberg, Suzanne
Schiller, Joan
Belinsky, Steven A.
TI SULF2 methylation is a prognostic biomarker for lung cancer survival and
increases sensitivity to camptothecin analogues via expression of ISG15
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Tessema, Mathewos Z.; Yingling, Christin M.; Thomas, Cynthia L.; Klinge, Donna M.; Bernauer, Amanda M.; Belinsky, Steven A.] Lovelace Resp Res Inst, Albuquerque, NM USA.
[Stidley, Chris; Joste, Nancy] Univ New Mexico, Albuquerque, NM 87131 USA.
[Dahlberg, Suzanne] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Schiller, Joan] Univ Texas Southwestern, Dallas, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 87
DI 10.1158/1538-7445.AM2011-87
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701403096
ER
PT J
AU Ueno, K
Hirata, H
Tabatabai, ZL
Hinoda, Y
Dahiya, R
AF Ueno, Koji
Hirata, Hiroshi
Tabatabai, Z. Laura
Hinoda, Yuji
Dahiya, Rajvir
TI IGFBP-4 activates the Wnt/beta-catenin signaling pathway and induces
M-CAM expression in human renal cell carcinoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Ueno, Koji; Hirata, Hiroshi; Dahiya, Rajvir] San Francisco VA Med Ctr, Dept Urol, San Francisco, CA USA.
[Ueno, Koji; Hirata, Hiroshi; Tabatabai, Z. Laura; Dahiya, Rajvir] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Tabatabai, Z. Laura] San Francisco VA Med Ctr, Dept Pathol, San Francisco, CA USA.
[Hinoda, Yuji] Yamaguchi Univ, Grad Sch Med, Dept Oncol & Lab Med, Ube, Yamaguchi 755, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 1124
DI 10.1158/1538-7445.AM2011-1124
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701403346
ER
PT J
AU van Bragt, M
Godinho, F
Orkin, S
Li, Z
AF van Bragt, Maaike
Godinho, Frank
Orkin, Stuart
Li, Zhe
TI ETV6-NTRK3 basal-like breast cancers originating from Wap plus breast
cells progress through a premalignant stage enriched in luminal
progenitors
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [van Bragt, Maaike; Li, Zhe] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Godinho, Frank] Childrens Hosp Boston, HHMI, Boston, MA USA.
[Orkin, Stuart] Childrens Hosp Boston, HHMI, DFCI, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-35
DI 10.1158/1538-7445.AM2011-LB-35
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701303386
ER
PT J
AU Venkatesan, N
Issakhanian, SP
Ginther, CG
Slamon, DJ
Srivatsan, ES
Veena, MS
AF Venkatesan, Natarajan
Issakhanian, Shawnt P.
Ginther, Charles G.
Slamon, Dennis J.
Srivatsan, Eri S.
Veena, Mysore S.
TI Involvement of somatic mutations in silencing cystatin E/M tumor
suppressor gene in breast cancer
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Venkatesan, Natarajan; Issakhanian, Shawnt P.; Ginther, Charles G.; Slamon, Dennis J.] Univ Calif Los Angeles, David Sch Med, Los Angeles, CA USA.
[Srivatsan, Eri S.; Veena, Mysore S.] Univ Calif Los Angeles, VA Greater Healthcare Syst, Los Angeles, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2201
DI 10.1158/1538-7445.AM2011-2201
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701402296
ER
PT J
AU Wade, H
McDonnell, D
Brown, M
AF Wade, Hilary
McDonnell, Donald
Brown, Myles
TI Dose-dependent effects of progestins on progesterone receptor activity
and target gene expression: less is more
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Wade, Hilary; Brown, Myles] Dana Farber Canc Inst, Boston, MA 02115 USA.
[McDonnell, Donald] Duke Univ, Med Ctr, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 4542
DI 10.1158/1538-7445.AM2011-4542
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701400204
ER
PT J
AU Wagle, N
Emery, C
Berger, MF
Davis, MJ
Sawyer, A
Pochanard, P
Kehoe, SM
Johannessen, CM
Macconaill, LE
Hahn, WC
Meyerson, M
Garraway, LA
AF Wagle, Nikhil
Emery, Caroline
Berger, Michael F.
Davis, Matthew J.
Sawyer, Allison
Pochanard, Panisa
Kehoe, Sarah M.
Johannessen, Cory M.
Macconaill, Laura E.
Hahn, William C.
Meyerson, Matthew
Garraway, Levi A.
TI Dissecting therapeutic resistance to RAF inhibition in melanoma by tumor
genomic profiling
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Wagle, Nikhil; Davis, Matthew J.; Sawyer, Allison; Pochanard, Panisa; Kehoe, Sarah M.; Macconaill, Laura E.; Hahn, William C.; Meyerson, Matthew; Garraway, Levi A.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Emery, Caroline] Novartis Inst Biomed Res, Cambridge, MA USA.
[Berger, Michael F.; Johannessen, Cory M.] Broad Inst MIT & Harvard, Cambridge, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 3933
DI 10.1158/1538-7445.AM2011-3933
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701403256
ER
PT J
AU Wargo, JA
Cogdill, A
Dang, P
Gupta, R
Piris, A
Boni, A
Garber, HR
Ott, H
Newton, LP
Flaherty, KT
Lawrence, DP
Tsao, H
Fisher, DE
AF Wargo, Jennifer A.
Cogdill, Alex
Dang, Ping
Gupta, Ridhi
Piris, Adriano
Boni, Andrea
Garber, Haven R.
Ott, Harald
Newton, Lindsay P.
Flaherty, Keith T.
Lawrence, Donald P.
Tsao, Hensin
Fisher, David E.
TI Treatment with a selective inhibitor of BRAFV600E increases melanocyte
antigen expression and CD8 T cell infiltrate in tumors of patients with
metastatic melanoma
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Wargo, Jennifer A.; Cogdill, Alex; Dang, Ping; Gupta, Ridhi; Piris, Adriano; Ott, Harald; Newton, Lindsay P.; Flaherty, Keith T.; Lawrence, Donald P.; Tsao, Hensin; Fisher, David E.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Boni, Andrea] Dartmouth Hitchcock Med Ctr, Lebanon, NH 03766 USA.
[Garber, Haven R.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 958
DI 10.1158/1538-7445.AM2011-958
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701400275
ER
PT J
AU Weigert, O
Lane, A
Kopp, N
Rodig, S
Yoda, A
Weinstock, DM
AF Weigert, Oliver
Lane, Andrew
Kopp, Nadja
Rodig, Scott
Yoda, Akinori
Weinstock, David M.
TI Functional oncogene identification in hematologic malignancies
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Weigert, Oliver; Lane, Andrew; Kopp, Nadja; Rodig, Scott; Yoda, Akinori; Weinstock, David M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-243
DI 10.1158/1538-7445.AM2011-LB-243
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701305387
ER
PT J
AU White, RM
Zon, LI
AF White, Richard M.
Zon, Leonard I.
TI DHODH regulates transcriptional elongation during melanoma evolution:
insights from zebrafish screening
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [White, Richard M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Zon, Leonard I.] Childrens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-335
DI 10.1158/1538-7445.AM2011-LB-335
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701303404
ER
PT J
AU Wilson, BG
Wang, X
Shen, XH
McKenna, ES
Lemieux, ME
Cho, YJ
Koelhoffer, EC
Pomeroy, SL
Orkin, SH
Roberts, CWM
AF Wilson, Boris G.
Wang, Xi
Shen, Xiaohua
McKenna, Elizabeth S.
Lemieux, Madeleine E.
Cho, Yoon-Jae
Koelhoffer, Edward C.
Pomeroy, Scott L.
Orkin, Stuart H.
Roberts, Charles W. M.
TI Epigenetic antagonism between Polycomb and SWI/SNF complexes
duringoncogenic transformation
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Wilson, Boris G.; Wang, Xi; Shen, Xiaohua; McKenna, Elizabeth S.; Lemieux, Madeleine E.; Koelhoffer, Edward C.; Pomeroy, Scott L.; Orkin, Stuart H.; Roberts, Charles W. M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Cho, Yoon-Jae] Childrens Hosp Boston, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-237
DI 10.1158/1538-7445.AM2011-LB-237
PG 1
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701300268
ER
PT J
AU Wong, CR
Stylianopoulos, T
Bhaumik, J
Cui, J
Martin, J
Chauhan, V
Popovic, Z
Chen, O
Jain, R
Fukumura, D
Bawendi, M
AF Wong, Cliff R.
Stylianopoulos, Triantafyllos
Bhaumik, Jayeeta
Cui, Jian
Martin, John
Chauhan, Vikash
Popovic, Zoran
Chen, Ou
Jain, Rakesh
Fukumura, Dai
Bawendi, Moungi
TI Multistage nanoparticle delivery system for deep penetration into solid
tumor
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Wong, Cliff R.; Cui, Jian; Popovic, Zoran; Chen, Ou; Bawendi, Moungi] MIT, Cambridge, MA 02139 USA.
[Stylianopoulos, Triantafyllos; Bhaumik, Jayeeta; Martin, John; Chauhan, Vikash; Jain, Rakesh; Fukumura, Dai] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Stylianopoulos, Triantafyllos; Bhaumik, Jayeeta; Martin, John; Chauhan, Vikash; Jain, Rakesh; Fukumura, Dai] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 3
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 548
DI 10.1158/1538-7445.AM2011-548
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701302195
ER
PT J
AU Woo, J
Morikawa, T
Ogino, S
Gilliland, DG
Shiydasani, RA
AF Woo, Janghee
Morikawa, Teppei
Ogino, Shuji
Gilliland, D. Gary
Shiydasani, Ramesh A.
TI Intestinal mesenchymal fibroblasts promote early epithelial
tumorigenesis through activation of integrin beta4 and receptor tyrosine
kinases, bypassing common mutational mechanisms
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Woo, Janghee; Morikawa, Teppei; Ogino, Shuji; Shiydasani, Ramesh A.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Gilliland, D. Gary] Merck Res Labs, N Wales, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 3106
DI 10.1158/1538-7445.AM2011-3106
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701402249
ER
PT J
AU Yamamura, S
Saini, S
Majid, S
Hirata, H
Ueno, K
Deng, GR
Tanaka, Y
Carroll, P
Dahiya, R
AF Yamamura, Soichiro
Saini, Sharanjot
Majid, Shahana
Hirata, Hiroshi
Ueno, Koji
Deng, Guoren
Tanaka, Yuichiro
Carroll, Peter
Dahiya, Rajvir
TI MicroRNA-34a inhibits proliferation and invasion by targeting c-Myc in
prostate cancer cells
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Yamamura, Soichiro; Saini, Sharanjot; Majid, Shahana; Hirata, Hiroshi; Ueno, Koji; Deng, Guoren; Tanaka, Yuichiro; Dahiya, Rajvir] San Francisco VA Med Ctr, San Francisco, CA USA.
[Carroll, Peter] Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 3968
DI 10.1158/1538-7445.AM2011-3968
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701403401
ER
PT J
AU Yang, XM
Locasale, J
Rahal, R
Breitkopf, S
VanderHeiden, M
Spentzos, D
Wu, CL
Perrimon, N
Cantley, L
Wong, E
Asara, J
AF Yang, Xuemei
Locasale, Jason
Rahal, Rami
Breitkopf, Susanne
VanderHeiden, Matthew
Spentzos, Dimitrios
Wu, Chin-Lee
Perrimon, Norbert
Cantley, Lewis
Wong, Eric
Asara, John
TI A mass spectrometry platform to quantitatively profile cancer cell
metabolism from cells, tumors, and fixed tissue
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Yang, Xuemei; Locasale, Jason; Breitkopf, Susanne; Spentzos, Dimitrios; Cantley, Lewis; Wong, Eric; Asara, John] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Rahal, Rami; Perrimon, Norbert] Harvard Univ, Sch Med, Boston, MA USA.
[VanderHeiden, Matthew] MIT, 77 Massachusetts Ave, Cambridge, MA 02139 USA.
[Wu, Chin-Lee] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA LB-255
DI 10.1158/1538-7445.AM2011-LB-255
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701306015
ER
PT J
AU Yeung, TL
Ghosh, S
Wong, KK
Birrer, MJ
Mok, SC
AF Yeung, Tsz-Lun
Ghosh, Sue
Wong, Kwong-Kwok
Birrer, Michael J.
Mok, Samuel C.
TI Up-regulation of stromal versican in advanced stage serous ovarian
cancer modifies tumor microenvironment and promotes cancer invasion
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Yeung, Tsz-Lun; Wong, Kwong-Kwok; Mok, Samuel C.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Ghosh, Sue] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Birrer, Michael J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 420
DI 10.1158/1538-7445.AM2011-420
PG 1
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701301006
ER
PT J
AU Zhai, RH
Zhao, Y
Liu, G
Ter-Minassian, M
Wang, ZX
Wu, IC
Su, L
Asomaning, K
Chen, F
Kulke, MH
Lin, XH
Heist, RS
Wain, JC
Christiani, DC
AF Zhai, Rihong
Zhao, Yang
Liu, Geoffrey
Ter-Minassian, Monica
Wang, Zhaoxi
Wu, I-Chen
Su, Li
Asomaning, Kofi
Chen, Feng
Kulke, Matthew H.
Lin, Xihong
Heist, Rebecca S.
Wain, John C.
Christiani, David C.
TI Gene-environment Interactions in esophageal adenocarcinoma risk: A
case-only analysis
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Zhai, Rihong; Zhao, Yang; Ter-Minassian, Monica; Wang, Zhaoxi; Wu, I-Chen; Su, Li; Asomaning, Kofi; Chen, Feng; Lin, Xihong; Christiani, David C.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Liu, Geoffrey] Princess Margaret Hosp, Ontario Canc Inst, Toronto, ON M4X 1K9, Canada.
[Kulke, Matthew H.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Heist, Rebecca S.; Wain, John C.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 3742
DI 10.1158/1538-7445.AM2011-3742
PG 2
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701305060
ER
PT J
AU Zhang, W
Fulci, G
Rabkin, SD
Zhang, X
Martuza, RL
AF Zhang, Wei
Fulci, Giulia
Rabkin, Samuel D.
Zhang, Xiang
Martuza, Robert L.
TI Combination treatment of bevacizumab and oncolytic HSV armed with
angiostatin show enhanced antitumoral and antiangiogenic effects
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Zhang, Wei; Fulci, Giulia; Rabkin, Samuel D.; Martuza, Robert L.] Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02114 USA.
[Zhang, Xiang] Fourth Mil Med Univ, Xijing Hosp, Dept Neurosurg, Xian 710032, Shaanxi, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 2568
DI 10.1158/1538-7445.AM2011-2568
PG 1
WC Oncology
SC Oncology
GA V43SP
UT WOS:000209701401245
ER
PT J
AU Zhu, SZ
Lee, JS
Shin, J
Perez-Atayde, AR
Kutok, JL
Rodig, SJ
Neuberg, DS
Guo, F
Helman, D
Feng, H
Stewart, RA
Wang, WC
George, RE
Kanki, JP
Look, AT
AF Zhu, Shizhen
Lee, Jeong-Soo
Shin, Jimann
Perez-Atayde, Antonio R.
Kutok, Jeffery L.
Rodig, Scott J.
Neuberg, Donna S.
Guo, Feng
Helman, Daniel
Feng, Hui
Stewart, Rodney A.
Wang, Wenchao
George, Rani E.
Kanki, John P.
Look, A. Thomas
TI Activated ALK accelerates the onset of neuroblastoma in MYCN-transgenic
zebrafish
SO CANCER RESEARCH
LA English
DT Meeting Abstract
C1 [Zhu, Shizhen; Lee, Jeong-Soo; Shin, Jimann; Neuberg, Donna S.; Guo, Feng; Helman, Daniel; Feng, Hui; Wang, Wenchao; George, Rani E.; Kanki, John P.; Look, A. Thomas] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Perez-Atayde, Antonio R.] Childrens Hosp, Boston, MA 02115 USA.
[Kutok, Jeffery L.; Rodig, Scott J.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Stewart, Rodney A.] Huntsman Canc Inst, Salt Lake City, UT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD APR 15
PY 2011
VL 71
SU 8
MA 4296
DI 10.1158/1538-7445.AM2011-4296
PG 1
WC Oncology
SC Oncology
GA V43SO
UT WOS:000209701301305
ER
PT J
AU Akeno, N
Smith, EP
Stefan, M
Huber, AK
Zhang, WJ
Keddache, M
Tomer, Y
AF Akeno, Nagako
Smith, Eric P.
Stefan, Mihaela
Huber, Amanda K.
Zhang, Weijia
Keddache, Mehdi
Tomer, Yaron
TI IFN-alpha Mediates the Development of Autoimmunity both by Direct Tissue
Toxicity and through Immune Cell Recruitment Mechanisms
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID CHRONIC HEPATITIS-C; INTERFERON-ALPHA; GENE-EXPRESSION; THYROID
AUTOIMMUNITY; I INTERFERONS; HASHIMOTOS-THYROIDITIS;
LUPUS-ERYTHEMATOSUS; SJOGRENS-SYNDROME; FAMILY PROTEINS; TRANSGENIC MICE
AB IFN-alpha is known to play a key role in autoimmunity, but the mechanisms are uncertain. Although the induction of autoimmunity by IFN-alpha is consistent with primarily immunomodulatory effects, the high frequency of nonautoimmune inflammation suggests other mechanisms. We used thyroiditis as a model to dissect these possibilities. IFN-alpha treatment of cultured thyrocytes increased expression of thyroid differentiation markers, thyroglobulin, thyroid-stimulating hormone receptor, thyroid peroxidase, and sodium iodide transporter. RNAseq analysis demonstrated that pathways of Ag presentation, pattern recognition receptors, and cytokines/chemokines were also stimulated. These changes were associated with markedly increased nonapoptotic thyroid cell death, suggesting direct toxicity. To corroborate these in vitro findings, we created transgenic mice with thyroid-specific overexpression of IFN-alpha under control of the thyroglobulin promoter. Transgenic mice developed marked inflammatory thyroid destruction associated with immune cell infiltration of thyroid and surrounding tissues leading to profound hypothyroidism, findings consistent with our in vitro results. In addition, transgenic mice thyroids showed upregulation of pathways similar to those observed in cultured thyrocytes. In particular, expression of granzyme B, CXCL10, a subset of the tripartite motif-containing family, and other genes involved in recruitment of bystander cytotoxic immune responses were increased. Pathways associated with apoptosis and autophagy were not induced. Taken together, our data demonstrate that the induction of tissue inflammation and autoimmunity by IFN-alpha involves direct tissue toxic effects as well as provocation of destructive bystander immune responses. The Journal of Immunology, 2011, 186: 4693-4706.
C1 [Stefan, Mihaela; Huber, Amanda K.; Tomer, Yaron] Mt Sinai Med Ctr, Dept Med, Div Endocrinol, Genome Ctr, New York, NY 10029 USA.
[Akeno, Nagako; Smith, Eric P.] Univ Cincinnati, Coll Med, Div Endocrinol, Cincinnati, OH 45267 USA.
[Zhang, Weijia] Mt Sinai Sch Med, Genome Ctr, Dept Med Bioinformat Core, New York, NY 10029 USA.
[Keddache, Mehdi] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
[Tomer, Yaron] James J Peters Vet Adm Med Ctr, New York, NY USA.
RP Tomer, Y (reprint author), Mt Sinai Med Ctr, Dept Med, Div Endocrinol, Genome Ctr, Box 1118,1 Gustave L Levy Pl, New York, NY 10029 USA.
EM yaron.tomer@mssm.edu
FU National Institute of Diabetes and Digestive and Kidney Diseases
[DK61659, DK073681]; Veterans Administration
FX This work was supported in part by Grants DK61659 and DK073681 from the
National Institute of Diabetes and Digestive and Kidney Diseases and by
a Veterans Administration Merit Award (to Y.T.).
NR 73
TC 27
Z9 29
U1 0
U2 4
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD APR 15
PY 2011
VL 186
IS 8
BP 4693
EP 4706
DI 10.4049/jimmunol.1002631
PG 14
WC Immunology
SC Immunology
GA 744FY
UT WOS:000289081500021
PM 21402899
ER
PT J
AU Kim, JI
O'Connor, MR
Duff, PE
Zhao, GP
Lee, KM
Eliades, P
Deng, SP
Yeh, H
Caton, AJ
Markmann, JF
AF Kim, James I.
O'Connor, Matthew R.
Duff, Patrick E.
Zhao, Gaoping
Lee, Kang Mi
Eliades, Philip
Deng, Shaoping
Yeh, Heidi
Caton, Andrew J.
Markmann, James F.
TI Generation of Adaptive Regulatory T Cells by Alloantigen Is Required for
Some But Not All Transplant Tolerance Protocols
SO TRANSPLANTATION
LA English
DT Article
DE Treg; Adaptive Tregs; Tolerance
ID TRANSCRIPTION FACTOR FOXP3; IMMUNOLOGICAL SELF-TOLERANCE;
GROWTH-FACTOR-BETA; IN-VIVO; ANTIGEN PRETREATMENT; THYMIC SELECTION;
TRANSGENIC MICE; INDUCTION; RAPAMYCIN; RECEPTOR
AB Background. Because CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs) are essential for the maintenance of self-tolerance, significant interest surrounds the developmental cues for thymic-derived natural Tregs (nTregs) and periphery-generated adaptive Tregs (aTregs). In the transplant setting, the allograft may play a role in the generation of alloantigen-specific Tregs, but this role remains undefined. We examined whether the immune response to a transplant allograft results in the peripheral generation of aTregs.
Methods. To identify generation of aTregs, purified graft-reactive CD4(+)CD25(-) T cells were adoptively transferred to mice-bearing skin allograft. To demonstrate that aTregs are necessary for tolerance, DBA/2 skin was transplanted onto C57BL/6-RAG-1-deficient recipients adoptively transferred with purified sorted CD4(+)CD25(-) T cells; half of the recipients undergo tolerance induction treatment.
Results. By tracking adoptively transferred cells, we show that purified graft-reactive CD4(+)CD25(-) T lymphocytes up-regulate Foxp3 in mice receiving skin allografts in the absence of any treatment. Interestingly, cotransfer of antigen-specific nTregs suppresses the up-regulation of Foxp3 by inhibiting the proliferation of allograft-responsive T cells. In vitro data are consistent with our in vivo data-Foxp3(+) cells are generated on antigen activation, and this generation is suppressed on coculture with antigen-specific nTregs. Finally, blocking aTreg generation in grafted, rapamycin-treated mice disrupts alloantigen-specific tolerance induction. In contrast, blocking aTreg generation in grafted mice treated with nondepleting anti-CD4 plus anti-CD40L antibodies does not disrupt graft tolerance.
Conclusions. We conclude that graft alloantigen stimulates the de novo generation of aTregs, and this generation may represent a necessary step in some but not all protocols of tolerance induction.
C1 [Kim, James I.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Surg,Div Transplantat, Boston, MA 02114 USA.
[Caton, Andrew J.] Wistar Inst Anat & Biol, Dept Immunol, Philadelphia, PA 19104 USA.
RP Kim, JI (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Surg,Div Transplantat, 55 Fruit St, Boston, MA 02114 USA.
EM jkim35@partners.org
OI Eliades, Philip/0000-0002-7985-6471
FU NIH [K01 DK079207 02, R01 AI-048820]
FX This work was supported by NIH K01 DK079207 02 (J.I.K.) and R01
AI-048820 (J.F.M.).
NR 46
TC 5
Z9 5
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0041-1337
EI 1534-6080
J9 TRANSPLANTATION
JI Transplantation
PD APR 15
PY 2011
VL 91
IS 7
BP 707
EP 713
DI 10.1097/TP.0b013e31820e50b3
PG 7
WC Immunology; Surgery; Transplantation
SC Immunology; Surgery; Transplantation
GA 740ID
UT WOS:000288784700009
PM 21386770
ER
PT J
AU Dryden-Peterson, S
Shapiro, RL
Hughes, MD
Powis, K
Ogwu, A
Moffat, C
Moyo, S
Makhema, J
Essex, M
Lockman, S
AF Dryden-Peterson, Scott
Shapiro, Roger L.
Hughes, Michael D.
Powis, Kathleen
Ogwu, Anthony
Moffat, Claire
Moyo, Sikhulile
Makhema, Joseph
Essex, Max
Lockman, Shahin
TI Increased Risk of Severe Infant Anemia After Exposure to Maternal HAART,
Botswana
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article; Proceedings Paper
CT 17th Conference on Retroviruses and Opportunistic Infections
CY FEB 16-19, 2010
CL San Francisco, CA
DE anemia; antiretroviral therapy; fetal drug exposure; Human
Immunodeficiency Virus; infant; mother-to-child transmission
ID ZIDOVUDINE COMBINATION THERAPY; TO-CHILD TRANSMISSION; ACTIVE
ANTIRETROVIRAL THERAPY; SINGLE-DOSE NEVIRAPINE; RED-CELL APLASIA;
TOTAL-BODY IRON; HIV TRANSMISSION; RANDOMIZED-TRIAL; EXPERIENCED
PATIENTS; UNINFECTED INFANTS
AB Background: Maternal highly-active antiretroviral therapy (HAART) reduces mother-to-child HIV transmission but may increase the risk for infant anemia.
Methods: The incidence of first severe anemia (grade 3 or 4, Division of AIDS 2004 Toxicity Table) was assessed among HIV-uninfected infants in the Mashi and Mma Bana mother-to-child HIV transmission prevention trials in Botswana. Severe anemia rates were compared between 3 groups: infants exposed to maternal HAART in utero and during breastfeeding (BF) and 1 month of postnatal zidovudine (ZDV) (HAART-BF); infants exposed to maternal ZDV in utero, 6 months of postnatal ZDV, and BF (ZDV-BF); and infants exposed to maternal ZDV in utero, 1 month of postnatal ZDV, and formula-feeding (ZDV-FF).
Results: A total of 1719 infants were analyzed-691 HAART-BF, 503 ZDV-BF, and 525 ZDV-FF. Severe anemia was detected in 118 infants (7.4%). By 6 months, 12.5% of HAART-BF infants experienced severe anemia, compared with 5.3% of ZDV-BF (P < 0.001) and 2.5% of ZDV-FF infants (P < 0.001). In adjusted analysis, HAART-BF infants were at greater risk of severe anemia than ZDV-BF or ZDV-FF infants (adjusted odds ratios 2.6 and 5.8, respectively; P < 0.001). Most anemias were asymptomatic and improved with iron/multivitamin supplementation and cessation of ZDV exposure. However, 11 infants (0.6% of all infants) required transfusion for symptomatic anemia. Microcytosis and hypochromia were common among infants with severe anemia.
Conclusions: Exposure to maternal HAART starting in utero was associated with severe infant anemia. Confirmation of this finding and possible strategies to mitigate hematologic toxicity warrant further study.
C1 [Dryden-Peterson, Scott; Lockman, Shahin] Brigham & Womens Hosp, Div Infect Dis, Dept Med, Boston, MA 02115 USA.
[Dryden-Peterson, Scott; Shapiro, Roger L.; Powis, Kathleen; Ogwu, Anthony; Essex, Max; Lockman, Shahin] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Cambridge, MA 02138 USA.
[Dryden-Peterson, Scott; Shapiro, Roger L.; Powis, Kathleen; Ogwu, Anthony; Moffat, Claire; Moyo, Sikhulile; Makhema, Joseph; Essex, Max; Lockman, Shahin] Botswana Harvard AIDS Inst Partnership, Gaborone, Botswana.
[Shapiro, Roger L.] Beth Israel Deaconess Med Ctr, Div Infect Dis, Dept Med, Boston, MA USA.
[Hughes, Michael D.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Cambridge, MA 02138 USA.
[Powis, Kathleen] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Powis, Kathleen] Massachusetts Gen Hosp, Dept Pediat, Boston, MA 02114 USA.
RP Dryden-Peterson, S (reprint author), Brigham & Womens Hosp, Div Infect Dis, Dept Med, 75 Francis St, Boston, MA 02115 USA.
EM scott_peterson@post.harvard.edu
RI Moyo, Sikhulile/E-1464-2015
OI Moyo, Sikhulile/0000-0003-3821-4592
FU FIC NIH HHS [R24 TW007988, R24 TW007988-05]; NIAID NIH HHS [P30
AI060354, U01 AI066454, U01 AI066454-01A1, UO1 AI066454]; NICHD NIH HHS
[R01 HD037793, R01 HD037793-05S1, R01 HD37793]
NR 59
TC 25
Z9 25
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 APR 15
PY 2011
VL 56
IS 5
BP 428
EP 436
DI 10.1097/QAI.0b013e31820bd2b6
PG 9
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 733DP
UT WOS:000288241800013
PM 21266910
ER
PT J
AU Goldstein, KE
Hazlett, EA
Savage, KR
Berlin, HA
Hamilton, HK
Zelmanova, Y
Look, AE
Koenigsberg, HW
Mitsis, EM
Tang, CY
McNamara, M
Siever, LJ
Cohen, BH
New, AS
AF Goldstein, Kim E.
Hazlett, Erin A.
Savage, Kimberley R.
Berlin, Heather A.
Hamilton, Holly K.
Zelmanova, Yuliya
Look, Amy E.
Koenigsberg, Harold W.
Mitsis, Effie M.
Tang, Cheuk Y.
McNamara, Margaret
Siever, Larry J.
Cohen, Barry H.
New, Antonia S.
TI Dorso- and ventro-lateral prefrontal volume and spatial working memory
in schizotypal personality disorder
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article
DE Working memory; Borderline personality disorder; Schizotypal personality
disorder; Dorsolateral prefrontal cortex; Ventrolateral prefrontal
cortex; MRI
ID UNMEDICATED SCHIZOPHRENIA-PATIENTS; BORDERLINE PERSONALITY;
FRONTAL-LOBE; INDIVIDUAL-DIFFERENCES; AUTOMATED BATTERY;
NONHUMAN-PRIMATES; FUNCTIONAL MRI; LARGE-SAMPLE; CORTEX; DEFICITS
AB Schizotypal personality disorder (SPD) individuals and borderline personality disorder (BPD) individuals have been reported to show neuropsychological impairments and abnormalities in brain structure. However, relationships between neuropsychological function and brain structure in these groups are not well understood. This study compared visual-spatial working memory (SWM) and its associations with dorsolateral prefrontal cortex (DLPFC) and ventrolateral prefrontal cortex (VLPFC) gray matter volume in 18 unmedicated SPD patients with no BPD traits, 18 unmedicated BPD patients with no SPD traits, and 16 healthy controls (HC). Results showed impaired SWM in SPD but not BPD, compared with HC. Moreover, among the HC group, but not SPD patients, better SWM performance was associated with larger VLPFC (BA44/45) gray matter volume (Fisher's Z p-values < 0.05). Findings suggest spatial working memory impairments may be a core neuropsychological deficit specific to SPD patients and highlight the role of VLPFC subcomponents in normal and dysfunctional memory performance. Published by Elsevier B.V.
C1 [Hazlett, Erin A.; Look, Amy E.; Koenigsberg, Harold W.; McNamara, Margaret; Siever, Larry J.; New, Antonia S.] James J Peters Vet Affairs Med Ctr, Bronx, NY 10468 USA.
[Hazlett, Erin A.; Look, Amy E.; Koenigsberg, Harold W.; McNamara, Margaret; Siever, Larry J.; New, Antonia S.] VISN 3 Mental Illness Res Educ & Clin Ctr MIRECC, Bronx, NY 10468 USA.
[Goldstein, Kim E.; Hazlett, Erin A.; Savage, Kimberley R.; Berlin, Heather A.; Hamilton, Holly K.; Zelmanova, Yuliya; Koenigsberg, Harold W.; Mitsis, Effie M.; McNamara, Margaret; Siever, Larry J.; New, Antonia S.] Mt Sinai Sch Med, Dept Psychiat, New York, NY USA.
[Mitsis, Effie M.] James J Peters Vet Affairs Med Ctr Rehabil Med, Bronx, NY USA.
[Tang, Cheuk Y.] Mt Sinai Sch Med, Dept Radiol, New York, NY USA.
[Cohen, Barry H.] NYU, Dept Psychol, New York, NY 10003 USA.
RP Hazlett, EA (reprint author), James J Peters Vet Affairs Med Ctr, 130 W Kingsbridge Rd,Rm 6A-45, Bronx, NY 10468 USA.
EM erin.hazlett@mssm.edu
FU NIMH [R01MH073911]; National Center for Research Resources (NCRR), a
component of the National Institutes of Health (NIH) [MO1-RR00071];
Mental Illness Research, Education and Clinical Center
FX This work was supported by NIMH grant R01MH073911 to Dr. Hazlett. Other
support came from Grant Number MO1-RR00071 from the National Center for
Research Resources (NCRR), a component of the National Institutes of
Health (NIH) and the Mental Illness Research, Education and Clinical
Center, VISN 3 Veterans Health Administration. We thank Dr. Monte
Buchsbaum who kindly allowed the use of in-house MIPS software.
NR 65
TC 9
Z9 9
U1 1
U2 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD APR 15
PY 2011
VL 218
IS 2
BP 335
EP 340
DI 10.1016/j.bbr.2010.11.042
PG 6
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 730OF
UT WOS:000288042600010
PM 21115066
ER
PT J
AU Hirata, H
Hinoda, Y
Nakajima, K
Kawamoto, K
Kikuno, N
Ueno, K
Yamamura, S
Zaman, MS
Khatri, G
Chen, Y
Saini, S
Majid, S
Deng, GR
Ishii, N
Dahiya, R
AF Hirata, Hiroshi
Hinoda, Yuji
Nakajima, Koichi
Kawamoto, Ken
Kikuno, Nobuyuki
Ueno, Koji
Yamamura, Soichiro
Zaman, Mohd S.
Khatri, Gaurav
Chen, Yi
Saini, Sharanjot
Majid, Shahana
Deng, Guoren
Ishii, Nobuhisa
Dahiya, Rajvir
TI Wnt antagonist DKK1 acts as a tumor suppressor gene that induces
apoptosis and inhibits proliferation in human renal cell carcinoma
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE DKK1; methylation; RCC; real-time RT-PCR; TCF/LEF reporter assay;
Immunohistochemistry; Western blot; ChIP assay; apoptosis; FACS; cell
cycle; invasion assay; in vivo
ID SIGNALING PATHWAY; CANCER-CELLS; EPIGENETIC INACTIVATION;
COLORECTAL-CANCER; BETA-CATENIN/TCF; DICKKOPF FAMILY; DNA METHYLATION;
PROGRESSION; EXPRESSION; REGULATOR
AB The functional significance of Wnt antagonist DKK1 has not been investigated in renal cell carcinoma (RCC). Therefore, we hypothesized that DKK1 may be a tumor suppressor gene and is epigenetically silenced, thus decreased DKK1 may cause progression of RCC. To assess the function of DKK1, we established stable DKK1 transfected cells and monitored them regarding cell viability, colony formation, apoptosis, cell cycle, and invasive capability. RCC cell lines had decreased levels of DKK1, which were increased after treatment with 5-Aza-20-deoxycytidine and trichostatin A. In chromatin immunoprecipitation assay, the level of dimethyl H3K9 and trimethyl H3K27 was decreased after 5-Aza-20-deoxycytidine/ trichostatin A treatment in RCC cell lines. Increased methylation was also associated with higher pathological stages in primary RCC tissues. T-cell factor/ lymphoid enhancer factor activity and nuclear beta-catenin expression were not changed in DKK1 transfectants. Also the expression of cyclinD1 and c-Myc was not changed in DKK1 transfectants. These results suggest that DKK1 may not be involved in the beta-catenin dependent pathway. We also evaluated the expression of various related genes. Cleaved caspase3, p53, p21 and puma expression were significantly upregulated in the DKK1 transfected cells. The population of apoptotic cells was increased in stable DKK1 cells and tumor growth suppression was also observed in nude mice with DKK1 transfected cells. In conclusion, this is the first report to show that DKK1 expression is epigenetically silenced in kidney cancer and its reexpression induces apoptosis and cell cycle arrest in RCC.
C1 [Hirata, Hiroshi; Kawamoto, Ken; Kikuno, Nobuyuki; Ueno, Koji; Yamamura, Soichiro; Zaman, Mohd S.; Khatri, Gaurav; Chen, Yi; Saini, Sharanjot; Majid, Shahana; Deng, Guoren; Dahiya, Rajvir] Univ Calif San Francisco, San Francisco, CA 94121 USA.
[Hirata, Hiroshi; Kawamoto, Ken; Kikuno, Nobuyuki; Ueno, Koji; Yamamura, Soichiro; Zaman, Mohd S.; Khatri, Gaurav; Chen, Yi; Saini, Sharanjot; Majid, Shahana; Deng, Guoren; Dahiya, Rajvir] San Francisco VA Med Ctr, Dept Urol, San Francisco, CA USA.
[Hinoda, Yuji] Yamaguchi Univ, Grad Sch Med, Dept Oncol & Lab Med, Yamaguchi, Japan.
[Nakajima, Koichi; Ishii, Nobuhisa] Toho Univ, Fac Med, Dept Urol, Tokyo, Japan.
RP Dahiya, R (reprint author), Vet Affairs Med Ctr, Urol Res Ctr 112F, 4150 Clement St, San Francisco, CA 94121 USA.
EM rdahiya@urology.ucsf.edu
RI Chen, Yi /J-4807-2012
FU NIH [RO1CA130860, RO1CA111470, T32-DK07790]; VA Research Enhancement
Award Program (REAP); Yamada Science Foundation
FX Grant sponsor: NIH; Grant numbers: RO1CA130860, RO1CA111470,
T32-DK07790; Grant sponsors: VA Research Enhancement Award Program
(REAP), Merit Review grants, and Yamada Science Foundation
NR 34
TC 43
Z9 49
U1 1
U2 11
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD APR 15
PY 2011
VL 128
IS 8
BP 1793
EP 1803
DI 10.1002/ijc.25507
PG 11
WC Oncology
SC Oncology
GA 730MM
UT WOS:000288037400005
PM 20549706
ER
PT J
AU Qureshi, AA
Karpen, CW
Qureshi, N
Papasian, CJ
Morrison, DC
Folts, JD
AF Qureshi, Asaf A.
Karpen, Charles W.
Qureshi, Nilofer
Papasian, Christopher J.
Morrison, David C.
Folts, John D.
