FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Gordon, A
Fiellin, D
Friedmann, P
Gourevitch, M
Kraemer, K
Arnsten, J
Saitz, R
AF Gordon, Adam J.
Fiellin, David A.
Friedmann, Peter D.
Gourevitch, Marc N.
Kraemer, Kevin L.
Arnsten, Julia H.
Saitz, Richard
CA Soc Gen Internal Med Subst Abuse
TI Update in Addiction Medicine for the Primary Care Clinician
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE substance-related disorders; primary health care; review literature
ID RANDOMIZED CONTROLLED-TRIAL; ALCOHOL-USE DISORDERS; SELF-HELP GROUPS;
OUTCOMES; BUPRENORPHINE; TOPIRAMATE; DEPENDENCE; ADULTS; AUDIT; ABUSE
C1 [Gordon, Adam J.] Univ Pittsburgh, Sch Med, VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA 15206 USA.
[Gordon, Adam J.] VA Pittsburgh Healthcare Syst, Mental Illness Res Educ & Clin Ctr, Pittsburgh, PA USA.
[Gordon, Adam J.; Kraemer, Kevin L.] Univ Pittsburgh, Ctr Res Hlth Care, Pittsburgh, PA USA.
[Fiellin, David A.] Yale Univ, Sch Med, New Haven, CT USA.
[Friedmann, Peter D.] Brown Univ, Alpert Med Sch, Rhode Isl Hosp,Div Gen Internal Med, Providence VA Med Ctr,Ctr Syst Outcomes & Qual Ch, Providence, RI 02912 USA.
[Gourevitch, Marc N.] NYU, Sch Med, New York, NY USA.
[Arnsten, Julia H.] Albert Einstein Coll Med, New York, NY USA.
[Arnsten, Julia H.] Montefiore Med Ctr, New York, NY USA.
[Saitz, Richard] Boston Med Ctr, Gen Internal Med Sect, CARE Unit, Boston, MA USA.
[Saitz, Richard] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Saitz, Richard] Boston Univ, Sch Publ Hlth, Youth Alcohol Prevent Ctr, Boston, MA 02215 USA.
[Saitz, Richard] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02215 USA.
RP Gordon, A (reprint author), Univ Pittsburgh, Sch Med, VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Mailcode 151-C-H,7180 Highland Dr 151 C-H, Pittsburgh, PA 15206 USA.
EM adam.gordon@va.gov
OI Fiellin, David/0000-0002-4006-010X; Gourevitch,
Marc/0000-0001-6865-2126; /0000-0002-2535-1427
FU Society of General Internal Medicine's Substance Abuse Interest Group
FX All authors are members of the Society of General Internal Medicine's
Substance Abuse Interest Group to which we are deeply indebted for its
support. The authors also wish to thank Margaret Krumm for her
contributions of coordinating the review and editing this paper.
NR 27
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U1 1
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 DEC
PY 2008
VL 23
IS 12
BP 2112
EP 2116
DI 10.1007/s11606-008-0806-7
PG 5
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 379VJ
UT WOS:000261424000026
PM 18830761
ER
PT J
AU Kadzielski, J
Malhotra, LR
Zurakowski, D
Lee, SGP
Jupiter, JB
Ring, D
AF Kadzielski, John
Malhotra, Leah R.
Zurakowski, David
Lee, Sang-Gil P.
Jupiter, Jesse B.
Ring, David
TI Evaluation of Preoperative Expectations and Patient Satisfaction After
Carpal Tunnel Release
SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME
LA English
DT Article
DE Carpal tunnel syndrome; patient expectations; outcome
ID TOTAL HIP-ARTHROPLASTY; IDIOPATHIC ARM PAIN; REPLACEMENT SURGERY;
BREAST-CANCER; KNEE SURGERY; OUTCOMES; HEALTH; OPTIMISM; PREDICT;
OSTEOARTHRITIS
AB Purpose We tested the hypothesis that preoperative expectations affect postoperative satisfaction and arm-specific, self-reported health Status after elective carpal tunnel release.
Methods Forty-nine patients having elective carpal tunnel release completed questionnaires evaluating self-rated upper extremity-specific disability using the Disabilities of the Arm Shoulder and Hand (DASH) questionnaire, expectations regarding surgery (Preop Expectations Score), personal importance of: upper-extremity function, measures of general optimism.. the Life Orientation Test (LOT), as well as health-specific optimism, and the Multidimensional Health Locus Of Control scale. Six months after surgery, patients completed a 10-point Likert scale to assess satisfaction, the DASH, and measures determining (1) fulfillment of expectations (Postop Met Expectations Score) and (2) relief of specific systems (Postop Help Score).
Results The DASH scores decreased significantly from an average of 37 points before surgery to an average of 15 points 6 months after carpal tunnel release (p <.001), and patients rated their satisfaction (mean +/- standard deviation) as 8 +/- 3. Preoperative expectations did not correlate with patient satisfaction or postoperative DASH scores. Multivariable analyses determined that patient satisfaction was best predicted by fulfillment of expectations (Postop Help Score alone, accounting for 41% of the variance in scores) and postoperative DASH scores were predicted by a combination of Postop Met Expectations Score and the LOT score (accounting for 31% of the variance in scores).
Conclusions As measured in this Study, the strongest predictor of satisfaction after carpal tunnel release was relief of symptoms, and the strongest predictors of postoperative disability were met expectations and optimism; however, the majority of the variance in postoperative satisfaction remains unexplained. (J Hand Surg 2008;33A:1783-1788. Copyright (c) 2008 by the American Society for Surgery of the Hand. All rights reserved.)
C1 [Ring, David] Massachusetts Gen Hosp, Dept Orthopaed Surg, Hand & Upper Extrem Serv, Boston, MA 02114 USA.
Childrens Hosp, Dept Orthoped Surg, Boston, MA 02115 USA.
RP Ring, D (reprint author), Massachusetts Gen Hosp, Dept Orthopaed Surg, Hand & Upper Extrem Serv, 55 Fruit St,YAW 2, Boston, MA 02114 USA.
EM dring@partners.org
NR 44
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U1 1
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0363-5023
J9 J HAND SURG-AM
JI J. Hand Surg.-Am. Vol.
PD DEC
PY 2008
VL 33A
IS 10
BP 1783
EP 1788
DI 10.1016/j.jhsa.2008.06.019
PG 6
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 388FT
UT WOS:000262006400014
PM 19084178
ER
PT J
AU Watson, J
Ring, D
AF Watson, Jeffrey
Ring, David
TI Influence of Psychological Factors on Grip Strength
SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME
LA English
DT Article
DE Depression; grip strength; performance-based; psychological distress;
upper extremity
ID PAIN CATASTROPHIZING SCALE; IDIOPATHIC ARM PAIN; DEPRESSIVE SYMPTOMS;
PHYSICAL FUNCTION; NORMATIVE DATA; OLDER PERSONS; HEALTH-STATUS;
PERFORMANCE; HAND; MEN
AB Purpose Grip strength is widely used to assess upper-extremity function. Although grip strength is a quantitative measure of function. gogrip strength is a reflection of both physical irnpaimient as well as subjective. psychological factors. We investigated the detern- nants of grip strength with the hypothesis that psychological factors are associated with diminished girp strength.
Methods One hundred thirty-four patients with an isolated, discrete upper-extremity condition had grip strength measurements, and, as part of one of several prospective clinical studies, during the same visit they completed 2 or more of the following surveys: the Center for Epidemlologic C Studies-Depression (CES-D) scale, Pain Anxiety Symptoms Scale, and Pain Catastrophizing Scale. Univariate and multivariable statistical analysis sought determinants of absolute grip strength and grip strength as a percentage of the opposite, uninvolved limb.
Results Determinants of absolute grip strength included gender and grip strength of the uninvolved limb. The association between CES-D score and absolute grip strength was near significant but very weak. Multivariable regression analysis produced a best-fit model that retained grip strength of the uninvolved limb and CES-D scores. When grip strength of the involved limb was evaluated as percentage of grip strength of the uninvolved limb, CES-D score was a weak but significant predictor, and patients recovering from a fracture of the distal radius had weaker grip strength than did patients with nontraumatic conditions.
Conclusions Depression scores were minimally associated with diminished grip strength. Psychological factors appear to affect disability (patient-reported health status) more than they affect performance-based measures of function. (J Hand Surg 2008;33A:1791-1795. Copyright (c) 2008 by the American Society for Surgery of the Hand. All rights reserved.)
C1 [Ring, David] Massachusetts Gen Hosp, Orthopaed Hand & Upper Extrem Serv, Yawkey Ctr, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Ring, D (reprint author), Massachusetts Gen Hosp, Orthopaed Hand & Upper Extrem Serv, Yawkey Ctr, Suite 2100,55 Fruit St, Boston, MA 02114 USA.
EM dring@partners.org
NR 33
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U1 3
U2 10
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0363-5023
J9 J HAND SURG-AM
JI J. Hand Surg.-Am. Vol.
PD DEC
PY 2008
VL 33A
IS 10
BP 1791
EP 1795
DI 10.1016/j.jhsa.2008.07.006
PG 5
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 388FT
UT WOS:000262006400016
PM 19084180
ER
PT J
AU Kong, BS
Kim, YJ
Suh, YS
Jawa, A
Nazzal, A
Lee, SG
AF Kong, Byeong Seon
Kim, Yong Jin
Suh, Young Suk
Jawa, Andrew
Nazzal, Adam
Lee, Sang Gil
TI Finger Soft Tissue Reconstruction Using Arterialized Venous Free Flaps
Having 2 Parallel Veins
SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME
LA English
DT Article
DE Arterialized venous free flap; finger; two parallel veins
ID SKIN DEFECTS; CLINICAL-APPLICATIONS; HAND
AB Purpose Arterialized venous free flaps with a single straight venous axis may require redirection of either the efferent or affere vein for anastornosis to the digital vessels. To simplify these flaps, the authors propose use of an arterialized venous free flap having 2 parallel veins that does not require redirection of the veins.
Methods The authors performed 44 arterialized venous free flaps having 2 parallel veins for the reconstruction of digital soft tissue defects. The mean area of coverage was 6.5 cm(2). The donor sites included the volar aspect of the distal forearm in 35 cases, the thenar area in 8 cases, and the dorsal aspect of the foot in 1 case.
Results Thirty-nine of the 44 flaps survived. Complete flap necrosis occurred in 5 cases, and flap congestion was seen in 28 cases.
Conclusions The authors had satisfactory results using arterialized venous free flaps having 2 parallel veins. By using these flaps, the authors were able to simplify the technique of arterialized venous flaps. (J Hand Surg 2008;33A: 1802-1806. (c) 2008 Published by Elsevier Inc. on behalf of the American Society for Surgery of the Hand.)
C1 [Kong, Byeong Seon] Busan Centum Hosp, Dept Orthoped Surg, Hand & Microsurg Ctr, Pusan, South Korea.
Massachusetts Gen Hosp, Dept Orthopaed Surg, Hand & Upper Extrem Serv, Boston, MA 02114 USA.
RP Kong, BS (reprint author), Busan Centum Hosp, Dept Orthoped Surg, Hand & Microsurg Ctr, 1077-1 Kwangan 3 Dong Suyoung Gu, Pusan, South Korea.
EM gongja2000@yahoo.co.kr
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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 0363-5023
J9 J HAND SURG-AM
JI J. Hand Surg.-Am. Vol.
PD DEC
PY 2008
VL 33A
IS 10
BP 1802
EP 1806
DI 10.1016/j.jhsa.2008.08.001
PG 5
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 388FT
UT WOS:000262006400018
PM 19084182
ER
PT J
AU Souer, JS
Mudgal, CS
AF Souer, J. S.
Mudgal, C. S.
TI PLATE FIXATION IN CLOSED IPSILATERAL MULTIPLE METACARPAL FRACTURES
SO JOURNAL OF HAND SURGERY-EUROPEAN VOLUME
LA English
DT Article
DE closed; multiple; metacarpal fractures; plating
ID PHALANGEAL FRACTURES; HAND; COMPLICATIONS; FINGERS; SCREWS; SHAFT
AB Closed multiple metacarpal fractures are uncommon. They are usually associated with significant soft tissue swelling. Early stable fixation and functional rehabilitation optimises outcome. We present a review of 19 patients with 43 metacarpal fractures treated by early open reduction and internal fixation with 2 mm plates. Eighteen patients recovered a full range of motion, while one patient was lost to follow-up. Implant removal on account of extensor irritation was required in only two metacarpals in two patients. Plating of multiple closed metacarpal fractures is a safe, reliable and consistently reproducible treatment method.
C1 [Mudgal, C. S.] Massachusetts Gen Hosp, Orthopaed Hand & Upper Extrem Serv, Yawkey Ctr, Boston, MA 02114 USA.
RP Mudgal, CS (reprint author), Massachusetts Gen Hosp, Orthopaed Hand & Upper Extrem Serv, Yawkey Ctr, Suite 2100,55 Fruit St, Boston, MA 02114 USA.
EM cmudgal@partners.org
NR 21
TC 10
Z9 11
U1 1
U2 1
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1753-1934
J9 J HAND SURG-EUR VOL
JI J. Hand Surg.-Eur. Vol.
PD DEC
PY 2008
VL 33E
IS 6
BP 740
EP 744
DI 10.1177/1753193408090101
PG 5
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 392VX
UT WOS:000262331400007
PM 18694922
ER
PT J
AU Frakt, AB
Pizer, SD
Hendricks, AM
AF Frakt, Austin B.
Pizer, Steven D.
Hendricks, Ann M.
TI Controlling Prescription Drug Costs: Regulation and the Role of Interest
Groups in Medicare and the Veterans Health Administration
SO JOURNAL OF HEALTH POLITICS POLICY AND LAW
LA English
DT Article
ID PRESSURE GROUPS; POLITICS; BENEFIT; PRICES; CARE; ACT
AB Medicare and the Veterans Health Administration (VA) both finance large outpatient prescription drug programs, though in very different ways. In the ongoing debate on how to control Medicare spending, some suggest that Medicare should negotiate directly with drug manufacturers, as the VA does. In this article we relate the role of interest groups to policy differences between Medicare and the VA and, in doing so, explain why such a large change to the Medicare drug program is unlikely. We argue that key policy differences are attributable to stable differences in interest group involvement. While this stability makes major changes in Medicare unlikely, it suggests the possibility of leveraging VA drug purchasing to achieve savings in Medicare. This could be done through a VA-administered drug-only benefit for Medicare-enrolled veterans. Such a partnership could incorporate key elements of both programs: capacity to accept large numbers of enrollees (like Medicare) and leverage to negotiate prescription drug prices (like the VA). Moreover, it could be implemented at no cost to the VA while achieving savings for Medicare and beneficiaries.
C1 [Frakt, Austin B.; Pizer, Steven D.; Hendricks, Ann M.] Boston Univ, Sch Publ Hlth, Boston, MA 02215 USA.
[Frakt, Austin B.; Pizer, Steven D.; Hendricks, Ann M.] VA Boston Healthcare Syst, Boston, MA USA.
RP Frakt, AB (reprint author), VA Boston Healthcare Syst, Boston, MA USA.
FU Department of Veterans Affairs Health Services Research and Development
Service [IIR 04-233-1]
FX This research was supported by the Department of Veterans Affairs Health
Services Research and Development Service Grant No. IIR 04-233-1. This
is an investigator-initiated, peer-reviewed grant. Although the authors
interviewed some current and former Medicare and Department of Veterans
Affairs administrators as part of this research, this article was
neither reviewed nor approved by Medicare or Department of Veterans
Affairs administrators prior to submission for publication. The views
expressed in this article are those of the authors and do not
necessarily reflect the positions of the Department of Veterans Affairs
or Boston University. We thank Dan Plafcan, Lynn Wolfsfeld, Julia
Prentice, and two anonymous reviewers for their helpful comments on
earlier versions of this article.
NR 66
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U1 1
U2 3
PU DUKE UNIV PRESS
PI DURHAM
PA 905 W MAIN ST, STE 18-B, DURHAM, NC 27701 USA
SN 0361-6878
J9 J HEALTH POLIT POLIC
JI J. Health Polit. Policy Law
PD DEC
PY 2008
VL 33
IS 6
BP 1079
EP 1106
DI 10.1215/03616878-2008-032
PG 28
WC Health Care Sciences & Services; Health Policy & Services; Medicine,
Legal; Social Issues; Social Sciences, Biomedical
SC Health Care Sciences & Services; Legal Medicine; Social Issues;
Biomedical Social Sciences
GA 383AV
UT WOS:000261647400005
PM 19038872
ER
PT J
AU Sussner, KM
Lindsay, AC
Greaney, ML
Peterson, KE
AF Sussner, Katarina M.
Lindsay, Ana C.
Greaney, Mary L.
Peterson, Karen E.