TI Tocotrienols-induced inhibition of platelet thrombus formation and
platelet aggregation in stenosed canine coronary arteries
SO LIPIDS IN HEALTH AND DISEASE
LA English
DT Article
ID LOW-DENSITY-LIPOPROTEIN; VITAMIN-E SUPPLEMENTATION; RICH FRACTION TRF25;
ALPHA-TOCOPHEROL; HYPERCHOLESTEROLEMIC HUMANS; ANTIOXIDANT ACTIVITY;
CARDIOVASCULAR-DISEASE; GAMMA-TOCOPHEROL; BRAN; ATHEROGENESIS
AB Background: Dietary supplementation with tocotrienols has been shown to decrease the risk of coronary artery disease. Tocotrienols are plant-derived forms of vitamin E, which have potent anti-inflammatory, antioxidant, anticancer, hypocholesterolemic, and neuroprotective properties. Our objective in this study was to determine the extent to which tocotrienols inhibit platelet aggregation and reduce coronary thrombosis, a major risk factor for stroke in humans. The present study was carried out to determine the comparative effects of alpha-tocopherol, alpha-tocotrienol, or tocotrienol rich fraction (TRF; a mixture of alpha(-) + gamma(-) + delta tocotrienols) on in vivo platelet thrombosis and ex vivo platelet aggregation (PA) after intravenous injection in anesthetized dogs, by using a mechanically stenosed circumflex coronary artery model (Folts' cyclic flow model).
Results: Collagen-induced platelet aggregation (PA) in platelet rich plasma (PRP) was decreased markedly after treatment with alpha-tocotrienol (59%; P < 0.001) and TRF (92%; P < 0.001). alpha-Tocopherol treatment was less effective, producing only a 22% (P < 0.05) decrease in PA. Adenosine diphosphate-induced (ADP) PA was also decreased after treatment with alpha-tocotrienol (34%; P < 0.05) and TRF (42%; P < 0.025). These results also indicate that intravenously administered tocotrienols were significantly better than tocopherols in inhibiting cyclic flow reductions (CFRs), a measure of the acute platelet-mediated thrombus formation. Tocotrienols (TRF) given intravenously (10 mg/kg), abolished CFRs after a mean of 68 min (range 22 - 130 min), and this abolition of CFRs was sustained throughout the monitoring period (50 - 160 min).
Next, pharmacokinetic studies were carried out and tocol levels in canine plasma and platelets were measured. As expected, alpha-Tocopherol treatment increased levels of total tocopherols in post-vs pre-treatment specimens (57 vs 18 mu g/mL in plasma, and 42 vs 10 mu g/mL in platelets). However, treatment with alpha-tocopherol resulted in slightly decreased levels of tocotrienols in post-vs pre-treatment samples (1.4 vs 2.9 mu g/mL in plasma and 2.3 vs 2.8 mu g/mL in platelets). alpha-Tocotrienol treatment increased levels of both tocopherols and tocotrienols in post-vs pre-treatment samples (tocopherols, 45 vs 10 mu g/mL in plasma and 28 vs 5 mu g/mL in platelets; tocotrienols, 2.8 vs 0.9 mu g/mL in plasma and 1.28 vs 1.02 mu g/mL in platelets). Treatment with tocotrienols (TRF) also increased levels of tocopherols and tocotrienols in post-vs pre-treatment samples (tocopherols, 68 vs 20 mu g/mL in plasma and 31.4 vs 7.9 mu g/mL in platelets; tocotrienols, 8.6 vs 1.7 mu g/mL in plasma and 3.8 vs 3.9 mu g/mL in platelets).
Conclusions: The present results indicate that intravenously administered tocotrienols inhibited acute platelet-mediated thrombus formation, and collagen and ADP-induced platelet aggregation. alpha-Tocotrienols treatment induced increases in alpha-tocopherol levels of 4-fold and 6-fold in plasma and platelets, respectively. Interestingly, tocotrienols (TRF) treatment induced a less pronounced increase in the levels of tocotrienols in plasma and platelets, suggesting that intravenously administered tocotrienols may be converted to tocopherols. Tocotrienols, given intravenously, could potentially prevent pathological platelet thrombus formation and thus provide a therapeutic benefit in conditions such as stroke and myocardial infarction.
C1 [Qureshi, Asaf A.; Qureshi, Nilofer; Papasian, Christopher J.; Morrison, David C.] Univ Missouri, Dept Basic Med Sci, Sch Med, Kansas City, MO 64108 USA.
[Qureshi, Asaf A.] Adv Med Res, Madison, WI 53719 USA.
[Karpen, Charles W.] Prairie Cardiovasc Consultants, Springfield, IL 62701 USA.
[Qureshi, Nilofer] Univ Missouri, Dept Pharmacol Toxicol, Kansas City, MO 64108 USA.
[Folts, John D.] William S Middleton Mem Vet Adm Med Ctr, Dept Med, Cardiovasc Sect, Madison, WI 53705 USA.
RP Qureshi, AA (reprint author), Univ Missouri, Dept Basic Med Sci, Sch Med, 2411 Holmes St, Kansas City, MO 64108 USA.
EM qureshia@umkc.edu
FU Advanced Medical Research (AMR); NIH [GM-50870]
FX We thank Ms. Lei He of Department of Nutrition Sciences, University of
Wisconsin, Madison for helpful discussions and technical assistance for
carrying out the estimation of tocols (tocopherols and tocotrienols) by
HPLC of all dog's samples (plasma and platelets) at Advanced Medical
Research, 8251 Raymond Road, Madison, Wisconsin, 53719, USA. We also
thank Mr. Keith Gilchrist (USDA, ARS, MWA, Cereals and Crops Research
Laboratory, Madison, WI, 53726, USA) for carrying out statistical
analyses of the data. The TRF (mixture of alpha-tocopherol + alpha-,
alpha-, delta-tocotrienols) of palm oil was supplied by Malaysian Palm
Oil Board, Kuala Lumpur, Malaysia (previously known as Palm Oil Research
Institute of Malaysia [PORIM]). This study was supported in part by
Advanced Medical Research (AMR) and NIH grant GM-50870 (NQ). The study
was carried out under a FDA approved IND number 36906.
NR 66
TC 7
Z9 7
U1 0
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1476-511X
J9 LIPIDS HEALTH DIS
JI Lipids Health Dis.
PD APR 14
PY 2011
VL 10
AR 58
DI 10.1186/1476-511X-10-58
PG 13
WC Biochemistry & Molecular Biology; Nutrition & Dietetics
SC Biochemistry & Molecular Biology; Nutrition & Dietetics
GA 765ME
UT WOS:000290710200001
PM 21489303
ER
PT J
AU Bolli, N
Payne, EM
Rhodes, J
Gjini, E
Johnston, AB
Guo, F
Lee, JS
Stewart, RA
Kanki, JP
Chen, AT
Zhou, Y
Zon, LI
Look, AT
AF Bolli, Niccolo
Payne, Elspeth M.
Rhodes, Jennifer
Gjini, Evisa
Johnston, Adam B.
Guo, Feng
Lee, Jeong-Soo
Stewart, Rodney A.
Kanki, John P.
Chen, Aye T.
Zhou, Yi
Zon, Leonard I.
Look, A. Thomas
TI cpsf1 is required for definitive HSC survival in zebrafish
SO BLOOD
LA English
DT Article
ID TRANSCRIPTION ELONGATION; EMBRYONIC-DEVELOPMENT; GENE-EXPRESSION;
HEMATOPOIESIS; MIGRATION; CELLS; DIFFERENTIATION; EMBRYOGENESIS;
MYELOPOIESIS; MUTANTS
AB A comprehensive understanding of the genes and pathways regulating hematopoiesis is needed to identify genes causally related to bone marrow failure syndromes, myelodysplastic syndromes, and hematopoietic neoplasms. To identify novel genes involved in hematopoiesis, we performed an ethyl-nitrosourea mutagenesis screen in zebrafish (Danio rerio) to search for mutants with defective definitive hematopoiesis. We report the recovery and analysis of the grechetto mutant, which harbors an inactivating mutation in cleavage and polyadenylation specificity factor 1 (cpsf1), a gene ubiquitously expressed and required for 3' untranslated region processing of a subset of pre-mRNAs. grechetto mutants undergo normal primitive hematopoiesis and specify appropriate numbers of definitive HSCs at 36 hours postfertilization. However, when HSCs migrate to the caudal hematopoietic tissue at 3 days postfertilization, their numbers start decreasing as a result of apoptotic cell death. Consistent with Cpsf1 function, c-myb:EGFP(+) cells in grechetto mutants also show defective polyadenylation of snrnp70, a gene required for HSC development. By 5 days postfertilization, definitive hematopoiesis is compromised and severely decreased blood cell numbers are observed across the myeloid, erythroid, and lymphoid cell lineages. These studies show that cpsf1 is essential for HSC survival and differentiation in caudal hematopoietic tissue. (Blood. 2011;117(15):3996-4007)
C1 [Bolli, Niccolo; Payne, Elspeth M.; Gjini, Evisa; Johnston, Adam B.; Guo, Feng; Lee, Jeong-Soo; Kanki, John P.; Look, A. Thomas] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Payne, Elspeth M.] Barts & London Queen Marys Sch Med & Dent, Inst Canc, London, England.
[Rhodes, Jennifer] Fox Chase Canc Ctr, Immune Cell Dev & Host Def Program, Philadelphia, PA 19111 USA.
[Stewart, Rodney A.] Univ Utah, Dept Oncol Sci, Huntsman Canc Inst, Salt Lake City, UT USA.
[Chen, Aye T.; Zhou, Yi; Zon, Leonard I.] Howard Hughes Med Inst, Boston, MA 02115 USA.
[Chen, Aye T.; Zhou, Yi; Zon, Leonard I.] Childrens Hosp, Stem Cell Program, Boston, MA 02115 USA.
[Chen, Aye T.; Zhou, Yi; Zon, Leonard I.] Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA.
[Chen, Aye T.; Zhou, Yi; Zon, Leonard I.] Harvard Univ, Sch Med, Harvard Stem Cell Inst, Boston, MA 02115 USA.
RP Bolli, N (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, Mayer Bldg,Rm M630,450 Brookline Ave, Boston, MA 02115 USA.
EM niccolo_bolli@dfci.harvard.edu; thomas_look@dfci.harvard.edu
RI Bolli, Niccolo/D-4057-2011;
OI Bolli, Niccolo/0000-0002-1018-5139; Stewart, Rodney/0000-0003-1220-1830
FU National Cancer Institute, National Institutes of Health [R01 CA93152];
Leukemia & Lymphoma Society; Leukaemia & Lymphoma Research, United
Kingdom; National Institute of Neurological Disorders and Stroke,
National Institutes of Health [R00 NS058608]
FX This work was supported by the National Cancer Institute, National
Institutes of Health (grant R01 CA93152 to A. T. L.); by a Leukemia &
Lymphoma Society Special Fellow Award (to N.B.); by Leukaemia & Lymphoma
Research, United Kingdom (to E. M. P.); and by the National Institute of
Neurological Disorders and Stroke, National Institutes of Health (award
R00 NS058608 to R.A.S.).
NR 45
TC 15
Z9 15
U1 1
U2 7
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD APR 14
PY 2011
VL 117
IS 15
BP 3996
EP 4007
DI 10.1182/blood-2010-08-304030
PG 12
WC Hematology
SC Hematology
GA 749YF
UT WOS:000289507200015
PM 21330472
ER
PT J
AU Jain, R
Kralovic, SM
Evans, ME
Ambrose, M
Simbartl, LA
Obrosky, DS
Render, ML
Freyberg, RW
Jernigan, JA
Muder, RR
Miller, LJ
Roselle, GA
AF Jain, Rajiv
Kralovic, Stephen M.
Evans, Martin E.
Ambrose, Meredith
Simbartl, Loretta A.
Obrosky, D. Scott
Render, Marta L.
Freyberg, Ron W.
Jernigan, John A.
Muder, Robert R.
Miller, LaToya J.
Roselle, Gary A.
TI Veterans Affairs Initiative to Prevent Methicillin-Resistant
Staphylococcus aureus Infections
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID INTENSIVE-CARE-UNIT; BLOOD-STREAM INFECTIONS; NOSOCOMIAL TRANSMISSION;
COLONIZATION PRESSURE; HOSPITAL ADMISSION; RISK; MRSA; SURVEILLANCE;
MULTICENTER; PRECAUTIONS
AB BACKGROUND
Health care-associated infections with methicillin-resistant Staphylococcus aureus (MRSA) have been an increasing concern in Veterans Affairs (VA) hospitals.
METHODS
A "MRSA bundle" was implemented in 2007 in acute care VA hospitals nationwide in an effort to decrease health care-associated infections with MRSA. The bundle consisted of universal nasal surveillance for MRSA, contact precautions for patients colonized or infected with MRSA, hand hygiene, and a change in the institutional culture whereby infection control would become the responsibility of everyone who had contact with patients. Each month, personnel at each facility entered into a central database aggregate data on adherence to surveillance practice, the prevalence of MRSA colonization or infection, and health care-associated transmissions of and infections with MRSA. We assessed the effect of the MRSA bundle on health care-associated MRSA infections.
RESULTS
From October 2007, when the bundle was fully implemented, through June 2010, there were 1,934,598 admissions to or transfers or discharges from intensive care units (ICUs) and non-ICUs (ICUs, 365,139; non-ICUs, 1,569,459) and 8,318,675 patient-days (ICUs, 1,312,840; and non-ICUs, 7,005,835). During this period, the percentage of patients who were screened at admission increased from 82% to 96%, and the percentage who were screened at transfer or discharge increased from 72% to 93%. The mean (+/- SD) prevalence of MRSA colonization or infection at the time of hospital admission was 13.6 +/- 3.7%. The rates of health care-associated MRSA infections in ICUs had not changed in the 2 years before October 2007 (P = 0.50 for trend) but declined with implementation of the bundle, from 1.64 infections per 1000 patient-days in October 2007 to 0.62 per 1000 patient-days in June 2010, a decrease of 62% (P<0.001 for trend). During this same period, the rates of health care-associated MRSA infections in non-ICUs fell from 0.47 per 1000 patient-days to 0.26 per 1000 patient-days, a decrease of 45% (P<0.001 for trend).
CONCLUSIONS
A program of universal surveillance, contact precautions, hand hygiene, and institutional culture change was associated with a decrease in health care-associated transmissions of and infections with MRSA in a large health care system.
C1 [Jain, Rajiv; Evans, Martin E.; Ambrose, Meredith; Miller, LaToya J.] Vet Affairs Cent Off, Patient Care Serv, Vet Hlth Adm MRSA Program Off, Pittsburgh, PA USA.
[Jain, Rajiv; Evans, Martin E.; Ambrose, Meredith; Miller, LaToya J.] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Jain, Rajiv; Muder, Robert R.] VA Pittsburgh Healthcare Syst, Dept Internal Med, Pittsburgh, PA USA.
[Jain, Rajiv; Muder, Robert R.] Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
[Obrosky, D. Scott] VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA USA.
[Kralovic, Stephen M.; Simbartl, Loretta A.; Roselle, Gary A.] VA Cent Off, Patient Care Serv, Natl Infect Dis Program Off, Cincinnati, OH USA.
[Kralovic, Stephen M.; Simbartl, Loretta A.; Roselle, Gary A.] Cincinnati VA Med Ctr, Cincinnati, OH USA.
[Kralovic, Stephen M.; Render, Marta L.; Roselle, Gary A.] Univ Cincinnati, Coll Med, Dept Internal Med, Cincinnati, OH USA.
[Render, Marta L.; Freyberg, Ron W.] VA Inpatient Evaluat Ctr, Cincinnati, OH USA.
[Evans, Martin E.] Univ Kentucky, Sch Med, Dept Internal Med, Lexington, KY 40506 USA.
[Jernigan, John A.] Ctr Dis Control & Prevent, Prevent & Response Branch, Div Healthcare Qual Promot, Atlanta, GA USA.
RP Evans, ME (reprint author), Lexington VAMC, VHA MDRO Program, 1101 Vet Dr,11I-CDD, Lexington, KY 40502 USA.
EM martin.evans@va.gov
NR 35
TC 238
Z9 252
U1 4
U2 21
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 APR 14
PY 2011
VL 364
IS 15
BP 1419
EP 1430
PG 12
WC Medicine, General & Internal
SC General & Internal Medicine
GA 749LD
UT WOS:000289467200006
PM 21488764
ER
PT J
AU Newton-Cheh, C
Lin, AE
Baggish, AL
Wang, H
AF Newton-Cheh, Christopher
Lin, Angela E.
Baggish, Aaron L.
Wang, He
TI Case 11-2011: A 47-Year-Old Man with Systemic Lupus Erythematosus and
Heart Failure Cardiac intracellular deposition disorder, consistent with
hydroxychloroquine toxicity
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID RESTRICTIVE CARDIOMYOPATHY; ULTRASTRUCTURAL FINDINGS; CHLOROQUINE;
THERAPY; DRUG; CLASSIFICATION; CARDIOLOGY
C1 [Newton-Cheh, Christopher] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Newton-Cheh, Christopher] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Newton-Cheh, Christopher; Baggish, Aaron L.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Lin, Angela E.] Massachusetts Gen Hosp, MassGen Hosp Children, Dept Pediat, Genet Unit, Boston, MA 02114 USA.
[Wang, He] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Newton-Cheh, Christopher; Baggish, Aaron L.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Lin, Angela E.] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
[Wang, He] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
RP Newton-Cheh, C (reprint author), Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
NR 26
TC 6
Z9 6
U1 0
U2 6
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 APR 14
PY 2011
VL 364
IS 15
BP 1450
EP 1460
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 749LD
UT WOS:000289467200011
PM 21488768
ER
PT J
AU Kapoor, R
Johnson, RA
AF Kapoor, Roger
Johnson, Richard A.
TI Necrolytic Acral Erythema
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Letter
ID CUTANEOUS MARKER; HEPATITIS-C
C1 [Kapoor, Roger; Johnson, Richard A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Kapoor, R (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 4
TC 4
Z9 4
U1 0
U2 0
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD APR 14
PY 2011
VL 364
IS 15
BP 1479
EP 1480
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 749LD
UT WOS:000289467200039
PM 21488794
ER
PT J
AU Eikermann-Haerter, K
Yuzawa, I
Qin, T
Wang, YM
Baek, K
Kim, YR
Hoffmann, U
Dilekoz, E
Waeber, C
Ferrari, MD
van den Maagdenberg, AMJM
Moskowitz, MA
Ayata, C
AF Eikermann-Haerter, Katharina
Yuzawa, Izumi
Qin, Tao
Wang, Yumei
Baek, Kwangyeol
Kim, Young Ro
Hoffmann, Ulrike
Dilekoz, Ergin
Waeber, Christian
Ferrari, Michel D.
van den Maagdenberg, Arn M. J. M.
Moskowitz, Michael A.
Ayata, Cenk
TI Enhanced Subcortical Spreading Depression in Familial Hemiplegic
Migraine Type 1 Mutant Mice
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID MINOR HEAD TRAUMA; DELAYED CEREBRAL EDEMA; CACNA1A GENE MUTATION;
CALCIUM-CHANNEL; CAUDATE-NUCLEUS; RATS; EXPRESSION; GUANOSINE; COMA;
ATAXIA
AB Familial hemiplegic migraine type 1, a monogenic migraine variant with aura, is linked to gain-of-function mutations in the CACNA1A gene encoding Ca(V)2.1 channels. The S218L mutation causes severe channel dysfunction, and paroxysmal migraine attacks can be accompanied by seizures, coma, and hemiplegia; patients expressing the R192Q mutation exhibit hemiplegia only. Familial hemiplegic migraine knock-in mice expressing the S218L or R192Q mutation are highly susceptible to cortical spreading depression, the electrophysiological surrogate for migraine aura, and develop severe and prolonged motor deficits after spreading depression. The S218L mutants also develop coma and seizures and sometimes die. To investigate underlying mechanisms for these symptoms, we used multielectrode electrophysiological recordings, diffusion-weighted magnetic resonance imaging, and c-fos immunohistochemistry to trace spreading depression propagation into subcortical structures. We showed that unlike the wild type, cortical spreading depression readily propagated into subcortical structures in both familial hemiplegic migraine type 1 mutants. Whereas the facilitated subcortical spread appeared limited to the striatum in R192Q, hippocampal and thalamic spread was detected in the S218L mutants with an allele-dosage effect. Both strains exhibited increased susceptibility to subcortical spreading depression and reverberating spreading depression waves. Altogether, these data show that spreading depression propagates between cortex, basal ganglia, diencephalon, and hippocampus in genetically susceptible brains, which could explain the prolonged hemiplegia, coma, and seizure phenotype in this variant of migraine with aura.
C1 [Eikermann-Haerter, Katharina; Yuzawa, Izumi; Qin, Tao; Wang, Yumei; Hoffmann, Ulrike; Dilekoz, Ergin; Waeber, Christian; Moskowitz, Michael A.; Ayata, Cenk] Harvard Univ, Massachusetts Gen Hosp, Dept Radiol, Stroke & Neurovasc Regulat Lab,Med Sch, Charlestown, MA 02129 USA.
[Baek, Kwangyeol; Kim, Young Ro] Harvard Univ, Massachusetts Gen Hosp, Dept Radiol, Athinoula A Martinos Ctr Biomed Imaging,Med Sch, Charlestown, MA 02129 USA.
[Ayata, Cenk] Harvard Univ, Massachusetts Gen Hosp, Dept Neurol, Stroke Serv,Med Sch, Charlestown, MA 02129 USA.
[Ayata, Cenk] Harvard Univ, Massachusetts Gen Hosp, Dept Neurol, Neurosci Intens Care Unit,Med Sch, Charlestown, MA 02129 USA.
[Ferrari, Michel D.; van den Maagdenberg, Arn M. J. M.] Leiden Univ, Dept Neurol, Med Ctr, NL-2333 ZC Leiden, Netherlands.
[van den Maagdenberg, Arn M. J. M.] Leiden Univ, Dept Human Genet, Med Ctr, NL-2333 ZC Leiden, Netherlands.
RP Ayata, C (reprint author), Massachusetts Gen Hosp, Neurovasc Res Lab, 149 13th St,Room 6403, Charlestown, MA 02129 USA.
EM cayata@partners.org
RI Waeber, Christian/A-8333-2009
OI Waeber, Christian/0000-0001-6078-0027
FU American Heart Association [SDG2610275, 0835451N]; National Institutes
of Health [NS061505, NS35611, EB002066]; Netherlands Organization for
Scientific Research [903-52-291, Vici 918.56.602]; European Union
"EUROHEAD" [LSHM-CT-2004-504837]; Centre for Medical Systems Biology,
Netherlands Genomics Initiative
FX This work was supported by the American Heart Association (Grants
SDG2610275 and 0835451N), the National Institutes of Health (Grants
NS061505, NS35611, and EB002066), the Netherlands Organization for
Scientific Research (Grants 903-52-291 and Vici 918.56.602), European
Union "EUROHEAD" (Grant LSHM-CT-2004-504837), and the Centre for Medical
Systems Biology in the framework of the Netherlands Genomics Initiative.
We thank Ludo Broos (Leiden University Medical Centre, Leiden, The
Netherlands) for confirmatory genotyping.
NR 55
TC 46
Z9 47
U1 0
U2 7
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 APR 13
PY 2011
VL 31
IS 15
BP 5755
EP 5763
DI 10.1523/JNEUROSCI.5346-10.2011
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 749MR
UT WOS:000289472400025
PM 21490217
ER
PT J
AU Tiyanont, K
Wales, TE
Aste-Amezaga, M
Aster, JC
Engen, JR
Blacklow, SC
AF Tiyanont, Kittichoat
Wales, Thomas E.
Aste-Amezaga, Miguel
Aster, Jon C.
Engen, John R.
Blacklow, Stephen C.
TI Evidence for Increased Exposure of the Notch1 Metalloprotease Cleavage
Site upon Conversion to an Activated Conformation
SO STRUCTURE
LA English
DT Article
ID FAMILIAL HYPERCHOLESTEROLEMIA; PROTEOLYTIC ACTIVATION; REGULATORY
REGION; LDL RECEPTOR; MUTATIONS; MODULE; DOMAIN; HETERODIMERIZATION;
LEUKEMIA; PATHWAY
AB Notch proteins are transmembrane receptors that normally adopt a resting state poised to undergo activating proteolysis upon ligand engagement. Receptor quiescence is maintained by three LIN12/Notch repeats (LNRs), which wrap around a heterodimerization domain (HD) divided by furin cleavage at site Si during maturation. Ligand binding initiates signaling by inducing sensitivity of the HD to proteolysis at the regulated S2 cleavage site. Here, we used hydrogen exchange mass spectrometry to examine the solution dynamics of the Notch1 negative regulatory region in autoinhibited states before and after Si cleavage, in a proteolytically sensitive "on" state, and in a complex with an inhibitory antibody. Conversion to the "on" state leads to accelerated deuteration in the S2 region and in nearby secondary structural elements within the HD. In contrast, complexation with the inhibitory antibody retards deuteration around the S2 site. Together, these studies reveal how S2 site exposure is promoted by receptor activation and suppressed by inhibitory antibodies.
C1 [Wales, Thomas E.; Engen, John R.] Northeastern Univ, Dept Chem & Chem Biol, Boston, MA 02115 USA.
[Tiyanont, Kittichoat; Blacklow, Stephen C.] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
[Tiyanont, Kittichoat; Blacklow, Stephen C.] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Aste-Amezaga, Miguel] Merck Res Labs, Dept Biol Res, West Point, PA 19486 USA.
[Aster, Jon C.; Blacklow, Stephen C.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
RP Engen, JR (reprint author), Northeastern Univ, Dept Chem & Chem Biol, Boston, MA 02115 USA.
EM j.engen@neu.edu; sblacklow@partners.org
FU NIH (National Institutes of Health) [R01 CA092433, P01 119070, R01
070590, R01 086507]; Leukemia and Lymphoma Society; Cancer Research
Institute; Waters
FX We are grateful to Wendy Gordon for helpful discussions. This work is
supported by NIH (National Institutes of Health) grants R01 CA092433
(S.C.B.), P01 119070 (S.C.B., J.C.A.), R01 070590 (J.R.E.) and R01
086507 (J.R.E.), and the Leukemia and Lymphoma Society (S.C.B., J.C.A.).
K.T. is supported by the Irvington Institute Postdoctoral Fellowship
program of the Cancer Research Institute. S.C.B., J.R.E.,. T.E.W., and
K.T. designed the study, with input from J.C.A. K.T. and T.E.W.
performed all HX MS experiments. K.T. purified all proteins and
performed reporter assays and immunoprecipitation studies. M.A.-A.
provided antibody. S.C.B., J.R.E., T.E.W., and K.T. analyzed data. K.T.
and S.C.B. wrote the manuscript with input from all authors. M. A.-A. is
an employee of Merck & Co., Inc. M.A.-A., J.C.A., and S.C.B. are
co-inventors of a patent application related to the antibody reported in
the study. J.E. is a consultant for the Waters Corporation and receives
funding from Waters through a cooperative research agreement.
NR 28
TC 27
Z9 27
U1 0
U2 9
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0969-2126
EI 1878-4186
J9 STRUCTURE
JI Structure
PD APR 13
PY 2011
VL 19
IS 4
BP 546
EP 554
DI 10.1016/j.str.2011.01.016
PG 9
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 751BN
UT WOS:000289592600013
PM 21481777
ER
PT J
AU Hysong, SJ
Sawhney, MK
Wilson, L
Sittig, DF
Esquivel, A
Singh, S
Singh, H
AF Hysong, Sylvia J.
Sawhney, Mona K.
Wilson, Lindsey
Sittig, Dean F.
Esquivel, Adol
Singh, Simran
Singh, Hardeep
TI Understanding the management of electronic test result notifications in
the outpatient setting
SO BMC MEDICAL INFORMATICS AND DECISION MAKING
LA English
DT Article
DE Decision Support Systems Clinical; Automated notification; diagnostic
errors; abnormal diagnostic test results; Medical Records Systems;
Computerized; patient follow-up; patient safety; health information
technology; communication; primary care
ID DRUG INTERACTION ALERTS; FOLLOW-UP; CLINICAL REMINDERS;
CANCER-DIAGNOSIS; OPPORTUNITIES; MEDICINE; BARRIERS; IMPROVE; SYSTEM;
RECORD
AB Background: Notifying clinicians about abnormal test results through electronic health record (EHR) -based "alert" notifications may not always lead to timely follow-up of patients. We sought to understand barriers, facilitators, and potential interventions for safe and effective management of abnormal test result delivery via electronic alerts.
Methods: We conducted a qualitative study consisting of six 6-8 member focus groups (N = 44) at two large, geographically dispersed Veterans Affairs facilities. Participants included full-time primary care providers, and personnel representing diagnostic services (radiology, laboratory) and information technology. We asked participants to discuss barriers, facilitators, and suggestions for improving timely management and follow-up of abnormal test result notifications and encouraged them to consider technological issues, as well as broader, human-factor-related aspects of EHR use such as organizational, personnel, and workflow.
Results: Providers reported receiving a large number of alerts containing information unrelated to abnormal test results, many of which were believed to be unnecessary. Some providers also reported lacking proficiency in use of certain EHR features that would enable them to manage alerts more efficiently. Suggestions for improvement included improving display and tracking processes for critical alerts in the EHR, redesigning clinical workflow, and streamlining policies and procedures related to test result notification.
Conclusion: Providers perceive several challenges for fail-safe electronic communication and tracking of abnormal test results. A multi-dimensional approach that addresses technology as well as the many non-technological factors we elicited is essential to design interventions to reduce missed test results in EHRs.
C1 [Hysong, Sylvia J.; Sawhney, Mona K.; Wilson, Lindsey; Singh, Hardeep] Baylor Coll Med, Houston VA Hlth Sci Res & Dev Ctr Excellence, Ctr Inquiry Improve Outpatient Safety Effect Elec, Michael E DeBakey Vet Affairs Med Ctr, Houston, TX 77030 USA.
[Hysong, Sylvia J.; Sawhney, Mona K.; Wilson, Lindsey; Singh, Hardeep] Baylor Coll Med, Dept Med, Sect Hlth Serv Res, Houston, TX 77030 USA.
[Sittig, Dean F.] Univ Texas Sch Biomed Informat, Houston, TX USA.
[Sittig, Dean F.] UT Mem Hermann Ctr Healthcare Qual & Safety, Houston, TX USA.
[Esquivel, Adol] St Lukes Episcopal Hlth Syst, Houston, TX USA.
[Singh, Simran] Louis Stokes Cleveland VA Med Ctr, Cleveland, OH USA.
RP Hysong, SJ (reprint author), Baylor Coll Med, Houston VA Hlth Sci Res & Dev Ctr Excellence, Ctr Inquiry Improve Outpatient Safety Effect Elec, Michael E DeBakey Vet Affairs Med Ctr, Houston, TX 77030 USA.
EM sylvia.hysong@va.gov
RI Hysong, Sylvia/B-8420-2008
OI Hysong, Sylvia/0000-0002-9063-5207
FU VA Career Development Award [CD2-07-0181]; NIH [K23CA125585]; VA
National Center of Patient Safety; Houston VA HSR&D Center of Excellence
[HFP90 020]; W. M. Keck Center for Interdisciplinary Bioscience Training
of the Gulf Coast Consortia [T32 HS017586]
FX This study was supported by a VA Career Development Award (CD2-07-0181)
to Dr. Hysong, an NIH K23 career development award (K23CA125585) awarded
to Dr Singh, the VA National Center of Patient Safety, and in part by
the Houston VA HSR&D Center of Excellence (HFP90 020) and AHRQ Training
Program of the W. M. Keck Center for Interdisciplinary Bioscience
Training of the Gulf Coast Consortia (AHRQ Grant No. T32 HS017586). The
views expressed in this article are solely those of the authors and do
not necessarily reflect the position or policy of the authors'
affiliated institutions or the granting agencies supporting this work.
NR 34
TC 18
Z9 18
U1 2
U2 7
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1472-6947
J9 BMC MED INFORM DECIS
JI BMC Med. Inform. Decis. Mak.
PD APR 12
PY 2011
VL 11
AR 22
DI 10.1186/1472-6947-11-22
PG 9
WC Medical Informatics
SC Medical Informatics
GA 768BT
UT WOS:000290907200001
PM 21486478
ER
PT J
AU Sheng, Q
Liu, J
AF Sheng, Q.
Liu, J.
TI The therapeutic potential of targeting the EGFR family in epithelial
ovarian cancer
SO BRITISH JOURNAL OF CANCER
LA English
DT Review
DE EGFR family; ErbB3; ovarian cancer
ID EPIDERMAL-GROWTH-FACTOR; GYNECOLOGIC-ONCOLOGY-GROUP; PHASE-II TRIAL;
CLINICAL ACTIVITY; EXPRESSION; RECURRENT; CARCINOMA; PROTEIN; HER2;
AMPLIFICATION
AB The epithelial growth factor receptor (EGFR) family of receptor tyrosine kinases has been reported to have an active role in a number of malignancies. Amplifications and overexpression of various EGFR family members, including EGFR, Her2, and ErbB3, have been reported in epithelial ovarian cancer. Although anti-EGFR-targeted therapy has shown limited clinical activity in ovarian cancer to date, a recent report suggests that activation of ErbB3, one of the members of the EGFR family, may support the growth and proliferation of ovarian cancer cells and that ErbB3 may therefore serve as a potential therapeutic target in this disease. Here, we review the EGFR family and the clinical experience with anti-EGFR family member-directed therapies in ovarian cancer to date. British Journal of Cancer (2011) 104, 1241-1245. doi:10.1038/bjc.2011.62 www.bjcancer.com Published online 1 March 2011 (C) 2011 Cancer Research UK
C1 [Liu, J.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Sheng, Q.] Nova Pharmaceut Corp, Novartis Oncol Translat Res, Cambridge, MA 02139 USA.
RP Liu, J (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA.
EM joyce_liu@dfci.harvard.edu
NR 32
TC 63
Z9 63
U1 4
U2 9
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
J9 BRIT J CANCER
JI Br. J. Cancer
PD APR 12
PY 2011
VL 104
IS 8
BP 1241
EP 1245
DI 10.1038/bjc.2011.62
PG 5
WC Oncology
SC Oncology
GA 749IL
UT WOS:000289458400001
PM 21364581
ER
PT J
AU Yi, CL
Troutman, S
Fera, D
Stemmer-Rachamimov, A
Avila, JL
Christian, N
Persson, NL
Shimono, A
Speicher, DW
Marmorstein, R
Holmgren, L
Kissil, JL
AF Yi, Chunling
Troutman, Scott
Fera, Daniela
Stemmer-Rachamimov, Anat
Avila, Jacqueline L.
Christian, Neepa
Persson, Nathalie Luna
Shimono, Akihiko
Speicher, David W.
Marmorstein, Ronen
Holmgren, Lars
Kissil, Joseph L.
TI A Tight Junction-Associated Merlin-Angiomotin Complex Mediates Merlin's
Regulation of Mitogenic Signaling and Tumor Suppressive Functions
SO CANCER CELL
LA English
DT Article
ID GTPASE-ACTIVATING PROTEIN; NEUROFIBROMATOSIS TYPE-2; P21-ACTIVATED
KINASES; ENDOTHELIAL-CELLS; POLARITY PROTEINS; HUMAN SCHWANNOMA;
RENAL-CARCINOMA; PLASMA-MEMBRANE; NF2 GENE; GROWTH
AB The Merlin/NF2 tumor suppressor restrains cell growth and tumorigenesis by controlling contact-dependent inhibition of proliferation. We have identified a tight-junction-associated protein complex comprising Merlin, Angiomotin, Patj, and Pals1. We demonstrate that Angiomotin functions downstream of Merlin and upstream of Rich1, a small GTPase Activating Protein, as a positive regulator of Rac1. Merlin, through competitive binding to Angiomotin, releases Rich1 from the Angiomotin-inhibitory complex, allowing Rich1 to inactivate Rac1, ultimately leading to attenuation of Rac1 and Ras-MAPK pathways. Patient-derived Merlin mutants show diminished binding capacities to Angiomotin and are unable to dissociate Rich1 from Angiomotin or inhibit MAPK signaling. Depletion of Angiomotin in Nf2(-/-) Schwann cells attenuates the Ras-MAPK signaling pathway, impedes cellular proliferation in vitro and tumorigenesis in vivo.
C1 [Yi, Chunling; Troutman, Scott; Avila, Jacqueline L.; Christian, Neepa; Speicher, David W.; Kissil, Joseph L.] Wistar Inst Anat & Biol, Mol & Cellular Oncogenesis Program, Philadelphia, PA 19104 USA.
[Fera, Daniela; Marmorstein, Ronen] Wistar Inst Anat & Biol, Gene Express & Regulat Program, Philadelphia, PA 19104 USA.
[Fera, Daniela; Marmorstein, Ronen] Univ Penn, Dept Chem, Philadelphia, PA 19104 USA.
[Stemmer-Rachamimov, Anat] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Persson, Nathalie Luna; Holmgren, Lars] Karolinska Inst, Ctr Canc, Dept Oncol Pathol, SE-17176 Stockholm, Sweden.
[Shimono, Akihiko] Natl Univ Singapore, Canc Sci Inst Singapore, Singapore 117456, Singapore.
RP Kissil, JL (reprint author), Wistar Inst Anat & Biol, Mol & Cellular Oncogenesis Program, Philadelphia, PA 19104 USA.
EM jkissil@wistar.org
FU Children's Tumor Foundation; FP7 EUCAAD project [200755]; Swedish Cancer
Society; Swedish Research Council; Cancer Society in Stockholm; Vinnova
and Karolinska Institutet; [CA124495]
FX We thank Dr. Marco Giovannini (House Ear Institute) for providing the
P0-Cre and Nf2 conditional knockout mice, Dr. Helen Morrison (Leibniz
Institute for Age Research) for RT4-67 and SC4 cells, Dr. Karen
Cichowski (Brigham and Women's Hospital) for MPNST 90-8TL cells, Dr.
Clark Wells (University of Indiana School of Medicine) for Patj-Myc and
Pals1-Flag constructs, Drs. Marianne James and Vijaya Ramesh
(Massachusetts General Hospital) for Flag-hNF2 construct, Dr. Wei Li
(Memorial Sloan-Ketttering Cancer Center) for Flag-HA-hNF2 construct,
and Jaleel Shujath for editorial comments. We are grateful for the
technical assistance of Drs. Sarah Wong and Steven Scherer (University
of Pennsylvania School of Medicine), Drs. Hon-Kit Andus Wong and
Emmanuelle di Tomaso (Massachusetts General Hospital). We thank the
Wistar Proteomics and Animal core facilities. This work was supported in
part by grant CA124495 (J.L.K). C.Y. is a recipient of Young
Investigator Award from the Children's Tumor Foundation. L.H. is
supported by grants from FP7 EUCAAD project 200755, Swedish Cancer
Society, Swedish Research Council and the Cancer Society in Stockholm.
N.L.P. is supported by grants from Vinnova and Karolinska Institutet.