TI The Influence of Immigrant Status and Acculturation on the Development
of Overweight in Latino Families: A Qualitative Study
SO JOURNAL OF IMMIGRANT AND MINORITY HEALTH
LA English
DT Article
DE Child obesity and overweight; Immigrants; Acculturation; Latino
AB Exposure to obesogenic environments in the U. S. may foster development of overweight in immigrants with greater acculturation. Few studies document mechanisms of the acculturation process from immigrants' own perspectives or describe implications on the children of immigrants. Focus groups and in-depth interviews were conducted with immigrant Latina mothers (N = 51) examining mothers' beliefs, attitudes and practices related to early child feeding and weight. Focus group participants completing the Marin Acculturation Scale more closely identified with Latino culture, although the mean score (2.04, SD = 0.59) was close to "bicultural''. Analysis revealed seven themes when mothers compared lifestyles between their native countries and the U. S., related to changes in (1) diet, perceived food quality and availability, (2) food and eating practices, (3) breastfeeding practices, (4) beliefs about food, child feeding and weight status, (5) weight status of mothers and children, (6) physical activity and sedentary lifestyles, and (7) social isolation and support.
C1 [Sussner, Katarina M.] Mt Sinai Sch Med, Dept Oncol Sci Canc Prevent & Control, New York, NY 10029 USA.
[Lindsay, Ana C.; Peterson, Karen E.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Greaney, Mary L.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Peterson, Karen E.] Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Boston, MA 02115 USA.
RP Sussner, KM (reprint author), Mt Sinai Sch Med, Dept Oncol Sci Canc Prevent & Control, 1425 Madison Ave,Box 1130, New York, NY 10029 USA.
EM katarina.sussner@mssm.edu
FU NCI NIH HHS [R03 CA108347, R03 CA108347-01]; NICHD NIH HHS [R01
HD037368, R01 HD37368]
NR 60
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U1 3
U2 21
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1557-1912
J9 J IMMIGR MINOR HEALT
JI J. Immigr. Minor. Health
PD DEC
PY 2008
VL 10
IS 6
BP 497
EP 505
DI 10.1007/s10903-008-9137-3
PG 9
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA V13DX
UT WOS:000207648600003
PM 18373200
ER
PT J
AU Fudaba, Y
Onoe, T
Chittenden, M
Shimizu, A
Shaffer, JM
Bronson, R
Sykes, M
AF Fudaba, Yasuhiro
Onoe, Takashi
Chittenden, Meredith
Shimizu, Akira
Shaffer, Juanita M.
Bronson, Roderick
Sykes, Megan
TI Abnormal Regulatory and Effector T Cell Function Predispose to
Autoimmunity following Xenogeneic Thymic Transplantation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID SKIN-GRAFT TOLERANCE; FETAL PIG THYMUS; NUDE-MICE; HOMEOSTATIC
PROLIFERATION; NEGATIVE SELECTION; THYMECTOMIZED MICE; POSITIVE
SELECTION; CUTTING EDGE; ATHYMIC MICE; PORCINE MHC
AB Porcine thymus grafts support robust murine and human thymopoiesis, generating a diverse T cell repertoire that is deleted of donor and host-reactive cells, achieving specific xenograft tolerance. Positive selection is mediated exclusively by the xenogeneic thymic MHC. Although thymectomized, T cell-depleted normal mice usually remain healthy following xenogeneic thymic transplantation, thymus-grafted congenitally athymic mice frequently develop multiorgan autoimmunity. We investigated the etiology of this syndrome by adoptively transferring lymphocyte populations from fetal pig thymus-grafted BALB/c nude mice to secondary BALB/c nude recipients. Fetal pig thymus-grafted nude mice generated normal numbers of CD25(+)Foxp3(+)CD4 T cells, but these cells lacked the capacity to block autoimmunity. Moreover, thymocytes and peripheral CD4(+)CD25(-) cells from fetal pig thymus-grafted nude mice, but not those from normal mice, induced autoimmunity in nude recipients. Injection of thymic epithelial cells from normal BALB/c mice into fetal pig thymus grafts reduced autoimmunity and enhanced regulatory function of splenocytes. Our data implicate abnormalities in postthymic maturation, expansion, and/or survival of T cells positively selected by a xenogeneic MHC, as well as incomplete intrathymic deletion of thymocytes recognizing host tissue-specific Ags, in autoimmune pathogenesis. Regulatory cell function is enhanced and negative selection of host-specific thymocytes may potentially also be improved by coimplantation of recipient thymic epithelial cells in the thymus xenograft. The Journal of Immunology, 2008, 181: 7649-7659.
C1 [Fudaba, Yasuhiro; Onoe, Takashi; Chittenden, Meredith; Shimizu, Akira; Shaffer, Juanita M.; Sykes, Megan] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Surg,Transplantat Biol Res Ctr, Boston, MA 02129 USA.
[Bronson, Roderick] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02114 USA.
RP Sykes, M (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Surg,Transplantat Biol Res Ctr, Massachusetts Gen Hosp E Bldg 149-5102,13th St, Boston, MA 02129 USA.
EM megan.sykes@tbrc.mgh.harvard.edu
FU National Institutes of Health [P01 A1045897, P01 HL18646]; Juvenile
Diabetes Research Foundation Basic Science [1-2007-723]; Japan Society
for the Promotion of Science
FX This work was supported by National Institutes of Health Grants P01
A1045897 and P01 HL18646, Juvenile Diabetes Research Foundation Basic
Science Grant 1-2007-723, and Immerge BT. Y.F. was supported in part by
the Uchara Memorial Foundation. T.O. was supported in part by a
Postdoctoral Fellowship for Research of Abroad front the Japan Society
for the Promotion of Science.
NR 49
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U1 1
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD DEC 1
PY 2008
VL 181
IS 11
BP 7649
EP 7659
PG 11
WC Immunology
SC Immunology
GA 376YX
UT WOS:000261220000026
PM 19017953
ER
PT J
AU Pazos, M
Siccardi, D
Mumy, KL
Bien, JD
Louie, S
Shi, HN
Gronert, K
Mrsny, RJ
McCormick, BA
AF Pazos, Michael
Siccardi, Dario
Mumy, Karen L.
Bien, Jeffrey D.
Louie, Steve
Shi, Hai Ning
Gronert, Karsten
Mrsny, Randall J.
McCormick, Beth A.
TI Multidrug Resistance-Associated Transporter 2 Regulates Mucosal
Inflammation by Facilitating the Synthesis of Hepoxilin A(3)
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID ENTERICA SEROTYPE TYPHIMURIUM; ARACHIDONATE 12-LIPOXYGENASE;
SALMONELLA-TYPHIMURIUM; INTESTINAL EPITHELIA; TRANSEPITHELIAL MIGRATION;
NEUTROPHIL MIGRATION; IN-VITRO; T-CELLS; COLITIS; DRUG
AB Neutrophil transmigration across mucosal surfaces contributes to dysfunction of epithelial barrier properties, a characteristic underlying many mucosal inflammatory diseases. Thus, insight into the directional movement of neutrophils across epithelial barriers will provide important information relating to the mechanisms of such inflammatory disorders. The eicosanoid hepoxilin A(3), an endogenous product of 12-lipoxygenase activity, is secreted from the apical surface of the epithelial barrier and establishes a chemotactic gradient to guide neutrophils from the submucosa across epithelia to the luminal site of an inflammatory stimulus, the final step in neutrophil recruitment. Currently, little is known regarding how hepoxilin A(3) is secreted from the intestinal epithelium during an inflammatory insult. In this study, we reveal that hepoxilin A(3) is a substrate for the apical efflux ATP-binding protein transporter multidrug resistance-associated protein 2 (MRP2). Moreover, using multiple in vitro and in vivo models, we show that induction of intestinal inflammation profoundly up-regulates apical expression of MRP2, and that interfering with hepoxilin A(3) synthesis and/or inhibition of MRP2 function results in a marked reduction in inflammation and severity of disease. Lastly, examination of inflamed intestinal epithelia in human biopsies revealed up-regulation of MRP2. Thus, blocking hepoxilin A(3) synthesis and/or inhibiting MRP2 may lead to the development of new therapeutic strategies for the treatment of epithelial-associated inflammatory conditions. The Journal of Immunology, 2008, 181: 8044-8052.
C1 [Pazos, Michael; Siccardi, Dario; Mumy, Karen L.; Bien, Jeffrey D.; Louie, Steve; Shi, Hai Ning; McCormick, Beth A.] Massachusetts Gen Hosp, Dept Pediat Gastroenterol & Nutr, Boston, MA 02129 USA.
[Siccardi, Dario; Mumy, Karen L.; McCormick, Beth A.] Harvard Univ, Sch Med, Dept Microbiol & Mol Genet, Boston, MA 02115 USA.
[Gronert, Karsten] Univ Calif Berkeley, Sch Optometry, Ctr Eye Dis & Dev, Berkeley, CA 94720 USA.
[Mrsny, Randall J.] Univ Bath, Dept Pharm & Pharmacol, Bath BA2 7AY, Avon, England.
[Mrsny, Randall J.] Unity Pharmaceut, Menlo Pk, CA 94025 USA.
RP McCormick, BA (reprint author), Massachusetts Gen Hosp, CNY 114 16th St 3503, Charlestown, MA 02129 USA.