NR 44
TC 99
Z9 100
U1 1
U2 15
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1535-6108
EI 1878-3686
J9 CANCER CELL
JI Cancer Cell
PD APR 12
PY 2011
VL 19
IS 4
BP 527
EP 540
DI 10.1016/j.ccr.2011.02.017
PG 14
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 751AN
UT WOS:000289589800012
PM 21481793
ER
PT J
AU Chen, JQ
Yao, YD
Gong, C
Yu, FY
Su, SC
Chen, JN
Liu, BD
Deng, H
Wang, FS
Lin, L
Yao, HR
Su, FX
Anderson, KS
Liu, QA
Ewen, ME
Yao, XB
Song, EW
AF Chen, Jingqi
Yao, Yandan
Gong, Chang
Yu, Fengyan
Su, Shicheng
Chen, Jianing
Liu, Bodu
Deng, Hui
Wang, Fengsong
Lin, Ling
Yao, Herui
Su, Fengxi
Anderson, Karen S.
Liu, Qiang
Ewen, Mark E.
Yao, Xuebiao
Song, Erwei
TI CCL18 from Tumor-Associated Macrophages Promotes Breast Cancer
Metastasis via PITPNM3
SO CANCER CELL
LA English
DT Article
ID CHEMOKINE RECEPTORS; ALTERNATIVE ACTIVATION; T-CELLS; PROTEIN;
EXPRESSION; CARCINOMA; INVASION; MICROENVIRONMENT; IDENTIFICATION;
ANGIOGENESIS
AB Tumor-associated macrophages (TAMs) can influence cancer progression and metastasis, but the mechanism remains unclear. Here, we show that breast TAMs abundantly produce CCL18, and its expression in blood or cancer stroma is associated with metastasis and reduced patient survival. CCL18 released by breast TAMs promotes the invasiveness of cancer cells by triggering integrin clustering and enhancing their adherence to extracellular matrix. Furthermore, we identify PITPNM3 as a functional receptor for CCL18 that mediates CCL18 effect and activates intracellular calcium signaling. CCL18 promotes the invasion and metastasis of breast cancer xenografts, whereas suppressing PITPNM3 abrogates these effects. These findings indicate that CCL18 derived from TAMs plays a critical role in promoting breast cancer metastasis via its receptor, PITPNM3.
C1 [Deng, Hui; Wang, Fengsong; Yao, Xuebiao] Hefei Natl Lab Phys Sci Nanoscale, Anhui Key Lab Cellular Dynam & Chem Biol, Hefei 230027, Anhui, Peoples R China.
[Deng, Hui; Wang, Fengsong; Yao, Xuebiao] Univ Sci & Technol China, Hefei 230027, Anhui, Peoples R China.
[Chen, Jingqi] Guangzhou Med Univ, Affiliated Hosp 2, Dept Med Oncol, Guangzhou 510260, Guangdong, Peoples R China.
[Chen, Jingqi; Yao, Yandan; Gong, Chang; Yu, Fengyan; Su, Shicheng; Chen, Jianing; Liu, Bodu; Lin, Ling; Yao, Herui; Su, Fengxi; Liu, Qiang; Song, Erwei] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Breast Tumor Ctr, Guangzhou 510120, Guangdong, Peoples R China.
[Anderson, Karen S.; Liu, Qiang; Ewen, Mark E.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Song, EW (reprint author), Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Breast Tumor Ctr, Guangzhou 510120, Guangdong, Peoples R China.
EM yaoxb@ustc.edu.cn; songerwei02@yahoo.com.cn
RI Liu, Bodu/G-5222-2016
OI Liu, Bodu/0000-0003-2097-725X
FU Ministry of Science and Technology of China [2010CB912800, 2011CB504203,
2009CB521706, 2008ZX10208, 2010CB912103]; Natural Science Foundation of
China [30921140312, 30831160515, 30830110, 30772550, 30671930, 30972785,
30973396, 30973505, 30801376, 90913016, 30900497]; Chinese Academy of
Science [KSCX1-YW-R65, KSCX2-YW-H-10, KSCX2-YW-R-195]; Natural Science
Foundation of Guangdong Province [8251008901000011]; Anhui Province
[08040102005]; Guangdong Higher Education Institutes, Sun Yat-sen
University [KLB09001]
FX This work was supported by grants from 973 (2010CB912800, 2011CB504203,
2009CB521706,2008ZX10208, 2010CB912103) Projects from Ministry of
Science and Technology of China, the Natural Science Foundation of China
(30921140312,30831160515, 30830110, 30772550, 30671930, 30972785,
30973396, 30973505, 30801376, 90913016, 30900497), Chinese Academy of
Science (KSCX1-YW-R65, KSCX2-YW-H-10, and KSCX2-YW-R-195), and Natural
Science Foundation of Guangdong Province (8251008901000011), Key
Laboratory of malignant tumor gene regulation and target therapy of
Guangdong Higher Education Institutes, Sun Yat-sen University
(KLB09001). A Key Project from Anhui Province (08040102005).
NR 36
TC 150
Z9 173
U1 11
U2 61
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1535-6108
J9 CANCER CELL
JI Cancer Cell
PD APR 12
PY 2011
VL 19
IS 4
BP 541
EP 555
DI 10.1016/j.ccr.2011.02.006
PG 15
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 751AN
UT WOS:000289589800013
PM 21481794
ER
PT J
AU Yosefy, C
Beeri, R
Guerrero, JL
Vaturi, M
Scherrer-Crosbie, M
Handschumacher, MD
Levine, RA
AF Yosefy, Chaim
Beeri, Ronen
Guerrero, J. Luis
Vaturi, Mordehay
Scherrer-Crosbie, Marielle
Handschumacher, Mark D.
Levine, Robert A.
TI Mitral Regurgitation After Anteroapical Myocardial Infarction New
Mechanistic Insights
SO CIRCULATION
LA English
DT Article
DE ischemia; mitral regurgitation; anterior wall myocardial infarction;
echocardiography, three-dimensional; remodeling
ID PAPILLARY-MUSCLE DYSFUNCTION; VENTRICULAR WALL COMPLEX; PROGNOSTIC
IMPLICATIONS; HEART-FAILURE; ECHOCARDIOGRAPHY; PATHOGENESIS; CLOSURE;
SHAPE; SIZE
AB Background-Mitral regurgitation (MR) generally accompanies inferobasal myocardial infarction (MI), with leaflet tethering by displaced papillary muscles. Mitral regurgitation is also reported with anteroapical MI without global dilatation or inferior wall motion abnormalities. We hypothesized that anteroapical MI extending to the inferior apex displaces the papillary muscles, tethering the mitral leaflets to cause MR.
Methods and Results-In the retrospective part of the study, consecutive anteroapical MI patients were studied. Moderate-severe MR occurred in 9% of 234 patients with only anteroapical MI versus 17% of 242 with inferoapical extension (P < 0.001). Ejection fraction was only mildly different (41 +/- 4% versus 46 +/- 5%; P < 0.01). In the human mechanistic portion of the study, 60 anteroapical MI patients (20 with only 2 apical segments involved and 40 with involvement of all 4 apical segments; 20 with MR and 20 without MR) were compared with 20 normal controls. Those with MR (>= moderate) had higher systolic papillary muscle-to-annulus tethering length (P < 0.01). Mitral regurgitation grade correlated most strongly with tethering length (r = 0.70) and its diminished systolic shortening (r = -0.65). In the animal study, 9 sheep with left anterior descending coronary artery ligation were analyzed. Four sheep that developed MR had inferoapical MI extension with tethering length increasing over 1.5 months (2.1 +/- 0.4 to 2.9 +/- 0.4 cm, P < 0.001) versus no significant increase in 5 sheep without MR (2.0 +/- 0.4 to 2.1 +/- 0.3 cm, P not statistically significant). In MR sheep, the normal decrease in tethering length from diastole to systole was eliminated (P < 0.01).
Conclusions-Anteroapical MI with inferoapical extension can mechanically displace papillary muscles, causing MR despite the absence of basal and midinferior wall motion abnormalities. This suggests the possibility of repositioning treatments for this condition. (Circulation. 2011;123:1529-1536.)
C1 [Yosefy, Chaim; Beeri, Ronen; Guerrero, J. Luis; Vaturi, Mordehay; Scherrer-Crosbie, Marielle; Handschumacher, Mark D.; Levine, Robert A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cardiac Ultrasound Lab, Boston, MA 02114 USA.
RP Levine, RA (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cardiac Ultrasound Lab, Yawkey 5068, Boston, MA 02114 USA.
EM rlevine@partners.org
RI Beeri, Ronen/A-4035-2009
OI Beeri, Ronen/0000-0002-8014-0702
FU National Institutes of Health, Bethesda, MD [R01 HL72265, K24 HL67434];
US-Israel Binational Science Foundation, Jerusalem, Israel [2005250]
FX The current study was supported in part by grants R01 HL72265 and K24
HL67434 from the National Institutes of Health, Bethesda, MD, and grant
2005250, from the US-Israel Binational Science Foundation, Jerusalem,
Israel.
NR 32
TC 21
Z9 23
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD APR 12
PY 2011
VL 123
IS 14
BP 1529
EP 1536
DI 10.1161/CIRCULATIONAHA.110.977843
PG 8
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 748QM
UT WOS:000289405600014
PM 21444880
ER
PT J
AU Scirica, BM
Braunwald, E
Hedgepeth, CM
Qin, J
Morrow, DA
Belardinelli, L
Wang, W
Karwatowska-Prokopczuk, E
Spinar, J
Verheugt, FWA
AF Scirica, Benjamin M.
Braunwald, Eugene
Hedgepeth, Chester M.
Qin, Jie
Morrow, David A.
Belardinelli, Luiz
Wang, Whedy
Karwatowska-Prokopczuk, Ewa
Spinar, Jindrich
Verheugt, Freek W. A.
TI Response to Letters Regarding Article, "Relationship Between
Nonsustained Ventricular Tachycardia After Non-ST-Elevation Acute
Coronary Syndrome and Sudden Cardiac Death: Observations From the
Metabolic Efficiency With Ranolazine for Less Ischemia in
Non-ST-Elevation Acute Coronary Syndrome-Thrombolysis in Myocardial
Infarction 36 (MERLIN-TIMI 36) Randomized Controlled Trial"
SO CIRCULATION
LA English
DT Letter
C1 [Scirica, Benjamin M.; Braunwald, Eugene; Hedgepeth, Chester M.; Qin, Jie; Morrow, David A.] Brigham & Womens Hosp, Dept Med, Div Cardiovasc, TIMI Study Grp, Boston, MA 02115 USA.
[Scirica, Benjamin M.; Braunwald, Eugene; Hedgepeth, Chester M.; Qin, Jie; Morrow, David A.] Harvard Univ, Sch Med, Boston, MA USA.
[Belardinelli, Luiz; Wang, Whedy; Karwatowska-Prokopczuk, Ewa] Gilead Sci Inc, Palo Alto, CA USA.
[Spinar, Jindrich] Univ Hosp Brno, Brno, Czech Republic.
[Verheugt, Freek W. A.] Onze Lieve Vrouw Hosp, Amsterdam, Netherlands.
RP Scirica, BM (reprint author), Brigham & Womens Hosp, Dept Med, Div Cardiovasc, TIMI Study Grp, Boston, MA 02115 USA.
RI Verheugt, F.W.A./H-8105-2014
NR 4
TC 0
Z9 0
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD APR 12
PY 2011
VL 123
IS 14
BP E405
EP E405
DI 10.1161/CIRCULATIONAHA.110.003525
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 748QM
UT WOS:000289405600004
ER
PT J
AU Bratzler, DW
Normand, SLT
Wang, Y
O'Donnell, WJ
Metersky, M
Han, LF
Rapp, MT
Krumholz, HM
AF Bratzler, Dale W.
Normand, Sharon-Lise T.
Wang, Yun
O'Donnell, Walter J.
Metersky, Mark
Han, Lein F.
Rapp, Michael T.
Krumholz, Harlan M.
TI An Administrative Claims Model for Profiling Hospital 30-Day Mortality
Rates for Pneumonia Patients
SO PLOS ONE
LA English
DT Article
ID QUALITY-OF-CARE; COMMUNITY-ACQUIRED PNEUMONIA; ACUTE
MYOCARDIAL-INFARCTION; PERFORMANCE-MEASURES; ELDERLY-PATIENTS;
HEART-FAILURE; US HOSPITALS; OUTCOMES; ISSUES
AB Background: Outcome measures for patients hospitalized with pneumonia may complement process measures in characterizing quality of care. We sought to develop and validate a hierarchical regression model using Medicare claims data that produces hospital-level, risk-standardized 30-day mortality rates useful for public reporting for patients hospitalized with pneumonia.
Methodology/Principal Findings: Retrospective study of fee-for-service Medicare beneficiaries age 66 years and older with a principal discharge diagnosis of pneumonia. Candidate risk-adjustment variables included patient demographics, administrative diagnosis codes from the index hospitalization, and all inpatient and outpatient encounters from the year before admission. The model derivation cohort included 224,608 pneumonia cases admitted to 4,664 hospitals in 2000, and validation cohorts included cases from each of years 1998-2003. We compared model-derived state-level standardized mortality estimates with medical record-derived state-level standardized mortality estimates using data from the Medicare National Pneumonia Project on 50,858 patients hospitalized from 1998-2001. The final model included 31 variables and had an area under the Receiver Operating Characteristic curve of 0.72. In each administrative claims validation cohort, model fit was similar to the derivation cohort. The distribution of standardized mortality rates among hospitals ranged from 13.0% to 23.7%, with 25(th), 50(th), and 75(th) percentiles of 16.5%, 17.4%, and 18.3%, respectively. Comparing model-derived risk-standardized state mortality rates with medical record-derived estimates, the correlation coefficient was 0.86 (Standard Error = 0.032).
Conclusions/Significance: An administrative claims-based model for profiling hospitals for pneumonia mortality performs consistently over several years and produces hospital estimates close to those using a medical record model.
C1 [Bratzler, Dale W.] Oklahoma Fdn Med Qual, Oklahoma City, OK 73134 USA.
[Normand, Sharon-Lise T.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Normand, Sharon-Lise T.] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
[Wang, Yun; Krumholz, Harlan M.] Yale Univ, Sch Med, Dept Internal Med, Sect Cardiovasc Med, New Haven, CT 06510 USA.
[Wang, Yun; Krumholz, Harlan M.] Yale New Haven Med Ctr, Ctr Outcomes Res & Evaluat, New Haven, CT 06504 USA.
[O'Donnell, Walter J.] Massachusetts Gen Hosp, Pulm & Crit Care Unit, Boston, MA 02114 USA.
[Metersky, Mark] Univ Connecticut, Sch Med, Div Pulm & Crit Care Med, Farmington, CT USA.
[Rapp, Michael T.] George Washington Univ, Sch Med & Hlth Sci, Dept Emergency Med, Washington, DC 20052 USA.
[Han, Lein F.; Rapp, Michael T.] Ctr Medicare & Medicaid Serv, Baltimore, MD USA.
[Krumholz, Harlan M.] Yale Univ, Sch Med, Sch Publ Hlth, Sect Hlth Policy & Adm, New Haven, CT USA.
[Krumholz, Harlan M.] Yale Univ, Sch Med, Dept Internal Med, Sch Publ Hlth,Robert Wood Johnson Clin Scholars P, New Haven, CT 06510 USA.
RP Bratzler, DW (reprint author), Oklahoma Fdn Med Qual, Oklahoma City, OK 73134 USA.
EM harlan.krumholz@yale.edu
FU Centers for Medicare and Medicaid Services, an agency of the U.S.
Department of Health and Human Services [500-02-OK-03, 500-05-CO01];
National Heart, Lung, and Blood Institute [U01 HL105270-01];
Massachusetts Department of Public Health
FX The analyses upon which this publication is based were performed in part
under Contract Numbers 500-02-OK-03 and Subcontract #500-05-CO01, funded
by the Centers for Medicare and Medicaid Services, an agency of the U.S.
Department of Health and Human Services. The content of this publication
does not necessarily reflect the views of 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. The
authors assume full responsibility for the accuracy and completeness of
the ideas presented. (025_HQMSS_OK0402_0407) CMS reviewed and approved
the use of its data for this work and approved submission of the
manuscript. The funder had no role in study design, data collection and
analysis, or manuscript preparation. Dr. Krumholz reports that he is a
consultant to UnitedHealthcare, and that he is supported by grant U01
HL105270-01 from the National Heart, Lung, and Blood Institute. Dr.
Normand reports that she is funded by the Massachusetts Department of
Public Health to monitor the quality of care following cardiac surgery
or percutaneous coronary intervention. The other authors report no
conflicts.
NR 24
TC 61
Z9 61
U1 0
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 12
PY 2011
VL 6
IS 4
AR e17401
DI 10.1371/journal.pone.0017401
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 748QE
UT WOS:000289404700004
PM 21532758
ER
PT J
AU Kemper, K
Bulla, S
Krueger, D
Ott, MJ
McCool, JA
Gardiner, P
AF Kemper, Kathi
Bulla, Sally
Krueger, Deborah
Ott, Mary Jane
McCool, Jane A.
Gardiner, Paula
TI Nurses' experiences, expectations, and preferences for mind-body
practices to reduce stress
SO BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE
LA English
DT Article
ID ALTERNATIVE THERAPIES; CRITICAL-CARE; ONCOLOGY NURSES; BLOOD-PRESSURE;
TAI-CHI; MINDFULNESS; BURNOUT; COMPLEMENTARY; INTERVENTION; MEDITATION
AB Background: Most research on the impact of mind-body training does not ask about participants' baseline experience, expectations, or preferences for training. To better plan participant-centered mind-body intervention trials for nurses to reduce occupational stress, such descriptive information would be valuable.
Methods: We conducted an anonymous email survey between April and June, 2010 of North American nurses interested in mind-body training to reduce stress. The e-survey included: demographic characteristics, health conditions and stress levels; experiences with mind-body practices; expected health benefits; training preferences; and willingness to participate in future randomized controlled trials.
Results: Of the 342 respondents, 96% were women and 92% were Caucasian. Most (73%) reported one or more health conditions, notably anxiety (49%); back pain (41%); GI problems such as irritable bowel syndrome (34%); or depression (33%). Their median occupational stress level was 4 (0 = none; 5 = extreme stress). Nearly all (99%) reported already using one or more mind-body practices to reduce stress: intercessory prayer (86%), breath-focused meditation (49%), healing or therapeutic touch (39%), yoga/tai chi/qi gong (34%), or mindfulness-based meditation (18%). The greatest expected benefits were for greater spiritual well-being (56%); serenity, calm, or inner peace (54%); better mood (51%); more compassion (50%); or better sleep (42%). Most (65%) wanted additional training; convenience (74% essential or very important), was more important than the program's reputation (49%) or scientific evidence about effectiveness (32%) in program selection. Most (65%) were willing to participate in a randomized trial of mind-body training; among these, most were willing to collect salivary cortisol (60%), or serum biomarkers (53%) to assess the impact of training.
Conclusions: Most nurses interested in mind-body training already engage in such practices. They have greater expectations about spiritual and emotional than physical benefits, but are willing to participate in studies and to collect biomarker data. Recruitment may depend more on convenience than a program's scientific basis or reputation. Knowledge of participants' baseline experiences, expectations, and preferences helps inform future training and research on mind-body approaches to reduce stress.
C1 [Kemper, Kathi; Bulla, Sally; Krueger, Deborah] Wake Forest Univ, Baptist Med Ctr, Ctr Integrat Med, Winston Salem, NC 27109 USA.
[Ott, Mary Jane] Dana Farber Canc Inst, Boston, MA 02115 USA.
[McCool, Jane A.] Northeastern Univ, Sch Nursing, Bouve Coll Hlth Sci, Boston, MA 02115 USA.
[Gardiner, Paula] Boston Univ, Sch Med, Boston, MA 02118 USA.
RP Kemper, K (reprint author), Wake Forest Univ, Baptist Med Ctr, Ctr Integrat Med, Winston Salem, NC 27109 USA.
EM kkemper@wfubmc.edu
OI Gardiner, Paula/0000-0002-3663-000X
NR 63
TC 11
Z9 11
U1 2
U2 46
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1472-6882
J9 BMC COMPLEM ALTERN M
JI BMC Complement. Altern. Med.
PD APR 11
PY 2011
VL 11
AR 26
DI 10.1186/1472-6882-11-26
PG 9
WC Integrative & Complementary Medicine
SC Integrative & Complementary Medicine
GA 756FM
UT WOS:000289997100001
PM 21481259
ER
PT J
AU White, MR
Jacobson, IG
Smith, B
Wells, TS
Gackstetter, GD
Boyko, EJ
Smith, TC
AF White, Martin R.
Jacobson, Isabel G.
Smith, Besa
Wells, Timothy S.
Gackstetter, Gary D.
Boyko, Edward J.
Smith, Tyler C.
CA Millennium Cohort Study Team
TI Health care utilization among complementary and alternative medicine
users in a large military cohort
SO BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE
LA English
DT Article
ID UNITED-STATES; MILLENNIUM COHORT; DRUG-INTERACTIONS; PREVALENCE;
THERAPIES; SELECTION; SYMPTOMS; PATTERNS; SCORES; TRENDS
AB Background: Complementary and Alternative Medicine use and how it impacts health care utilization in the United States Military is not well documented. Using data from the Millennium Cohort Study we describe the characteristics of CAM users in a large military population and document their health care needs over a 12-month period. The aim of this study was to determine if CAM users are requiring more physician-based medical services than users of conventional medicine.
Methods: Inpatient and outpatient medical services were documented over a 12-month period for 44,287 participants from the Millennium Cohort Study. Equal access to medical services was available to anyone needing medical care during this study period. The number and types of medical visits were compared between CAM and non-CAM users. Chi square test and multivariable logistic regression was applied for the analysis.
Results: Of the 44,287 participants, 39% reported using at least one CAM therapy, and 61% reported not using any CAM therapies. Those individuals reporting CAM use accounted for 45.1% of outpatient care and 44.8% of inpatient care. Individuals reporting one or more health conditions were 15% more likely to report CAM use than non-CAM users and 19% more likely to report CAM use if reporting one or more health symptoms compared to non-CAM users. The unadjusted odds ratio for hospitalizations in CAM users compared to non-CAM users was 1.29 (95% CI: 1.16-1.43). The mean number of days receiving outpatient care for CAM users was 7.0 days and 5.9 days for non-CAM users (p < 0.001).
Conclusions: Our study found those who report CAM use were requiring more physician-based medical services than users of conventional medicine. This appears to be primarily the result of an increase in the number of health conditions and symptoms reported by CAM users.
C1 [White, Martin R.; Jacobson, Isabel G.; Smith, Besa; Wells, Timothy S.; Smith, Tyler C.] USN, Dept Def Ctr Deployment Hlth Res, Hlth Res Ctr, San Diego, CA 92152 USA.
[Gackstetter, Gary D.] Analyt Serv Inc ANSER, Arlington, VA USA.
[Boyko, Edward J.] Vet Affairs Puget Sound Hlth Care Syst, Seattle Epidemiol Res & Informat Ctr, Seattle, WA USA.
RP White, MR (reprint author), USN, Dept Def Ctr Deployment Hlth Res, Hlth Res Ctr, San Diego, CA 92152 USA.
EM martin.white@med.navy.mil
FU Department of Veterans Affairs; Henry M. Jackson Foundation
FX We appreciate the support of the Henry M. Jackson Foundation for the
Advancement of Military Medicine, Rockville, MD.; The views expressed in
this article are those of the authors and do not reflect the official
policy or position of the Department of the Navy, Department of the
Army, Department of the Air Force, Department of Defense, or the US
Government. The Department of Veterans Affairs supported Dr. Boyko's
involvement in this research. This research has been conducted in
compliance with all applicable federal regulations governing the
protection of human subjects in research (protocol NHRC.2000.0007).
NR 39
TC 14
Z9 14
U1 1
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1472-6882
J9 BMC COMPLEM ALTERN M
JI BMC Complement. Altern. Med.
PD APR 11
PY 2011
VL 11
AR 27
DI 10.1186/1472-6882-11-27
PG 11
WC Integrative & Complementary Medicine
SC Integrative & Complementary Medicine
GA 755SF
UT WOS:000289956000001
PM 21481260
ER
PT J
AU Tomas, E
Stanojevic, V
Habener, JF
AF Tomas, Eva
Stanojevic, Violeta
Habener, Joel F.
TI GLP-1-derived nonapeptide GLP-1(28-36)amide targets to mitochondria and
suppresses glucose production and oxidative stress in isolated mouse
hepatocytes
SO REGULATORY PEPTIDES
LA English
DT Article
DE Diabetes; Metabolic syndrome; Insulin resistance; Liver; NEP 24.11
ID GLUCAGON-LIKE PEPTIDE-1; GLP-1 9-36 AMIDE; NEUTRAL ENDOPEPTIDASE-24.11;
INSULIN-RESISTANCE; METABOLIC SYNDROME; PROTEIN; RECEPTOR; DEGRADATION;
HEART; MICE
AB Background: Uncontrolled hepatic glucose production (gluconeogenesis), and glycogenolysis, is a major contributor to the fasting hyperglycemia associated with type 2 diabetes. Here we report the discovery of a C-terminal nonapeptide (FIAWLVKGRamide) derived from GLP-1 that suppresses glucose production and oxidative stress in isolated mouse hepatocytes. The nonapeptide, GLP-1(28-36)amide, was reported earlier to be a major product derived from the cleavage of GLP-1 by the endopeptidase NEP 24.11.
Methods and results: Hepatocytes were isolated from the livers of normal and diet-induced obese mice. We find that the GLP-1(28-36)amide nonapeptide rapidly enters isolated mouse hepatocytes by GLP-1 receptor-independent mechanisms, and targets to mitochondria where it inhibits gluconeogenesis and oxidative stress.
Conclusions: These findings suggest that GLP-1 not only acts on a cell surface G-protein coupled receptor activating kinase-regulated signaling pathways, but a small C-terminal peptide derived from GLP-1 also enters cells, targets mitochondria, and exerts insulin-like actions by modulating oxidative phosphorylation. GLP-1(28-36)amide, or a peptide mimetic derived there from, might prove to be a useful treatment for fasting hyperglycemia and metabolic syndrome in type 2 diabetes. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Tomas, Eva; Stanojevic, Violeta; Habener, Joel F.] Massachusetts Gen Hosp, Mol Endocrinol Lab, Boston, MA 02114 USA.
RP Habener, JF (reprint author), Massachusetts Gen Hosp, Mol Endocrinol Lab, Boston, MA 02114 USA.
EM jhabener@partners.org
FU Merck Co.; Novo Nordisk
FX We thank Zhenghu Liu and Karen McManus for helpful comments and for help
in the assays, and Robert Tyszkowski in the MGH PMB Microscopy Core for
confocal imaging. Early phases of the studies were supported in part by
a one-year Investigator Initiated Studies Program grant from Merck &
Co.; Later studies were supported in part by a Basic Science Grant from
Novo Nordisk.
NR 36
TC 37
Z9 38
U1 0
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-0115
J9 REGUL PEPTIDES
JI Regul. Pept.
PD APR 11
PY 2011
VL 167
IS 2-3
BP 177
EP 184
DI 10.1016/j.regpep.2011.01.003
PG 8
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA 755JT
UT WOS:000289927000004
PM 21256872
ER
PT J
AU Stengel, A
Coskun, T
Goebel-Stengel, M
Craft, LS
Alsina-Fernandez, J
Wang, LX
Rivier, J
Tache, Y
AF Stengel, Andreas
Coskun, Tamer
Goebel-Stengel, Miriam
Craft, Libbey S.
Alsina-Fernandez, Jorge
Wang, Lixin
Rivier, Jean
Tache, Yvette
TI Chronic injection of pansomatostatin agonist ODT8-SST differentially
modulates food intake and decreases body weight gain in lean and
diet-induced obese rats
SO REGULATORY PEPTIDES
LA English
DT Article
DE Body weight; Brain; Diet-induced obesity; Fat mass; Lean body mass;
Somatostatin
ID CORTICOTROPIN-RELEASING-FACTOR; GROWTH-HORMONE-SECRETION;
CENTRAL-NERVOUS-SYSTEM; SOMATOSTATIN RECEPTOR; NEUROPEPTIDE-Y;
PERIVENTRICULAR NUCLEUS; STIMULATING HORMONE; INHIBITS SECRETION;
FEEDING RESPONSE; BARREL ROTATION
AB The aim of this study was to investigate the central actions of the stable pansomatostatin peptide agonist. ODT8-SST on body weight. ODT8-SST or vehicle was acutely (1 mu g/rat) injected or chronically infused (5 mu g/rat/d, 14 d) intracerebroventricularly and daily food intake, body weight and composition were monitored. In lean rats, neither acute nor chronic ODT8-SST influenced daily food intake while body weight was reduced by 2.2% after acute injection and there was a 14 g reduction of body weight gain after 14 d compared to vehicle (p < 0.01). In diet-induced obese (DIO) rats, chronic ODT8-SST increased cumulative 2-week food intake compared to vehicle (+14%, p < 0.05) and also blunted body weight change (-11 g, p<0.05). ODT8-SST for 14 d reduced lean mass (-22 g and -25 g respectively, p < 0.001) and total water (-19g and -22 g respectively, p<0.001) in lean and DIO rats and increased fat mass in DIO (+16 g, p<0.001) but not lean rats (+1 g, p > 0.05) compared to vehicle. In DIO rats, ODT8-SST reduced ambulatory (-27%/24 h, p<0.05) and fine movements (-38%, p<0.01) which was associated with an increased positive energy balance compared to vehicle (+ 50g. p<0.01). Chronic central somatostatin receptor activation in lean rats reduces body weight gain and lean mass independently of food intake which is likely related to growth hormone inhibition. In DIO rats, ODT8-SST reduces lean mass but promotes food intake and fat mass, indicating differential responsiveness to somatostatin under obese conditions. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Tache, Yvette] VA Greater Los Angeles Healthcare Syst, Ctr Neurobiol Stress, Los Angeles, CA 90073 USA.
[Stengel, Andreas; Goebel-Stengel, Miriam; Wang, Lixin; Tache, Yvette] Univ Calif Los Angeles, Dept Med, CURE Digest Dis Res Ctr, Ctr Neurobiol Stress,Digest Dis Div, Los Angeles, CA 90024 USA.
[Coskun, Tamer; Craft, Libbey S.; Alsina-Fernandez, Jorge] Eli Lilly & Co, Biotechnol Discovery Res, Indianapolis, IN 46285 USA.
[Rivier, Jean] Salk Inst Biol Studies, Peptide Biol Labs, La Jolla, CA USA.
RP Tache, Y (reprint author), VA Greater Los Angeles Healthcare Syst, Ctr Neurobiol Stress, CURE Bldg 115,Room 117,11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM ytache@mednet.ucla.edu
FU German Research Foundation [STE 1765/1-1, GO 1718/1-1, NIH R01 DK-33061,
DK-41301]; VA
FX This study was supported by German Research Foundation Grants STE
1765/1-1 (A.S.), GO 1718/1-1 (M.G.-S.), NIH R01 DK-33061, Center Grant
DK-41301 (Animal Core) (Y.T.), VA Research Career Scientist Award (Y.T.)
and VA Rehabilitation Research and Development Grant (Y.T., A.S.). J.R.
is the Dr. Frederik Paulsen Chair in Neurosciences Professor. We are
grateful to Mrs. Honghui Liang and Mrs. Hsui-Chiung Yang for their
excellent technical support and we thank Ms. Eugenia Hu for reviewing
the manuscript.
NR 47
TC 2
Z9 2
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-0115
J9 REGUL PEPTIDES
JI Regul. Pept.
PD APR 11
PY 2011
VL 167
IS 2-3
BP 201
EP 208
DI 10.1016/j.regpep.2011.01.006
PG 8
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA 755JT
UT WOS:000289927000007
PM 21315111
ER
PT J
AU Casarett, D
Johnson, M
Smith, D
Richardson, D
AF Casarett, David
Johnson, Megan
Smith, Dawn
Richardson, Diane
TI The Optimal Delivery of Palliative Care A National Comparison of the
Outcomes of Consultation Teams vs Inpatient Units
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Article
ID RANDOMIZED CONTROLLED-TRIAL; LIFE CARE; ADVANCED CANCER; FAMILY-MEMBERS;
QUALITY MEASURE; TERMINALLY-ILL; END; IMPACT; DEATH; COMMUNICATION
AB Background: Growing attention to end-of-life care has led to intensive efforts to provide better palliative care. However, it is not known whether palliative care is best provided by consultative teams or in dedicated units.
Methods: This nationwide telephone survey was conducted in 77 Veterans Affairs medical centers that offer palliative care consultation services and dedicated palliative care units. One family member per patient who died at a participating Veterans Affairs medical center between July 1, 2008, and December 31, 2009, was invited to participate. The telephone survey included 1 global rating item and 9 core items describing the patient's care in the last month of life.
Results: Interviews were completed with family members for 5901 of 9546 patients. Of these, 1873 received usual care, 1549 received a palliative care consultation, and 2479 received care in a palliative care unit. After non-response weighting and propensity score adjustment, families of patients who received a palliative care consultation were more likely than those who received usual care to report that the patient's care in the last month of life had been "excellent" (adjusted proportions: 51% vs 46%; odds ratio [OR], 1.25; 95% confidence interval [CI], 1.02-1.55; P=.04). However, families of patients who received care in a palliative care unit were even more likely to report excellent care (adjusted proportions: 63% vs 53%; OR, 1.52; 95% CI, 1.25-1.85; P <.001).
Conclusion: Care received in palliative care units may offer more improvements in care than those achieved with palliative care consultations.
C1 [Casarett, David] Univ Penn, Div Geriatr Med, Sch Med, Philadelphia, PA 19104 USA.
[Johnson, Megan; Smith, Dawn; Richardson, Diane] Ctr Hlth Equ Res & Promot, Dept Vet Affairs, Med Ctr, Philadelphia, PA USA.
RP Casarett, D (reprint author), Univ Penn, Div Geriatr Med, Sch Med, 3615 Chestnut St, Philadelphia, PA 19104 USA.
EM Casarett@mail.med.upenn.edu
FU Department of Veterans Affairs, Veterans Health Administration, Office
of Research and Development, Human Services Research and Development;
Department of Veterans Affairs Comprehensive End-of-Life Care Initiative
FX This material is based on work supported by the Department of Veterans
Affairs, Veterans Health Administration, Office of Research and
Development, Human Services Research and Development. This work was
funded as part of a grant from the Department of Veterans Affairs
Comprehensive End-of-Life Care Initiative (Dr Casarett).
NR 46
TC 38
Z9 38
U1 0
U2 3
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 APR 11
PY 2011
VL 171
IS 7
BP 649
EP 655
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA 754PI
UT WOS:000289867700009
PM 21482838
ER
PT J
AU Correa-Rocha, R
Anghel, SI
Budinska, E
Boligan, KF
Abraham, S
Colombetti, S
Fontao, L
Mariotti, A
Rimoldi, D
Ghanem, GE
Fisher, DE
Bracco, L
Levy, F
Delorenzi, M
Piguet, V
AF Correa-Rocha, R.
Anghel, S. I.
Budinska, E.
Boligan, K. F.
Abraham, S.
Colombetti, S.
Fontao, L.
Mariotti, A.
Rimoldi, D.
Ghanem, G. E.
Fisher, D. E.
Bracco, L.
Levy, F.
Delorenzi, M.
Piguet, V.
TI Global analysis of transcription reveals BCSC-1 as a melanoma tumor
suppressor that downregulates MITF
SO BRITISH JOURNAL OF DERMATOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the British-Society-for-Investigative-Dermatology
CY APR 11-13, 2011
CL Univ Manchester, Manchester, ENGLAND
SP British Soc Investigat Dermatol
HO Univ Manchester
C1 [Correa-Rocha, R.; Anghel, S. I.; Boligan, K. F.; Abraham, S.; Fontao, L.; Piguet, V.] Microbiol Univ Hosp, Dept Dermatol & Venereol, Geneva, Switzerland.
[Correa-Rocha, R.; Anghel, S. I.; Boligan, K. F.; Abraham, S.; Fontao, L.; Piguet, V.] Mol Med Univ Hosp, Geneva, Switzerland.
[Correa-Rocha, R.; Anghel, S. I.; Boligan, K. F.; Abraham, S.; Fontao, L.; Piguet, V.] Med Sch Geneva, Geneva, Switzerland.
[Correa-Rocha, R.] Hosp Gen Univ Gregorio Maranon, Lab Mol Immunobiol, Madrid, Spain.
[Budinska, E.; Delorenzi, M.] Univ Lausanne, Swiss Inst Bioinformat, Lausanne, Switzerland.
[Budinska, E.] Masaryk Univ, Inst Biostat & Anal, Brno, Czech Republic.
[Colombetti, S.; Rimoldi, D.; Levy, F.] Univ Lausanne, Ludwig Inst Canc Res, CH-1066 Epalinges, Switzerland.
[Mariotti, A.] Univ Lausanne, Fac Biol & Med, Div Expt Oncol, CH-1066 Epalinges, Switzerland.
[Ghanem, G. E.] Univ Libre Bruxelles, Inst J Bordet, Lab Oncol & Chirurg Expt, Brussels, Belgium.
[Fisher, D. E.] Harvard Univ, Sch Med, Dept Dermatol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Bracco, L.] ExonHit Therapeut Inc, Gaithersburg, MD USA.
[Levy, F.] Debiopharm SA, Lausanne, Switzerland.
[Delorenzi, M.] CHU Vaudois, Dept Format & Rech, CH-1011 Lausanne, Switzerland.
[Delorenzi, M.] ISREC SV EPFL, Natl Ctr Competence Res Mol Oncol, Lausanne, Switzerland.
[Piguet, V.] Cardiff Univ, Welsh Inst Dermatol, Dept Dermatol & Wound Healing, Cardiff, S Glam, Wales.
[Piguet, V.] Univ Wales Hosp, Cardiff CF4 4XW, S Glam, Wales.
EM Piguetv@cardiff.ac.uk
RI Correa-Rocha, Rafael/C-8213-2011; Budinska, Eva/F-2698-2011
OI Correa-Rocha, Rafael/0000-0003-3456-9986; Budinska,
Eva/0000-0002-9004-9187
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 0007-0963
J9 BRIT J DERMATOL
JI Br. J. Dermatol.
PD APR 11
PY 2011
VL 164
IS 4
BP 933
EP 933
PG 1
WC Dermatology
SC Dermatology
GA 745FF
UT WOS:000289150600118
ER
PT J
AU Li, XY
Sanda, T
Look, AT
Novina, CD
von Boehmer, H
AF Li, Xiaoyu
Sanda, Takaomi
Look, A. Thomas
Novina, Carl D.
von Boehmer, Harald
TI Repression of tumor suppressor miR-451 is essential for NOTCH1-induced
oncogenesis in T-ALL
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; C-MYC; LYMPHOCYTIC-LEUKEMIA; CELL
DEVELOPMENT; GLIOMA-CELLS; NOTCH1; EXPRESSION; GENE; TARGETS; CANCER
AB The NOTCH1 signaling pathway is a critical determinant of cell fate decisions and drives oncogenesis through mechanisms that are incompletely understood. Using an established mouse model of T cell acute lymphoblastic leukemia (T-ALL), here we report that induction of intracellular Notch1 (ICN1) leads to repression of miR-451 and miR-709. ICN1 decreases expression of these miRNAs by inducing degradation of the E2a tumor suppressor, which transcriptionally activates the genes encoding miR-451 and miR-709. Both miR-451 and miR-709 directly repress Myc expression. In addition, miR-709 directly represses expression of the Akt and Ras-GRF1 oncogenes. We also show that repression of miR-451 and miR-709 expression is required for initiation and maintenance of mouse T-ALL. miR-451 but not miR-709 is conserved in humans, and human T-ALLs with activating NOTCH1 mutations have decreased miR-451 and increased MYC levels compared with T-ALLs with wild-type NOTCH1. Thus, miR-451 and miR-709 function as potent suppressors of oncogenesis in NOTCH1-induced mouse T-ALL, and miR-451 influences MYC expression in human T-ALL bearing NOTCH1 mutations.