EM mccormic@helix.mgh.harvard.edu
FU National Institutes of Health [DK 56754, DK 33506]; National Eye
Institute [EY01613604]; Harvard Medical School; Department of Surgery at
Massachusetts General Hospital; National Institutes of Health Minority
Supplement Award
FX This research was supported by National Institutes of Health Grants DK
56754 and DK 33506 (to B.A.M.), National Eye Institute Grant EY01613604
(to K.G.), and a T32 Training Grant sponsored by Harvard Medical School
and the Department of Surgery at Massachusetts General Hospital (to
K.L.M.). M.P. was supported by a National Institutes of Health Minority
Supplement Award.
NR 49
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Z9 19
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD DEC 1
PY 2008
VL 181
IS 11
BP 8044
EP 8052
PG 9
WC Immunology
SC Immunology
GA 376YX
UT WOS:000261220000070
PM 19017997
ER
PT J
AU Huang, SH
Dunkley-Thompson, J
Tang, YH
Macklin, EA
Steel-Duncan, J
Singh-Minott, I
Ryland, EG
Smikle, M
Walker, BD
Christie, CDC
Feeney, ME
AF Huang, SiHong
Dunkley-Thompson, Jacqueline
Tang, YanHua
Macklin, Eric A.
Steel-Duncan, Julianne
Singh-Minott, Indira
Ryland, Elizabeth G.
Smikle, Monica
Walker, Bruce D.
Christie, Celia D. C.
Feeney, Margaret E.
TI Deficiency of HIV-Gag-Specific T Cells in Early Childhood Correlates
with Poor Viral Containment
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; INFECTED CHILDREN; DISEASE PROGRESSION;
HIV-1-INFECTED INFANTS; LYMPHOCYTE RESPONSES; CD8-T-CELL MEMORY;
IMMUNE-RESPONSES; TYPE-1 INFECTION; CD4-T-CELL HELP; 1ST YEAR
AB Perinatal HIV infection is characterized by a sustained high-level viremia and a high risk of rapid progression to AIDS, indicating a failure of immunologic containment of the virus. We hypothesized that age-related differences in the specificity or function of HIV-specific T cells may influence HIV RNA levels and clinical outcome following perinatal infection. In this study, we defined the HIV epitopes targeted by 76 pediatric subjects (47 HIV infected and 29 HIV exposed, but uninfected), and assessed the ability of HIV-specific CD8 and CD4 T cells to degranulate and produce IFN-gamma, TNF-alpha, and IL-2. No responses were detected among HIV-uninfected infants, whereas responses among infected subjects increased in magnitude and breadth with age. Gag-specific responses were uncommon during early infancy, and their frequency was significantly lower among children younger than 24 mo old (p = 0.014). Importantly, Gag responders exhibited significantly lower HIV RNA levels than nonresponders (log viral load 5.8 vs 5.0; p = 0.005). Both the total and Gag-specific T cell frequency correlated inversely with viral load after correction for age, whereas no relationship with targeting of other viral proteins was observed. Functional assessment of HIV-specific T cells by multiparameter flow cytometry revealed that polyfunctional CD8 cells were less prevalent in children before 24 mo of age, and that HIV-specific CD4 cell responses were of universally low frequency among anti retroviral-naive children and absent in young infants. These cross-sectional data suggest that qualitative differences in the CD8 response, combined with a deficiency of HIV-specific CD4 cells, may contribute to the inability of young infants to limit replication of HIV. The Journal of Immunology, 2008, 181: 8103-8111.
C1 [Huang, SiHong; Tang, YanHua; Ryland, Elizabeth G.; Walker, Bruce D.; Feeney, Margaret E.] Massachusetts Gen Hosp, Partners AIDS Res Ctr, Boston, MA 02115 USA.
[Huang, SiHong; Tang, YanHua; Ryland, Elizabeth G.; Walker, Bruce D.; Feeney, Margaret E.] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02115 USA.
[Huang, SiHong; Tang, YanHua; Ryland, Elizabeth G.; Walker, Bruce D.; Feeney, Margaret E.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Dunkley-Thompson, Jacqueline; Steel-Duncan, Julianne; Singh-Minott, Indira; Smikle, Monica; Christie, Celia D. C.] Univ W Indies, Kingston Perinatal AIDS Program, Kingston 7, Jamaica.
[Dunkley-Thompson, Jacqueline; Steel-Duncan, Julianne; Singh-Minott, Indira; Smikle, Monica; Christie, Celia D. C.] Univ W Indies, Dept Obstet Gynecol & Pediat, Kingston 7, Jamaica.
[Huang, SiHong; Feeney, Margaret E.] Childrens Hosp, Boston, MA 02115 USA.
[Macklin, Eric A.] Massachusetts Gen Hosp, Ctr Biostat, Boston, MA 02114 USA.
[Macklin, Eric A.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Huang, SiHong] Pfizer & Merck, Beth Israel Deaconess Med Ctr, Harvard Massachusetts Inst Technol Hlth Sci & Tec, Clin Investigator Training Program, Boston, MA 02215 USA.
[Walker, Bruce D.] Howard Hughes Med Inst, Chevy Chase, MD 20815 USA.
RP Feeney, ME (reprint author), Massachusetts Gen Hosp East, 5th Floor,149 13th St, Charlestown, MA 02129 USA.
EM mfeency@partners.org
RI Macklin, Eric/E-2955-2013
OI Macklin, Eric/0000-0003-1618-3502
FU Elizabeth Glaser Pediatric AIDS Foundation; Charles H. Hood Foundation;
National Institutes of Health [R01-AI068497]; Children Elizabeth Glaser
Scientist Award
FX This work was supported by grants From the Elizabeth Glaser Pediatric
AIDS Foundation (to M.E.F. and C.D.C.C.), Jewelers for Children, Charles
H. Hood Foundation (to M.E.F.), and National Institutes of Health
(R01-AI068497, to M.E.F.). S.H. is supported by the Clinical
Investigator Training Program. B.D.W. is a Doris Duke Distinguished
Clinical Scientist and a Howard Hughes Investigator. C.D.C.C. is a
recipient of the International Leadership Award from the Elizabeth
Glaser Pediatric AIDS Foundation. KEY. is a recipient of the 2006
Jewelers for Children Elizabeth Glaser Scientist Award.
NR 58
TC 24
Z9 24
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD DEC 1
PY 2008
VL 181
IS 11
BP 8103
EP 8111
PG 9
WC Immunology
SC Immunology
GA 376YX
UT WOS:000261220000076
PM 19018003
ER
PT J
AU Sun, BK
Tsao, H
AF Sun, Bryan K.
Tsao, Hensin
TI X-Chromosome Inactivation and Skin Disease
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Review
ID INCONTINENTIA PIGMENTI; DNA METHYLATION; WILMS-TUMOR; XIST GENE;
EXPRESSION; LINES; RNA; MUTATION; BLASCHKO; FEMALES
AB X-chromosome inactivation (XCI) is the process in which females transcriptionally silence one of their two X chromosomes in early embryonic development, equalizing X chromosome gene expression between males and females. XCI depends on a gene called XIST, a functional RNA molecule that does not code for a protein. Recent studies indicate abundant intergenic transcription and nonprotein coding RNAs in the human genome, which are suspected to function in modulating gene expression. XCI may therefore serve as a useful model to learn and understand the potential function of these elements, as well as their effects on human disease. Here, we review the genetic and molecular basis of XCI and describe how the mechanistics of this process lead to the phenotypes of X-linked skin diseases, most notably in the pattern of lines, swirls, and whorls first noted by the dermatologist Alfred Blaschko. We suggest that XCI, and other epigenetic phenomena, will continue to impact our understanding of the genetic mechanisms of disease.
C1 [Tsao, Hensin] Harvard Univ, Sch Med, Dept Dermatol, Boston, MA 02114 USA.
[Tsao, Hensin] Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA.
[Tsao, Hensin] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Tsao, Hensin] Massachusetts Gen Hosp, MGH Canc Ctr, Boston, MA 02114 USA.
RP Tsao, H (reprint author), Harvard Univ, Sch Med, Dept Dermatol, Bartlett 622,50 Blossom St, Boston, MA 02114 USA.
EM htsao@partners.org
OI Sun, Bryan/0000-0002-0740-0125
NR 37
TC 24
Z9 24
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD DEC
PY 2008
VL 128
IS 12
BP 2753
EP 2759
DI 10.1038/jid.2008.145
PG 7
WC Dermatology
SC Dermatology
GA 374RX
UT WOS:000261062500004
PM 18509358
ER
PT J
AU Dadras, SS
Skrzypek, A
Nguyen, L
Shin, JW
Schulz, MMP
Arbiser, J
Mihm, MC
Detmar, M
AF Dadras, Soheil S.