C1 [Li, Xiaoyu; Novina, Carl D.; von Boehmer, Harald] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02215 USA.
[Sanda, Takaomi; Look, A. Thomas] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02215 USA.
RP von Boehmer, H (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, 44 Binney St, Boston, MA 02215 USA.
EM carl_novina@dfci.harvard.edu; Harald_von_boehmer@dfci.harvard.edu
FU National Cancer Institute [5P01CA109901, 5P01CA68484]; Jose Carreras
International Leukemia Foundation; Claudia Adams Barr grant; Children's
Leukemia Research Association
FX This work was funded by National Cancer Institute grants 5P01CA109901
(A.T. Look and H. von Boehmer) and 5P01CA68484 (A.T. Look); by a Jose
Carreras International Leukemia Foundation grant (C.D. Novina); by the
Claudia Adams Barr grant (X. Li); and by the Children's Leukemia
Research Association (T. Sandal.
NR 48
TC 55
Z9 63
U1 1
U2 10
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0022-1007
EI 1540-9538
J9 J EXP MED
JI J. Exp. Med.
PD APR 11
PY 2011
VL 208
IS 4
BP 663
EP 675
DI 10.1084/jem.20102384
PG 13
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 748QF
UT WOS:000289404800004
PM 21464222
ER
PT J
AU Kim, TH
Shivdasani, RA
AF Kim, Tae-Hee
Shivdasani, Ramesh A.
TI Notch signaling in stomach epithelial stem cell homeostasis
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID GENE-EXPRESSION; SECRETASE INHIBITORS; PROGENITOR CELLS; MOUSE STOMACH;
SELF-RENEWAL; DIFFERENTIATION; INTESTINE; IDENTIFICATION; PATHWAY;
CANCER
AB The mammalian adult gastric epithelium self-renews continually through the activity of stem cells located in the isthmus of individual gland units. Mechanisms facilitating stomach stem and progenitor cell homeostasis are unknown. Here, we show that Notch signaling occurs in the mouse stomach epithelium during development and becomes restricted mainly to the isthmus in adult glands, akin to its known localization in the proliferative compartment of intestinal villi. Using genetic and chemical inhibition, we demonstrate that Notch signaling is required to maintain the gastric stem cell compartment. Activation of Notch signaling in lineage-committed stomach epithelial cells is sufficient to induce dedifferentiation into stem and/or multipotential progenitors that populate the mucosa with all major cell types. Prolonged Notch activation within dedifferentiated parietal cells eventually enhances cell proliferation and induces adenomas that show focal Wnt signaling. In contrast, Notch activation within native antral stomach stem cells does not affect cell proliferation. These results establish a role for Notch activity in the foregut and highlight the importance of cellular context in gastric tumorigenesis.
C1 [Kim, Tae-Hee; Shivdasani, Ramesh A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Kim, Tae-Hee; Shivdasani, Ramesh A.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Kim, Tae-Hee; Shivdasani, Ramesh A.] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
RP Shivdasani, RA (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
EM ramesh_shivdasani@dfci.harvard.edu
FU Caring for Carcinoid Foundation; National Institutes of Health
[R01DK081113]; Dana-Farber/Harvard Cancer Center [P50CA127003]
FX Supported by the Caring for Carcinoid Foundation, grant R01DK081113 from
the National Institutes of Health, and the Dana-Farber/Harvard Cancer
Center SPORE Program in GI Cancers (P50CA127003).
NR 43
TC 35
Z9 41
U1 1
U2 5
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0022-1007
EI 1540-9538
J9 J EXP MED
JI J. Exp. Med.
PD APR 11
PY 2011
VL 208
IS 4
BP 677
EP 688
DI 10.1084/jem.20101737
PG 12
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 748QF
UT WOS:000289404800005
PM 21402740
ER
PT J
AU Bhattacharyya, S
Deb, J
Patra, AK
Duong, ATP
Chen, W
Vaeth, M
Berberich-Siebelt, F
Klein-Hessling, S
Lamperti, ED
Reifenberg, K
Jellusova, J
Schweizer, A
Nitschke, L
Leich, E
Rosenwald, A
Brunner, C
Engelmann, S
Bommhardt, U
Avots, A
Muller, MR
Kondo, E
Serfling, E
AF Bhattacharyya, Sankar
Deb, Jolly
Patra, Amiya K.
Duong Anh Thuy Pham
Chen, Wen
Vaeth, Martin
Berberich-Siebelt, Friederike
Klein-Hessling, Stefan
Lamperti, Edward D.
Reifenberg, Kurt
Jellusova, Julia
Schweizer, Astrid
Nitschke, Lars
Leich, Ellen
Rosenwald, Andreas
Brunner, Cornelia
Engelmann, Swen
Bommhardt, Ursula
Avots, Andris
Mueller, Martin R.
Kondo, Eisaku
Serfling, Edgar
TI NFATc1 affects mouse splenic B cell function by controlling the
calcineurin-NFAT signaling network
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID EFFECTOR T-CELLS; TRANSCRIPTION FACTOR; GENE-EXPRESSION; IN-VIVO;
PHOSPHOLIPASE C-GAMMA-2; AUTOIMMUNE-DISEASES; NEGATIVE REGULATOR;
IMMUNE-RESPONSE; DUAL ROLES; MICE
AB By studying mice in which the Nfatc1 gene was inactivated in bone marrow, spleen, or germinal center B cells, we show that NFATc1 supports the proliferation and suppresses the activation-induced cell death of splenic B cells upon B cell receptor (BCR) stimulation. BCR triggering leads to expression of NFATc1/alpha A, a short isoform of NFATc1, in splenic B cells. NFATc1 ablation impaired Ig class switch to IgG3 induced by T cell-independent type II antigens, as well as IgG31(+) plasmablast formation. Mice bearing NFATc1(-/-) B cells harbor twofold more interleukin 10-producing B cells. NFATc1(-/-) B cells suppress the synthesis of interferon-gamma by T cells in vitro, and these mice exhibit a mild clinical course of experimental autoimmune encephalomyelitis. In large part, the defective functions of NFATc1(-/-) B cells are caused by decreased BCR-induced Ca2+ flux and calcineurin (Cn) activation. By affecting CD22, Rcan1, CnA, and NFATc1/alpha A expression, NFATc1 controls the Ca2+-dependent Cn-NFAT signaling network and, thereby, the fate of splenic B cells upon BCR stimulation.
C1 [Bhattacharyya, Sankar; Deb, Jolly; Patra, Amiya K.; Duong Anh Thuy Pham; Chen, Wen; Vaeth, Martin; Berberich-Siebelt, Friederike; Klein-Hessling, Stefan; Avots, Andris; Serfling, Edgar] Univ Wurzburg, Dept Mol Pathol, D-97080 Wurzburg, Germany.
[Leich, Ellen; Rosenwald, Andreas] Univ Wurzburg, Inst Pathol, D-97080 Wurzburg, Germany.
[Lamperti, Edward D.; Mueller, Martin R.] Immune Dis Inst, Boston, MA 02114 USA.
[Lamperti, Edward D.; Mueller, Martin R.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Reifenberg, Kurt] Johannes Gutenberg Univ Mainz, Cent Anim Facil, D-55101 Mainz, Germany.
[Jellusova, Julia; Schweizer, Astrid; Nitschke, Lars] Univ Erlangen Nurnberg, Dept Genet, D-91058 Erlangen, Germany.
[Brunner, Cornelia] Univ Ulm, Dept Physiol Chem, D-89081 Ulm, Germany.
[Engelmann, Swen; Bommhardt, Ursula] Univ Magdeburg, Inst Med & Clin Immunol, D-39120 Magdeburg, Germany.
[Kondo, Eisaku] Okayama Univ, Dept Pathol, Grad Sch Med Dent & Pharmaceut Sci, Okayama 7008558, Japan.
RP Serfling, E (reprint author), Univ Wurzburg, Dept Mol Pathol, D-97080 Wurzburg, Germany.
EM serflinge@mail.uni-wuerzburg.de
RI Brunner, Cornelia/L-1291-2013
FU Deutsche Forschungsgemeinschaft [TRR52, SFB643, FOR832, BO 1054-212];
Wilhelm-Sander and Scheel foundations
FX The work was supported by the Deutsche Forschungsgemeinschaft grant
TRR52 (to F. Berberich-Siebelt, A. Avots, and E. Serfling), SFB643 and
FOR832 Erlangen (to L Nitschke), and BO 1054-212 (to U. Bommhardtb the
Land Sachsen-Anhalt (N2/C2 to U. Bommhardt) and the Wilhelm-Sander and
Scheel foundations (to E. Setting).
NR 82
TC 45
Z9 46
U1 0
U2 2
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0022-1007
EI 1540-9538
J9 J EXP MED
JI J. Exp. Med.
PD APR 11
PY 2011
VL 208
IS 4
BP 823
EP 839
DI 10.1084/jem.20100945
PG 17
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 748QF
UT WOS:000289404800016
PM 21464221
ER
PT J
AU Matthews, LT
Giddy, J
Ghebremichael, M
Hampton, J
Guarino, AJ
Ewusi, A
Carver, E
Axten, K
Geary, MC
Gandhi, RT
Bangsberg, DR
AF Matthews, Lynn T.
Giddy, Janet
Ghebremichael, Musie
Hampton, Jane
Guarino, Anthony J.
Ewusi, Aba
Carver, Emma
Axten, Karen
Geary, Meghan C.
Gandhi, Rajesh T.
Bangsberg, David R.
TI A Risk-Factor Guided Approach to Reducing Lactic Acidosis and
Hyperlactatemia in Patients on Antiretroviral Therapy
SO PLOS ONE
LA English
DT Article
ID HIV-INFECTED PATIENTS; SYMPTOMATIC HYPERLACTATEMIA; SOUTH-AFRICA;
COMPLICATIONS; MANAGEMENT; STAVUDINE; LACTATE; COHORT; ADULTS; WOMEN
AB Background: Stavudine continues to be used in antiretroviral treatment (ART) regimens in many resource-limited settings. The use of zidovudine instead of stavudine in higher-risk patients to reduce the likelihood of lactic acidosis and hyperlactatemia (LAHL) has not been examined.
Methods: Antiretroviral-naive, HIV-infected adults initiating ART between 2004 and 2007 were divided into cohorts of those initiated on stavudine- or zidovudine-containing therapy. We evaluated stavudine or zidovudine use, age, sex, body mass index (BMI), baseline CD4 cell count, creatinine, hemoglobin, alanine aminotransferase, and albumin as predictors of time to LAHL with Cox Proportional Hazards (PH) regression models.
Results: Among 2062 patients contributing 2747 patient years (PY), the combined incidence of LAHL was 3.2/100 PY in those initiating stavudine- and 0.34/100 PY in those initiating zidovudine-containing ART (RR 9.26, 95% CI: 1.28-66.93). In multivariable Cox PH analysis, stavudine exposure (HR 14.31, 95% CI: 5.79-35.30), female sex (HR 3.41, 95% CI: 1.89-6.19), higher BMI (HR 3.21, 95% CI: 2.16-4.77), higher creatinine (1.63, 95% CI: 1.12-2.36), higher albumin (HR 1.04, 95% CI: 1.011.07), and lower CD4 cell count (HR 0.96, 95% CI: 0.92-1.0) at baseline were associated with higher LAHL rates. Among participants who started on stavudine, switching to zidovudine was associated with lower LAHL rates (HR 0.15, 95% CI: 0.06-0.35). Subgroup analysis limited to women with higher BMI >= 25 kg/m(2) initiated on stavudine also showed that switch to zidovudine was protective when controlling for other risk factors (HR 0.21, 95% CI.07-0.64).
Conclusions: Stavudine exposure, female sex, and higher BMI are strong, independent predictors for developing LAHL. Patients with risk factors for lactic acidosis have less LAHL while on zidovudine-rather than stavudine-containing ART. Switching patients from stavudine to zidovudine is protective. Countries continuing to use stavudine should avoid this drug in women and patients with higher BMI.
C1 [Matthews, Lynn T.] Beth Israel Deaconess Med Ctr, Div Infect Dis, Boston, MA 02215 USA.
[Giddy, Janet; Hampton, Jane] McCord Hosp, HIV Program, Durban, South Africa.
[Ghebremichael, Musie; Axten, Karen; Gandhi, Rajesh T.; Bangsberg, David R.] Ragon Inst Massachusetts Gen Hosp Massachusetts I, Boston, MA USA.
[Guarino, Anthony J.] Massachusetts Gen Hosp, Inst Hlth Profess, Boston, MA 02114 USA.
[Ewusi, Aba] Harvard Vanguard Med Associates, Div Internal Med, Boston, MA USA.
[Carver, Emma] Univ Wales Hosp, Dept Emergency Med, Cardiff CF4 4XW, S Glam, Wales.
[Geary, Meghan C.] Albany Med Coll, Albany, NY 12208 USA.
[Gandhi, Rajesh T.] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
[Bangsberg, David R.] Mbarara Univ Sci & Technol, Mbarara, Uganda.
[Bangsberg, David R.] Massachusetts Gen Hosp, Ctr Global Hlth, Boston, MA 02114 USA.
RP Matthews, LT (reprint author), Beth Israel Deaconess Med Ctr, Div Infect Dis, Boston, MA 02215 USA.
EM ltmatthe@bidmc.harvard.edu
FU Mark and Lisa Schwartz Family Foundation; Burroughs Wellcome
Fund/American Society for Tropical Medicine and Hygiene; NIH [R01
AI066992-04A1, NIH G08LM008830-01, MH K-24 87227]; Harvard University
Center for AIDS Research [NIH 2P30 AI06035406]; [NIH U01 AI 694722]
FX Dr. Matthews' work was supported by the Mark and Lisa Schwartz Family
Foundation and by a postdoctoral fellowship in tropical infectious
diseases from the Burroughs Wellcome Fund/American Society for Tropical
Medicine and Hygiene. Dr. Gandhi is supported by NIH R01 AI066992-04A1
and NIH G08LM008830-01 and by grants to the AIDS Clinical Trials Group
(NIH U01 AI 694722) and the Harvard University Center for AIDS Research
(NIH 2P30 AI06035406). Dr. Bangsberg was supported by NIH grant MH K-24
87227. The authors are also grateful to Dr. Heather Ribaudo of the
Harvard University Center for AIDS Research Biostatistical Core (NIH
#AI060354). The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 29
TC 10
Z9 10
U1 0
U2 0
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 11
PY 2011
VL 6
IS 4
AR e18736
DI 10.1371/journal.pone.0018736
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 747XH
UT WOS:000289354100037
PM 21494566
ER
PT J
AU Tamayo, P
Cho, YJ
Tsherniak, A
Greulich, H
Ambrogio, L
Schouten-van Meeteren, N
Zhou, TN
Buxton, A
Kool, M
Meyerson, M
Pomeroy, SL
Mesirov, JP
AF Tamayo, Pablo
Cho, Yoon-Jae
Tsherniak, Aviad
Greulich, Heidi
Ambrogio, Lauren
Schouten-van Meeteren, Netteke
Zhou, Tianni
Buxton, Allen
Kool, Marcel
Meyerson, Matthew
Pomeroy, Scott L.
Mesirov, Jill P.
TI Predicting Relapse in Patients With Medulloblastoma by Integrating
Evidence From Clinical and Genomic Features
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID WIDE EXPRESSION PROFILES; CHILDRENS CANCER GROUP; BREAST-CANCER;
GENE-EXPRESSION; CHILDHOOD MEDULLOBLASTOMA; RISK; MYC; PROGNOSIS;
STRATIFICATION; TRIAL
AB Purpose
Despite significant progress in the molecular understanding of medulloblastoma, stratification of risk in patients remains a challenge. Focus has shifted from clinical parameters to molecular markers, such as expression of specific genes and selected genomic abnormalities, to improve accuracy of treatment outcome prediction. Here, we show how integration of high-level clinical and genomic features or risk factors, including disease subtype, can yield more comprehensive, accurate, and biologically interpretable prediction models for relapse versus no-relapse classification. We also introduce a novel Bayesian nomogram indicating the amount of evidence that each feature contributes on a patient-by-patient basis.
Patients and Methods
A Bayesian cumulative log-odds model of outcome was developed from a training cohort of 96 children treated for medulloblastoma, starting with the evidence provided by clinical features of metastasis and histology (model A) and incrementally adding the evidence from gene-expression-derived features representing disease subtype-independent (model B) and disease subtype-dependent (model C) pathways, and finally high-level copy-number genomic abnormalities (model D). The models were validated on an independent test cohort (n = 78).
Results
On an independent multi-institutional test data set, models A to D attain an area under receiver operating characteristic (au-ROC) curve of 0.73 (95% CI, 0.60 to 0.84), 0.75 (95% CI, 0.64 to 0.86), 0.80 (95% CI, 0.70 to 0.90), and 0.78 (95% CI, 0.68 to 0.88), respectively, for predicting relapse versus no relapse.
Conclusion
The proposed models C and D outperform the current clinical classification schema (au-ROC, 0.68), our previously published eight-gene outcome signature (au-ROC, 0.71), and several new schemas recently proposed in the literature for medulloblastoma risk stratification. J Clin Oncol 29: 1415-1423. (C) 2011 by American Society of Clinical Oncology
C1 MIT, Eli & Edythe Broad Inst, Cambridge, MA 02139 USA.
Harvard Univ, Cambridge, MA 02138 USA.
Harvard Univ, Brigham & Womens Hosp, Childrens Hosp, Dana Farber Canc Inst,Med Sch, Boston, MA 02115 USA.
Childrens Oncol Grp, Arcadia, CA USA.
Univ Amsterdam, Acad Med Ctr, NL-1105 AZ Amsterdam, Netherlands.
RP Mesirov, JP (reprint author), Broad Inst MIT & Harvard, Cambridge Ctr 7, Cambridge, MA 02142 USA.
EM mesirov@broad.mit.edu
RI Meyerson, Matthew/E-7123-2012; Kool, Marcel/H-2541-2013
FU [R01-CA109467]; [R01-CA105607]; [R01-CA121941]; [R01-GM074024];
[P50-CA112962]; [P30-HD018655]
FX Supported by Grants No. R01-CA109467, R01-CA105607, R01-CA121941,
R01-GM074024, P50-CA112962, and P30-HD018655.
NR 53
TC 32
Z9 32
U1 1
U2 4
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 APR 10
PY 2011
VL 29
IS 11
BP 1415
EP 1423
DI 10.1200/JCO.2010.28.1675
PG 9
WC Oncology
SC Oncology
GA 746VW
UT WOS:000289276900021
PM 21357789
ER
PT J
AU Shinagare, AB
Ramaiya, NH
O'Regan, K
Jagannathan, JP
Hornick, JL
LaCasce, AS
AF Shinagare, Atul B.
Ramaiya, Nikhil H.
O'Regan, Kevin
Jagannathan, Jyothi P.
Hornick, Jason L.
LaCasce, Ann S.
TI Helicobacter pylori-Negative Gastric Mucosa-Associated Lymphoid Tissue
Lymphoma
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID MALT LYMPHOMA; INFECTION
C1 [Shinagare, Atul B.; Ramaiya, Nikhil H.; O'Regan, Kevin; Jagannathan, Jyothi P.; LaCasce, Ann S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Shinagare, Atul B.; Ramaiya, Nikhil H.; O'Regan, Kevin; Jagannathan, Jyothi P.; Hornick, Jason L.] Brigham & Womens Hosp, Boston, MA 02115 USA.
RP Shinagare, AB (reprint author), Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 13
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
EI 1527-7755
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD APR 10
PY 2011
VL 29
IS 11
BP E297
EP E300
DI 10.1200/JCO.2010.33.2320
PG 4
WC Oncology
SC Oncology
GA 746VW
UT WOS:000289276900004
PM 21245429
ER
PT J
AU Cho, YJ
Tsherniak, A
Tamayo, P
Santagata, S
Ligon, A
Greulich, H
Berhoukim, R
Amani, V
Goumnerova, L
Eberhart, CG
Lau, CC
Olson, JM
Gilbertson, RJ
Gajjar, A
Delattre, O
Kool, M
Ligon, K
Meyerson, M
Mesirov, JP
Pomeroy, SL
AF Cho, Yoon-Jae
Tsherniak, Aviad
Tamayo, Pablo
Santagata, Sandro
Ligon, Azra
Greulich, Heidi
Berhoukim, Rameen
Amani, Vladimir
Goumnerova, Liliana
Eberhart, Charles G.
Lau, Ching C.
Olson, James M.
Gilbertson, Richard J.
Gajjar, Amar
Delattre, Olivier
Kool, Marcel
Ligon, Keith
Meyerson, Matthew
Mesirov, Jill P.
Pomeroy, Scott L.
TI Integrative Genomic Analysis of Medulloblastoma Identifies a Molecular
Subgroup That Drives Poor Clinical Outcome
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID COPY NUMBER ABNORMALITIES; CENTRAL-NERVOUS-SYSTEM; BETA-CATENIN STATUS;
EXPRESSION PROFILES; PEDIATRIC MEDULLOBLASTOMAS; GENE-EXPRESSION; HUMAN
CANCERS; PATHWAY; CELLS; HYBRIDIZATION
AB Purpose
Medulloblastomas are heterogeneous tumors that collectively represent the most common malignant brain tumor in children. To understand the molecular characteristics underlying their heterogeneity and to identify whether such characteristics represent risk factors for patients with this disease, we performed an integrated genomic analysis of a large series of primary tumors.
Patients and Methods
We profiled the mRNA transcriptome of 194 medulloblastomas and performed high-density single nucleotide polymorphism array and miRNA analysis on 115 and 98 of these, respectively. Non-negative matrix factorization-based clustering of mRNA expression data was used to identify molecular subgroups of medulloblastoma; DNA copy number, miRNA profiles, and clinical outcomes were analyzed for each. We additionally validated our findings in three previously published independent medulloblastoma data sets.
Results
Identified are six molecular subgroups of medulloblastoma, each with a unique combination of numerical and structural chromosomal aberrations that globally influence mRNA and miRNA expression. Wereveal the relative contribution of each subgroup to clinical outcome as a whole and show that a previously unidentified molecular subgroup, characterized genetically by c-MYC copy number gains and transcriptionally by enrichment of photoreceptor pathways and increased miR-183 similar to 96 similar to 182 expression, is associated with significantly lower rates of event-free and overall survivals.
Conclusion
Our results detail the complex genomic heterogeneity of medulloblastomas and identify a previously unrecognized molecular subgroup with poor clinical outcome for which more effective therapeutic strategies should be developed. J Clin Oncol 29: 1424- 1430. (C) 2010 by American Society of Clinical Oncology
C1 Harvard Univ, Brigham & Womens Hosp, Childrens Hosp Boston, Sch Med, Boston, MA 02115 USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Broad Inst Massachusetts Inst Technol & Harvard, Cambridge, MA USA.
Johns Hopkins Univ, Med Ctr, Baltimore, MD 21218 USA.
Baylor Coll Med, Texas Childrens Canc Ctr, Houston, TX 77030 USA.
Univ Washington, Fred Hutchinson Canc Res Ctr, Seattle, WA 98195 USA.
St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
Lab Genet & Biol Canc, Paris, France.
Univ Amsterdam, Acad Med Ctr, NL-1105 AZ Amsterdam, Netherlands.
RP Pomeroy, SL (reprint author), Childrens Hosp, 300 Longwood Ave, Boston, MA 02115 USA.
EM scott.pomeroy@childrens.harvard.edu
RI Meyerson, Matthew/E-7123-2012; Kool, Marcel/H-2541-2013
FU [NIH-R01-109467]; [NIH-R33-CA97556-01]; [NIH-6R01-CA-121941-04];
[NIH-R01-GM074024]; [NIH-P50-CA112962]; [NIH-R01-NS055089]
FX Supported by Grants No. NIH-R01-109467, NIH-R33-CA97556-01,
NIH-6R01-CA-121941-04, NIH-R01-GM074024, NIH-P50-CA112962, and
NIH-R01-NS055089.
NR 36
TC 239
Z9 244
U1 3
U2 13
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 APR 10
PY 2011
VL 29
IS 11
BP 1424
EP 1430
DI 10.1200/JCO.2010.28.5148
PG 7
WC Oncology
SC Oncology
GA 746VW
UT WOS:000289276900022
PM 21098324
ER
PT J
AU Lee, PT
Kerry, VB
Stone, VE
Freedberg, KA
Bangsberg, DR
AF Lee, Patrick T.
Kerry, Vanessa Bradford
Stone, Valerie E.
Freedberg, Kenneth A.
Bangsberg, David R.
TI Transforming health professionals' education
SO LANCET
LA English
DT Letter
C1 [Lee, Patrick T.] Massachusetts Gen Hosp, Boston, MA 02130 USA.
Harvard Univ, Sch Med, Boston, MA 02130 USA.
RP Lee, PT (reprint author), Massachusetts Gen Hosp, Boston, MA 02130 USA.
EM drpatricktlee@gmail.com
NR 5
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0140-6736
EI 1474-547X
J9 LANCET
JI Lancet
PD APR 9
PY 2011
VL 377
IS 9773
BP 1235
EP 1235
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 751DI
UT WOS:000289597300019
PM 21481695
ER
PT J
AU Andrews, JR
Basu, S
AF Andrews, Jason R.
Basu, Sanjay
TI Transmission dynamics and control of cholera in Haiti: an epidemic model
SO LANCET
LA English
DT Article
ID ENDEMIC CHOLERA; BANGLADESH; OUTBREAK; EXPERTS; SCALE
AB Background Official projections of the cholera epidemic in Haiti have not incorporated existing disease trends or patterns of transmission, and proposed interventions have been debated without comparative estimates of their effect. We used a mathematical model of the epidemic to provide projections of future morbidity and mortality, and to Produce comparative estimates of the effects of proposed interventions.
Methods We designed mathematical models of cholera transmission based on existing models and fitted them to incidence data reported in Haiti for each province from Oct 31, 2010, to Jan 24, 2011. We then simulated future epidemic trajectories from March 1 to Nov 30, 2011, to estimate the effect of clean water, vaccination, and enhanced antibiotic distribution programmes.
Findings We project 779 000 cases of cholera in Haiti (95% CI 599 000-914 000) and 11 100 deaths (7300-17 400) between March 1 and Nov 30, 2011. We expect that a 1% per week reduction in consumption of contaminated water would avert 105 000 cases (88 000-116 000) and 1500 deaths (1100-2300). We predict that the vaccination of 10% of the population, from March 1, will avert 63 000 cases (48 000-78 000) and 900 deaths (600-1500). The proposed extension of the use of antibiotics to all patients with severe dehydration and half of patients with moderate dehydration is expected to avert 9000 cases (8000-10 000) and 1300 deaths (900-2000).
Interpretation A decline in cholera prevalence in early 2011 is part of the natural course of the epidemic, and should not be interpreted as indicative of successful intervention. Substantially more cases of cholera are expected than official estimates used for resource allocation. Combined, clean water provision, vaccination, and expanded access to antibiotics might avert thousands of deaths.
C1 [Andrews, Jason R.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
[Andrews, Jason R.] Harvard Univ, Sch Publ Hlth, Ctr Communicable Dis Dynam, Boston, MA 02114 USA.
[Basu, Sanjay] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Basu, Sanjay] San Francisco Gen Hosp, Div Gen Internal Med, San Francisco, CA 94110 USA.
RP Andrews, JR (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Infect Dis, Cox 5, Boston, MA 02114 USA.
EM jandrews6@partners.org
OI Andrews, Jason/0000-0002-5967-251X
FU National Institutes of Health (NIGMS) [U54 GM088558]
FX JRA is supported by the National Institutes of Health (NIGMS grant
number U54 GM088558). This report is solely the responsibility of the
authors and does not necessarily represent the official views of the
National Institutes of Health. We thank Marc Lipsitch for his helpful
comments.
NR 34
TC 65
Z9 69
U1 0
U2 34
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0140-6736
EI 1474-547X
J9 LANCET
JI Lancet
PD APR 9
PY 2011
VL 377
IS 9773
BP 1248
EP 1255
DI 10.1016/S0140-6736(11)60273-0
PG 8
WC Medicine, General & Internal
SC General & Internal Medicine
GA 751DI
UT WOS:000289597300031
PM 21414658
ER
PT J
AU Talkowski, ME
Ernst, C
Heilbut, A
Chiang, C
Hanscom, C
Lindgren, A
Kirby, A
Liu, ST
Muddukrishna, B
Ohsumi, TK
Shen, YP
Borowsky, M
Daly, MJ
Morton, CC
Gusella, JF
AF Talkowski, Michael E.
Ernst, Carl
Heilbut, Adrian
Chiang, Colby
Hanscom, Carrie
Lindgren, Amelia
Kirby, Andrew
Liu, Shangtao
Muddukrishna, Bhavana
Ohsumi, Toshiro K.
Shen, Yiping
Borowsky, Mark
Daly, Mark J.
Morton, Cynthia C.
Gusella, James F.
TI Next-Generation Sequencing Strategies Enable Routine Detection of
Balanced Chromosome Rearrangements for Clinical Diagnostics and Genetic
Research
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID GENOMIC ENRICHMENT
AB The contribution of balanced chromosomal rearrangements to complex disorders remains unclear because they are not detected routinely by genome-wide microarrays and clinical localization is imprecise. Failure to consider these events bypasses a potentially powerful complement to single nucleotide polymorphism and copy-number association approaches to complex disorders, where much of the heritability remains unexplained. To capitalize on this genetic resource, we have applied optimized sequencing and analysis strategies to test whether these potentially high-impact variants can be mapped at reasonable cost and throughput. By using a whole-genome multiplexing strategy, rearrangement breakpoints could be delineated at a fraction of the cost of standard sequencing. For rearrangements already mapped regionally by karyotyping and fluorescence in situ hybridization, a targeted approach enabled capture and sequencing of multiple breakpoints simultaneously. Importantly, this strategy permitted capture and unique alignment of up to 97% of repeat-masked sequences in the targeted regions. Genome-wide analyses estimate that only 3.7% of bases should be routinely omitted from genomic DNA capture experiments. Illustrating the power of these approaches, the rearrangement breakpoints were rapidly defined to base pair resolution and revealed unexpected sequence complexity, such as co-occurrence of inversion and translocation as an underlying feature of karyotypically balanced alterations. These findings have implications ranging from genome annotation to de novo assemblies and could enable sequencing screens for structural variations at a cost comparable to that of microarrays in standard clinical practice.
C1 [Talkowski, Michael E.; Ernst, Carl; Heilbut, Adrian; Chiang, Colby; Hanscom, Carrie; Kirby, Andrew; Liu, Shangtao; Shen, Yiping; Daly, Mark J.; Gusella, James F.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Talkowski, Michael E.; Ernst, Carl; Ohsumi, Toshiro K.; Borowsky, Mark; Gusella, James F.] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
[Talkowski, Michael E.; Ernst, Carl; Ohsumi, Toshiro K.; Borowsky, Mark; Gusella, James F.] Harvard Univ, Sch Med, Dept Neurol, Boston, MA 02115 USA.
[Muddukrishna, Bhavana; Ohsumi, Toshiro K.; Borowsky, Mark] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
[Lindgren, Amelia; Morton, Cynthia C.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Obstet & Gynecol, Boston, MA 02115 USA.
[Lindgren, Amelia; Morton, Cynthia C.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Talkowski, Michael E.; Kirby, Andrew; Daly, Mark J.; Morton, Cynthia C.; Gusella, James F.] Broad Inst Harvard & MIT, Program Med & Populat Genet, Cambridge, MA 02143 USA.
RP Gusella, JF (reprint author), Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
EM gusella@helix.mgh.harvard.edu
RI Sincan, Murat /A-3794-2010; Heilbut, Adrian/J-9427-2012;
OI Heilbut, Adrian/0000-0002-8169-7967; Chiang, Colby/0000-0002-4113-6065
FU National Institutes of Health [GM061354, HD065286]; Simons Foundation
Autism Research Initiative and Autism Speaks; National Institute of
Mental Health [F32MH087123]; MGH Executive Committee; Canadian
Institutes of Health Research
FX We thank Tammy Gillis, Mary Anne Anderson, and Diane Lucente at the
Center for Human Genetic Research of Massachusetts General Hospital
(MGH) and the Genome Sequencing Platform at the Broad Institute for
technical assistance. We also thank Oleg Iartchouk, Madelyn Light, Peter
Rossetti, and colleagues at the Partners Center for Personalized Genomic
Medicine for contributing the HiSeq 2000 data and Dennis Gurgul of
Partners Research Computing at Massachusetts General Hospital for
assistance with computational resources. This work was funded by grants
GM061354 and HD065286 from the National Institutes of Health and by the
Simons Foundation Autism Research Initiative and Autism Speaks. M.E.T.
was supported by an National Institute of Mental Health National
Research Service Award (F32MH087123) and an MGH Executive Committee on
Research Fund for Medical Discovery. C.E. was supported by a Canadian
Institutes of Health Research Bisby Fellowship.
NR 22
TC 78
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U1 1
U2 6
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD APR 8
PY 2011
VL 88
IS 4
BP 469
EP 481
DI 10.1016/j.ajhg.2011.03.013
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 752BY
UT WOS:000289664300007
PM 21473983
ER
PT J
AU Goessling, W
Allen, RS
Guan, X
Jin, P
Uchida, N
Dovey, M
Harris, JM
Metzger, ME
Bonifacino, AC
Stroncek, D
Stegner, J
Armant, M
Schlaeger, T
Tisdale, JF
Zon, LI
Donahue, RE
North, TE
AF Goessling, Wolfram
Allen, Robyn S.
Guan, Xiao
Jin, Ping
Uchida, Naoya
Dovey, Michael
Harris, James M.
Metzger, Mark E.
Bonifacino, Aylin C.
Stroncek, David
Stegner, Joseph
Armant, Myriam
Schlaeger, Thorsten
Tisdale, John F.
Zon, Leonard I.
Donahue, Robert E.
North, Trista E.
TI Prostaglandin E2 Enhances Human Cord Blood Stem Cell Xenotransplants and
Shows Long-Term Safety in Preclinical Nonhuman Primate Transplant Models
SO CELL STEM CELL
LA English
DT Article
ID BONE-MARROW; PROGENITOR CELLS; EXPANSION; MOBILIZATION; REPOPULATION;
ENGRAFTMENT; RECEPTOR; DONORS
AB Hematopoietic stem cells (HSCs) are used in transplantation therapy to reconstitute the hematopoietic system. Human cord blood (hCB) transplantation has emerged as an attractive alternative treatment option when traditional HSC sources are unavailable; however, the absolute number of hCB HSCE.; transplanted is significantly lower than bone marrow or mobilized peripheral blood stem cells (MPBSCs). We previously demonstrated that dimethyl-prostaglandin E2 (dmPGE2), increased HSCs in vertebrate models. Here, we describe preclinical analyses of the therapeutic potential of dmPGE2 treatment by using human and nonhuman primate HSCs. dmPGE2 significantly increased total human hematopoietic colony formation in vitro and enhanced engraftment of unfractionated and CD34(+) hCB after xenotransplantation. In nonhuman primate autologous transplantation, dmPGE2-treated CD34(+) MPBSCs showed stable multilineage engraftment over 1 year postinfusion. Together, our analyses indicated that dmPGE2 mediates conserved responses in HSCs from human and nonhuman primates and provided sufficient preclinical information to support proceeding to an FDA-approved phase 1 clinical trial.
C1 [Goessling, Wolfram; Zon, Leonard I.; North, Trista E.] Harvard Stem Cell Inst, Boston, MA 02115 USA.
[Goessling, Wolfram; Zon, Leonard I.; North, Trista E.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Goessling, Wolfram] Brigham & Womens Hosp, Dana Farber Canc Inst, Gastrointestinal Canc Ctr, Div Genet, Boston, MA 02115 USA.
[Goessling, Wolfram] Brigham & Womens Hosp, Dana Farber Canc Inst, Gastrointestinal Canc Ctr, Div Gastroenterol, Boston, MA 02115 USA.
[Allen, Robyn S.; Metzger, Mark E.; Bonifacino, Aylin C.; Donahue, Robert E.] NHLBI, Hematol Branch, NIH, Rockville, MD 20850 USA.
[Guan, Xiao; Schlaeger, Thorsten; Zon, Leonard I.] Childrens Hosp, Stem Cell Program, Boston, MA 02115 USA.
[Jin, Ping; Stroncek, David] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Uchida, Naoya; Tisdale, John F.] NIDDK, Mol & Clin Hematol Branch, NHLBI, NIH, Bethesda, MD 20892 USA.
[Dovey, Michael; Harris, James M.; North, Trista E.] Beth Israel Deaconess Med Ctr, Dept Pathol, Boston, MA 02115 USA.
[Stegner, Joseph; Armant, Myriam] Immune Dis Inst, Ctr Human Cell Therapy, Boston, MA 02115 USA.
[Zon, Leonard I.] Howard Hughes Med Inst, Boston, MA 02115 USA.
RP North, TE (reprint author), Harvard Stem Cell Inst, Boston, MA 02115 USA.
EM tnorth@bidmc.harvard.edu
RI Guan, Xiao/D-5656-2013;
OI Goessling, Wolfram/0000-0001-9972-1569
FU Harvard Stern Cell Institute; NIH NIDDK; Howard Hughes Medical
Institute; National Institutes of Health, NHLBI; NIDDK; Department of
Transfusion Medicine at the NIH Clinical Center; FATE Therapeutics
FX The HMS researchers thank J. Trowbridge, C. Walkley, G.O. Daley J. Ritz,
L. Silberstein, G. Kao, J. Antin, R. Soiffer, K. Ballen, C. Cutler, and
the members of the Center for Human Cell Therapy at Harvard Medical
School, Dana-Farber Cancer Institute for helpful discussions and
guidance on the clinical application of dmPGE2 and the FDA application
process. We are grateful to the Carolinas Cord Blood Bank for providing
us with discarded cord blood units. The NIH researchers thank K.
Keyvanfar for cell-sorting assistance, Y. Tian for assisting with the
processing of the microarray data, and the veterinary and animal care
staff at 5 Research Court and Poolesville for maintaining the nonhuman
primates used in this study. This research was supported by the Harvard
Stern Cell Institute (VV.G., LIZ., T.E.N.), NIH NIDDK (W.G., LIZ.,
TEN.), Howard Hughes Medical Institute (LIZ.), the Intramural Research
Program of the National Institutes of Health, NHLBI, and/or NIDDK
(R.S.A., N.U., M.E.M., A.C.B., J.F.T., RED.), and the Department of
Transfusion Medicine at the NIH Clinical Center (P.J., D.S.). T.E.N. and
W.G. receive patent royalties and consulting fees from FATE
Therapeutics; L.I.Z. is a scientific founder and stockholder of and
receives patent royalties from FATE Therapeutics, which is currently
testing the use of prostaglandin E2 to enhance the efficacy of hCB
transplants in an independently conducted phase I clinical trial.
NR 32
TC 124
Z9 128
U1 0
U2 10
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1934-5909
EI 1875-9777
J9 CELL STEM CELL
JI Cell Stem Cell
PD APR 8
PY 2011
VL 8
IS 4
BP 445
EP 458
DI 10.1016/j.stem.2011.02.003
PG 14
WC Cell & Tissue Engineering; Cell Biology
SC Cell Biology
GA 752QI
UT WOS:000289707100016
PM 21474107
ER
PT J
AU Laitman, BM
DaSilva, JK
Ross, RJ
Tejani-Butt, S
Morrison, AR
AF Laitman, Benjamin M.
DaSilva, Jamie K.
Ross, Richard J.
Tejani-Butt, Shanaz
Morrison, Adrian R.
TI Reduced gamma range activity at REM sleep onset and termination in
fear-conditioned Wistar-Kyoto rats
SO NEUROSCIENCE LETTERS
LA English
DT Article
DE Gamma power; Rapid eye movement sleep; Fear conditioning; Posttraumatic
stress disorder
ID POSTTRAUMATIC-STRESS-DISORDER; WKY RATS; DEPENDENT PLASTICITY;
DEPRESSIVE BEHAVIOR; SPRAGUE-DAWLEY; TWIN; OSCILLATION; PERFORMANCE;
MECHANISMS; STATES
AB Recent investigations of rapid eye movement sleep (REMS) continuity have emphasized the importance of transitions both into and out of REMS. We have previously reported that, compared to Wistar rats (WIS), Wistar-Kyoto rats (WIN) responded to fear conditioning (FC) with more fragmented REMS. Gamma oscillations in the electroencephalogram (EEG) are synchronized throughout the brain in periods of focused attention, and such synchronization of cell assemblies in the brain may represent a temporal binding mechanism. Therefore, we examined the effects of FC on EEG gamma range activity (30-50 Hz) at REMS transitions in WKY compared to WIS. Relative power in the gamma range (measured as a percent of total power) at Baseline and upon re-exposure to the fear-inducing conditioning stimulus was measured 35s before REMS onset to 105s after REMS onset (ARO) and 85s before REMS termination (BRT) to 35 s after REMS termination. After baseline recording, rats received 10 tones, each co-terminating with an electric foot shock. On Days 1 and 14 post-conditioning, rats were re-exposed to three tones. Fast-Fourier transforms created power spectral data in the gamma frequency domain. Relative power was extracted from an average of 4-5 REMS transitions. Relative gamma power was always higher in WIS. On Day 14, at 15 s and 25s ARO, WIN had significant increases in relative gamma power from Baseline. WIS had a significant increase on Day 1 at 25 s ARO. Despite the increases in relative gamma power, WIN never achieved levels attained by WIS. Moreover, at 5 s BRT, only WKY had a significant decrease in relative gamma power from Baseline to Day 14. Gamma range activity may indicate neural activity underlying maintenance of REMS continuity. Low relative gamma power at REMS transitions may be associated with increased REMS fragmentation in WKY after FC. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
C1 [Laitman, Benjamin M.; Ross, Richard J.; Morrison, Adrian R.] Univ Penn, Sch Vet Med, Dept Anim Biol, Philadelphia, PA 19104 USA.
[DaSilva, Jamie K.; Tejani-Butt, Shanaz] Univ Sci Philadelphia, Dept Pharmaceut Sci, Philadelphia, PA 19104 USA.
[Ross, Richard J.] Univ Penn, Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA.
[Ross, Richard J.] Philadelphia VA Med Ctr, Behav Hlth Serv, Philadelphia, PA 19104 USA.
RP Laitman, BM (reprint author), Univ Penn, Sch Vet Med, Dept Anim Biol, 3800 Spruce St, Philadelphia, PA 19104 USA.
EM laitman@sas.upenn.edu
FU UPSHS [MH072897, AA015921]
FX Supported by UPSHS grants MH072897 to Adrian R. Morrison and AA015921 to
Shanaz Tejani-Butt. The content of this article does not reflect the
views of the Department of Veterans Affairs or of the U.S. Government.
We also gratefully acknowledge contributions of Graziella L Mann and Dr.
Philip R. Gehrman.
NR 35
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U1 1
U2 3
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0304-3940
J9 NEUROSCI LETT
JI Neurosci. Lett.
PD APR 8
PY 2011
VL 493
IS 1-2
BP 14
EP 17
DI 10.1016/j.neulet.2011.02.003
PG 4
WC Neurosciences
SC Neurosciences & Neurology
GA 745QN
UT WOS:000289180800003
PM 21316420
ER
PT J
AU Hersperger, AR
Martin, JN
Shin, LY
Sheth, PM
Kovacs, CM
Cosma, GL
Makedonas, G
Pereyra, F
Walker, BD
Kaul, R
Deeks, SG
Betts, MR
AF Hersperger, Adam R.
Martin, Jeffrey N.
Shin, Lucy Y.
Sheth, Prameet M.
Kovacs, Colin M.
Cosma, Gabriela L.
Makedonas, George
Pereyra, Florencia
Walker, Bruce D.
Kaul, Rupert
Deeks, Steven G.
Betts, Michael R.
TI Increased HIV-specific CD8(+) T-cell cytotoxic potential in HIV elite
controllers is associated with T-bet expression
SO BLOOD
LA English
DT Article
ID GRANULE EXOCYTOSIS PATHWAY; TRANSCRIPTION FACTOR; PERFORIN EXPRESSION;
EFFECTOR MOLECULES; IMMUNE CONTROL; VIRUS CONTROL; UP-REGULATION;
GRANZYME-B; MEMORY; DEATH
AB Recent data suggest that CD8(+) T-cell effector activity is an important component in the control of HIV replication in elite controllers (ECs). One critical element of CD8(+) T-cell effector function and differentiation is the T-box transcription factor T-bet. In the present study, we assessed T-bet expression, together with the effector proteins perforin, granzyme A(Grz A), granzyme B(Grz B), and granulysin, in HIV-specific CD8(+) T cells from ECs (n = 20), chronically infected progressors (CPs; n = 18), and highly active anti-retroviral therapy (HAART)-suppressed individuals (n = 19). Compared with the other cohort groups, HIV-specific CD8(+) T cells among ECs demonstrated a superior ability to express perforin and Grz B, but with no detectable difference in the levels of Grz A or granulysin. We also observed higher levels of T-bet in HIV-specific CD8(+) T cells from ECs, with an ensuing positive correlation between T-bet and levels of both perforin and Grz B. Moreover, HIV-specific CD8(+) T cells in ECs up-regulated T-bet to a greater extent than CPs after in vitro expansion, with concomitant up-regulation of perforin and Grz B. These results suggest that T-bet may play an important role in driving effector function, and its modulation may lead to enhanced effector activity against HIV. (Blood. 2011;117(14):3799-3808)
C1 [Hersperger, Adam R.; Cosma, Gabriela L.; Makedonas, George; Betts, Michael R.] Univ Penn, Dept Microbiol, Philadelphia, PA 19104 USA.
[Martin, Jeffrey N.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Shin, Lucy Y.; Sheth, Prameet M.; Kaul, Rupert] Univ Toronto, Dept Med, Toronto, ON, Canada.
[Kovacs, Colin M.] Canadian Immunodeficiency Res Collaborat, Toronto, ON, Canada.
[Pereyra, Florencia; Walker, Bruce D.] Harvard Univ, Boston, MA 02115 USA.
[Pereyra, Florencia; Walker, Bruce D.] Massachusetts Gen Hosp, MIT, Ragon Inst, Boston, MA 02114 USA.
[Walker, Bruce D.] Howard Hughes Med Inst, Chevy Chase, MD USA.
[Deeks, Steven G.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
RP Betts, MR (reprint author), 402C Johnson Pavil,3610 Hamilton Walk, Philadelphia, PA 19104 USA.
EM betts@mail.med.upenn.edu
FU National Institutes of Health [RO1 AI076066, HHSN272200800063C]; Centers
for AIDS Research at the University of California-San Francisco [PO
AI27763]; Center for AIDS Research Network of Integrated Systems [R24
AI067039]; University of California-San Francisco Clinical and
Translational Science Institute [UL1 RR024131]; National Institute of
Allergy and Infectious Diseases [RO1 AI087145, K24AI069994, AI 76174];
American Foundation for AIDS Research; Ragon Institute
FX This work was supported by many sources, including the National
Institutes of Health (grants RO1 AI076066 and HHSN272200800063C to
M.B.), the Centers for AIDS Research at the University of California-San
Francisco (grant PO AI27763), the Center for AIDS Research Network of
Integrated Systems (grant R24 AI067039), the University of
California-San Francisco Clinical and Translational Science Institute
(grant UL1 RR024131), the National Institute of Allergy and Infectious
Diseases (grants RO1 AI087145, K24AI069994, and AI 76174), the American
Foundation for AIDS Research, and the Ragon Institute.
NR 49
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U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD APR 7
PY 2011
VL 117
IS 14
BP 3799
EP 3808
DI 10.1182/blood-2010-12-322727
PG 10
WC Hematology
SC Hematology
GA 746RV
UT WOS:000289265500015
PM 21289310
ER
PT J
AU Reed, MC
Dhaliwal, G
Saint, S
Nallamothu, BK
AF Reed, Michael C.
Dhaliwal, Gurpreet
Saint, Sanjay
Nallamothu, Brahmajee K.
TI The Right Angle
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID CENTRAL VENOUS-PRESSURE; CONSTRICTIVE PERICARDITIS; RESTRICTIVE
CARDIOMYOPATHY; CRITICALLY ILL; MODERN-ERA; PATIENT; IMPACT
C1 [Reed, Michael C.; Saint, Sanjay; Nallamothu, Brahmajee K.] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Saint, Sanjay; Nallamothu, Brahmajee K.] Ann Arbor Vet Affairs Med Ctr, Hlth Serv Res & Dev Ctr Excellence, Ann Arbor, MI USA.
[Dhaliwal, Gurpreet] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Dhaliwal, Gurpreet] San Francisco VA Med Ctr, Dept Internal Med, San Francisco, CA USA.
RP Reed, MC (reprint author), Univ Michigan, Dept Internal Med, 1500 E Med Ctr Dr,SPC 5869, Ann Arbor, MI 48109 USA.
EM micreed@med.umich.edu
NR 15
TC 0
Z9 0
U1 0
U2 1
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD APR 7
PY 2011
VL 364
IS 14
BP 1350
EP 1356
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA 745WS
UT WOS:000289202800012
PM 21470013
ER
PT J
AU Pascual-Figal, DA
Sanchez-Mas, J
Januzzi, JL
AF Pascual-Figal, Domingo A.
Sanchez-Mas, Jesus
Januzzi, James L.
TI Eplerenone in Mild Heart Failure
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Letter
ID SPIRONOLACTONE
C1 [Pascual-Figal, Domingo A.; Sanchez-Mas, Jesus] Univ Hosp Virgen de la Arrixaca, Murcia, Spain.
[Januzzi, James L.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Pascual-Figal, DA (reprint author), Univ Hosp Virgen de la Arrixaca, Murcia, Spain.
EM dapascual@servicam.com
RI Pascual Figal, Domingo /B-3794-2008
OI Pascual Figal, Domingo /0000-0002-4993-9540
NR 4
TC 0
Z9 0
U1 1
U2 3
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD APR 7
PY 2011
VL 364
IS 14
BP 1370
EP 1370
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 745WS
UT WOS:000289202800017
PM 21470020
ER
PT J
AU Handschin, C
Spiegelman, BM
AF Handschin, Christoph
Spiegelman, Bruce M.
TI PGC-1 Coactivators and the Regulation of Skeletal Muscle Fiber-Type
Determination
SO CELL METABOLISM
LA English
DT Letter
C1 [Handschin, Christoph] Univ Basel, Div Pharmacol Neurobiol, Biozentrum, CH-4056 Basel, Switzerland.
[Spiegelman, Bruce M.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Spiegelman, Bruce M.] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
RP Handschin, C (reprint author), Univ Basel, Div Pharmacol Neurobiol, Biozentrum, CH-4056 Basel, Switzerland.
EM handschin@unibas.ch; bruce_spiegelman@dfci.harvard.edu
RI Handschin, Christoph/E-6886-2015
OI Handschin, Christoph/0000-0003-0603-1097
NR 5
TC 16
Z9 18
U1 0
U2 8
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1550-4131
EI 1932-7420
J9 CELL METAB
JI Cell Metab.
PD APR 6
PY 2011
VL 13
IS 4
BP 351
EP 351
DI 10.1016/j.cmet.2011.03.008
PG 1
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 748HM
UT WOS:000289381300001
PM 21459315
ER
PT J
AU Tsou, L
Zheng, B
Hsu, CH
Sasaki, AT
Cantley, LC
AF Tsou, Ling
Zheng, Bin
Hsu, Chia-Hsien
Sasaki, Atsuo T.
Cantley, Lewis C.
TI A Fluorescent Reporter of AMPK Activity and Cellular Energy Stress
SO CELL METABOLISM
LA English
DT Article
ID ACTIVATED PROTEIN-KINASE; UPSTREAM KINASE; LKB1; BETA; HOMEOSTASIS;
CELLS; FRET; VARIABILITY; SPECIFICITY; APOPTOSIS
AB AMP-activated protein kinase (AMPK) is activated when the AMP/ATP ratio in cells is elevated due to energy stress. Here, we describe a biosensor, AMPKAR, that exhibits enhanced fluorescence resonance energy transfer (FRET) in response to phosphorylation by AMPK, allowing spatiotemporal monitoring of AMPK activity in single cells. We show that this reporter responds to a variety of stimuli that are known to induce energy stress and that the response is dependent on AMPK alpha l and alpha 2 and on the upstream kinase LKB1. Interestingly, we found that AMPK activation is confined to the cytosol in response to energy stress but can be observed in both the cytosol and nucleus in response to calcium elevation. Finally, using this probe with U2OS cells in a microfluidic device, we observed a very high cell-to-cell variability in the amplitude and time course of AMPK activation and recovery in response to pulses of glucose deprivation.
C1 [Tsou, Ling; Zheng, Bin; Sasaki, Atsuo T.; Cantley, Lewis C.] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA.
[Tsou, Ling; Zheng, Bin; Sasaki, Atsuo T.; Cantley, Lewis C.] Beth Israel Deaconess Med Ctr, Div Signal Transduct, Boston, MA 02115 USA.
[Hsu, Chia-Hsien] Harvard Univ, Sch Med, Massachusetts Gen Hosp, BioMEMS Resource Ctr,Ctr Engn Med & Surg Serv, Boston, MA 02114 USA.
RP Cantley, LC (reprint author), Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA.
EM lewis_cantley@hms.harvard.edu
RI Hsu, Chia-Hsien /E-3946-2010; Cantley, Lewis/D-1800-2014
OI Cantley, Lewis/0000-0002-1298-7653
FU National Institutes of Health [R01-GM56203, P01-CAl20964, R00-CA133245]
FX We thank Jin Zhang for providing AKAR3 construct, Alexandra Newton for
DKAR plasmid, and Keith R. Laderoute for AMPK null MEFs, Mike Begley for
providing lentiviral reagents and assistance with establishing stable
cell lines, Irimia Daniel and Octavio Hurtado for valuable assistance
with microfluidic device microfabrication, the Nikon Imaging Center at
Harvard Medical School for imaging assistance, Rebacca Ward, Ken
Swanson, and Jason Localsale for critical reading of the manuscript, and
members of the Cantley Lab for helpful discussion. This work was
supported by National Institutes of Health grants R01-GM56203 and
P01-CAl20964 to L.C.C., and R00-CA133245 to B.Z.
NR 38
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U1 1
U2 14
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1550-4131
EI 1932-7420
J9 CELL METAB
JI Cell Metab.
PD APR 6
PY 2011
VL 13
IS 4
BP 476
EP 486
DI 10.1016/j.cmet.2011.03.006
PG 11
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 748HM
UT WOS:000289381300018
ER
PT J
AU Campbell, JH
Burdo, TH
Autissier, P
Bombardier, JP
Westmoreland, SV
Soulas, C
Gonzalez, RG
Ratai, EM
Williams, KC
AF Campbell, Jennifer H.
Burdo, Tricia H.
Autissier, Patrick
Bombardier, Jeffrey P.
Westmoreland, Susan V.
Soulas, Caroline
Gonzalez, R. Gilberto
Ratai, Eva-Maria
Williams, Kenneth C.
TI Minocycline Inhibition of Monocyte Activation Correlates with Neuronal
Protection in SIV NeuroAIDS
SO PLOS ONE
LA English
DT Article
ID SIMIAN IMMUNODEFICIENCY VIRUS; AMYOTROPHIC-LATERAL-SCLEROSIS;
PERIVASCULAR MACROPHAGES; NONHUMAN PRIMATE; HIV-INFECTION; CD8(+)
LYMPHOCYTES; TYPE-1 INFECTION; T-CELLS; DEMENTIA; DISEASE
AB Background: Minocycline is a tetracycline antibiotic that has been proposed as a potential conjunctive therapy for HIV-1 associated cognitive disorders. Precise mechanism(s) of minocycline's functions are not well defined.
Methods: Fourteen rhesus macaques were SIV infected and neuronal metabolites measured by proton magnetic resonance spectroscopy ((1)H MRS). Seven received minocycline (4 mg/kg) daily starting at day 28 post-infection (pi). Monocyte expansion and activation were assessed by flow cytometry, cell traffic to lymph nodes, CD16 regulation, viral replication, and cytokine production were studied.
Results: Minocycline treatment decreased plasma virus and pro-inflammatory CD14+CD16+ and CD14(lo)CD16+ monocytes, and reduced their expression of CD11b, CD163, CD64, CCR2 and HLA-DR. There was reduced recruitment of monocyte/macrophages and productively infected cells in axillary lymph nodes. There was an inverse correlation between brain NAA/Cr (neuronal injury) and circulating CD14+CD16+ and CD14(lo)CD16+ monocytes. Minocycline treatment in vitro reduced SIV replication CD16 expression on activated CD14+CD16+ monocytes, and IL-6 production by monocytes following LPS stimulation.
Conclusion: Neuroprotective effects of minocycline are due in part to reduction of activated monocytes, monocyte traffic. Mechanisms for these effects include CD16 regulation, reduced viral replication, and inhibited immune activation.
C1 [Campbell, Jennifer H.; Burdo, Tricia H.; Autissier, Patrick; Soulas, Caroline; Williams, Kenneth C.] Boston Coll, Dept Biol, Chestnut Hill, MA 02167 USA.
[Gonzalez, R. Gilberto; Ratai, Eva-Maria] Harvard Univ, Sch Med, Boston, MA USA.
[Bombardier, Jeffrey P.; Westmoreland, Susan V.] New England Reg Primate Res Ctr, Southborough, MA 01772 USA.
[Gonzalez, R. Gilberto; Ratai, Eva-Maria] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Boston, MA 02114 USA.
[Gonzalez, R. Gilberto; Ratai, Eva-Maria] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
RP Campbell, JH (reprint author), Boston Coll, Dept Biol, Chestnut Hill, MA 02167 USA.
EM williauy@bc.edu
FU NIH [RO1NS40237, R01NS37654, U19MH081835, R01NS06897, R21NS059331,
R01NS050041]
FX This work was supported by NIH (www.nih.gov) grants RO1NS40237 (KCW),
R01NS37654(KCW), U19MH081835 (KCW), R01NS06897 (KCW), R21NS059331 (EMR),
and R01NS050041 (RGG). In vivo CD8 T lymphocyte depletion antibodies
used in these studies were provided by the NIH Nonhuman Primate Reagent
Resource (nhpreagents.bidmc.harvard.edu; R24 RR016001, N01 AI040101).
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 55
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PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 6
PY 2011
VL 6
IS 4
AR e18688
DI 10.1371/journal.pone.0018688
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 745UM
UT WOS:000289192400043
PM 21494695
ER
PT J
AU Fang, F
Kasperzyk, JL
Shui, I
Hendrickson, W
Hollis, BW
Fall, K
Ma, J
Gaziano, JM
Stampfer, MJ
Mucci, LA
Giovannucci, E
AF Fang, Fang
Kasperzyk, Julie L.
Shui, Irene
Hendrickson, Whitney
Hollis, Bruce W.
Fall, Katja
Ma, Jing
Gaziano, J. Michael
Stampfer, Meir J.
Mucci, Lorelei A.
Giovannucci, Edward
TI Prediagnostic Plasma Vitamin D Metabolites and Mortality among Patients
with Prostate Cancer
SO PLOS ONE
LA English
DT Article
ID UNITED-STATES; SUBSEQUENT DEVELOPMENT; D-RECEPTOR; RISK;
1,25-DIHYDROXYVITAMIN-D; 25-HYDROXYVITAMIN-D; RADIOIMMUNOASSAY;
CALCITRIOL; DIAGNOSIS; PROGNOSIS
AB Background: Laboratory evidence suggests that vitamin D might influence prostate cancer prognosis.
Methodology/Principal Findings: We examined the associations between prediagnostic plasma levels of 25(OH) vitamin D [25(OH)D] and 1,25(OH)(2)vitamin D [1,25(OH)(2)D] and mortality among 1822 participants of the Health Professionals Follow-up Study and Physicians' Health Study who were diagnosed with prostate cancer. Cox proportional hazards models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) of total mortality (n = 595) and lethal prostate cancer (death from prostate cancer or development of bone metastases; n = 202). In models adjusted for age at diagnosis, BMI, physical activity, and smoking, we observed a HR of 1.22 (95% CI: 0.97, 1.54) for total mortality, comparing men in the lowest to the highest quartile of 25(OH) D. There was no association between 1,25(OH) 2D and total mortality. Men with the lowest 25(OH) D quartile were more likely to die of their cancer (HR: 1.59; 95% CI: 1.06, 2.39) compared to those in the highest quartile (P(trend) = 0.006). This association was largely explained by the association between low 25(OH) D levels and advanced cancer stage and higher Gleason score, suggesting that these variables may mediate the influence of 25(OH) D on prognosis. The association also tended to be stronger among patients with samples collected within five years of cancer diagnosis. 1,25(OH)(2)D levels were not associated with lethal prostate cancer.
Conclusions/Significance: Although potential bias of less advanced disease due to more screening activity among men with high 25(OH) D levels cannot be ruled out, higher prediagnostic plasma 25(OH) D might be associated with improved prostate cancer prognosis.
C1 [Fang, Fang; Kasperzyk, Julie L.; Hendrickson, Whitney; Ma, Jing; Stampfer, Meir J.; Mucci, Lorelei A.; Giovannucci, Edward] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA.
[Fang, Fang; Kasperzyk, Julie L.; Hendrickson, Whitney; Ma, Jing; Stampfer, Meir J.; Mucci, Lorelei A.; Giovannucci, Edward] Harvard Univ, Sch Med, Boston, MA USA.
[Fang, Fang] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Kasperzyk, Julie L.; Shui, Irene; Hendrickson, Whitney; Fall, Katja; Stampfer, Meir J.; Mucci, Lorelei A.; Giovannucci, Edward] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Hollis, Bruce W.] Med Univ S Carolina, Dept Pediat, Charleston, SC 29425 USA.
[Fall, Katja] Orebro Univ Hosp, Clin Epidemiol & Biostat Unit, Orebro, Sweden.
[Gaziano, J. Michael] Brigham & Womens Hosp, Dept Med, Div Prevent Med, Boston, MA 02115 USA.
[Gaziano, J. Michael] Brigham & Womens Hosp, Dept Med, Div Aging, Boston, MA 02115 USA.
[Gaziano, J. Michael] VA Boston Healthcare Syst, Massachusetts Vet Epidemiol Res & Informat Ctr, Geriatr Res Educ & Clin Ctr, Boston, MA USA.
[Stampfer, Meir J.; Giovannucci, Edward] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
RP Fang, F (reprint author), Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA.
EM fang.fang@channing.harvard.edu
OI Fang, Fang/0000-0002-3310-6456; Fall, Katja/0000-0002-3649-2639
FU National Institutes of Health [CA133891, CA141298, CA34933, CA40360,
CA091793, CA055075, CA42182, HL26490, HL34595]; Prostate Cancer
Foundation, Santa Monica, CA, USA; National Cancer Institute National
Research Service [T32 CA09001]
FX This work was supported by the National Institutes of Health research
grants CA133891, CA141298, CA34933, CA40360, CA091793, CA055075,
CA42182, HL26490 and HL34595; Prostate Cancer Foundation, Santa Monica,
CA, USA and National Cancer Institute National Research Service Award
T32 CA09001. The funders had no role in study design, data collection
and analysis, decision to publish, or preparation of the manuscript.
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PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 6
PY 2011
VL 6
IS 4
AR e18625
DI 10.1371/journal.pone.0018625
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 745UM
UT WOS:000289192400041
PM 21494639
ER
PT J
AU Shulman, M
Cohen, M
Soto-Gutierrez, A
Yagi, H
Wang, HY
Goldwasser, J
Lee-Parsons, CW
Benny-Ratsaby, O
Yarmush, ML
Nahmias, Y
AF Shulman, Maria
Cohen, Merav
Soto-Gutierrez, Alejandro
Yagi, Hiroshi
Wang, Hongyun
Goldwasser, Jonathan
Lee-Parsons, Carolyn W.
Benny-Ratsaby, Ofra
Yarmush, Martin L.
Nahmias, Yaakov
TI Enhancement of Naringenin Bioavailability by Complexation with
Hydroxypropoyl-beta-Cyclodextrin
SO PLOS ONE
LA English
DT Article
ID CITRUS FLAVONOID NARINGENIN; ORAL BIOAVAILABILITY; GRAPEFRUIT JUICE;
INSULIN-RECEPTOR; B SECRETION; APO-B; HESPERETIN; INHIBITION;
EXPRESSION; PHARMACOKINETICS
AB The abundant flavonoid aglycone, naringenin, which is responsible for the bitter taste in grapefruits, has been shown to possess hypolipidemic and anti-inflammatory effects both in vitro and in vivo. Recently, our group demonstrated that naringenin inhibits hepatitis C virus (HCV) production, while others demonstrated its potential in the treatment of hyperlipidemia and diabetes. However, naringenin suffers from low oral bioavailability critically limiting its clinical potential. In this study, we demonstrate that the solubility of naringenin is enhanced by complexation with beta-cyclodextrin, an FDA approved excipient. Hydroxypropoyl-beta-cyclodextrin (HP beta CD), specifically, increased the solubility of naringenin by over 400-fold, and its transport across a Caco-2 model of the gut epithelium by 11-fold. Complexation of naringenin with HP beta CD increased its plasma concentrations when fed to rats, with AUC values increasing by 7.4-fold and C(max) increasing 14.6-fold. Moreover, when the complex was administered just prior to a meal it decreased VLDL levels by 42% and increased the rate of glucose clearance by 64% compared to naringenin alone. These effects correlated with increased expression of the PPAR co-activator, PGC1 alpha in both liver and skeletal muscle. Histology and blood chemistry analysis indicated this route of administration was not associated with damage to the intestine, kidney, or liver. These results suggest that the complexation of naringenin with HP beta CD is a viable option for the oral delivery of naringenin as a therapeutic entity with applications in the treatment of dyslipidemia, diabetes, and HCV infection.
C1 [Shulman, Maria; Cohen, Merav; Nahmias, Yaakov] Hebrew Univ Jerusalem, Inst Life Sci, Sch Comp Sci & Engn, Ctr Bioengn, IL-91904 Jerusalem, Israel.
[Soto-Gutierrez, Alejandro; Yagi, Hiroshi; Wang, Hongyun; Goldwasser, Jonathan; Yarmush, Martin L.; Nahmias, Yaakov] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Engn Med, Boston, MA USA.
[Goldwasser, Jonathan] MIT, Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
[Benny-Ratsaby, Ofra] Harvard Univ, Sch Med, Childrens Hosp Boston, Boston, MA USA.
[Lee-Parsons, Carolyn W.] Northeastern Univ, Dept Chem Engn, Boston, MA 02115 USA.
[Yarmush, Martin L.] Rutgers State Univ, Dept Biomed Engn, Piscataway, NJ USA.
RP Shulman, M (reprint author), Hebrew Univ Jerusalem, Inst Life Sci, Sch Comp Sci & Engn, Ctr Bioengn, IL-91904 Jerusalem, Israel.
EM ynahmias@cs.huji.ac.il
RI Nahmias, Yaakov/H-4725-2013
FU National Institute of Diabetes and Digestive and Kidney Diseases
[K01DK080241]; Harvard Clinical Nutrition Research Center
[P30-DK040561]; European Research Council [TMIHCV 242699]
FX This work was supported by the National Institute of Diabetes and
Digestive and Kidney Diseases (K01DK080241) and the Harvard Clinical
Nutrition Research Center (P30-DK040561). Resources were provided by
European Research Council Starting Grant (TMIHCV 242699), the BioMEMS
Resource Center (P41 EB-002503), and the Alexander Silberman Institute
of Life Sciences. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 31
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U1 3
U2 27
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 6
PY 2011
VL 6
IS 4
AR e18033
DI 10.1371/journal.pone.0018033
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 745UM
UT WOS:000289192400007
PM 21494673
ER
PT J
AU Bauer, KA
AF Bauer, Kenneth A.
TI Long-term Management of Venous Thromboembolism A 61-Year-Old Woman With
Unprovoked Venous Thromboembolism
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID DEEP-VEIN-THROMBOSIS; FACTOR-V-LEIDEN; ORAL ANTICOAGULANT-THERAPY;
LOW-INTENSITY WARFARIN; PATIENT-LEVEL METAANALYSIS;
COAGULATION-FACTOR-V; ACTIVATED PROTEIN-C; D-DIMER; PULMONARY-EMBOLISM;
RISK-FACTORS
AB Numerous randomized clinical trials have compared various durations of anticoagulant therapy with a vitamin K antagonist (ie, warfarin) for an initial episode of venous thromboembolism (VTE). Despite major advances in understanding the pathophysiology of thrombosis and its genetic basis, clinical risk factors at presentation have emerged as the primary determinant of recurrence risk. Following a minimum of 3 months of anticoagulant therapy, patients with VTE in association with transient risk factors (eg, major surgery, trauma, pregnancy) have a low annual recurrence risk, while patients without identifiable provocative risk factors have a recurrence risk of approximately 25% at 4 years with the highest annual rates occurring in the first 2 years. Extending warfarin therapy is highly effective in preventing recurrences but is associated with increased rates of major and minor bleeding. Clinical decision making therefore requires individualized assessment of recurrence and bleeding risk, coupled with patient preference. After 3 months of anticoagulant therapy for a first episode of unprovoked VTE, male sex, age older than 65 years, and an elevated D-dimer level 1 month after discontinuing anticoagulant therapy are useful parameters in identifying patients with an increased recurrence risk. The case of Ms W, a woman with unprovoked venous thromboembolism and hemorrhagic event while receiving anticoagulation, is used to illustrate clinical decision making to determine ongoing treatment. JAMA. 2011;305(13):1336-1345 www.jama.com
C1 [Bauer, Kenneth A.] Beth Israel Deaconess Med Ctr, Boston, MA 02492 USA.
[Bauer, Kenneth A.] Harvard Univ, Sch Med, Boston, MA USA.
[Bauer, Kenneth A.] VA Boston Healthcare Syst, Hematol Sect, Boston, MA USA.
RP Bauer, KA (reprint author), Beth Israel Deaconess Med Ctr, 330 Brookline Ave, Boston, MA 02492 USA.
EM kbauer@bidmc.harvard.edu
NR 73
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U1 0
U2 0
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 APR 6
PY 2011
VL 305
IS 13
BP 1336
EP 1345
DI 10.1001/jama.2011.361
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 745JT
UT WOS:000289162400023
PM 21386068
ER
PT J
AU Lee, SJ
Eng, C
AF Lee, Sei J.
Eng, Catherine
TI Goals of Glycemic Control in Frail Older Patients With Diabetes
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
ID POPULATION; DISABILITY
C1 [Lee, Sei J.] San Francisco VA Med Ctr, Div Geriatr, San Francisco, CA 94121 USA.
[Lee, Sei J.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Eng, Catherine] On Lok Lifeways, San Francisco, CA USA.
RP Lee, SJ (reprint author), San Francisco VA Med Ctr, Div Geriatr, 4150 Clement St,Bldg 1,Room 211A, San Francisco, CA 94121 USA.
EM sei.lee@ucsf.edu
FU NCRR NIH HHS [KL2 RR024130]
NR 10
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U1 0
U2 4
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD APR 6
PY 2011
VL 305
IS 13
BP 1350
EP 1351
DI 10.1001/jama.2011.404
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 745JT
UT WOS:000289162400026
PM 21467289
ER
PT J
AU Onnela, JP
Arbesman, S
Gonzalez, MC
Barabasi, AL
Christakis, NA
AF Onnela, Jukka-Pekka
Arbesman, Samuel
Gonzalez, Marta C.
Barabasi, Albert-Laszlo
Christakis, Nicholas A.
TI Geographic Constraints on Social Network Groups
SO PLOS ONE
LA English
DT Article
ID MOBILE COMMUNICATION-NETWORKS; PATTERNS
AB Social groups are fundamental building blocks of human societies. While our social interactions have always been constrained by geography, it has been impossible, due to practical difficulties, to evaluate the nature of this restriction on social group structure. We construct a social network of individuals whose most frequent geographical locations are also known. We also classify the individuals into groups according to a community detection algorithm. We study the variation of geographical span for social groups of varying sizes, and explore the relationship between topological positions and geographic positions of their members. We find that small social groups are geographically very tight, but become much more clumped when the group size exceeds about 30 members. Also, we find no correlation between the topological positions and geographic positions of individuals within network communities. These results suggest that spreading processes face distinct structural and spatial constraints.
C1 [Onnela, Jukka-Pekka; Arbesman, Samuel; Christakis, Nicholas A.] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
[Gonzalez, Marta C.] MIT, Dept Civil & Environm Engn & Engn Syst, Cambridge, MA 02139 USA.
[Barabasi, Albert-Laszlo] Northeastern Univ, Dept Phys Biol & Comp Sci, Ctr Complex Network Res, Boston, MA 02115 USA.
[Barabasi, Albert-Laszlo] Dana Farber Canc Inst, Ctr Canc Syst Biol, Boston, MA 02115 USA.
[Barabasi, Albert-Laszlo] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med, Boston, MA 02115 USA.
[Christakis, Nicholas A.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Christakis, Nicholas A.] Harvard Fac Arts & Sci, Dept Sociol, Cambridge, MA USA.
RP Onnela, JP (reprint author), Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
EM onnela@med.harvard.edu
RI Gonzalez, Marta/E-9456-2011
OI Gonzalez, Marta/0000-0002-8482-0318
FU National Institute on Aging [P01 AG-031093]; Office of Naval Research
[ONR N000141010968]; Network Science Collaborative Technology Alliance
[ARL NS-CTA W911NF-09-2-0053]; Defense Threat Reduction Agency [DTRA
BRBAA08-Per4-C-2-0033, DTRA WMD BRBAA07-J-2-0035]; National Science
Foundation [NSF BCS-0826958]; James S. McDonnell Foundation [JSMF
220020084]
FX JPO, SA, and NAC are supported by the National Institute on Aging (grant
P01 AG-031093); ALB and MCG by the Office of Naval Research (grant ONR
N000141010968), the Network Science Collaborative Technology Alliance
(grant ARL NS-CTA W911NF-09-2-0053), the Defense Threat Reduction Agency
(grants DTRA BRBAA08-Per4-C-2-0033 and DTRA WMD BRBAA07-J-2-0035), the
National Science Foundation (grant NSF BCS-0826958), and the James S.
McDonnell Foundation (grant JSMF 220020084). The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
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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 APR 5
PY 2011
VL 6
IS 4
AR e16939
DI 10.1371/journal.pone.0016939
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 745UD
UT WOS:000289191300004
PM 21483665
ER
PT J
AU Santosuosso, M
Righi, E
Hill, ED
Leblanc, PR
Kodish, B
Mylvaganam, HN
Siddappa, NB
Stevceva, L
Hu, SL
Ghebremichael, M
Chenine, AL
Hovav, AH
Ruprecht, RM
Poznansky, MC
AF Santosuosso, Michael
Righi, Elda
Hill, E. David
Leblanc, Pierre R.
Kodish, Brett
Mylvaganam, Hari N.
Siddappa, Nagadenahalli B.
Stevceva, Liljana
Hu, Shiu-Lok
Ghebremichael, Musie
Chenine, Agnes-L.
Hovav, Avi-Hai
Ruprecht, Ruth M.
Poznansky, Mark C.
TI R5-SHIV Induces Multiple Defects in T Cell Function during Early
Infection of Rhesus Macaques Including Accumulation of T Reg Cells in
Lymph Nodes
SO PLOS ONE
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; HIV-1 INFECTION; INDUCED APOPTOSIS;
ENVELOPE PROTEIN; IMMUNE-RESPONSES; VIRAL-INFECTION; DENDRITIC CELLS;
TYPE-1 GP120; IN-VIVO; INDIVIDUALS
AB Background: HIV-1 is a pathogen that T cell responses fail to control. HIV-1gp120 is the surface viral envelope glycoprotein that interacts with CD4 T cells and mediates entry. HIV-1gp120 has been implicated in immune dysregulatory functions that may limit anti-HIV antigen-specific T cell responses. We hypothesized that in the context of early SHIV infection, immune dysregulation of antigen-specific T-effector cell and regulatory functions would be detectable and that these would be associated or correlated with measurable concentrations of HIV-1gp120 in lymphoid tissues.
Methods: Rhesus macaques were intravaginally inoculated with a Clade C CCR5-tropic simian-human immunodeficiency virus, SHIV-1157ipd3N4. HIV-1gp120 levels, antigen-specificity, levels of apoptosis/anergy and frequency and function of Tregs were examined in lymph node and blood derived T cells at 5 and 12 weeks post inoculation.