Skrzypek, Adrienne
Nguyen, Lynh
Shin, Jay W.
Schulz, Martin M. P.
Arbiser, Jack
Mihm, Martin C.
Detmar, Michael
TI Prox-1 Promotes Invasion of Kaposiform Hemangioendotheliomas
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Article
ID KASABACH-MERRITT PHENOMENON; ENDOTHELIAL-CELLS; DIFFERENTIATION;
HERPESVIRUS; EXPRESSION; SARCOMA; SYSTEM; BLOOD; MODEL; GENE
AB Kaposi's sarcoma (KS) is the most frequently occurring malignant tumor in patients infected with HIV. Recent studies have revealed that infection of vascular endothelial cells with KS-associated herpes virus in vitro results in a lymphatic reprogramming of these cells, with potent induction of the lymphatic marker genes podoplanin and vascular endothelial growth factor receptor-3, which is mediated by upregulation of the transcription factor Prox1. However, the potential effects of Prox1 expression on the biology of KS and, in particular, on the aggressive and invasive behavior of KS tumors in vivo have remained unknown. We stably expressed Prox1 cDNA in the two mouse hemangioendothelioma cell lines EOMA and Py-4-1, well-established murine models for kaposiform hemangioendothelioma. Surprisingly, we found that expression of Prox1 was sufficient to induce a more aggressive behavior of tumors growing in syngenic mice, leading to enhanced local invasion into the muscular layer and to cellular anaplasia in vivo, and increased migration rate in vitro. This enhanced malignant phenotype was associated with upregulation of several genes involved in proteolysis, cell adhesion, and migration. Together, these results indicate that Prox1 plays an important, previously unanticipated role in mediating the aggressive behavior of vascular neoplasms such as KS.
C1 [Dadras, Soheil S.; Skrzypek, Adrienne; Nguyen, Lynh; Shin, Jay W.; Detmar, Michael] Cutaneous Biol Res Ctr, Dept Dermatol, Boston, MA USA.
[Dadras, Soheil S.; Mihm, Martin C.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Dadras, Soheil S.; Mihm, Martin C.] Harvard Univ, Sch Med, Boston, MA USA.
[Shin, Jay W.; Schulz, Martin M. P.; Detmar, Michael] ETH, Swiss Fed Inst Technol, Inst Pharmaceut Sci, Zurich, Switzerland.
[Arbiser, Jack] Emory Univ, Dept Dermatol, Atlanta, GA 30322 USA.
RP Dadras, SS (reprint author), Stanford Univ, Med Ctr, 300 Pasteur Dr, Stanford, CA 94305 USA.
EM sdadras@stanford.edu
FU NIH/NCI [CA69184, CA86410, CA92644]; Susan G. Komen Breast Cancer
Foundation; American Cancer Society Program Project [9923901]; Swiss
National Fund [3100A0-108207]; Austrian Science Foundation [S9408-B11];
Commission of the European Communities [LSHC-CT-2005-518178]; NIH
Pathology Training Grant; Cutaneous Biology Research Center;
Massachusetts General Hospital/Shiseido Co. Ltd. Agreement
FX We thank L. Janes and J. Bertoncini for expert technical assistance, Dr
S. I. Tomarev for providing the pcDNA3/hProx-1 cDNA, Dr D. G. Jackson
for the mouse anti-LYVE-1 antibody, and Drs K. Alitalo and Y. Hong for
the antiProx-1 antibodies. This work was supported by NIH/NCI grants
CA69184, CA86410, and CA92644 (M. D.), the Susan G. Komen Breast Cancer
Foundation (M. D.), American Cancer Society Program Project Grant
9923901 (M. D.), Swiss National Fund grant 3100A0-108207 (M. D.),
Austrian Science Foundation grant S9408-B11 (M. D.), Commission of the
European Communities grant LSHC-CT-2005-518178 (M. D.), an NIH Pathology
Training Grant (S. S. D.), and by the Cutaneous Biology Research Center
through the Massachusetts General Hospital/Shiseido Co. Ltd. Agreement
(M. D.).
NR 31
TC 23
Z9 25
U1 1
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD DEC
PY 2008
VL 128
IS 12
BP 2798
EP 2806
DI 10.1038/jid.2008.176
PG 9
WC Dermatology
SC Dermatology
GA 374RX
UT WOS:000261062500010
PM 18580962
ER
PT J
AU Jackonis, MJ
Deyton, L
Hess, WJ
AF Jackonis, Michael J.
Deyton, Lawrence
Hess, William J.
TI War, Its Aftermath, and US Health Policy: Toward a Comprehensive Health
Program for America's Military Personnel, Veterans, and Their Families
SO JOURNAL OF LAW MEDICINE & ETHICS
LA English
DT Article
AB This essay discusses the challenges faced by veterans returning to society in light of the current organization and structure of the military, veterans', and overall U.S. health care systems. It also addresses the need for an integrated health care financing and delivery system to ensure a continuum of care for service members, veterans, dependents, and other family members. The health care systems of both the Department of Defense and the Department of Veterans Affairs execute their responsibilities to active duty service members, while their families and retirees/veterans are under separate legal authorities. Although they perform their mandates with extraordinary commitment and demonstrably high quality, both systems need to explore improved communication, coordination, and sharing, as well as increased collaboration with the Department of Health and Human Services programs serving the same populations, far beyond current efforts. The health care-related missions and the locus of health care delivery of each agency are admittedly unique, but their distinctions must not be permitted to impede system integration and coordination of a continuum of care provided to the men and women who serve the nation, and their families.
C1 [Deyton, Lawrence] US Dept Vet Affairs, Washington, DC USA.
[Deyton, Lawrence] George Washington Univ, Med Ctr, Sch Publ Hlth & Hlth Sci, Washington, DC 20052 USA.
[Hess, William J.] Natl Naval Med Ctr, Bethesda, MD USA.
NR 39
TC 10
Z9 10
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1073-1105
J9 J LAW MED ETHICS
JI J. Law Med. Ethics
PD WIN
PY 2008
VL 36
IS 4
BP 677
EP 689
DI 10.1111/j.1748-720X.2008.00322.x
PG 13
WC Ethics; Law; Medical Ethics; Medicine, Legal
SC Social Sciences - Other Topics; Government & Law; Medical Ethics; Legal
Medicine
GA 378ZR
UT WOS:000261364300008
PM 19093991
ER
PT J
AU Goldstein, MM
Blumenthal, D
AF Goldstein, Melissa M.
Blumenthal, David
TI Building an Information Technology Infrastructure
SO JOURNAL OF LAW MEDICINE & ETHICS
LA English
DT Article
ID ELECTRONIC HEALTH RECORDS; CARE
AB The widespread adoption of health information technology (HIT) has been recognized as both a necessary element of health reform and a required building block of a modern, high performing health care system.
C1 [Goldstein, Melissa M.] George Washington Univ, Med Ctr, Sch Publ Hlth & Hlth Serv, Dept Hlth Policy, Washington, DC 20037 USA.
[Goldstein, Melissa M.] George Washington Univ, Med Ctr, Dept Clin Management, Washington, DC 20037 USA.
[Goldstein, Melissa M.] George Washington Univ, Med Ctr, Sch Med & Hlth Sci, Washington, DC 20037 USA.
[Blumenthal, David] Massachusetts Gen Hosp, Partners Healthcare Syst, Inst Hlth Policy & Phys, Boston, MA 02114 USA.
[Blumenthal, David] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
RP Goldstein, MM (reprint author), George Washington Univ, Med Ctr, Sch Publ Hlth & Hlth Serv, Dept Hlth Policy, Washington, DC 20037 USA.
NR 25
TC 4
Z9 4
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1073-1105
J9 J LAW MED ETHICS
JI J. Law Med. Ethics
PD WIN
PY 2008
VL 36
IS 4
BP 709
EP 715
DI 10.1111/j.1748-720X.2008.00326.x
PG 7
WC Ethics; Law; Medical Ethics; Medicine, Legal
SC Social Sciences - Other Topics; Government & Law; Medical Ethics; Legal
Medicine
GA 378ZR
UT WOS:000261364300012
PM 19093995
ER
PT J
AU Morone, JA
Blumenthal, D
AF Morone, James A.
Blumenthal, David
TI Nine Lessons for Health Reform: Or Will We Finally Learn from the Past ?
SO JOURNAL OF LAW MEDICINE & ETHICS
LA English
DT Article
AB Health care reform sits, once again, in the eye of the political storm. This article, based on an analysis of past health care debates, offers nine historical lessons for contemporary reformers. We describe the most important political do's and don'ts.
C1 [Morone, James A.] Brown Univ, Providence, RI 02912 USA.
[Blumenthal, David] Massachusetts Gen Hosp, Partners Healthcare Syst, Inst Hlth Policy, Boston, MA 02114 USA.
[Blumenthal, David] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
RP Morone, JA (reprint author), Brown Univ, Providence, RI 02912 USA.
NR 8
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1073-1105
J9 J LAW MED ETHICS
JI J. Law Med. Ethics
PD WIN
PY 2008
VL 36
IS 4
BP 722
EP 724
DI 10.1111/j.1748-720X.2008.00328.x
PG 3
WC Ethics; Law; Medical Ethics; Medicine, Legal
SC Social Sciences - Other Topics; Government & Law; Medical Ethics; Legal
Medicine
GA 378ZR
UT WOS:000261364300014
PM 19093997
ER
PT J
AU Ascon, DB
Ascon, M
Satpute, S
Lopez-Briones, S
Racusen, L
Colvin, RB
Soloski, MJ
Rabb, H
AF Ascon, Dolores B.
Ascon, Miguel
Satpute, Shailesh
Lopez-Briones, Sergio
Racusen, Lorraine
Colvin, Robert B.
Soloski, Mark J.
Rabb, Hamid
TI Normal mouse kidneys contain activated and CD3(+)CD4(-)CD8(-)
double-negative T lymphocytes with a distinct TCR repertoire
SO JOURNAL OF LEUKOCYTE BIOLOGY
LA English
DT Article
DE DN T cells; NK cells; cytokines; ischemia; rodents
ID RENAL ISCHEMIA-REPERFUSION; CELL-ACTIVATION; INTERFERON-GAMMA; HUMAN
LIVER; INJURY; MICE; ALPHA; POPULATIONS; CYTOKINES; MODEL
AB Healthy liver, intestine, lung, and skin harbor resident lymphocytes with conventional and unconventional phenotypes. Lymphocytes also have been detected in healthy mice kidneys; however, these cells have not been well studied and have been largely overlooked. To better characterize the intra-renal lymphocytes, we extensively perfused C57BL/6J mice with PBS and then isolated mononuclear cells for flow cytometry analysis. We observed T cells, B cells, and NK cells in normal mice kidneys after extensive perfusion. Approximately 50% of kidney T lymphocytes expressed intermediate levels of CD3 (CD3(int) T cells). Similar to liver and lung, a high percentage of unconventional CD3(+)CD4(-)CD8(-) double-negative T cells was observed in normal mice kidneys, from which 11% expressed B220 antigen. Unlike the spleen and blood, the classic CD4(+) and CD8(+) T lymphocytes in the kidney had a high proportion of activated CD69(+) and effector/memory CD44CD62L ligand phenotypes. Also, a small percentage of CD4(+)CD25(+) forkhead box p3(+) and NKT cells was observed in perfused and exanguinated kidneys. In addition, a distinct TCR repertoire was found on intra-renal conventional and unconventional T cells compared with those from the spleen. Finally, after 24 h of renal ischemia reperfusion injury (IRI), increased production of cytokines IFN-gamma and TNF-alpha by CD4(+) and CD8(+) T cells, isolated from perfused kidneys, was observed. These data suggest that some of these cells harbored in the kidney could be implicated in the immune response of the IRI pathogenic process. J. Leukoc. Biol. 84: 1400-1409; 2008.
C1 [Ascon, Dolores B.; Ascon, Miguel; Satpute, Shailesh; Lopez-Briones, Sergio; Racusen, Lorraine; Soloski, Mark J.; Rabb, Hamid] Johns Hopkins Univ, Sch Med, Dept Pathol & Med, Baltimore, MD USA.
[Colvin, Robert B.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol, Boston, MA USA.
RP Ascon, DB (reprint author), BriJen Biotech, UMBC Technol Ctr, Baltimore, MD 21227 USA.
EM dascon@brijenbiotech.com; hrabb1@jhmi.edu
OI Lopez-Briones, Sergio/0000-0003-0273-0958
FU National Institutes of Health [R01 DK54770, 3R01DK054770-05S1,
3R01DK054770-06A1, HL073944, RO1 AI42287, R21 AI063133]
FX This study was supported by National Institutes of Health grants R01
DK54770 (H. R.), 3R01DK054770-05S1 (D.B.A.), 3R01DK054770-06A1 (M.A.),
SCCOR HL073944 (H.R.), RO1 AI42287 (M.J.S.), and R21 AI063133 (M.J.S.).
We thank Dr. Abdel Hamad for advice with DN T cells. We also thank Dr.
Hye Ryoun Jang for help in kidney surgery.
NR 38
TC 31
Z9 32
U1 0
U2 4
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0741-5400
J9 J LEUKOCYTE BIOL
JI J. Leukoc. Biol.
PD DEC 1
PY 2008
VL 84
IS 6
BP 1400
EP 1409
DI 10.1189/jlb.0907651
PG 10
WC Cell Biology; Hematology; Immunology
SC Cell Biology; Hematology; Immunology
GA 374GR
UT WOS:000261032300007
PM 18765477
ER
PT J
AU McCaslin, SE
Inslicht, SS
Metzler, TJ
Henn-Haase, C
Maguen, S
Neylan, TC
Choucroun, G
Marmar, CR
AF McCaslin, Shannon E.
Inslicht, Sabra S.
Metzler, Thomas J.
Henn-Haase, Clare
Maguen, Shira
Neylan, Thomas C.
Choucroun, Gerard
Marmar, Charles R.
TI Trait Dissociation Predicts Posttraumatic Stress Disorder Symptoms in a
Prospective Study of Urban Police Officers
SO JOURNAL OF NERVOUS AND MENTAL DISEASE
LA English
DT Article
DE Dissociation; traumatic stress; police officers
ID EMERGENCY SERVICES PERSONNEL; CIVILIAN MISSISSIPPI SCALE; SEXUAL-ABUSE;
PERITRAUMATIC DISSOCIATION; VIETNAM VETERANS; NEUROPEPTIDE-Y; PTSD
SYMPTOMS; RISK-FACTORS; TRAUMA; RELIABILITY
AB The current study prospectively examines the predictive relationship of trait dissociation, assessed during academy training, to PTSD symptoms assessed at 12 months of active police duty in relatively young and healthy police academy recruits (N = 180). The roles of pre-academy trauma exposure, exposure to life-threatening critical incidents during police duty, and peritraumatic dissociation at the time of the officer's worst critical incident were also examined. Utilizing path analytic techniques, greater trait dissociation, assessed during academy training, was predictive of both peritraumatic dissociation, and PTSD symptoms assessed at 12 months of police service. Moreover, after accounting for trait dissociation and peritraumatic dissociation, the relationship of previous trauma to later PTSD symptoms was no longer significant, demonstrating that the effect of previous trauma on later vulnerability to PTSD symptoms in this sample may be mediated by both trait and peritraumatic dissociation.
C1 [McCaslin, Shannon E.; Inslicht, Sabra S.; Metzler, Thomas J.; Henn-Haase, Clare; Maguen, Shira; Neylan, Thomas C.; Marmar, Charles R.] San Francisco VA Med Ctr, Mental Hlth Serv, San Francisco, CA USA.
[McCaslin, Shannon E.; Inslicht, Sabra S.; Metzler, Thomas J.; Henn-Haase, Clare; Maguen, Shira; Neylan, Thomas C.; Marmar, Charles R.] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA.
[Choucroun, Gerard] No Calif Inst Res & Educ, San Francisco, CA USA.
RP McCaslin, SE (reprint author), Vet Affairs Med Ctr, PTSD Res Program, 4150 Clement St 116P, San Francisco, CA 94121 USA.
EM Shannon.McCaslin@ucsf.edu
FU NIMH NIH HHS [R01 MH056350]
NR 54
TC 22
Z9 22
U1 0
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-3018
J9 J NERV MENT DIS
JI J. Nerv. Ment. Dis.
PD DEC
PY 2008
VL 196
IS 12
BP 912
EP 918
DI 10.1097/NMD.0b013e31818ec95d
PG 7
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 383DE
UT WOS:000261653500008
PM 19077859
ER
PT J
AU Kim, SP
Simeral, JD
Hochberg, LR
Donoghue, JP
Black, MJ
AF Kim, Sung-Phil
Simeral, John D.
Hochberg, Leigh R.
Donoghue, John P.
Black, Michael J.