Results/Conclusions: We observed reduced responses to Gag in CD4 and gp120 in CD8 lymph node-derived T cells compared to the peripheral blood at 5 weeks post-inoculation. Reduced antigen-specific responses were associated with higher levels of PD-1 on lymph node-derived CD4 T cells as compared to peripheral blood and uninfected lymph node-derived CD4 T cells. Lymph nodes contained increased numbers of Tregs as compared to peripheral blood, which positively correlated with gp120 levels; T regulatory cell depletion restored CD8 T cell responses to Gag but not to gp120. HIV gp120 was also able to induce T regulatory cell chemotaxis in a dose-dependent, CCR5-mediated manner. These studies contribute to our broader understanding of the ways in which HIV-1 dysregulates T cell function and localization during early infection.
C1 [Santosuosso, Michael; Righi, Elda; Hill, E. David; Leblanc, Pierre R.; Kodish, Brett; Mylvaganam, Hari N.; Stevceva, Liljana; Poznansky, Mark C.] Massachusetts Gen Hosp, Vaccine & Immunotherapy Ctr, Infect Dis Med Div, Charlestown, MA USA.
[Siddappa, Nagadenahalli B.; Chenine, Agnes-L.; Ruprecht, Ruth M.] Dana Farber Canc Inst, Dept Canc Immunol, Boston, MA 02115 USA.
[Siddappa, Nagadenahalli B.; Chenine, Agnes-L.; Ruprecht, Ruth M.] Dana Farber Canc Inst, AIDS, Boston, MA 02115 USA.
[Hu, Shiu-Lok] Univ Washington, Dept Pharmaceut, Seattle, WA 98195 USA.
[Ghebremichael, Musie] Harvard Univ, Sch Publ Hlth, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Hovav, Avi-Hai] Hebrew Univ Jerusalem, Fac Med Dent, Inst Dent Sci, Jerusalem, Israel.
RP Santosuosso, M (reprint author), Massachusetts Gen Hosp, Vaccine & Immunotherapy Ctr, Infect Dis Med Div, Charlestown, MA USA.
EM mpoznansky@partners.org
OI Byrareddy, Siddappa /0000-0002-7423-1763
FU National Institutes of Health (NIH) [RO1 AI49757, PO1 AI048240, RO1
DE016013]; Yerkes National Primate Research center [RR00165]
FX This work was completed via support of MCP (National Institutes of
Health (NIH) RO1 AI49757), RMR (NIH grants PO1 AI048240 and RO1
DE016013) and Yerkes National Primate Research center (Grant #RR00165).
MS is a research fellow of the Canadian Institute of Health. The funders
had no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
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U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 5
PY 2011
VL 6
IS 4
AR e18465
DI 10.1371/journal.pone.0018465
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 745UD
UT WOS:000289191300023
PM 21483689
ER
PT J
AU Streb, JW
Long, XC
Lee, TH
Sun, QA
Kitchen, CM
Georger, MA
Slivano, OJ
Blaner, WS
Carr, DW
Gelman, IH
Miano, JM
AF Streb, Jeffrey W.
Long, Xiaochun
Lee, Ting-Hein
Sun, Qiang
Kitchen, Chad M.
Georger, Mary A.
Slivano, Orazio J.
Blaner, William S.
Carr, Daniel W.
Gelman, Irwin H.
Miano, Joseph M.
TI Retinoid-Induced Expression and Activity of an Immediate Early Tumor
Suppressor Gene in Vascular Smooth Muscle Cells
SO PLOS ONE
LA English
DT Article
ID PROLIFERATION IN-VITRO; SERUM RESPONSE FACTOR; KINASE-C SUBSTRATE;
PROTEIN-KINASE; INTIMAL HYPERPLASIA; NEOINTIMA FORMATION;
ANGIOTENSIN-II; CYTOSKELETAL ARCHITECTURE; BALLOON ANGIOPLASTY; NUCLEAR
RECEPTORS
AB Retinoids are used clinically to treat a number of hyper-proliferative disorders and have been shown in experimental animals to attenuate vascular occlusive diseases, presumably through nuclear receptors bound to retinoic acid response elements (RARE) located in target genes. Here, we show that natural or synthetic retinoids rapidly induce mRNA and protein expression of a specific isoform of A-Kinase Anchoring Protein 12 (AKAP12 beta) in cultured smooth muscle cells (SMC) as well as the intact vessel wall. Expression kinetics and actinomycin D studies indicate Akap12 beta is a retinoid-induced, immediate-early gene. Akap12 beta promoter analyses reveal a conserved RARE mildly induced with atRA in a region that exhibits hyperacetylation. Immunofluorescence microscopy and protein kinase A (PKA) regulatory subunit overlay assays in SMC suggest a physical association between AKAP12 beta and PKA following retinoid treatment. Consistent with its designation as a tumor suppressor, inducible expression of AKAP12 beta attenuates SMC growth in vitro. Further, immunohistochemistry studies establish marked decreases in AKAP12 expression in experimentally-injured vessels of mice as well as atheromatous lesions in humans. Collectively, these results demonstrate a novel role for retinoids in the induction of an AKAP tumor suppressor that blocks vascular SMC growth thus providing new molecular insight into how retiniods may exert their anti-proliferative effects in the injured vessel wall.
C1 [Streb, Jeffrey W.; Long, Xiaochun; Lee, Ting-Hein; Sun, Qiang; Kitchen, Chad M.; Georger, Mary A.; Slivano, Orazio J.; Miano, Joseph M.] Univ Rochester, Sch Med & Dent, Aab Cardiovasc Res Inst, Rochester, NY 14627 USA.
[Miano, Joseph M.] Univ Rochester, Sch Med & Dent, Dept Pathol & Lab Med, Rochester, NY USA.
[Blaner, William S.] Columbia Univ, Dept Med, New York, NY USA.
[Carr, Daniel W.] Portland VA Med Ctr, Portland, OR USA.
[Gelman, Irwin H.] Roswell Pk Canc Inst, Dept Canc Genet, Buffalo, NY 14263 USA.
RP Streb, JW (reprint author), Univ Rochester, Sch Med & Dent, Aab Cardiovasc Res Inst, Rochester, NY 14627 USA.
EM j.m.miano@rochester.edu
FU National Institutes of Health [HL070077, CA094108, DK079221, DK068437,
T32HL07949]; Department of Veterans Affairs, Veterans Health
Administration, Office of Research and Development, Biomedical
Laboratory Research and Development Service
FX This research was supported by National Institutes of Health grants
HL070077 to JMM; CA094108 to IHG; DK079221 and DK068437 to WSB; and
Department of Veterans Affairs, Veterans Health Administration, Office
of Research and Development, Biomedical Laboratory Research and
Development Service to DWC. JWS was funded through an NIH training grant
(#T32HL07949). The funders had no role in study design, data collection
and analysis, decision to publish, or preparation of the manuscript.
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PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 5
PY 2011
VL 6
IS 4
AR e18538
DI 10.1371/journal.pone.0018538
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 745UD
UT WOS:000289191300028
PM 21483686
ER
PT J
AU Yeh, RW
Kennedy, K
Spertus, JA
Parikh, SA
Sakhuja, R
Anderson, HV
White, CJ
Rosenfield, K
AF Yeh, Robert W.
Kennedy, Kevin
Spertus, John A.
Parikh, Sahil A.
Sakhuja, Rahul
Anderson, H. Vernon
White, Christopher J.
Rosenfield, Kenneth
TI Do Postmarketing Surveillance Studies Represent Real-World Populations?
A Comparison of Patient Characteristics and Outcomes After Carotid
Artery Stenting
SO CIRCULATION
LA English
DT Article
DE carotid arteries; carotid stenting; outcomes research; registries
ID DRUG-ELUTING STENTS; HIGH-RISK PATIENTS; CLINICAL-TRIAL; EMBOLIC
PROTECTION; RANDOMIZED-TRIALS; CAPTURE REGISTRY; PROPENSITY-SCORE;
ENDARTERECTOMY; GENERALIZABILITY; STENOSIS
AB Background-To evaluate outcomes after carotid artery stenting in larger real-world populations, the Food and Drug Administration mandated that companies conduct postmarketing surveillance (PMS) studies of approved stent systems. Whether PMS studies are representative of carotid artery stenting in routine clinical practice has not been established.
Methods and Results-Within the National Cardiovascular Database Registry-Carotid Artery Revascularization and Endarterectomy (NCDR CARE) Registry, we compared patient and procedural characteristics, in-hospital outcomes, and subsequent all-cause mortality after carotid artery stenting in PMS study participants and nonparticipants. We conducted both crude and propensity score-adjusted comparisons for all outcomes between groups. Compared with nonparticipants, participants in PMS studies had lower rates of symptomatic carotid artery disease within the preceding 6 months, prior stroke, and acute evolving stroke at baseline. The PMS study participants had lower unadjusted rates of combined in-hospital death, stroke, or myocardial infarction (2.3% versus 4.1%; P<0.001), driven by lower rates of stroke (1.7% versus 2.7%; P=0.005) and death (0.3% versus 1.4%; P<0.001). Differences in survival persisted after propensity score adjustment (odds ratio, 0.44; 95% confidence interval, 0.21 to 0.95; P=0.04 for in-hospital mortality; and hazard ratio, 0.80; 95% confidence interval, 0.66 to 0.97; P=0.02 for 2-year mortality). Baseline differences in neurological history explained the largest proportion of the difference in outcomes between groups.
Conclusions-Participants in PMS studies for carotid artery stenting have different clinical and procedural characteristics and lower mortality compared with nonparticipants. Extrapolating results from PMS studies of carotid artery stenting to larger real-world settings should be done only with great caution. (Circulation. 2011;123:1384-1390.)
C1 [Yeh, Robert W.; Sakhuja, Rahul; Rosenfield, Kenneth] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Cardiol,Dept Med, Boston, MA 02144 USA.
[Kennedy, Kevin; Spertus, John A.] St Lukes Mid Amer Heart Inst, Kansas City, MO USA.
[Kennedy, Kevin; Spertus, John A.] Univ Missouri, Kansas City, MO USA.
[Parikh, Sahil A.] Univ Hosp Case Med Ctr, Harrington McLaughlin Heart & Vasc Inst, Cleveland, OH USA.
[Parikh, Sahil A.] Case Western Reserve Univ, Sch Med, Cleveland, OH USA.
[Anderson, H. Vernon] Univ Texas Hlth Sci Ctr, Houston, TX USA.
[White, Christopher J.] Ochsner Clin Fdn, Dept Cardiovasc Dis, New Orleans, LA USA.
RP Yeh, RW (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Cardiol,Dept Med, GRB 800, Boston, MA 02144 USA.
EM ryeh@partners.org
RI White, Christopher/J-6686-2012
OI White, Christopher/0000-0001-8618-7539
FU American College of Cardiology Foundation's NCDR; Abbott Vascular; Bard
Peripheral Vascular; Medtronic/Invatec; Atrium; Boston Scientific Corp.;
Complete Conference Management; Harvard Clinical Research Institute;
Contego; Micell; Becker Ventures
FX This research was supported by the American College of Cardiology
Foundation's NCDR. The views expressed in this article represent those
of the authors and do not necessarily represent the official views of
the NCDR or its associated professional societies identified at
www.ncdr.com.; Dr Yeh is an investigator for the Harvard Clinical
Research Institute and a consultant for the Kaiser Permanente Division
of Research. Dr Spertus has a contract with the American College of
Cardiology Foundation to conduct analyses for the CARE registry. Dr
White reports a consulting relationship as the principle investigator
for the Carotid Stenting Boston Scientific Surveillance Program (CABANA)
trial from Boston Scientific Corp. Dr Rosenfield reports receiving
research grants from Abbott Vascular, Bard Peripheral Vascular,
Medtronic/Invatec, and Atrium; receiving consulting/advisory board fees
from Abbott Vascular, Boston Scientific Corp, Complete Conference
Management, Harvard Clinical Research Institute, Contego, Micell, and
Becker Ventures; having equity in Lumen Biomedical, Medical Stimulation
Corp, Angioguard (Cordis), and Micell; and serving on the board of
directors for VIVA Physicians (501C3). The other authors report no
conflicts.
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PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD APR 5
PY 2011
VL 123
IS 13
BP 1384
EP 1390
DI 10.1161/CIRCULATIONAHA.110.991075
PG 7
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 744FO
UT WOS:000289080500011
PM 21422383
ER
PT J
AU Afilalo, J
Rudski, LG
Sebag, IA
Eisenberg, MJ
Alexander, KP
Morin, JF
Langlois, Y
Noiseux, N
Perrault, LP
Monette, J
Bergman, H
Picard, MH
AF Afilalo, Jonathan
Rudski, Lawrence G.
Sebag, Igal A.
Eisenberg, Mark J.
Alexander, Karen P.
Morin, Jean-Francois
Langlois, Yves
Noiseux, Nicolas
Perrault, Louis P.
Monette, Johanne
Bergman, Howard
Picard, Michael H.
TI HYPERDYNAMIC LEFT VENTRICULAR FUNCTION IS ASSOCIATED WITH ADVERSE EVENTS
IN ELDERLY PATIENTS UNDERGOING CARDIAC SURGERY
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 SMBD Jewish Gen Hosp, Montreal, PQ, Canada.
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 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E1010
EP E1010
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695101013
ER
PT J
AU Bhardwaj, A
Truong, QA
Storrow, A
Peacock, WF
Lee, HK
Yeo, KTJ
Curtis, KM
Foote, RS
Thomas, S
Miller, KF
Januzzi, JL
AF Bhardwaj, Anju
Truong, Quynh A.
Storrow, Alan
Peacock, W. Frank
Lee, Hong K.
Yeo, Kiang-Teck J.
Curtis, Kevin M.
Foote, Robert S.
Thomas, Stephen
Miller, Karen F.
Januzzi, James L.
TI SERIAL MEASUREMENT OF UNBOUND FREE FATTY ACIDS ADDS TO HIGHLY SENSITIVE
TROPONIN I IN THE DIAGNOSTIC EVALUATION OF CHEST PAIN
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 [Bhardwaj, Anju; Truong, Quynh A.; Storrow, Alan; Peacock, W. Frank; Lee, Hong K.; Yeo, Kiang-Teck J.; Curtis, Kevin M.; Foote, Robert S.; Thomas, Stephen; Miller, Karen F.; Januzzi, James L.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
NR 0
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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 APR 5
PY 2011
VL 57
IS 14
SU 1
BP E936
EP E936
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695100937
ER
PT J
AU Cohen, L
Spano-Brennan, LM
Thomas, DK
Gandhi, SK
Kostis, WJ
Kostis, JB
AF Cohen, Liliana
Spano-Brennan, Liana M.
Thomas, Dwithiya K.
Gandhi, Sampada K.
Kostis, William J.
Kostis, John B.
TI IMPACT OF THE RED DRESS CAMPAIGN (R) ON INCIDENCE, MORTALITY, AND
MANAGEMENT OF ACUTE MYOCARDIAL INFARCTION IN WOMEN
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 UMDNJ, Robert Wood Johnson Med Sch, New Brunswick, NJ USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
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U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E1165
EP E1165
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695101168
ER
PT J
AU Engel, LC
Verdini, D
Major, GP
Abbara, S
Hoffmann, U
Kalra, M
Brady, TJ
Ghoshhajra, B
AF Engel, Leif-Christophe
Verdini, Dan
Major, Gyoengyi Petra
Abbara, Suhny
Hoffmann, Udo
Kalra, Mannudeep
Brady, Thomas J.
Ghoshhajra, Brian
TI ANTHROPOMORPHIC MEASUREMENTS ON CT IMAGES: A POTENTIAL SURROGATE OR
REPLACEMENT FOR BMI WHEN SELECTING CARDIOTHORACIC CT DOSE PARAMETERS?
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 [Engel, Leif-Christophe; Verdini, Dan; Major, Gyoengyi Petra; Abbara, Suhny; Hoffmann, Udo; Kalra, Mannudeep; Brady, Thomas J.; Ghoshhajra, Brian] Massachusetts Gen Hosp, Cardiac MR PET CT Program, Boston, MA 02114 USA.
NR 0
TC 0
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U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E820
EP E820
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695100821
ER
PT J
AU Fifer, K
Subramanian, S
Fontanez, SI
Figueroa, A
Brady, TJ
Tawakol, A
AF Fifer, Kenneth
Subramanian, Sharath
Fontanez, Sara I.
Figueroa, Amparo
Brady, Thomas J.
Tawakol, Ahmed
TI HIGH PERIODONTAL DISEASE ACTIVITY IS ASSOCIATED WITH SUBSEQUENT CAROTID
ARTERY STENOSIS PROGRESSION
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 [Fifer, Kenneth; Subramanian, Sharath; Fontanez, Sara I.; Figueroa, Amparo; Brady, Thomas J.; Tawakol, Ahmed] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
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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 APR 5
PY 2011
VL 57
IS 14
SU 1
BP E1571
EP E1571
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695101574
ER
PT J
AU Gilstrap, L
Fernandez-Golarz, C
Cantu, S
Rosenfield, H
Scott, N
Wood, M
AF Gilstrap, Lauren
Fernandez-Golarz, Carina
Cantu, Stephanie
Rosenfield, Hannah
Scott, Nandita
Wood, Malissa
TI THE CHALLENGE OF CARDIAC PREVENTION IN AN ACADEMIC MEDICAL CENTER
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
NR 0
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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 APR 5
PY 2011
VL 57
IS 14
SU 1
BP E1189
EP E1189
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695101192
ER
PT J
AU Goehler, A
Nolte, J
Neumann, A
Mostardt, S
Manne, JM
Abbara, S
Brady, TJ
Hoffmann, U
Gazelle, GS
Wasem, J
Neumann, T
AF Goehler, Alexander
Nolte, Julia
Neumann, Anja
Mostardt, Sarah
Manne, Jennifer M.
Abbara, Suhny
Brady, Thomas J.
Hoffmann, Udo
Gazelle, G. Scott
Wasem, Juergen
Neumann, Till
TI CLINICAL BENEFIT AND COST-EFFECTIVENESS OF CARDIOVASCULAR DISEASE
SCREENING IN HIV-INFECTED PATIENTS
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 Massachusetts Gen Hosp, Inst Technol Assessment, Boston, MA 02114 USA.
Univ Duisburg Essen, Essen, Germany.
NR 0
TC 0
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U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E1186
EP E1186
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695101189
ER
PT J
AU Goehler, A
McMahon, PM
Gupta, S
Gilmore, M
Brady, TJ
Gazelle, GS
Hoffmann, U
Truong, QA
AF Goehler, Alexander
McMahon, Pamela M.
Gupta, Supriya
Gilmore, Mike
Brady, Thomas J.
Gazelle, G. Scott
Hoffmann, Udo
Truong, Quynh A.
TI COST-EFFECTIVENESS OF FOLLOW-UP OF INCIDENTAL LUNG NODULES DETECTED
DURING CONTRAST ENHANCED CORONARY CTA IN PATIENTS WITH CHEST PAIN
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 Massachusetts Gen Hosp, Dep Radiol, Boston, MA 02114 USA.
Univ Duisburg Essen, Insitute Healthcare Management, Essen, Germany.
NR 0
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U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E781
EP E781
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695100782
ER
PT J
AU Hage, FG
Bhatia, V
Dean, P
Iqbal, F
Heo, J
Iskandrian, AE
AF Hage, Fadi G.
Bhatia, Vikas
Dean, Phillip
Iqbal, Fahad
Heo, Jaekyeong
Iskandrian, Ami E.
TI THE HEART RATE RESPONSE TO ADENOSINE CAN RISK STRATIFY PATIENTS WITH
DIABETES MELLITUS UNDERGOING MYOCARDIAL PERFUSION IMAGING
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 Univ Alabama, Birmingham, AL USA.
Birmingham Vet Affairs Med Ctr, Birmingham, AL USA.
NR 0
TC 0
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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 APR 5
PY 2011
VL 57
IS 14
SU 1
BP E743
EP E743
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695100744
ER
PT J
AU Hou, JB
Han, ZG
Yang, S
Meng, LB
Xing, L
Jia, HB
Zhang, SS
Yu, B
Jang, IK
AF Hou, Jingbo
Han, Zhigang
Yang, Shuang
Meng, Lingbo
Xing, Lei
Jia, Haibo
Zhang, Shaosong
Yu, Bo
Jang, Ik-Kyung
TI THE SAFETY AND FEASIBILITY OF INTRAVASCULAR OPTICAL COHERENCE TOMOGRAPHY
IN PATIENTS WITH ACUTE CORONARY SYNDROME: A SINGLE CENTER EXPERIENCE OF
689 PATIENTS
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 HMU, Affiliated Hosp 2, Dept Cardiol, Harbin, Peoples R China.
Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
NR 0
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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 APR 5
PY 2011
VL 57
IS 14
SU 1
BP E975
EP E975
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695100976
ER
PT J
AU Kim, HN
Mohammed, AA
Bhardwaj, A
Rehman, S
Gregory, SA
Barajas, JA
Barajas, LJ
Weiner, RB
Baggish, AL
Moore, SA
Semigran, MJ
Januzzi, JL
AF Kim, Han-Na
Mohammed, Asim A.
Bhardwaj, Anju
Rehman, Shafiq
Gregory, Shawn A.
Barajas, Justine A.
Barajas, Linda J.
Weiner, Rory B.
Baggish, Aaron L.
Moore, Stephanie A.
Semigran, Marc J.
Januzzi, James L.
TI DO ELDERLY PATIENTS WITH HEART FAILURE DUE TO LEFT VENTRICULAR SYSTOLIC
DYSFUNCTION BENEFIT FROM NT-PROBNP-GUIDED HEART FAILURE MANAGEMENT?
RESULTS FROM THE PROBNP OUTPATIENT TAILORED CHRONIC HEART FAILURE
THERAPY (PROTECT) STUDY
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 [Kim, Han-Na; Mohammed, Asim A.; Bhardwaj, Anju; Rehman, Shafiq; Gregory, Shawn A.; Barajas, Justine A.; Barajas, Linda J.; Weiner, Rory B.; Baggish, Aaron L.; Moore, Stephanie A.; Semigran, Marc J.; Januzzi, James L.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
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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 APR 5
PY 2011
VL 57
IS 14
SU 1
BP E394
EP E394
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695100395
ER
PT J
AU Kim, HN
Rehman, S
Mohammed, AA
Bhardwaj, A
Parks, KA
Sullivan, DA
Chen-Tournoux, A
Moore, SA
Barajas, JA
Barajas, LJ
Weiner, RB
Baggish, AL
Semigran, MJ
Januzzi, JL
AF Kim, Han-Na
Rehman, Shafiq
Mohammed, Asim A.
Bhardwaj, Anju
Parks, Kimberly A.
Sullivan, Dorothy A.
Chen-Tournoux, Annabel
Moore, Stephanie A.
Barajas, Justine A.
Barajas, Linda J.
Weiner, Rory B.
Baggish, Aaron L.
Semigran, Marc J.
Januzzi, James L.
TI CHARACTERIZING THE "NON-RESPONDER" TO NT-PROBNP GUIDED HEART FAILURE
TREATMENT: RESULTS FROM THE PROBNP OUTPATIENT TAILORED CHRONIC HEART
FAILURE (PROTECT) STUDY
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 [Kim, Han-Na; Rehman, Shafiq; Mohammed, Asim A.; Bhardwaj, Anju; Parks, Kimberly A.; Sullivan, Dorothy A.; Chen-Tournoux, Annabel; Moore, Stephanie A.; Barajas, Justine A.; Barajas, Linda J.; Weiner, Rory B.; Baggish, Aaron L.; Semigran, Marc J.; Januzzi, James L.] 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 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E295
EP E295
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695100296
ER
PT J
AU Kostis, WJ
Moreyra, AE
Kostis, JB
AF Kostis, William J.
Moreyra, Abel E.
Kostis, John B.
TI CONTINUATION OF MORTALITY REDUCTION AFTER THE END OF RANDOMIZED THERAPY
IN CLINICAL TRIALS OF LIPID-LOWERING MEDICATIONS
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
UMDNJ, Robert Wood Johnson Med Sch, New Brunswick, NJ USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E500
EP E500
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695100501
ER
PT J
AU Medina, H
Cannon, CC
Fonarow, GC
Peacock, FW
Laskey, WK
Grau-Sepulveda, MV
Fernandez, AF
Peterson, ED
Schwamm, LH
Bhatt, DL
AF Medina, Hector
Cannon, Christopher C.
Fonarow, Gregg C.
Peacock, Frank W.
Laskey, Warren K.
Grau-Sepulveda, Maria V.
Fernandez, Adrian F.
Peterson, Eric D.
Schwamm, Lee H.
Bhatt, Deepak L.
TI QUALITY OF CARE AND OUTCOMES IN 5,339 PATIENTS AGED 80 OR ABOVE
PRESENTING WITH ST-ELEVATION MYOCARDIAL INFARCTION: ANALYSIS FROM
AMERICAN HEART ASSOCIATION GET WITH THE GUIDELINES: CORONARY ARTERY
DISEASE
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E1285
EP E1285
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695101288
ER
PT J
AU Mercado, N
Cohen, DJ
Spertus, JA
House, J
Kennedy, K
Chan, PS
Rosenfield, KA
Marso, SP
AF Mercado, Nestor
Cohen, David J.
Spertus, John A.
House, John
Kennedy, Kevin
Chan, Paul S.
Rosenfield, Kenneth A.
Marso, Steven P.
TI IN-HOSPITAL OUTCOMES OF CAROTID ARTERY STENTING IN PATIENTS WITH A
CONTRALATERAL CAROTID OCCLUSION: ANALYSIS FROM THE CAROTID ARTERY
REVASCULARIZATION AND ENDARTERECTOMY (CARE) REGISTRY
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 St Lukes Mid Amer Heart & Vasc Inst, Kansas City, MO USA.
Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E1421
EP E1421
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695101424
ER
PT J
AU Noseworthy, P
Porthan, K
Tikkanen, J
Peloso, G
Merchant, F
Pietila, A
Havulinna, A
Oikarinen, L
Hwang, SJ
O'Donnell, C
Salomaa, V
Newton-Cheh, C
Huikuri, H
AF Noseworthy, Peter
Porthan, Kimmo
Tikkanen, Jani
Peloso, Gina
Merchant, Faisal
Pietila, Arto
Havulinna, Aki
Oikarinen, Lasse
Hwang, Shi-Jen
O'Donnell, Christopher
Salomaa, Veikko
Newton-Cheh, Christopher
Huikuri, Heikki
TI THE EARLY REPOLARIZATION PATTERN: CLINICAL CORRELATES AND HERITABILITY
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
Univ Helsinki, Cent Hosp, Helsinki, Finland.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E109
EP E109
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695100110
ER
PT J
AU O'Donnell, TFX
Morrow, DA
O'Donoghue, M
Jarolim, P
Sloan, S
Simon, DI
Libby, P
Sabatine, MS
AF O'Donnell, Thomas F. X.
Morrow, David A.
O'Donoghue, Michelle
Jarolim, Petr
Sloan, Sarah
Simon, Daniel I.
Libby, Peter
Sabatine, Marc S.
TI ASSOCIATION OF MRP-8/14 LEVELS AND FUTURE CORONARY EVENTS IN PATIENTS
WITH STABLE CAD
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 [O'Donnell, Thomas F. X.; Morrow, David A.; O'Donoghue, Michelle; Jarolim, Petr; Sloan, Sarah; Simon, Daniel I.; Libby, Peter; Sabatine, Marc S.] Brigham & Womens Hosp, Thrombolysis Myocardial Infarct TIMI Study Grp, Boston, MA 02115 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 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E1123
EP E1123
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695101126
ER
PT J
AU O'Malley, RG
Bonaca, MP
Sabatine, MS
Scirica, BM
Murphy, SA
Jarolim, P
Braunwald, E
Morrow, DA
AF O'Malley, Ryan G.
Bonaca, Marc P.
Sabatine, Marc S.
Scirica, Benjamin M.
Murphy, Sabina A.
Jarolim, Petr
Braunwald, Eugene
Morrow, David A.
TI C-TERMINAL PROVASOPRESSIN (COPEPTIN), MID-REGION PRO-ADRENOMEDULLIN
(MR-PROADM) AND MID-REGION PRO-ATRIAL NATRIURETIC PEPTIDE (MR-PROANP) AS
NOVEL PROGNOSTIC BIOMARKERS AFTER NON-ST ELEVATION ACUTE CORONARY
SYNDROME: ANALYSIS FROM MERLIN TIMI-36
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 [O'Malley, Ryan G.; Bonaca, Marc P.; Sabatine, Marc S.; Scirica, Benjamin M.; Murphy, Sabina A.; Jarolim, Petr; Braunwald, Eugene; Morrow, David A.] Brigham & Womens Hosp, TIMI Study Grp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E1020
EP E1020
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695101023
ER
PT J
AU Parikh, NI
Rosenthal, EJ
Honeycutt, E
Roe, M
Mittleman, MA
Ho, KKL
Carrozza, JP
AF Parikh, Nisha I.
Rosenthal, Eric J.
Honeycutt, Emily
Roe, Matthew
Mittleman, Murray A.
Ho, Kalon K. L.
Carrozza, Joseph P.
TI LEFT-DOMINANT CORONARY ARTERY CIRCULATION IS ASSOCIATED WITH HIGHER
IN-HOSPITAL MORTALITY AMONG PATIENTS UNDERGOING PERCUTANEOUS CORONARY
INTERVENTION IN ACUTE CORONARY SYNDROME: DATA FROM THE AMERICAN COLLEGE
OF CARDIOLOGY NATIONAL CARDIOVASCULAR DATA REGISTRY FOR CATHETERIZATION
PERCUTANEOUS CORONARY INTERVENTION
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 Kaiser Permanente Hawaii, Honolulu, HI USA.
Harvard Beth Israel Deaconess Med Ctr, Boston, MA USA.
NR 0
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 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E903
EP E903
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695100904
ER
PT J
AU Perlowski, A
Jaff, M
O'Shaughnessy, D
Brueggeman, C
Rosenfield, K
AF Perlowski, Alice
Jaff, Michael
O'Shaughnessy, Deborah
Brueggeman, Cristina
Rosenfield, Kenneth
TI STARCLOSE DEVICE CLOSURE OF FEMORAL ARTERIOTOMY SITE VERSUS MANUAL
COMPRESSION IN PATIENTS WITH PERIPHERAL ARTERIAL DISEASE: THE CLIPIT
TRIAL
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 [Perlowski, Alice; Jaff, Michael; O'Shaughnessy, Deborah; Brueggeman, Cristina; Rosenfield, Kenneth] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
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 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E1982
EP E1982
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695101985
ER
PT J
AU Sakhuja, R
Gandhi, S
Rogers, RK
Margey, RJP
Jaff, MR
Schainfeld, R
Rosenfield, K
AF Sakhuja, Rahul
Gandhi, Sanjay
Rogers, Robert K.
Margey, Ronan J. P.
Jaff, Michael R.
Schainfeld, Robert
Rosenfield, Kenneth
TI A NOVEL ENDOVENOUS APPROACH FOR TREATMENT OF MASSIVE CENTRAL VENOUS OR
PULMONARY ARTERIAL THROMBUS, MASS, OR VEGETATION: THE ANGIOVAC SUCTION
CANNULA AND CIRCUIT
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 [Sakhuja, Rahul; Gandhi, Sanjay; Rogers, Robert K.; Margey, Ronan J. P.; Jaff, Michael R.; Schainfeld, Robert; Rosenfield, Kenneth] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 4
Z9 4
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E1535
EP E1535
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695101538
ER
PT J
AU Shah, RV
McNulty, S
Lee, K
Felker, GM
O'Connor, CM
Givertz, MM
AF Shah, Ravi V.
McNulty, Steven
Lee, Kerry
Felker, G. Michael
O'Connor, Christopher M.
Givertz, Michael M.
TI EFFECT OF ADMISSION ORAL DIURETIC DOSE ON RESPONSE TO CONTINUOUS VERSUS
BOLUS INTRAVENOUS DIURETICS IN ACUTE HEART FAILURE: AN ANALYSIS FROM
DOSE-AHF
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
Duke Univ, Med Ctr, Duke Clin Res Ctr, Durham, NC USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E216
EP E216
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695100217
ER
PT J
AU Subramanian, S
Lawler, M
Vijayakumar, J
Abdelbaky, A
Brady, T
Fayad, Z
Chen, J
Tawakol, A
AF Subramanian, Sharath
Lawler, Meredith
Vijayakumar, Jayanthi
Abdelbaky, Amr
Brady, Thomas
Fayad, Zahi
Chen, John
Tawakol, Ahmed
TI 18 F-FLUORODEOXYGLUCOSE POSITRON EMISSION TOMOGRAPHY AND MAGNETIC
RESONANCE IMAGING FOR LOCALIZATION OF INFLAMED AND LIPID-RICH AORTIC
PLAQUES
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
Mt Sinai Sch Med, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E846
EP E846
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695100847
ER
PT J
AU Todoran, TM
Connors, G
Engleson, BA
Sobieszczyk, PS
Eisenhauer, AC
Kinlay, S
AF Todoran, Thomas M.
Connors, Gerard
Engleson, 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 JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 VA Boston Healthcare Syst, W Roxbury, MA USA.
Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E1962
EP E1962
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695101965
ER
PT J
AU Vora, A
Morrow, DA
O'Donoghue, M
Jarolim, P
Sloan, S
Sabatine, MS
AF Vora, Amit
Morrow, David A.
O'Donoghue, Michelle
Jarolim, Petr
Sloan, Sarah
Sabatine, Marc S.
TI ASSOCIATION OF SVCAM-1 WITH MAJOR ADVERSE CARDIAC EVENTS IN PATIENTS
WITH STABLE CAD
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 Brigham & Womens Hosp, Boston, MA 02115 USA.
TIMI Study Grp, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E1122
EP E1122
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695101125
ER
PT J
AU Vorasettakarnkij, Y
Verdini, DJ
Deeprasertkul, P
Medina, HM
Goehler, A
Halpern, EF
Ahmed, W
Uthamalingam, S
Figueroa, AL
Major, GP
Brady, TJ
Sosnovik, DE
Ghoshhajra, BB
Holmvang, G
AF Vorasettakarnkij, Yongkasem
Verdini, Daniel J.
Deeprasertkul, Peerawut
Medina, Hector M.
Goehler, Alexander
Halpern, Elkan F.
Ahmed, Waleed
Uthamalingam, Shanmugam
Figueroa, Amparo L.
Major, Gyongyi P.
Brady, Thomas J.
Sosnovik, David E.
Ghoshhajra, Brian B.
Holmvang, Godtfred
TI CORRELATION OF LEFT VENTRICULAR NON-COMPACTED/COMPACTED MASS RATIO AND
CLINICAL OUTCOMES IN PATIENTS WITH LEFT VENTRICULAR NON-COMPACTION
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
Chulalongkorn Univ, Fac Med, Dept Med, Bangkok 10330, Thailand.
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 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E789
EP E789
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695100790
ER
PT J
AU Weiner, RB
Baggish, AL
Chen-Tournoux, AA
Marshall, JE
Kim, HN
Bhardwaj, A
Mohammed, AA
Rehman, SU
Barajas, L
Barajas, J
Gregory, SA
Moore, SA
Semigran, MJ
Januzzi, JL
AF Weiner, Rory B.
Baggish, Aaron L.
Chen-Tournoux, Annabel A.
Marshall, Jane E.
Kim, Han-Na
Bhardwaj, Anju
Mohammed, Asim A.
Rehman, Shafiq U.
Barajas, Linda
Barajas, Justine
Gregory, Shawn A.
Moore, Stephanie A.
Semigran, Marc J.
Januzzi, James L.
TI IMPROVEMENT OF ECHOCARDIOGRAPHIC PARAMETERS ASSOCIATED WITH NT-PROBNP
GUIDED HEART FAILURE MANAGEMENT: MECHANISTIC INSIGHTS FROM THE PROBNP
OUTPATIENT TAILORED CHRONIC HEART FAILURE (PROTECT) STUDY
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 [Weiner, Rory B.; Baggish, Aaron L.; Chen-Tournoux, Annabel A.; Marshall, Jane E.; Kim, Han-Na; Bhardwaj, Anju; Mohammed, Asim A.; Rehman, Shafiq U.; Barajas, Linda; Barajas, Justine; Gregory, Shawn A.; Moore, Stephanie A.; Semigran, Marc J.; Januzzi, James L.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E2030
EP E2030
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695102035
ER
PT J
AU White, HD
Chew, DP
Dauerman, HL
Mahaffey, KW
Gibson, CM
Harrington, RA
Bhatt, DL
AF White, Harvey D.
Chew, Derek P.
Dauerman, Harold L.
Mahaffey, Kenneth W.
Gibson, C. Michael
Harrington, Robert A.
Bhatt, Deepak L.
TI REDUCED IMMEDIATE ISCHEMIC EVENTS WITH CANGRELOR IN PCI USING THE
UNIVERSAL DEFINITION OF MI: POOLED ANALYSIS OF THE CANGRELOR VERSUS
STANDARD THERAPY TO ACHIEVE OPTIMAL MANAGEMENT OF PLATELET INHIBITION
TRIALS
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 Auckland City Hosp, Auckland, New Zealand.
Brigham & Womens Hosp, Boston, MA 02115 USA.
VA Boston Healthcare Syst, Boston, MA 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 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E1097
EP E1097
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695101100
ER
PT J
AU Zilinski, JL
Shah, RV
Barajas, L
Barajas, JA
Wang, TJ
Januzzi, JL
AF Zilinski, Jodi L.
Shah, Ravi V.
Barajas, Linda
Barajas, Justine A.
Wang, Thomas J.
Januzzi, James L.
TI MEASUREMENT OF SOLUBLE ST2 IN ADVANCED STAGE HEART FAILURE PATIENTS
TREATED WITH INVASIVE HEMODYNAMIC "TAILORED" THERAPY
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 60th Annual Scientific Session and Expo of the
American-College-of-Cardiology
CY APR 03-05, 2011
CL New Orleans, LA
SP Amer Coll Cardiol
C1 [Zilinski, Jodi L.; Shah, Ravi V.; Barajas, Linda; Barajas, Justine A.; Wang, Thomas J.; Januzzi, James L.] Massachusetts Gen Hosp, Boston, MA 02114 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 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD APR 5
PY 2011
VL 57
IS 14
SU 1
BP E279
EP E279
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 778HR
UT WOS:000291695100280
ER
PT J
AU Ryan, G
Berrebi, C
Beckett, M
Taylor, S
Quiter, E
Cho, M
Pincus, H
Kahn, K
AF Ryan, Gery
Berrebi, Claude
Beckett, Megan
Taylor, Stephanie
Quiter, Elaine
Cho, Michelle
Pincus, Harold
Kahn, Katherine
TI Reengineering the clinical research enterprise to involve more community
clinicians
SO IMPLEMENTATION SCIENCE
LA English
DT Article
ID NIH ROADMAP; TRANSLATION; NETWORKS; TRIALS; US
AB Background: The National Institutes of Health has called for expansion of practice-based research to improve the clinical research enterprise.
Methods: This paper presents a model for the reorganization of clinical research to foster long-term participation by community clinicians.
Based on the literature and interviews with clinicians and other stakeholders, we posited a model, conducted further interviews to test the viability of the model, and further adapted it.
Results: We propose a three-dimensional system of checks and balances to support community clinicians using research support organizations, community outreach, a web-based registry of clinicians and studies, web-based training services, quality audits, and a feedback mechanism for clinicians engaged in research.
Conclusions: The proposed model is designed to offer a systemic mechanism to address current barriers that prevent clinicians from participation in research. Transparent mechanisms to guarantee the safety of patients and the integrity of the research enterprise paired with efficiencies and economies of scale are maintained by centralizing some of the functions. Assigning other responsibilities to more local levels assures flexibility with respect to the size of the clinician networks and the changing needs of researchers.
C1 [Ryan, Gery; Berrebi, Claude; Beckett, Megan; Taylor, Stephanie; Kahn, Katherine] RAND Hlth, Santa Monica, CA USA.
[Pincus, Harold] RAND Univ Pittsburgh, Hlth Inst, Pittsburgh, PA USA.
[Pincus, Harold] Columbia Univ, Dept Psychiat, New York, NY USA.
[Pincus, Harold] New York Presbyterian Hosp, New York, NY USA.
[Kahn, Katherine] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90095 USA.
[Taylor, Stephanie] VA Greater Los Angeles Healthcare Syst, Hlth Serv Res & Dev Off, US Dept Vet Affairs, Los Angeles, CA USA.
[Quiter, Elaine] Univ Calif Los Angeles, Sch Publ Hlth, Los Angeles, CA 90024 USA.
[Cho, Michelle] Compass Lexecon, Oakland, CA USA.
RP Kahn, K (reprint author), RAND Hlth, Santa Monica, CA USA.
EM kahn@rand.org
RI Berrebi, Claude/K-8329-2012
FU National Institute of Child Health and Human Development (NICHD)
[HHSN275200403390C]
FX This publication was made possible by Contract Number HHSN275200403390C
from the National Institute of Child Health and Human Development
(NICHD).
NR 21
TC 4
Z9 4
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1748-5908
J9 IMPLEMENT SCI
JI Implement. Sci.
PD APR 4
PY 2011
VL 6
AR 36
DI 10.1186/1748-5908-6-36
PG 7
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 754MN
UT WOS:000289858900001
PM 21463518
ER
PT J
AU Fiamegos, YC
Kastritis, PL
Exarchou, V
Han, H
Bonvin, AMJJ
Vervoort, J
Lewis, K
Hamblin, MR
Tegos, GP
AF Fiamegos, Yiannis C.
Kastritis, Panagiotis L.
Exarchou, Vassiliki
Han, Haley
Bonvin, Alexandre M. J. J.
Vervoort, Jacques
Lewis, Kim
Hamblin, Michael R.
Tegos, George P.
TI Antimicrobial and Efflux Pump Inhibitory Activity of Caffeoylquinic
Acids from Artemisia absinthium against Gram-Positive Pathogenic
Bacteria
SO PLOS ONE
LA English
DT Article
ID STAPHYLOCOCCUS-AUREUS; MULTIDRUG-RESISTANCE; ANTIBIOTIC-ACTIVITY;
CHLOROGENIC ACIDS; NORA; TRANSPORTER; DERIVATIVES; BERBERINE; ANALOGS;
PROTEIN
AB Background: Traditional antibiotics are increasingly suffering from the emergence of multidrug resistance amongst pathogenic bacteria leading to a range of novel approaches to control microbial infections being investigated as potential alternative treatments. One plausible antimicrobial alternative could be the combination of conventional antimicrobial agents/antibiotics with small molecules which block multidrug efflux systems known as efflux pump inhibitors. Bioassay-driven purification and structural determination of compounds from plant sources have yielded a number of pump inhibitors which acted against gram positive bacteria.
Methodology/Principal Findings: In this study we report the identification and characterization of 4',5'-O-dicaffeoylquinic acid (4',5'-ODCQA) from Artemisia absinthium as a pump inhibitor with a potential of targeting efflux systems in a wide panel of Gram-positive human pathogenic bacteria. Separation and identification of phenolic compounds (chlorogenic acid, 3',5'-ODCQA, 4',5'-ODCQA) was based on hyphenated chromatographic techniques such as liquid chromatography with post column solid-phase extraction coupled with nuclear magnetic resonance spectroscopy and mass spectroscopy. Microbial susceptibility testing and potentiation of well know pump substrates revealed at least two active compounds; chlorogenic acid with weak antimicrobial activity and 4',5'-ODCQA with pump inhibitory activity whereas 3',5'-ODCQA was ineffective. These intitial findings were further validated with checkerboard, berberine accumulation efflux assays using efflux-related phenotypes and clinical isolates as well as molecular modeling methodology.
Conclusions/Significance: These techniques facilitated the direct analysis of the active components from plant extracts, as well as dramatically reduced the time needed to analyze the compounds, without the need for prior isolation. The calculated energetics of the docking poses supported the biological information for the inhibitory capabilities of 4',5'-ODCQA and furthermore contributed evidence that CQAs show a preferential binding to Major Facilitator Super family efflux systems, a key multidrug resistance determinant in gram-positive bacteria.
C1 [Fiamegos, Yiannis C.] Univ Ioannina, Analyt Chem Lab, GR-45110 Ioannina, Greece.
[Kastritis, Panagiotis L.; Bonvin, Alexandre M. J. J.] Univ Utrecht, Bijvoet Ctr Biomol Res, Fac Sci, Utrecht, Netherlands.
[Exarchou, Vassiliki] Univ Ioannina, NMR Ctr, GR-45110 Ioannina, Greece.
[Han, Haley; Hamblin, Michael R.; Tegos, George P.] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Vervoort, Jacques] Wageningen NMR Ctr, Biophys Lab, Wageningen, Netherlands.
[Lewis, Kim] Northeastern Univ, Dept Biol, Boston, MA 02115 USA.
[Lewis, Kim] Northeastern Univ, Antimicrobial Drug Discovery Ctr, Boston, MA 02115 USA.
[Hamblin, Michael R.; Tegos, George P.] Harvard Univ, Sch Med, Dept Dermatol, Boston, MA 02115 USA.
[Hamblin, Michael R.] MIT, Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
RP Fiamegos, YC (reprint author), Univ Ioannina, Analyt Chem Lab, GR-45110 Ioannina, Greece.
EM gtegos@salud.unm.edu
RI Tegos, George/C-8830-2011; Bonvin, Alexandre/A-5420-2009; Kastritis,
Panagiotis/F-2498-2010;
OI Bonvin, Alexandre/0000-0001-7369-1322; Kastritis,
Panagiotis/0000-0002-1463-8422; Hamblin, Michael/0000-0001-6431-4605
FU E.U. [HPRI-CT-2001-00178, 2002-31, 2003-011]; National Institutes of
Health (NIH) [5U54MH084690-02, R01GM59903R01AI050875]; Massachusetts
Technology Transfer Center (MTTC); Netherlands Organization for
Scientific Research [700.56.442]
FX Funding for Y. Fiamegos was provided by E.U. Large Scale Facilities
program, contracts HPRI-CT-2001-00178, 'LC-NMR analysis of traditional
herbal pharmaceuticals' (project no 2002-31) and 'On line LC-SPE-NMR
system in analyzing the bioactive constituents of Artemisia extract',
(Project no 2003-011) of the Wageningen NMR center. Funding was provided
for G. Tegos by the National Institutes of Health (NIH, 5U54MH084690-02,
Center Driven Initiative 1) and Massachusetts Technology Transfer Center
(MTTC), by the National Institutes of Health for K. Lewis (NIH,
R01GM59903) and M. R. Hamblin (NIH, R01AI050875). Funding for P.
Kastritis was provided by the Netherlands Organization for Scientific
Research through a VICI grant (700.56.442) to A. Bonvin. The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 62
TC 37
Z9 40
U1 2
U2 27
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 APR 4
PY 2011
VL 6
IS 4
AR e18127
DI 10.1371/journal.pone.0018127
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 743ZC
UT WOS:000289058700009
PM 21483731
ER
PT J
AU Deliolanis, NC
Wurdinger, T
Pike, L
Tannous, BA
Breakefield, XO
Weissleder, R
Ntziachristos, V
AF Deliolanis, Nikolaos C.
Wurdinger, Thomas
Pike, Lisa
Tannous, Bakhos A.
Breakefield, Xandra O.
Weissleder, Ralph
Ntziachristos, Vasilis
TI In vivo tomographic imaging of red-shifted fluorescent proteins
SO BIOMEDICAL OPTICS EXPRESS
LA English
DT Article
ID OPTICAL TOMOGRAPHY; SMALL ANIMALS; MOLECULAR TOMOGRAPHY; DIFFUSE
TOMOGRAPHY; MONOMERIC RED; RECONSTRUCTION; MICROSCOPY; TISSUES; DESIGN;
SYSTEM
AB We have developed a spectral inversion method for three-dimensional tomography of far-red and near-infrared fluorescent proteins in animals. The method was developed in particular to address the steep light absorption transition of hemoglobin from the visible to the far-red occurring around 600 nm. Using an orthotopic mouse model of brain tumors expressing the red-shifted fluorescent protein mCherry, we demonstrate significant improvements in imaging accuracy over single-wavelength whole body reconstructions. Furthermore, we show an improvement in sensitivity of at least an order of magnitude over green fluorescent protein (GFP) for whole body imaging. We discuss how additional sensitivity gains are expected with the use of further red-shifted fluorescent proteins and we explain the differences and potential advantages of this approach over two-dimensional planar imaging methods. (C) 2011 Optical Society of America
C1 [Deliolanis, Nikolaos C.; Wurdinger, Thomas; Tannous, Bakhos A.; Breakefield, Xandra O.; Weissleder, Ralph; Ntziachristos, Vasilis] Harvard Univ, Sch Med, Dept Radiol, Ctr Mol Imaging Res,Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Wurdinger, Thomas; Pike, Lisa; Tannous, Bakhos A.; Breakefield, Xandra O.] Harvard Univ, Sch Med, Dept Neurol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Deliolanis, Nikolaos C.; Ntziachristos, Vasilis] Tech Univ Munich, Inst Biol & Med Imaging, Munich, Germany.
[Deliolanis, Nikolaos C.; Ntziachristos, Vasilis] Helmholtz Zentrum Munchen, Munich, Germany.
[Wurdinger, Thomas] Vrije Univ Amsterdam Med Ctr, Neurooncol Res Grp, Dept Neurosurg, Amsterdam, Netherlands.
[Deliolanis, Nikolaos C.; Weissleder, Ralph] Harvard Univ, Ctr Syst Biol, Massachusetts Gen Hosp, Dept Syst Biol,Med Sch, Boston, MA USA.
RP Deliolanis, NC (reprint author), Harvard Univ, Sch Med, Dept Radiol, Ctr Mol Imaging Res,Massachusetts Gen Hosp, Boston, MA 02115 USA.
EM ndeliolanis@yahoo.com
OI Deliolanis, Nikolaos/0000-0002-6392-3035
FU National Institutes of Health [R01EB004382, P50CA86355, U24CA092782];
European Community
FX We thank Claudio Vinegoni, Jason Gaglia, Diane Mathis, and Christophe
Benoist for many helpful discussions and Jenny Chan for the MR imaging.
The research was supported by the National Institutes of Health grants
R01EB004382, P50CA86355, U24CA092782 and a Marie Curie Intra-European
Fellowship within the 7th European Community Framework Programme.
NR 37
TC 17
Z9 17
U1 0
U2 4
PU OPTICAL SOC AMER
PI WASHINGTON
PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA
SN 2156-7085
J9 BIOMED OPT EXPRESS
JI Biomed. Opt. Express
PD APR 1
PY 2011
VL 2
IS 4
BP 887
EP 900
PG 14
WC Biochemical Research Methods; Optics; Radiology, Nuclear Medicine &
Medical Imaging
SC Biochemistry & Molecular Biology; Optics; Radiology, Nuclear Medicine &
Medical Imaging
GA 886TN
UT WOS:000299876900014
PM 21483611
ER
PT J
AU Wang, Y
Hancock, AM
Bradner, J
Chung, KA
Quinn, JF
Peskind, ER
Galasko, D
Jankovic, J
Zabetian, CP
Kim, HM
Leverenz, JB
Montine, TJ
Ginghina, C
Edwards, KL
Snapinn, KW
Goldstein, DS
Shi, M
Zhang, J
AF Wang, Yu
Hancock, Aneeka M.
Bradner, Joshua
Chung, Kathryn A.
Quinn, Joseph F.
Peskind, Elaine R.
Galasko, Douglas
Jankovic, Joseph
Zabetian, Cyrus P.
Kim, Hojoong M.
Leverenz, James B.
Montine, Thomas J.
Ginghina, Carmen
Edwards, Karen L.
Snapinn, Katherine W.
Goldstein, David S.
Shi, Min
Zhang, Jing
TI Complement 3 and Factor H in Human Cerebrospinal Fluid in Parkinson's
Disease, Alzheimer's Disease, and Multiple-System Atrophy
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID CSF AMYLOID-BETA; CONSENSUS STATEMENT; COGNITIVE DECLINE;
NERVOUS-SYSTEM; PHOSPHO-TAU; LEWY BODY; DEMENTIA; BIOMARKERS; DIAGNOSIS;
EXPRESSION
AB Complement activation, a key component of neuroinflammation, has been reported in both Parkinson's disease (PD) and Alzheimer's disease (AD). However, it is unclear whether complement activation and neuroinflammation in general are distinctly different from each another in major neurodegenerative disorders. In the present study, cerebrospinal fluid complement 3 (C3) and factor H (FH) were measured and evaluated together with amyloid-beta(42) (A beta(42)), which in recent investigations was decreased in patients with PD, in particular those with cognitive impairment. The study included 345 participants: 126 patients with PD at various stages with or without cognitive impairment, 50 with AD, and 32 with multiple-system atrophy, and 137 healthy control individuals. In addition to changes in A beta(42) concentrations, there were clear differences in the patterns of complement profiles among neurodegenerative disorders. The C3/FH ratio demonstrated high sensitivity and specificity in differentiating patients with multiple-system atrophy from those with AD or PD and control individuals. In addition, the C3/A beta(42) and FH/A beta(42) ratios not only correlated with PD severity approximated using the Unified Parkinson's Disease Rating Scale but also with the presence of cognitive impairment or dementia in PD. Both C3 and FH correlated with the severity of impairment in AD as indicated using Mini-Mental State Examination scores. (Am J Pathol 2011, 178:1509-1516; DOI: 10.1016/j.ajpath.2011.01.006)
C1 [Wang, Yu; Hancock, Aneeka M.; Bradner, Joshua; Montine, Thomas J.; Ginghina, Carmen; Shi, Min; Zhang, Jing] Univ Washington, Sch Med, Dept Pathol, Seattle, WA 98104 USA.
[Peskind, Elaine R.; Leverenz, James B.] Univ Washington, Sch Med, Dept Psychiat & Behav Sci, Seattle, WA 98104 USA.
[Zabetian, Cyrus P.; Kim, Hojoong M.; Leverenz, James B.] Univ Washington, Sch Med, Dept Neurol, Seattle, WA 98104 USA.
[Wang, Yu] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Neurosurg, Wuhan 430074, Peoples R China.
[Chung, Kathryn A.; Quinn, Joseph F.] Oregon Hlth & Sci Univ, Dept Neurol, Portland, OR 97201 USA.
[Peskind, Elaine R.; Leverenz, James B.] Vet Affairs Puget Sound Hlth Care Syst, Mental Illness Res Educ & Clin Ctr, Seattle, WA USA.
[Zabetian, Cyrus P.] Vet Affairs Puget Sound Hlth Care Syst, Geriatr Res Educ & Clin Ctr, Seattle, WA USA.
[Kim, Hojoong M.] Vet Affairs Puget Sound Hlth Care Syst, Dept Neurol, Seattle, WA USA.
[Galasko, Douglas] Univ Calif San Diego, Dept Neurosci, San Diego, CA 92103 USA.
[Jankovic, Joseph] Baylor Coll Med, Parkinsons Dis Ctr, Dept Neurol, Houston, TX 77030 USA.
[Jankovic, Joseph] Baylor Coll Med, Movement Disorders Clin, Dept Neurol, Houston, TX 77030 USA.
[Edwards, Karen L.; Snapinn, Katherine W.] Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA.
[Goldstein, David S.] NINDS, Clin Neurocardiol Sect, Clin Neurosci Program, Div Intramural Res,NIH, Bethesda, MD 20892 USA.
RP Zhang, J (reprint author), Univ Washington, Sch Med, Dept Pathol, HMC Box 359635,325 9th Ave, Seattle, WA 98104 USA.
EM zhangj@uw.edu
RI Shi, Min/G-6165-2012;
OI Shi, Min/0000-0002-6901-2558; Zabetian, Cyrus/0000-0002-7739-4306
FU National Institutes of Health [ES004696, NS057567, AG025327, AG033398,
NS060252, NS062684, AG005136, AG008017]; Michael J. Fox Foundation;
Cheng-Mei Shaw Endowment; Nancy and Buster Alvord Endowment
FX Supported by grants ES004696, NS057567, AG025327, AG033398, and NS060252
(J.Z.), NS062684 (T.J.M., C.P.Z., J.B.L., and J.Z.), AG005136 (ERR. and
T.J.M.), and AG008017 (K.A.C. and J.F.Q.) from the National Institutes
of Health, and grants from the Michael J. Fox Foundation and the
Cheng-Mei Shaw Endowment (J.Z.) and the Nancy and Buster Alvord
Endowment (T.J.M.).
NR 37
TC 38
Z9 41
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD APR
PY 2011
VL 178
IS 4
BP 1509
EP 1516
DI 10.1016/j.ajpath.2011.01.006
PG 8
WC Pathology
SC Pathology
GA 865JH
UT WOS:000298306700012
PM 21435440
ER
PT J
AU Miyajima, M
Chase, CM
Alessandrini, A
Farkash, EA
Della Pelle, P
Benichou, G
Graham, JA
Madsen, JC
Russell, PS
Colvin, RB
AF Miyajima, Masahiro
Chase, Catharine M.
Alessandrini, Alessandro
Farkash, Evan A.
Della Pelle, Patricia
Benichou, Gilles
Graham, Jay A.
Madsen, Joren C.
Russell, Paul S.
Colvin, Robert B.
TI Early Acceptance of Renal Allografts in Mice Is Dependent on Foxp3(+)
Cells
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID REGULATORY T-CELLS; TRANSPLANT TOLERANCE; LYMPHOID NEOGENESIS;
KIDNEY-TRANSPLANTS; CARDIAC ALLOGRAFTS; PROTOCOL BIOPSIES; CHRONIC
REJECTION; MINIATURE SWINE; DISEASE; EXPRESSION
AB Mouse renal allografts have a remarkable ability to promote acceptance across full major histocompatibility complex incompatibilities in certain strain combinations without immunosuppression. The mechanism is unknown but is believed to involve immunoregulation. This study tests whether Foxp3(+) T-regulatory cells are responsible in the early phase of graft acceptance, using B6.Foxp3(DTR) mice that express diphtheria toxin receptor (DTR) in Foxp3(+) cells. The administration of DT to B6.Foxp3(DTR) recipients with accepted DBA/2 kidneys, 3 weeks to 3 months after transplantation, caused a marked depletion of Foxp3 cells and triggered acute cellular rejection, manifested by a sudden increase in blood urea nitrogen within a week. None of the controls showed an increase in blood urea nitrogen, including DT-treated B6 wild-type recipients of DBA/2 kidneys or B6.Foxp3(DTR) recipients of isografts. Accepted DBA/2 allografts showed prominent lymphoid sheaths around arteries containing numerous CD3(+)Foxp3(+) cells, CD4(+) cells, dedritic cells, and B cells, which was independent of CCR4. The lymphoid sheaths disintegrate after Foxp3 depletion, accompanied by widespread CD8 interstitial mononuclear inflammation, tubulitis, and endarteritis. The Foxp3 depletion caused an increased frequency of donor-reactive cells in the spleen by interferon (IFN) gamma enzyme-linked immunosorbent spot (ELISPOT) assays and increased expression of the maturation markers, CD86 and IA(b), on dendritic cells in the spleen and kidney. We conclude that Foxp3(+) cells are needed to maintain acceptance of major histocompatibility complex-incompatible renal allografts in the first 3 months after transplantation and may act by inhibiting DC maturation. (Am J Pathol 2011, 178:1635-1645; DOI: 10.1016/j.ajpath.2010.12.024)
C1 [Miyajima, Masahiro; Alessandrini, Alessandro; Benichou, Gilles; Graham, Jay A.; Madsen, Joren C.; Russell, Paul S.; Colvin, Robert B.] Massachusetts Gen Hosp, Transplantat Ctr, Boston, MA 02114 USA.
[Farkash, Evan A.; Della Pelle, Patricia; Colvin, Robert B.] Massachusetts Gen Hosp, Pathol Serv, Boston, MA 02114 USA.
[Madsen, Joren C.] Massachusetts Gen Hosp, Div Cardiac Surg, Boston, MA 02114 USA.
[Miyajima, Masahiro; Chase, Catharine M.; Alessandrini, Alessandro; Benichou, Gilles; Madsen, Joren C.; Russell, Paul S.] Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA.
[Colvin, Robert B.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
RP Colvin, RB (reprint author), Massachusetts Gen Hosp, Transplantat Ctr, Thier 831, Boston, MA 02114 USA.
EM colvin@helix.mgh.harvard.edu
RI Graham, Jay/A-4896-2014
OI Graham, Jay/0000-0003-2054-1253
FU International Society for Heart and Lung Transplantation; NIH
[R01HL071932-05A11, R56AI081734, RO1AI081734]
FX Supported by a research award from the International Society for Heart
and Lung Transplantation (M.M.) and grants from the NIH
(R01HL071932-05A11 to J.C.M.; R56AI081734 and RO1AI081734 to R.B.C.).
NR 53
TC 32
Z9 32
U1 0
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD APR
PY 2011
VL 178
IS 4
BP 1635
EP 1645
PG 11
WC Pathology
SC Pathology
GA 865JH
UT WOS:000298306700023
PM 21435448
ER
PT J
AU Nakao, S
Noda, K
Zandi, S
Sun, DW
Taher, M
Schering, A
Xie, F
Mashima, Y
Hafezi-Moghadam, A
AF Nakao, Shintaro
Noda, Kousuke
Zandi, Souska
Sun, Dawei
Taher, Mandi
Schering, Alexander
Xie, Fang
Mashima, Yukihiko
Hafezi-Moghadam, Ali
TI VAP-1 Mediated M2 Macrophage Infiltration Underlies IL-1 beta- but Not
VEGF-A-Induced Lymph- and Angiogenesis
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID VASCULAR ADHESION PROTEIN-1; IN-VIVO; ENDOTHELIAL INJURY;
LYMPHANGIOGENESIS; NEOVASCULARIZATION; INFLAMMATION; SELECTIN;
INTEGRINS; MECHANISM; GROWTH
AB Vascular adhesion protein-1 (YAP-1) contributes to inflammatory and angiogenic diseases, including cancer and age-related macular degeneration. It is expressed in blood vessels and contributes to inflammatory leukocyte recruitment. The cytokines IL-1 beta and vascular endothelial growth factor A (VEGF-A) modulate angiogenesis, lymphangiogenesis, and leukocyte infiltration. The lymphatic endothelium expresses intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, which facilitate leukocyte transmigration into the lymphatic vessels. However, whether lymphatics express YAP-1 and whether they contribute to cytokine-dependent lymph- and angiogenesis are unknown. We investigated the role of VAP-1 in IL-1 beta- and VEGF-A-induced lymph- and angiogenesis using the established corneal tnicropocket assay. IL-1 beta increased YAP-1 expression in the inflamed cornea. Our in vivo molecular imaging revealed significantly higher YAP-1 expression in neovasculature than in the preexisting vessels. YAP-1 was expressed in blood but not lymphatic vessels in vivo. IL-1 beta-induced M2 macrophage infiltration and lymph- and angiogenesis were blocked by YAP-1 inhibition. In contrast, VEGF-A-induced lymph- and angiogenesis were unaffected by YAP-1 inhibition. Our results indicate a key role for YAP-1 in lymph- and angiogenesis-related macrophage recruitment. YAP-1 might become a new target for treatment of inflammatory lymph- and angiogenic diseases, including cancer. (Am J Pathol 2011, 178:1913-1921; DOI: 10.1016/j.ajpath.2011.01.011)
C1 [Hafezi-Moghadam, Ali] Harvard Univ, Brigham & Womens Hosp, Sch Med, Ctr Excellence Funct & Mol Imaging, Boston, MA 02115 USA.
[Nakao, Shintaro; Noda, Kousuke; Zandi, Souska; Sun, Dawei; Taher, Mandi; Schering, Alexander; Xie, Fang; Hafezi-Moghadam, Ali] Harvard Univ, Angiogenesis Lab, Sch Med, Massachusetts Eye & Ear Infirm, Boston, MA 02115 USA.
[Nakao, Shintaro; Noda, Kousuke; Zandi, Souska; Sun, Dawei; Taher, Mandi; Schering, Alexander; Xie, Fang; Hafezi-Moghadam, Ali] Harvard Univ, Dept Ophthalmol, Sch Med, Boston, MA 02115 USA.
[Zandi, Souska; Sun, Dawei; Taher, Mandi; Schering, Alexander; Xie, Fang; Hafezi-Moghadam, Ali] Harvard Univ, Dept Radiol, Sch Med, Boston, MA 02115 USA.
[Mashima, Yukihiko] R Tech Ueno Ltd, Tokyo, Japan.
RP Hafezi-Moghadam, A (reprint author), Harvard Univ, Brigham & Womens Hosp, Sch Med, Ctr Excellence Funct & Mol Imaging, 221 Longwood Ave,3rd Floor, Boston, MA 02115 USA.
EM ahm@bwh.harvard.edu
OI Hafezi-Moghadam, Ali/0000-0002-5336-0697
FU National Institutes of Health [AI050775]; Malaysian Palm Oil Board;
American Health Assistance Foundation; Bausch Lomb; Japan Eye Bank
Association; Tear Film & Ocular Surface Society
FX Supported by National Institutes of Health grant AI050775, the Malaysian
Palm Oil Board, American Health Assistance Foundation, an overseas
Research Fellowship Award from Bausch & Lomb, a Fellowship Award from
the Japan Eye Bank Association, and Tear Film & Ocular Surface Society
Young Investigator Fellowship (to S.N. under the mentorship of A.H.-M.).
NR 28
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Z9 24
U1 1
U2 14
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD APR
PY 2011
VL 178
IS 4
BP 1913
EP 1921
DI 10.1016/j.ajpath.2011.01.011
PG 9
WC Pathology
SC Pathology
GA 865JH
UT WOS:000298306700047
PM 21435467
ER
PT J
AU Jin, YP
Chauhan, SK
Annan, JEI
Sage, PT
Sharpe, AH
Dana, R
AF Jin, Yiping
Chauhan, Sunil K.
Annan, Jaafar E. I.
Sage, Peter T.
Sharpe, Arlene H.
Dana, Reza
TI A Novel Function for Programmed Death Ligand-1 Regulation of
Angiogenesis
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID ORTHOTOPIC CORNEAL ALLOGRAFTS; ANTIGEN-PRESENTING CELLS;
ENDOTHELIAL-CELLS; IMMUNE PRIVILEGE; B7 FAMILY; T-CELLS; EXPRESSION;
PD-L1; NEOVASCULARIZATION; B7-H1
AB Programmed death ligand-1 (PD-L1) plays a critical role in T-cell regulatory function. Here, we report a newly discovered effect of PD-L1 on angiogenesis. We demonstrate that PD-L1 and its receptor CD80, but not PD-1, are expressed by primary murine lung and heart vascular endothelial cells and the miscrovascular endothelial cell line (Ms1) at both the mRNA and protein levels in vitro. The inhibition of PD-L1 or CD80 expression in MS1 cells, by small-interfering RNA transfection, led to a significant up-regulation of vascular endothelial growth factor receptor 2 expression and cell proliferation levels in MS1 cells. Furthermore, MS1 cells were found to have a significantly lower proliferation and vascular endothelial growth factor receptor 2 expression levels when they were co-cultured with PD-L1-expressing normal corneal epithelial cells, as compared to MS1 cells co-cultured with PD-L1(-/-) corneal epithelial cells. In a suture-induced corneal angiogenesis model, we observed a significantly higher level of angiogenic response in PD-L1(-/-) knockout mice as compared to wild-type mice, although there was no significant difference in the expression of inflammatory cytokines (interleukin-1 alpha, interleukin-1 beta, or tumor necrosis factor-alpha) or the infiltration of innate immune cells (neutrophils and macrophages) between the two groups. We conclude that the expression of PD-L1 in both vascular endothelial cells and corneal epithelial cells regulates corneal angiogenesis. (Am J Pathol 2011, 178:1922-1929; DOI: 10.1016/j.ajpath.2010.12.027)
C1 [Jin, Yiping; Chauhan, Sunil K.; Annan, Jaafar E. I.; Dana, Reza] Harvard Univ, Sch Med, Schepens Eye Res Inst, Dept Ophthalmol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
[Sage, Peter T.; Sharpe, Arlene H.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02114 USA.
RP Dana, R (reprint author), Harvard Univ, Sch Med, Schepens Eye Res Inst, Dept Ophthalmol, 20 Staniford St, Boston, MA 02114 USA.
EM reza.dana@schepens.harvard.edu
FU National Institutes of Health [R01 EY 12963, RO1 AI 40614, T32 AI
070085-03]
FX Supported by National Institutes of Health grants R01 EY 12963 (R.D.),
RO1 AI 40614 (A.H.S.), and T32 AI 070085-03 (P.T.S.).
NR 30
TC 16
Z9 17
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD APR
PY 2011
VL 178
IS 4
BP 1922
EP 1929
DI 10.1016/j.ajpath.2010.12.027
PG 8
WC Pathology
SC Pathology
GA 865JH
UT WOS:000298306700048
PM 21435468
ER
PT J
AU Tyler, DA
Parker, VA
AF Tyler, Denise A.
Parker, Victoria A.
TI Staff Teamwork in Long-Term Care Facilities The Influence of Management
Style, Training, and Feedback
SO RESEARCH IN GERONTOLOGICAL NURSING
LA English
DT Article
ID TURNOVER; EXPLORATION; PERFORMANCE; QUALITY; JOB
AB The purpose of this study was to describe the organizational factors associated with high and low amounts of teamwork among direct-care workers in long-term care (LTC) facilities. A systematic analysis of observation data collected at 20 LTC facilities was first used to categorize facilities as high-, moderate-, or low-teamwork facilities. Next, qualitative analysis of 59 interviews collected in 4 high-teamwork and 5 low-teamwork facilities was used to identify the organizational factors associated with high and low teamwork. Findings showed that high- and low-teamwork LTC facilities in this study differed in three organizational areas: management style, training, and feedback and recognition. As such, improved teamwork in LTC facilities may result from changes to basic management practices, such as training and employee feedback.
C1 [Tyler, Denise A.] Brown Univ, Ctr Gerontol & Hlth Care Res, Dept Community Hlth, Providence, RI 02912 USA.
[Parker, Victoria A.] Boston Univ, Sch Publ Hlth, Div Hlth Policy & Management, Boston, MA USA.
[Parker, Victoria A.] VA Boston Healthcare Syst, Ctr Org Leadership & Management Res, Boston, MA USA.
RP Tyler, DA (reprint author), Brown Univ, Ctr Gerontol & Hlth Care Res, Dept Community Hlth, Box G-S121-6, Providence, RI 02912 USA.
EM denise_tyler@brown.edu
FU Agency for Healthcare Research and Quality [1 R01 HS12031]; Commonwealth
Corporation
FX The authors disclose that they have no significant financial interests
in any product or class of products discussed directly or indirectly in
this activity. This research was supported by the Agency for Healthcare
Research and Quality (grant 1 R01 HS12031, Task Design, Motivation, and
Nursing Home Care Quality) and by the Commonwealth Corporation's Susan
Eaton Memorial Dissertation Fellowship.
NR 25
TC 4
Z9 4
U1 1
U2 3
PU SLACK INC
PI THOROFARE
PA 6900 GROVE RD, THOROFARE, NJ 08086 USA
SN 1940-4921
EI 1938-2464
J9 RES GERONTOL NURS
JI Res. Gerontol. Nurs.
PD APR
PY 2011
VL 4
IS 2
BP 135
EP 146
DI 10.3928/19404921-20100706-01
PG 12
WC Nursing
SC Nursing
GA 864YJ
UT WOS:000298276100007
PM 20669862
ER
PT J
AU Leong, JVB
Boro, MS
Winter, ME
AF Leong, Julie V. B.
Boro, Maureen S.
Winter, Michael E.
TI Determining vancomycin clearance in an overweight and obese population
SO AMERICAN JOURNAL OF HEALTH-SYSTEM PHARMACY
LA English
DT Article
DE Antibiotics; Dosage; Excretion; Hospitals; Methodology; Obesity;
Vancomycin; Weight
ID PHARMACOKINETIC PARAMETERS; CREATININE CLEARANCE; VETERANS; THERAPY
AB Purpose. Two methods of calculating vancomycin clearance were compared to determine the best body weight measure to use when dosing vancomycin for overweight and obese patients.
Methods. Hospitalized veterans weighing more than 120% of their ideal body weight (IBW) with serum vancomycin concentrations (SVCs) drawn between January 1, 2003, and June 30, 2005, were eligible for study inclusion. Exclusion criteria included weight of more than 300% the IBW, unstable renal function, dialysis, uncertain vancomycin dosing or sampling times, and distribution-phase sampling. Data from January 1 through December 31, 2003 (phase 1) determined the best-fit weight for vancomycin clearance for the Leonard and Boro method. The bias and precision of the modified Leonard and Boro method using the best-fit weight for vancomycin clearance were then compared with those of the Rushing and Ambrose method for predicting SVCs from January 1, 2004, through June 30, 2005 (phase 2).
Results. Forty-eight patients were included in phase 1, with 67 SVCs for analysis. During phase 1, adjusted body weight (ABW), using the Leonard and Boro method, was superior in predicting vancomycin clearance and the resultant SVCs.. A total of 96 patients were included in phase 2 of the study, with 160 SVCs for analysis. The modified Leonard and Boro method was significantly more precise than the Rushing and Ambrose method in predicting vancomycin clearance.
Conclusion. Use of ABW proved to be superior compared with total body weight when estimating vancomycin clearance in overweight and obese patients. While there was no difference in bias between methods, the modified Leonard and Boro method was significantly more precise than the Rushing and Ambrose method in predicting SVCs when dosing vancomycin for obese patients.
C1 [Boro, Maureen S.] San Francisco VA Med Ctr, Pharm Informat & Pharmacokinet Program, San Francisco, CA 94121 USA.
[Boro, Maureen S.; Winter, Michael E.] Univ Calif San Francisco, Sch Pharm, San Francisco, CA 94143 USA.
RP Boro, MS (reprint author), San Francisco VA Med Ctr, Pharm Informat & Pharmacokinet Program, 4150 Clement St, San Francisco, CA 94121 USA.
EM maureen.boro@va.gov
NR 21
TC 12
Z9 13
U1 2
U2 6
PU AMER SOC HEALTH-SYSTEM PHARMACISTS
PI BETHESDA
PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 USA
SN 1079-2082
J9 AM J HEALTH-SYST PH
JI Am. J. Health-Syst. Pharm.
PD APR 1
PY 2011
VL 68
IS 7
BP 599
EP 603
DI 10.2146/ajhp100410
PG 5
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 858CF
UT WOS:000297772800011
PM 21411801
ER
PT J
AU Steensma, DP
AF Steensma, David P.
TI ASH 2010 meeting report-Top 10 clinically-oriented abstracts in
myelodysplastic syndromes (MDS)
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Editorial Material
ID INTERNATIONAL WORKING GROUP; PROGNOSTIC SCORING SYSTEM; IRON
CHELATION-THERAPY; ANTITHYMOCYTE GLOBULIN; IMMUNOSUPPRESSIVE THERAPY;
DNA METHYLTRANSFERASE; PREDICTING SURVIVAL; RESPONSE CRITERIA; MYELOID
CANCERS; PHASE-II
AB The December 2010 American Society of Hematology (ASH) annual meeting in Orlando, Florida included more than 150 abstracts in the myelodysplastic syndromes (MDS) category. Thirty-six MDS-focused abstracts were presented in 6 oral sessions, and 120 additional abstracts were presented in 3 poster sessions. Although the 2010 ASH annual meeting included relatively little new MDS clinical trial data, with only one large randomized trial presented (the Intergroup E1905 study), it was an exciting conference from the standpoint of molecular discoveries in myeloid neoplasms, as various investigative groups presented results offering novel insights into MDS pathobiology, generated via high-throughput genomic sequencing and other innovative laboratory techniques. Here I summarize and discuss 10 MDS-related abstracts of special interest, which contain information that informs clinical practice. All 10 of these abstracts are published in full in the November 19, 2010 issue of Blood (volume 116, issue 21) and are identified here by their abstract number and title.
C1 Dana Farber Canc Inst, Div Hematol Malignancies, Boston, MA 02115 USA.
RP Steensma, DP (reprint author), Dana Farber Canc Inst, Div Hematol Malignancies, 44 Binney St,Suite D1B30, Boston, MA 02115 USA.
EM david_steensma@dfci.harvard.edu
OI Steensma, David/0000-0001-5130-9284
NR 67
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U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0361-8609
J9 AM J HEMATOL
JI Am. J. Hematol.
PD APR
PY 2011
VL 86
IS 4
BP 385
EP 391
DI 10.1002/ajh.21975
PG 7
WC Hematology
SC Hematology
GA 740JW
UT WOS:000288790200016
ER
PT J
AU Sano, M
Raman, R
Emond, J
Thomas, RG
Petersen, R
Schneider, LS
Aisen, PS
AF Sano, Mary
Raman, Rema
Emond, Jennifer
Thomas, Ronald G.
Petersen, Ronald
Schneider, Lon S.
Aisen, Paul S.
TI Adding Delayed Recall to the Alzheimer Disease Assessment Scale is
Useful in Studies of Mild Cognitive Impairment But Not Alzheimer Disease
SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS
LA English
DT Article
DE Alzheimer disease; mild cognitive impairment; Alzheimer Disease
Assessment Scale; delayed recall; clinical trial outcomes
ID CLINICAL-TRIALS; INSTRUMENTS; PLACEBO
AB Objective: To determine if the addition of delayed recall (DR) assessment adds sensitivity to the cognitive subscale of the Alzheimer Disease Assessment Scale (ADAS-cog) in clinical trials in mild cognitive impairment (MCI) and Alzheimer Disease (AD).