TI Neural control of computer cursor velocity by decoding motor cortical
spiking activity in humans with tetraplegia
SO JOURNAL OF NEURAL ENGINEERING
LA English
DT Article
ID PRIMATE PRIMARY MOTOR; FREE ARM MOVEMENTS; 3-DIMENSIONAL SPACE;
INTERNAL-MODELS; VISUAL TARGETS; CELL DISCHARGE; KALMAN FILTER; CORTEX;
POPULATION; DIRECTION
AB Computer-mediated connections between human motor cortical neurons and assistive devices promise to improve or restore lost function in people with paralysis. Recently, a pilot clinical study of an intracortical neural interface system demonstrated that a tetraplegic human was able to obtain continuous two-dimensional control of a computer cursor using neural activity recorded from his motor cortex. This control, however, was not sufficiently accurate for reliable use in many common computer control tasks. Here, we studied several central design choices for such a system including the kinematic representation for cursor movement, the decoding method that translates neuronal ensemble spiking activity into a control signal and the cursor control task used during training for optimizing the parameters of the decoding method. In two tetraplegic participants, we found that controlling a cursor's velocity resulted in more accurate closed-loop control than controlling its position directly and that Cursor velocity control was achieved more rapidly than position control. Control quality was further improved over conventional linear filters by using a probabilistic method, the Kalman filter, to decode human motor cortical activity. Performance assessment based on standard metrics used for the evaluation of a wide range of pointing devices demonstrated significantly improved cursor control with velocity rather than position decoding.
C1 [Kim, Sung-Phil; Black, Michael J.] Brown Univ, Dept Comp Sci, Providence, RI 02912 USA.
[Simeral, John D.; Hochberg, Leigh R.; Donoghue, John P.] Ctr Restorat & Regenerat Med, Rehabil R&D Serv, Dept Vet Affairs, Providence, RI 02912 USA.
[Simeral, John D.; Hochberg, Leigh R.; Donoghue, John P.] Brown Univ, Dept Neurosci, Providence, RI 02912 USA.
[Hochberg, Leigh R.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Hochberg, Leigh R.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Boston, MA 02114 USA.
[Hochberg, Leigh R.] Harvard Univ, Sch Med, Spaulding Rehabil Hosp, Boston, MA 02114 USA.
[Donoghue, John P.] Cyberkinet Neurotechnol Syst Inc, Foxboro, MA 02035 USA.
RP Kim, SP (reprint author), Brown Univ, Dept Comp Sci, Box 1910,115 Waterman St, Providence, RI 02912 USA.
EM spkim@cs.brown.edu; black@cs.brown.edu
OI Hochberg, Leigh/0000-0003-0261-2273
FU NIH-NINDS [R01 NS 50867-01, NS25074]; Katie Sarnson Foundation; Office
of Naval Research [N0014-04-1-082, N0014-07-1-0803]; European
Neurobotics Program [FP6-IST-001917]; Rehabilitation Research and
Development Service, Department of Veterans Affairs
FX This work is partially supported by NIH-NINDS R01 NS 50867-01 as part of
the NSF/NIH Collaborative Research in Computational Neuroscience
Program, NIH-NINDS NS25074, the Katie Sarnson Foundation, and by the
Office of Naval Research (awards N0014-04-1-082 and N0014-07-1-0803).
This material is based upon work supported in part by the Office of
Research and Development, Rehabilitation R&D Service, Department of
Veterans Affairs (JDS, LRH). We also thank the European Neurobotics
Program FP6-IST-001917 and Rehabilitation Research and Development
Service, Department of Veterans Affairs. The clinical trial from which
these data are derived is sponsored by Cyberkinetics Neurotechnology
Systems, Inc. We thank Gregory Shakhnarovich, Frank Wood and Wilson
Truccolo for comments and assistance. We also thank Abe Caplan, Eric
Peterson, Michael Fritz and Cyberkinetics Neurotechnology Systems. Inc.
for running the recording sessions described here.
NR 49
TC 155
Z9 157
U1 1
U2 17
PU IOP PUBLISHING LTD
PI BRISTOL
PA DIRAC HOUSE, TEMPLE BACK, BRISTOL BS1 6BE, ENGLAND
SN 1741-2560
J9 J NEURAL ENG
JI J. Neural Eng.
PD DEC
PY 2008
VL 5
IS 4
BP 455
EP 476
DI 10.1088/1741-2560/5/4/010
PG 22
WC Engineering, Biomedical; Neurosciences
SC Engineering; Neurosciences & Neurology
GA 388LD
UT WOS:000262020400010
PM 19015583
ER
PT J
AU Liu, Y
Dinkin, MJ
Loewenstein, JI
Rizzo, JF
Cestari, DM
AF Liu, Yao
Dinkin, Marc J.
Loewenstein, John I.
Rizzo, Joseph F., III
Cestari, Dean M.
TI Multifocal Electroretinographic Abnormalities in Ethambutol-Induced
Visual Loss
SO JOURNAL OF NEURO-OPHTHALMOLOGY
LA English
DT Article
ID TOXICITY
AB Two patients who developed decreased visual acuity after several months of ethambutol treatment for Mycobacterium avium-intracellulare infection had bitemporal visual field defects that suggested optic chiasm damage. Multifocal electroretinography (mfERG) disclosed markedly low-amplitude responses at fixation and in the regions corresponding to the visual field defects. These results suggested that the visual dysfunction might be entirely attributable to retinal rather than optic nerve toxicity. These are the first reported patients to show mfERG abnormalities that correspond to bitemporal visual field defects and add to the growing evidence that ethambutol damages the retina.
C1 [Cestari, Dean M.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Neuroophthalmol,Neuroophthalmol Serv, Boston, MA 02114 USA.
Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Retina Serv DMP, Boston, MA 02114 USA.
[Dinkin, Marc J.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Neurol, Boston, MA 02115 USA.
RP Cestari, DM (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Neuroophthalmol,Neuroophthalmol Serv, 243 Charles St,9th Floor Massachusetts Eye & Ear, Boston, MA 02114 USA.
EM dean_cestari@meei.harvard.edu
NR 8
TC 9
Z9 10
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1070-8022
J9 J NEURO-OPHTHALMOL
JI J. Neuro-Ophthal.
PD DEC
PY 2008
VL 28
IS 4
BP 278
EP 282
PG 5
WC Clinical Neurology; Ophthalmology
SC Neurosciences & Neurology; Ophthalmology
GA 380BI
UT WOS:000261440100003
PM 19145124
ER
PT J
AU Theodore, S
Cao, S
McLean, PJ
Standaert, DG
AF Theodore, Shaji
Cao, Shuwen
McLean, Pamela J.
Standaert, David G.
TI Targeted Overexpression of Human alpha-Synuclein Triggers Microglial
Activation and an Adaptive Immune Response in a Mouse Model of Parkinson
Disease
SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
LA English
DT Article
DE Adeno-associated virus; Dopamine; Glia; Immunoglobulin; Lymphocytes;
Neurodegeneration; Neuroinflammation
ID ADENOASSOCIATED VIRUS TYPE-2; MEDIATED GENE-TRANSFER;
CENTRAL-NERVOUS-SYSTEM; SUBSTANTIA-NIGRA; DOPAMINERGIC-NEURONS;
ALTERNATIVE ACTIVATION; REACTIVE MICROGLIA; PROTEIN-KINASE; LEWY BODIES;
CELL INJURY
AB Microglial activation and adaptive immunity have been implicated in the neurodegenerative processes in Parkinson disease. It has been proposed that these responses may be triggered by modified forms of alpha-synuclein (alpha-SYN), particularly nitrated species, which are released as a consequence of dopaminergic neurodegeneration. To examine the relationship between alpha-SYN, microglial activation, Mouse model of Parkinson and adaptive immunity, We used a disease in which human alpha-SYN is overexpressed by a recombinant adeno-associated virus vector, serotype 2 (AAV2-SYN); this overexpression leads to slow degeneration of dopaminergic neurons. Microglial activation and components of the adaptive immune response were assessed using immunohistochemistry; quantitative polymerase chain reaction was used to examine cytokine expression. Four weeks after injection, there was a marked increase in CD68-positive microglia and greater infiltration of B and T lymphocytes in the substantia nigra pars compacta of the AAV2-SYN group than in controls. At 12 weeks, CD68 staining declined, but B- and T-cell infiltration persisted. Expression of proinflammatory cytokines was enhanced, whereas markets of alternative activation (i.e. arginase I and interleukins 4 and 13) were not altered. Increased immunoreactivity activity for mouse immunoglobulin was detected at all time points in the AAV2-SYN animals. These data show that overexpression of alpha-SYN alone, in the absence of overt neurodegeneration, is sulficient to trigger neuroinflammation with both microglial activation and stimulation of adaptive immunity.
C1 [Theodore, Shaji; Cao, Shuwen; Standaert, David G.] Univ Alabama, Ctr Neurodegenerat & Expt Therapeut, Birmingham, AL 35294 USA.
[McLean, Pamela J.] Massachusetts Gen Hosp, Mass Gen Inst Neurodegenerat Dis, Dept Neurol, Charlestown, MA USA.
RP Standaert, DG (reprint author), Univ Alabama, Ctr Neurodegenerat & Expt Therapeut, 1719 6th Ave S,CIRC 516, Birmingham, AL 35294 USA.