Background: Memory, particularly DR, is the most sensitive test for early detection of AD and MCI. However, it is not clear that assessment of DR adds benefit for measuring change over time after a diagnosis is made or in clinical trials. The ADAS-cog is the most commonly used tool to assess treatment efficacy in AD clinical trials. In an attempt to improve sensitivity to change, assessment of DR after the 3-trial, 10-word list was added to the standard 11-item ADAS-cog. We examined the added value of the DR in participants with MCI and AD followed for at least 1 year.
Design/Methods: Data from 111 subjects with AD and 259 subjects with MCI who were randomly assigned to the placebo arm of 2 clinical trials were included. Participants with AD had Mini-Mental State Examination scores of 13 to 27 and those with MCI had 24 to 30. We calculated the ADAS-cog11 score based on the original 11 items (range: best to worse, 0 to 70), the DR item score (range: 0 to 10 words not recalled), and the ADAS-cog12 (range: 0 to 80). We assessed the rate of missing items for DR over time, the change scores, the association between scores and baseline performance, and used longitudinal mixed effects regression models to examine the rate of change.
Results: At baseline AD subjects were near floor on DR (8.93 +/- 1.6 SD) and showed little change over 1 year (0.12 +/- 1.34); the MCI subjects baseline DR was 6.2 +/- 2.2 with 1-year change of 0.20 +/- 1.7. We compared standardized change (change/SD) for ADAS-cog11, and 12 in MCI and found a 10% improvement with ADAS-cog12; there was no improvement in the AD group. In a subset of MCI and AD cases with matching Mini-Mental State Examination (23 to 27), the ADAS-cog12 provided an 18% improvement in standardized change in MCI subjects, with no benefit in the AD cohort, primarily owing to increased variance.
Conclusions/Relevance: The addition of DR to the ADAS-cog score increased the ability to detect change in subjects with MCI over 1 year compared with the ADAS-cog11 but increased the variance in subjects with AD, even in those with mild impairment These findings speak to the need to tailor outcome measures to the specific study population and diagnosis for maximal efficiency and economy when conducting clinical trials.
C1 [Sano, Mary] James J Peters VAMC, Bronx, NY 10468 USA.
[Sano, Mary] Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA.
[Raman, Rema; Thomas, Ronald G.] UCSD, Dept Family & Prevent Med, La Jolla, CA USA.
[Raman, Rema; Thomas, Ronald G.] UCSD, Dept Neurosci, La Jolla, CA USA.
[Emond, Jennifer] UCSD, Alzheimers Dis Res Ctr, La Jolla, CA USA.
[Aisen, Paul S.] UCSD, Dept Neurosci, La Jolla, CA USA.
[Schneider, Lon S.] Univ So Calif, Keck Sch Med, Dept Psychiat, Los Angeles, CA 90033 USA.
[Schneider, Lon S.] Univ So Calif, Keck Sch Med, Dept Neurol, Los Angeles, CA 90033 USA.
[Petersen, Ronald] Mayo Clin, Dept Neurol, Rochester, MN USA.
RP Sano, M (reprint author), James J Peters VAMC, 130 W Kingsbridge Rd,Code 150,Room 1F01, Bronx, NY 10468 USA.
EM Mary.sano@mssm.edu
FU NIA [U01AG10483, AG005138, P50 AG05142]; California Alzheimer Disease
Center
FX Supported by the following NIA grants: U01AG10483 and AG005138, P50
AG05142, and California Alzheimer Disease Center Program.
NR 14
TC 12
Z9 12
U1 3
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0893-0341
J9 ALZ DIS ASSOC DIS
JI Alzheimer Dis. Assoc. Dis.
PD APR-JUN
PY 2011
VL 25
IS 2
BP 122
EP 127
DI 10.1097/WAD.0b013e3181f883b7
PG 6
WC Clinical Neurology; Pathology
SC Neurosciences & Neurology; Pathology
GA 766MR
UT WOS:000290787700004
PM 20921876
ER
PT J
AU Rathmell, JP
Michna, E
Fitzgibbon, DR
Stephens, LS
Posner, KL
Domino, KB
AF Rathmell, James P.
Michna, Edward
Fitzgibbon, Dermot R.
Stephens, Linda S.
Posner, Karen L.
Domino, Karen B.
TI Injury and Liability Associated with Cervical Procedures for Chronic
Pain
SO ANESTHESIOLOGY
LA English
DT Article
ID EPIDURAL STEROID INJECTIONS; SPINAL-CORD-INJURY; REGIONAL ANESTHESIA;
TRANSFORAMINAL INJECTION; INTERVENTIONAL TECHNIQUES; GENERAL-ANESTHESIA;
TASK-FORCE; NECK PAIN; COMPLICATIONS; POPULATION
AB Background: Prompted by an increase in interventional pain treatments performed at the level of the cervical spine, we investigated the characteristics and patterns of injury in malpractice claims collected from January 1, 2005 to December 31, 2008.
Methods: We compared claims arising from cervical pain treatments with all other chronic pain claims collected from the American Society of Anesthesiologists' closed claims database between 2005 and 2008. Claims for spinal cord injury underwent in-depth analysis for mechanisms of injury and use of sedation during the procedure.
Results: Claims related to cervical interventions represented 22% (64/294) of chronic pain treatment claims. Patients who underwent cervical procedures were healthier (American Society of Anesthesiologists' score, 1-2; P < 0.001) and were more often women (P = 0.011). Of the patients who underwent a cervical procedure, 59% experienced spinal cord damage compared with 11% of patients with other chronic pain (P < 0.001), with direct needle trauma as the predominant cause (31%). General anesthesia or sedation was used in 67% of cervical procedure claims associated with spinal cord injuries but in only 19% of cervical procedure claims not associated with spinal cord injuries (P < 0.001). Of the patients who underwent cervical procedures and had spinal cord injuries, 25% were nonresponsive during the procedure compared with 5% of the patients who underwent cervical procedures and did not have spinal cord injuries (P < 0.05, kappa = 0.52).
Conclusions: Injuries related to cervical interventional pain treatment were often severe and related to direct needle trauma to the spinal cord. Traumatic spinal cord injury was more common in patients who received sedation or general anesthesia and in those who were unresponsive during the procedure. Further studies are crucial to define the usefulness of cervical interventions and to improve their safety.
C1 [Rathmell, James P.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Pain Ctr, Div Pain Med, Boston, MA 02114 USA.
[Rathmell, James P.] Harvard Univ, Sch Med, Boston, MA USA.
[Michna, Edward] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Fitzgibbon, Dermot R.; Stephens, Linda S.; Posner, Karen L.; Domino, Karen B.] Univ Washington, Dept Anesthesiol & Pain Med, Seattle, WA 98195 USA.
RP Rathmell, JP (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Pain Ctr, Div Pain Med, 55 Fruit St,Gray Bigelow 444, Boston, MA 02114 USA.
EM jprathmell@partners.org
FU American Society of Anesthesiologists (ASA), Park Ridge, Illinois
FX Received from Massachusetts General Hospital, Boston, Massachusetts;
Brigham and Women's Hospital, Boston, Massachusetts; and the University
of Washington School of Medicine, Seattle, Washington. Submitted for
publication July 27, 2010. Accepted for publication December 27, 2010.
Supported in part by the American Society of Anesthesiologists (ASA),
Park Ridge, Illinois. All opinions expressed herein are those of the
authors and do not reflect the policy of the ASA.
NR 33
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Z9 35
U1 2
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-3022
J9 ANESTHESIOLOGY
JI Anesthesiology
PD APR
PY 2011
VL 114
IS 4
BP 918
EP 926
DI 10.1097/ALN.0b013e31820fc7f2
PG 9
WC Anesthesiology
SC Anesthesiology
GA 739DT
UT WOS:000288694400023
PM 21386702
ER
PT J
AU Kim, J
Artinyan, A
Mailey, B
Christopher, S
Lee, W
McKenzie, S
Chen, SL
Bhatia, S
Pigazzi, A
Garcia-Aguilar, J
AF Kim, Joseph
Artinyan, Avo
Mailey, Brian
Christopher, Stefanie
Lee, Wendy
McKenzie, Shaun
Chen, Steven L.
Bhatia, Smita
Pigazzi, Alessio
Garcia-Aguilar, Julio
TI An Interaction of Race and Ethnicity With Socioeconomic Status in Rectal
Cancer Outcomes
SO ANNALS OF SURGERY
LA English
DT Article
ID COLORECTAL-CANCER; AFRICAN-AMERICANS; TREATMENT DISPARITIES; RACIAL
DISPARITIES; UNITED-STATES; SURVIVAL; STAGE; POPULATION; CARCINOMA
AB Objective: Because appropriate rectal cancer care and subsequent outcomes can be influenced by several variables, our objective was to investigate how race, ethnicity, and socioeconomic status (SES) may impact rectal cancer outcomes.
Background: The management of rectal cancer requires a multidisciplinary approach utilizing medical and surgical subspecialties.
Methods: We performed an investigation of patients with rectal adenocarcinoma from Los Angeles County from 1988 to 2006 using the Los Angeles County Cancer Surveillance Program. Clinical and pathologic characteristics were compared among groups and overall survival was stratified by race/ethnicity and SES.
Results: Of 9504 patients with rectal cancer, 53% (n = 4999) were white, 10% black, 18% Hispanic, and 14% Asian. Stratified by race/ethnicity, Asians had the best overall survival followed by Hispanics, whites, and blacks (median survival 7.7 vs. 5.7, 5.5, and 3.4 years, respectively; P < 0.001). Stratified by SES group, the highest group had the best overall survival followed by middle and lowest groups (median survival 8.4 vs. 5.1 and 3.8 years, respectively, P < 0.001). Similar results were observed for surgical patients. On multivariate analysis, race/ethnicity, and SES remained independent predictors of overall survival in patients with rectal adenocarcinoma. Furthermore, interaction analysis indicated that the improved survival for select racial/ethnic groups was not dependent on SES classification.
Conclusions: Within the diverse Los Angeles County population, both race/ethnicity, and SES result in inequities in rectal cancer outcomes. Although SES may directly impact outcomes via access to care, the reasons for the association between race/ethnicity and outcomes remain uncertain.
C1 [Kim, Joseph; Mailey, Brian; Christopher, Stefanie; Lee, Wendy; McKenzie, Shaun; Pigazzi, Alessio; Garcia-Aguilar, Julio] Div Surg Oncol, Dept Surg, Duarte, CA 91010 USA.
[Artinyan, Avo] Baylor Coll Med, Michael E DeBakey Dept Surg, Houston, TX 77030 USA.
[Artinyan, Avo] Baylor Coll Med, Houston Hlth Serv, Houston, TX 77030 USA.
[Artinyan, Avo] Baylor Coll Med, Res Ctr Excellence, Michael E DeBakey Vet Affairs Med Ctr, Houston, TX 77030 USA.
[Chen, Steven L.] Univ Calif Davis, Dept Surg, Sacramento, CA 95817 USA.
[Bhatia, Smita] Dept Populat Sci, Duarte, CA USA.
RP Kim, J (reprint author), Div Surg Oncol, Dept Surg, 1500 E Duarte Rd, Duarte, CA 91010 USA.
EM jokim@coh.org
FU Houston VA HSR&D Center of Excellence [HFP90-020]
FX Supported in part by the Houston VA HSR&D Center of Excellence
(HFP90-020) for Dr. Avo Artinyan.
NR 20
TC 19
Z9 19
U1 2
U2 5
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 APR
PY 2011
VL 253
IS 4
BP 647
EP 654
DI 10.1097/SLA.0b013e3182111102
PG 8
WC Surgery
SC Surgery
GA 734VQ
UT WOS:000288368600003
PM 21475002
ER
PT J
AU Conrad, C
Podolsky, MJ
Cusack, JC
AF Conrad, Claudius
Podolsky, Michael J.
Cusack, James C.
TI Antiproteasomal agents in rectal cancer
SO ANTI-CANCER DRUGS
LA English
DT Article
DE antiproteasomal agents; chemotherapy; colorectal cancer;
radiosensitizing agent; ubiquitin-proteasome system
ID FACTOR-KAPPA-B; PROTEASOME INHIBITOR BORTEZOMIB; HUMAN COLON-CANCER;
EXTERNAL-BEAM RADIATION; SQUAMOUS-CELL CARCINOMA; ADVANCED SOLID TUMORS;
PHASE-I TRIAL; COLORECTAL-CANCER; BETA-CATENIN; MULTIPLE-MYELOMA
AB Colorectal cancer (CRC) is a prevalent and highly morbid condition. An improved understanding of the molecular pathogenesis of CRC in recent years has led to novel therapies complementing traditional chemotherapy, radiotherapy, and surgery. As in other cancers, it has become clear that the ubiquitin-proteasome system represents important cellular machinery that plays a complex role in the carcinogenesis of CRC, and may be a promising target for modulation in the treatment of CRC. In particular, there has been promise in targeting nuclear factor-kappa B and cell-cycle pathways in CRC through proteasome inhibition. Proteasome inhibition may be an important means of sensitizing cancers to traditional chemotherapy and radiotherapy through these pathways. In this review, we outline the basic science of the ubiquitin-proteasome system in CRC pathogenesis, highlight the use of proteasome inhibitors in cancers other than CRCs, and weigh the accumulating evidence and data, both preclinical and clinical, for the use of proteasome inhibition in CRC. Furthermore, we review the emerging evidence of proteasome inhibition as a possible radiosensitizing agent in rectal cancer and elucidate some possible future directions for this novel therapeutic option. Anti-Cancer Drugs 22: 341-350 (C) 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins.
C1 [Cusack, James C.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Surg,Surg Oncol Associates, Boston, MA 02114 USA.
RP Cusack, JC (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Surg,Surg Oncol Associates, 55 Fruit St,Yawkey 7B, Boston, MA 02114 USA.
EM jcusack@partners.org
NR 129
TC 5
Z9 6
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0959-4973
J9 ANTI-CANCER DRUG
JI Anti-Cancer Drugs
PD APR
PY 2011
VL 22
IS 4
BP 341
EP 350
DI 10.1097/CAD.0b013e328342fedb
PG 10
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 732OT
UT WOS:000288197400007
PM 21200315
ER
PT J
AU Wang, WL
Soslow, R
Hensley, M
Asad, H
Zannoni, GF
de Nictolis, M
Branton, P
Muzikansky, A
Oliva, E
AF Wang, Wei-Lien
Soslow, Robert
Hensley, Martee
Asad, Haider
Zannoni, Gian Franco
de Nictolis, Michele
Branton, Philip
Muzikansky, Alona
Oliva, Esther
TI Histopathologic Prognostic Factors in Stage I Leiomyosarcoma of the
Uterus: A Detailed Analysis of 27 Cases
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE uterus; leiomyosarcoma; stage I; age; tumor size; histologic subtypes;
cytologic atypia; tumor cell necrosis; mitotic rate; prognosis
ID SMOOTH-MUSCLE TUMORS; GYNECOLOGIC-ONCOLOGY-GROUP; UTERINE
LEIOMYOSARCOMA; MYXOID LEIOMYOSARCOMA; ADJUVANT CHEMOTHERAPY; TREATMENT
FAILURES; SARCOMAS; EXPRESSION; SURVIVAL; P53
AB Uterine leiomyosarcomas (Ut-LMSs) are aggressive tumors with an overall poor prognosis (15% to 25% 5-year survival rate). However, patients with stage I Ut-LMSs are reported to have a relatively better outcome when compared with the overall group with a 5-year survival rate ranging from 25% to 75%. The purpose of this study was to evaluate the histopathologic parameters that may impact outcome in stage I Ut-LMSs. Twenty-seven patients with stage I Ut-LMSs were identified from the files of 5 tertiary care hospitals between 1974 and 2006. Tumors were primarily staged based on pathologic information, supplemented with radiologic findings (10 cases) and clinical records (1 case). Patients with stage I tumors with no additional clinical or radiologic staging information were included in the study if no recurrence was documented after 6 months from the initial staging operation (16 cases). Clinicopathologic parameters that were statistically evaluated included age [mean, 54 y (37 to 73)], tumor size [mean, 9.5 cm (5.5 to 16)], cell type (17 spindled, 5 epithelioid, 2 myxoid, and 3 mixed), mitotic activity [mean count, 24 (4 to 69)/10 high-power fields], marked cytologic atypia (26 of 27 cases), tumor cell necrosis (12 of 27 cases), and lymphovascular invasion (6 of 27 cases). Follow-up was available for all the patients. Poor outcome was defined when patients either died of disease or were alive with disease. Overall, accounting for any length of follow-up, 16 of 27 (59%) patients with stage I Ut-LMSs had poor outcome; 7 died of disease (mean follow-up, 13 mo) and 9 were alive with disease (mean follow-up, 31 mo). The remaining 11 patients were alive and well with a mean follow-up of 48 months. However, at 2 years of follow-up by univariate analysis, only nonspindle morphology (P < 0.0183) and diffuse high-grade cytologic atypia (P < 0.02) were statistically associated with poor outcome. No statistically significant association with survival was identified by univariate analysis when evaluating mean age, count, or lymphovascular invasion. In conclusion, stage I leiomyosarcoma is associated with poor prognosis. No conclusive differences were observed among different clinicopathologic parameters and prognosis, although it seemed that spindle cell morphology and diffuse high-grade cytologic atypia were associated with longer overall survival and higher death rates, respectively.
C1 [Oliva, Esther] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Soslow, Robert; Hensley, Martee; Asad, Haider] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Zannoni, Gian Franco] Univ Cattolica, Rome, Italy.
[de Nictolis, Michele] Ist Anat & Istol Pathol, Ancona, Italy.
[Branton, Philip] Inova Fairfax Hosp, Church Falls, VA USA.
RP Oliva, E (reprint author), Massachusetts Gen Hosp, Dept Pathol, 55 Fruit St, Boston, MA 02114 USA.
EM eoliva@partners.org
OI Soslow, Robert/0000-0002-7269-5898
NR 71
TC 11
Z9 12
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0147-5185
EI 1532-0979
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD APR
PY 2011
VL 35
IS 4
BP 522
EP 529
DI 10.1097/PAS.0b013e31820ca624
PG 8
WC Pathology; Surgery
SC Pathology; Surgery
GA 736JT
UT WOS:000288491600007
PM 21383611
ER
PT J
AU Richler, JJ
Cheung, OS
Gauthier, I
AF Richler, Jennifer J.
Cheung, Olivia S.
Gauthier, Isabel
TI Holistic Processing Predicts Face Recognition
SO PSYCHOLOGICAL SCIENCE
LA English
DT Article
DE face perception; individual differences; holistic processing
ID SPATIAL-FREQUENCIES; OBJECT RECOGNITION; PERCEPTION; EXPERTISE; CHILDREN
AB The concept of holistic processing is a cornerstone of face-recognition research. In the study reported here, we demonstrated that holistic processing predicts face-recognition abilities on the Cambridge Face Memory Test and on a perceptual face-identification task. Our findings validate a large body of work that relies on the assumption that holistic processing is related to face recognition. These findings also reconcile the study of face recognition with the perceptual-expertise work it inspired; such work links holistic processing of objects with people's ability to individuate them. Our results differ from those of a recent study showing no link between holistic processing and face recognition. This discrepancy can be attributed to the use in prior research of a popular but flawed measure of holistic processing. Our findings salvage the central role of holistic processing in face recognition and cast doubt on a subset of the face-perception literature that relies on a problematic measure of holistic processing.
C1 [Richler, Jennifer J.] Vanderbilt Univ, Dept Psychol, Nashville, TN 37240 USA.
[Cheung, Olivia S.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Martinos Ctr, Cambridge, MA 02138 USA.
RP Richler, JJ (reprint author), Vanderbilt Univ, Dept Psychol, 301 Wilson Hall,111 21st Ave S, Nashville, TN 37240 USA.
EM jennifer.j.richler@vanderbilt.edu
OI Gauthier, Isabel/0000-0002-6249-4769
FU NEI NIH HHS [P30 EY008126, P30-EY008126, R01 EY013441, R01
EY013441-06A2, R01 EY013441-08]
NR 30
TC 117
Z9 119
U1 5
U2 56
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0956-7976
J9 PSYCHOL SCI
JI Psychol. Sci.
PD APR
PY 2011
VL 22
IS 4
BP 464
EP 471
DI 10.1177/0956797611401753
PG 8
WC Psychology, Multidisciplinary
SC Psychology
GA 817WZ
UT WOS:000294709000009
PM 21393576
ER
PT J
AU Safren, SA
Blashill, AJ
O'Cleirigh, CM
AF Safren, Steven A.
Blashill, Aaron J.
O'Cleirigh, Conall M.
TI Promoting the Sexual Health of MSM in the Context of Comorbid Mental
Health Problems
SO AIDS AND BEHAVIOR
LA English
DT Article
DE Men who have sex with men; MSM; Syndemics; HIV prevention; Mental health
ID HIV BEHAVIORAL INTERVENTIONS; RISK BEHAVIOR; PSYCHIATRIC-DISORDERS;
COGNITIVE MODEL; UNITED-STATES; DEPRESSION; ADULTS; TRANSMISSION;
CHILDHOOD; PEOPLE
AB Despite the moderate efficacy of HIV prevention interventions for at risk gay, bisexual, and other men who have sex with men (MSM), MSM continue to represent the largest group of new HIV infections and the largest number of individuals living with HIV in the US. Environmental factors such as sexual minority stress increase the vulnerability of MSM for mental health problems. These mental health problems can be a barrier to consistently engaging in self-care health behaviors such as sexual risk reduction. We consider the following observations critical to identifying priorities for HIV prevention among MSM: (1) gay, bisexual and other MSM have higher rates of mental health problems than general population estimates; (2) these mental health problems co-occur with each other and interact synergistically to increase HIV risk; and (3) comorbid mental health problems may compromise the impact of prevention programs, and integrating treatment of mental health issues into prevention programs may improve program efficacy. Novel prevention interventions for at risk MSM that integrate programming with the treatment of co-occurring and interfering mental health issues are the most promising avenue to increase prevention intervention efficacy and effectiveness. By addressing significant mental health issues and supporting broad based prevention efforts at the individual and community level, there is also the potential to improve the overall quality of life and public mental health of gay, bisexual, and other MSM.
C1 [Safren, Steven A.; Blashill, Aaron J.; O'Cleirigh, Conall M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Safren, Steven A.; Blashill, Aaron J.; O'Cleirigh, Conall M.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Safren, Steven A.; O'Cleirigh, Conall M.] Fenway Community Hlth, Boston, MA USA.
[Blashill, Aaron J.] St Louis Univ, St Louis, MO 63103 USA.
RP Safren, SA (reprint author), Massachusetts Gen Hosp, 1 Bowdoin Sq,7th Floor, Boston, MA 02114 USA.
EM ssafren@partners.org
FU NIMH NIH HHS [5R34MH081760, MH084757, R01 MH084757, R34 MH081760]
NR 47
TC 25
Z9 25
U1 1
U2 9
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1090-7165
J9 AIDS BEHAV
JI AIDS Behav.
PD APR
PY 2011
VL 15
SU 1
BP S30
EP S34
DI 10.1007/s10461-011-9898-x
PG 5
WC Public, Environmental & Occupational Health; Social Sciences, Biomedical
SC Public, Environmental & Occupational Health; Biomedical Social Sciences
GA 814EG
UT WOS:000294428800005
PM 21331799
ER
PT J
AU Vance, DE
Eagerton, G
Harnish, B
McKie, P
Fazeli, PL
AF Vance, David E.
Eagerton, Greg
Harnish, Brenna
McKie, Peggy
Fazeli, Pariya L.
TI Cognitive Prescriptions: A Nursing Approach to Increasing Cognitive
Reserve
SO JOURNAL OF GERONTOLOGICAL NURSING
LA English
DT Article
ID OLDER-ADULTS; TAXI DRIVERS; NEUROPLASTICITY; INTERVENTION; NEUROGENESIS;
DEMENTIA; PROTECT; NUTRITION; BEHAVIOR; LIFE
AB Nonpathological cognitive declines occur with aging and negatively affect everyday functioning and reduce quality of life. Many older adults, aware of such cognitive changes, seek ways to bolster their cognitive functioning. Evidence based on the cognitive aging literature supports a number of factors associated with cognitive functioning. These factors include physical exercise, intellectual exercise, nutrition, sleep hygiene, social interaction, and mood and emotional state. These factors can be manipulated and woven together by nurses and other health professionals to develop an easy-to-use, non-invasive cognitive prescription for improving the cognitive health of older adults. An example and directions for developing and implementing cognitive prescriptions are described.
C1 [Vance, David E.; Harnish, Brenna] Univ Alabama, Sch Nursing, Birmingham, AL 35294 USA.
[McKie, Peggy] Univ Alabama, Dept Pathol, Birmingham, AL 35294 USA.
[Fazeli, Pariya L.] Univ Alabama, Dept Psychol, Birmingham, AL 35294 USA.
[Fazeli, Pariya L.] Univ Alabama, Ctr Res Appl Gerontol, Birmingham, AL 35294 USA.
[Eagerton, Greg] Birmingham Vet Affairs Med Ctr, Birmingham, AL USA.
RP Vance, DE (reprint author), Univ Alabama, Sch Nursing, Room 456,1701 Univ Blvd, Birmingham, AL 35294 USA.
EM devance@uab.edu
RI AUDIFFREN, MICHEL/H-5649-2011;
OI Vance, David/0000-0002-0498-6263
FU University of Alabama at Birmingham Edward R. Roybal Center [2 P30
AG022838-06]
FX Dr. Vance, Dr. Eagerton, Ms. Harnish, Ms. McKie, and Ms. Fazeli disclose
that they have no significant financial interests in any product or
class of products discussed directly or indirectly in this activity.
This article was written with partial support from the University of
Alabama at Birmingham Edward R. Roybal Center for Translational Research
on Aging and Mobility Project (grant 2 P30 AG022838-06).
NR 37
TC 18
Z9 18
U1 1
U2 7
PU SLACK INC
PI THOROFARE
PA 6900 GROVE RD, THOROFARE, NJ 08086 USA
SN 0098-9134
J9 J GERONTOL NURS
JI J. Gerontol. Nurs.
PD APR
PY 2011
VL 37
IS 4
BP 22
EP 29
DI 10.3928/00989134-20101202-03
PG 8
WC Geriatrics & Gerontology; Gerontology; Nursing
SC Geriatrics & Gerontology; Nursing
GA 811WW
UT WOS:000294249700006
PM 21175110
ER
PT J
AU Corcoran, RB
Settleman, J
Engelman, JA
AF Corcoran, Ryan B.
Settleman, Jeffrey
Engelman, Jeffrey A.
TI Potential Therapeutic Strategies to Overcome Acquired Resistance to BRAF
or MEK Inhibitors in BRAF Mutant Cancers
SO ONCOTARGET
LA English
DT Article
DE BRAF; MEK; acquired resistance; melanoma; colorectal cancer; NRAS;
IGF1R; PDGFR
ID SMALL-CELL LUNG; B-RAF; METASTATIC MELANOMA; AZD6244 ARRY-142886;
MEDIATES RESISTANCE; KINASE INHIBITORS; PHASE-II; BCR-ABL; MUTATION;
PATHWAY
AB Recent clinical trials with selective inhibitors of the BRAF and MEK kinases have shown promising results in patients with tumors harboring BRAF V600 mutations. However, as has been observed previously with similarly successful targeted therapies, acquired resistance to these agents is an emerging problem that limits their clinical benefit. Several recent studies from our laboratory and others have investigated the causes of acquired resistance to BRAF and MEK inhibitors, and multiple resistance mechanisms have been identified. Here, we review these mechanisms and suggest that they can be broadly grouped into two main classes: ERK-dependent and ERK-independent. We also propose distinct therapeutic strategies that might be employed to overcome each class of acquired resistance.
C1 [Corcoran, Ryan B.; Engelman, Jeffrey A.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02129 USA.
[Corcoran, Ryan B.; Engelman, Jeffrey A.] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[Settleman, Jeffrey] Genentech Inc, San Francisco, CA 94080 USA.
RP Engelman, JA (reprint author), Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02129 USA.
EM jengelman@partners.org
NR 54
TC 67
Z9 69
U1 0
U2 9
PU IMPACT JOURNALS LLC
PI ALBANY
PA 6211 TIPTON HOUSE, STE 6, ALBANY, NY 12203 USA
SN 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD APR
PY 2011
VL 2
IS 4
BP 336
EP 346
PG 11
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 802KM
UT WOS:000293509600013
PM 21505228
ER
PT J
AU Coopey, SB
Buckley, J
Smith, BL
Hughes, K
Gadd, M
Specht, M
AF Coopey, Suzanne Brooks
Buckley, Julliette
Smith, Barbara Lynn
Hughes, Kevin
Gadd, Michele
Specht, Michelle
TI Lumpectomy Cavity Shaved Margins Do Not Impact Re-Excision Rates
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 12th Annual Meeting of the American-Society-of-Breast-Surgeons
CY APR 27-MAY 01, 2011
CL Washington, DC
SP Amer Soc Breast Surg
C1 [Coopey, Suzanne Brooks; Buckley, Julliette; Smith, Barbara Lynn; Hughes, Kevin; Gadd, Michele; Specht, Michelle] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
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 APR
PY 2011
VL 18
SU 2
BP S154
EP S154
PG 1
WC Oncology; Surgery
SC Oncology; Surgery
GA 791HP
UT WOS:000292656100005
ER
PT J
AU Dominici, L
Lester, S
Guo, LF
Specht, M
Smith, B
Golshan, M
AF Dominici, Laura
Lester, Susan
Guo, Lifei
Specht, Michelle
Smith, Barbara
Golshan, Mehra
TI Modern Surgical Approach to Paget Disease
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Meeting Abstract
CT 12th Annual Meeting of the American-Society-of-Breast-Surgeons
CY APR 27-MAY 01, 2011
CL Washington, DC
SP Amer Soc Breast Surg
C1 [Dominici, Laura; Lester, Susan; Guo, Lifei; Golshan, Mehra] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Specht, Michelle; Smith, Barbara] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
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 APR
PY 2011
VL 18
SU 2
BP S167
EP S167
PG 1
WC Oncology; Surgery
SC Oncology; Surgery
GA 791HP
UT WOS:000292656100038
ER
PT J
AU Church, EC
Mauldin, PD
Bosso, JA
AF Church, E. Chandler
Mauldin, Patrick D.
Bosso, John A.
TI Antibiotic Resistance in Pseudomonas aeruginosa Related to Quinolone
Formulary Changes: An Interrupted Time Series Analysis
SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY
LA English
DT Editorial Material
ID STAPHYLOCOCCUS-AUREUS; RATES; SUSCEPTIBILITY
C1 [Church, E. Chandler; Mauldin, Patrick D.; Bosso, John A.] S Carolina Coll Pharm, Dept Pharm & Clin Sci, Charleston, SC 29425 USA.
[Mauldin, Patrick D.] S Carolina Coll Pharm, Ctr Medicat Safety, Charleston, SC 29425 USA.
[Mauldin, Patrick D.] Ralph H Johnson VA Med Ctr, Charleston, SC USA.
[Bosso, John A.] Med Univ S Carolina, Dept Med, Coll Med, Charleston, SC USA.
RP Bosso, JA (reprint author), S Carolina Coll Pharm, Dept Clin Pharm & Outcome Sci, Med Univ S Carolina Campus, Charleston, SC 29425 USA.
EM bossoja@musc.edu
NR 10
TC 2
Z9 2
U1 0
U2 1
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 0899-823X
J9 INFECT CONT HOSP EP
JI Infect. Control Hosp. Epidemiol.
PD APR
PY 2011
VL 32
IS 4
BP 400
EP 402
DI 10.1086/659157
PG 5
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA 790UO
UT WOS:000292614900015
PM 21460495
ER
PT J
AU Pandolfi, F
Cianci, R
Casciano, F
Pagliari, D
De Pasquale, T
Landolfi, R
Di Sante, G
Kurnick, JT
Ria, F
AF Pandolfi, F.
Cianci, R.
Casciano, F.
Pagliari, D.
De Pasquale, T.
Landolfi, R.
Di Sante, G.
Kurnick, J. T.
Ria, F.
TI SKEWED T-CELL RECEPTOR REPERTOIRE: MORE THAN A MARKER OF MALIGNANCY, A
TOOL TO DISSECT THE IMMUNOPATHOLOGY OF INFLAMMATORY DISEASES
SO JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS
LA English
DT Editorial Material
DE T-cell receptor; solid tumors melanoma; auto immune diseases; skewed TCR
repertoire; spectratyping; rheumatoid arthritis
ID ACTIVE ANTIRETROVIRAL THERAPY; GRANULAR LYMPHOCYTE LEUKEMIA; MYELIN
BASIC-PROTEIN; RHEUMATOID-ARTHRITIS; MULTIPLE-SCLEROSIS;
PERIPHERAL-BLOOD; SYNOVIAL-FLUID; THYMIC OUTPUT; INFILTRATING
LYMPHOCYTES; OLIGOCLONAL EXPANSION
AB The highly diverse heterodimeric surface T cell receptor (TCR) gives the T lymphocyte its specificity for MHC-bound peptides needed to initiate antigen-recognition. In normal peripheral blood, spleen and lymph nodes, the TCR repertoire of the T lymphocytes is usually polyclonal. However, in malignancies such as leukemias, as well as in lymphoproliferative diseases of mature T cells, the TCR is a reflection of the clonality of the malignant cells and is therefore monoclonal. Several clinical conditions (mainly solid tumors and autoimmune diseases) have been described where the TCR repertoire is restricted. The ability to demonstrate clonal TCR usage provides a useful tool to dissect the immunopathology of inflammatory diseases. In this review we discuss these findings and propose to sub-divide diseases with restricted TCR repertoire into a group of conditions in which there is a known TCR ligand, as opposed to diseases in which the restricted TCR repertoire is the result of impaired T-cell development. This classification sheds light on the pathogenesis of several inflammatory diseases.
C1 [Ria, F.] Univ Cattolica, Ist Patol Gen, I-00168 Rome, Italy.
[Pandolfi, F.; Cianci, R.; Casciano, F.; Pagliari, D.; De Pasquale, T.; Landolfi, R.] Univ Cattolica, Dept Internal Med, I-00168 Rome, Italy.
[Kurnick, J. T.] Harvard Univ, Sch Med, Boston, MA USA.
[Kurnick, J. T.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Ria, F (reprint author), Univ Cattolica, Ist Patol Gen, Largo F Vito 1, I-00168 Rome, Italy.
EM fria@rm.unicatt.it
RI Casciano, Fabio/H-3219-2015; Di Sante, Gabriele/K-8629-2016;
OI Di Sante, Gabriele/0000-0001-6608-3388; Casciano,
Fabio/0000-0002-6431-3335
NR 60
TC 13
Z9 13
U1 1
U2 5
PU BIOLIFE SAS
PI SILVA MARINA (TE)
PA VIA S STEFANO 39 BIS, 64029 SILVA MARINA (TE), ITALY
SN 0393-974X
J9 J BIOL REG HOMEOS AG
JI J. Biol. Regul. Homeost. Agents
PD APR-JUN
PY 2011
VL 25
IS 2
BP 153
EP 161
PG 9
WC Endocrinology & Metabolism; Immunology; Medicine, Research &
Experimental; Physiology
SC Endocrinology & Metabolism; Immunology; Research & Experimental
Medicine; Physiology
GA 793VS
UT WOS:000292852600002
PM 21880203
ER
PT J
AU Conti, CM
Fulcheri, M
Anogeianaki, A
Maccauro, G
Tete, S
Salini, V
Tripidi, D
Toniato, E
Caraffa, A
Antionolfi, P
Galzio, R
Neri, G
Pandolfi, F
Doyle, R
AF Conti, C. M.
Fulcheri, M.
Anogeianaki, A.
Maccauro, G.
Tete, S.
Salini, V.
Tripidi, D.
Toniato, E.
Caraffa, A.
Antionolfi, P.
Galzio, R.
Neri, G.
Pandolfi, F.
Doyle, R.
TI PSYCHOLOGICAL STRESS AND VITAMINS
SO JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS
LA English
DT Editorial Material
DE stress; vitamins
ID ENDOTHELIAL GROWTH-FACTOR; RHEUMATOID-ARTHRITIS; SIGNALING PATHWAYS;
CELLS; ASSOCIATION; DEPRESSION; CHILDREN; THERAPY; SYSTEM; INFLAMMATION
AB Conditions of stress and anxiety have complex interactions with insufficient vitamin intake and malnutrition. This study, based on literature research in Medline, analyzes the inter-relationship between vitamins and stress. This report concerns a number of vitamins that have been receiving much attention in earlier reviews of the literature, for their potential to protect against stress-related events, and focus is placed upon recent findings.
C1 [Conti, C. M.; Fulcheri, M.] Univ G dAnnunzio, Dept Clin Psychol, Chieti, Italy.
[Anogeianaki, A.] Aristotle Univ Thessaloniki, Sch Med, Dept Physiol, Thessaloniki, Greece.
[Maccauro, G.] Univ Cattolica Sacro Cuore, Dept Orthopaed, Rome, Italy.
[Tete, S.; Tripidi, D.] Univ G dAnnunzio, Sch Dent, Chieti, Italy.
[Salini, V.] Univ G dAnnunzio, Orthopaed Div, Chieti, Italy.
[Toniato, E.] Univ G dAnnunzio, Div Immunol, Chieti, Italy.
[Caraffa, A.; Antionolfi, P.] Univ Perugia, Orthopaed Div, I-06100 Perugia, Italy.
[Galzio, R.] Univ Aquila, Dept Hlth Sci, I-67100 Laquila, Italy.
[Neri, G.] Univ G dAnnunzio, ENT Div, Chieti, Italy.
[Pandolfi, F.] Univ Cattolica Sacro Cuore, Dept Internal Med, Rome, Italy.
[Doyle, R.] Massachusetts Gen Hosp, Dept Pediat Psychopharmacol, Boston, MA 02114 USA.
RP Conti, CM (reprint author), Gabriele dAnnunzio Univ, Dept Clin Psychol, Via Vestini, I-66013 Chieti, Italy.
RI Galzio, Renato/I-4826-2012;
OI Galzio, Renato/0000-0003-1933-1355; Fulcheri, Mario/0000-0002-2389-9800;
MACCAURO, Giulio/0000-0002-7359-268X
NR 64
TC 4
Z9 4
U1 0
U2 3
PU BIOLIFE SAS
PI SILVA MARINA (TE)
PA VIA S STEFANO 39 BIS, 64029 SILVA MARINA (TE), ITALY
SN 0393-974X
J9 J BIOL REG HOMEOS AG
JI J. Biol. Regul. Homeost. Agents
PD APR-JUN
PY 2011
VL 25
IS 2
BP 163
EP 168
PG 6
WC Endocrinology & Metabolism; Immunology; Medicine, Research &
Experimental; Physiology
SC Endocrinology & Metabolism; Immunology; Research & Experimental
Medicine; Physiology
GA 793VS
UT WOS:000292852600003
PM 21880204
ER
EF