EM dstandaert@uab.edu
RI Cao, Shuwen/E-1924-2016
FU National Institutes of Health [P50 NS38372, P30 NS057098]; American
Parkinson's Disease Association
FX This work was supported by the National Institutes of Health (Grant No.
P50 NS38372 and P30 NS057098) and by the American Parkinson's Disease
Association.
NR 63
TC 93
Z9 98
U1 2
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-3069
J9 J NEUROPATH EXP NEUR
JI J. Neuropathol. Exp. Neurol.
PD DEC
PY 2008
VL 67
IS 12
BP 1149
EP 1158
DI 10.1097/NEN.0b013e31818e5e99
PG 10
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 378VH
UT WOS:000261352100004
PM 19018246
ER
PT J
AU Freeman, SH
Kandel, R
Cruz, L
Rozkalne, A
Newell, K
Frosch, MP
Hedley-Whyte, ET
Locascio, JJ
Lipsitz, LA
Hyman, BT
AF Freeman, Stefanie H.
Kandel, Ruth
Cruz, Luis
Rozkalne, Anete
Newell, Kathy
Frosch, Matthew P.
Hedley-Whyte, E. Tessa
Locascio, Joseph J.
Lipsitz, Lewis A.
Hyman, Bradley T.
TI Preservation of Neuronal Number Despite Age-Related Cortical Brain
Atrophy in Elderly Subjects Without Alzheimer Disease
SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
LA English
DT Article
DE Aging; Cerebral cortex; Neurons; Stereology
ID HUMAN CEREBRAL-CORTEX; RHESUS-MONKEY; HUMAN NEOCORTEX; GRAY-MATTER;
IN-VIVO; LAYER 1; DECLINE; MRI
AB Cerebral volume loss has long been associated with normal aging, bill Whether this is due to aging itself or to age-related diseases, including incipient Alzheimer disease, is uncertain. To understand the changes that occur in the aging brain, we examined the cerebral cortex of 27 normal individuals ranging in age from 56 to 103 years. None fulfilled the criteria for the neuropathologic diagnosis of, Alzheimer disease or other neurodegenerative disease. Seventeen of the elderly participants had cognitive testing an average of 6.7 months prior to death. we used quantitative approaches to analyze cortical thickness, neuronal number, and density. Frontal and temporal neocortical regions had clear evidence of cortical thinning with age, but total neuronal numbers in frontal and temporal neocortical regions remained relatively constant during a 50-year age range. These data suggest that loss of neuronal and dendritic architecture, rather than loss of neurons. underlies neocortical volume loss with increasing age in the absence of Alzheimer disease.
C1 [Freeman, Stefanie H.; Frosch, Matthew P.; Hedley-Whyte, E. Tessa; Hyman, Bradley T.] Massachusetts Gen Hosp, Dept Pathol, CS Kubik Lab Neuropathol, Boston, MA 02114 USA.
[Freeman, Stefanie H.; Rozkalne, Anete; Frosch, Matthew P.; Locascio, Joseph J.; Hyman, Bradley T.] Massachusetts Gen Hosp, Dept Neurol, MassGen Inst Neurodegenerat Dis, Alzheimer Res Unit, Boston, MA 02114 USA.
[Kandel, Ruth; Lipsitz, Lewis A.] Harvard Univ, Sch Med, Hebrew Senior Life & Beth Israel Deaconess Med Ct, Boston, MA USA.
[Cruz, Luis] Boston Univ, Ctr Polymer Studies, Dept Phys, Boston, MA 02215 USA.
[Newell, Kathy] Univ Kansas, Med Ctr, Dept Pathol, Kansas City, KS 66103 USA.
[Locascio, Joseph J.] MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA.
RP Freeman, SH (reprint author), 200 Abbott Pk Rd, Abbott Pk, IL 60064 USA.
EM freestefanie@gmail.com
RI Cruz Cruz, Luis/B-2685-2013
FU Massachusetts Alzheimer Disease Research Center [AG05134, AG09487,
AG004390, R01-AG021133, R21-AG023661, R03-AG024633]
FX Supportcd by Grant Nos. AG05134. AG09487, AG004390. R01-AG021133,
R21-AG023661, and R03-AG024633 from the Massachusetts Alzheimer Disease
Research Center.
NR 35
TC 68
Z9 70
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-3069
J9 J NEUROPATH EXP NEUR
JI J. Neuropathol. Exp. Neurol.
PD DEC
PY 2008
VL 67
IS 12
BP 1205
EP 1212
DI 10.1097/NEN.0b013e31818fc72f
PG 8
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 378VH
UT WOS:000261352100009
PM 19018241
ER
PT J
AU Vincent, JL
Kahn, I
Snyder, AZ
Raichle, ME
Buckner, RL
AF Vincent, Justin L.
Kahn, Itamar
Snyder, Abraham Z.
Raichle, Marcus E.
Buckner, Randy L.
TI Evidence for a Frontoparietal Control System Revealed by Intrinsic
Functional Connectivity
SO JOURNAL OF NEUROPHYSIOLOGY
LA English
DT Article
ID ANTERIOR CINGULATE CORTEX; DEFAULT-MODE NETWORK; BOLD SIGNAL
FLUCTUATIONS; HUMAN PREFRONTAL CORTEX; RESTING-STATE NETWORKS; HUMAN
CEREBRAL-CORTEX; COGNITIVE CONTROL; MEMORY RETRIEVAL; EPISODIC MEMORY;
WORKING-MEMORY
AB Vincent JL, Kahn I, Snyder AZ, Raichle ME, Buckner RL. Evidence for a frontoparietal control system revealed by intrinsic functional connectivity. J Neurophysiol 100: 3328-3342, 2008. First published September 17, 2008; doi: 10.1152/jn.90355.2008. Two functionally distinct, and potentially competing, brain networks have been recently identified that can be broadly distinguished by their contrasting roles in attention to the external world versus internally directed mentation involving long-term memory. At the core of these two networks are the dorsal attention system and the hippocampal-cortical memory system, a component of the brain's default network. Here spontaneous blood-oxygenation-level-dependent ( BOLD) signal correlations were used in three separate functional magnetic resonance imaging data sets ( n = 105) to define a third system, the frontoparietal control system, which is spatially interposed between these two previously defined systems. The frontoparietal control system includes many regions identified as supporting cognitive control and decision-making processes including lateral prefrontal cortex, anterior cingulate cortex, and inferior parietal lobule. Detailed analysis of frontal and parietal cortex, including use of high-resolution data, revealed clear evidence for contiguous but distinct regions: in general, the regions associated with the frontoparietal control system are situated between components of the dorsal attention and hippocampal-cortical memory systems. The frontoparietal control system is therefore anatomically positioned to integrate information from these two opposing brain systems.
C1 [Vincent, Justin L.; Buckner, Randy L.] Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA.
[Vincent, Justin L.; Buckner, Randy L.] Harvard Univ, Ctr Brain Sci, Cambridge, MA 02138 USA.
[Vincent, Justin L.; Snyder, Abraham Z.; Raichle, Marcus E.] Washington Univ, Sch Med, Mallinckrodt Inst Radiol, St Louis, MO USA.
[Snyder, Abraham Z.; Raichle, Marcus E.] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA.
[Raichle, Marcus E.] Washington Univ, Sch Med, Dept Anat & Neurobiol, St Louis, MO 63110 USA.
[Raichle, Marcus E.] Washington Univ, Sch Med, Dept Biomed Engn, St Louis, MO USA.
[Vincent, Justin L.; Kahn, Itamar; Buckner, Randy L.] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Boston, MA 02114 USA.
[Kahn, Itamar; Buckner, Randy L.] Howard Hughes Med Inst, Chevy Chase, MD USA.
RP Vincent, JL (reprint author), Harvard Univ, Dept Psychol, 33 Kirkland St,WJH 274, Cambridge, MA 02138 USA.
EM vincent@nmr.mgh.harvard.edu
FU National Institutes of Health [AG-021910, NS-06833]; Mallinckrodt
Institute of Radiology; AAMCBR; McDonnell Foundation; Howard Hughes
Medical Institute
FX This work was supported by National Institutes of Health Grants
AG-021910 and NS-06833, the Mallinckrodt Institute of Radiology, AAMCBR,
the James S McDonnell Foundation, and the Howard Hughes Medical
Institute.
NR 97
TC 600
Z9 608
U1 18
U2 74
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-3077
J9 J NEUROPHYSIOL
JI J. Neurophysiol.
PD DEC
PY 2008
VL 100
IS 6
BP 3328
EP 3342
DI 10.1152/jn.90355.2008
PG 15
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA 380EQ
UT WOS:000261449400030
PM 18799601
ER
PT J
AU McMurtray, AM
Sultzer, DL
Monserratt, L
Yeo, T
Mendez, MF
AF McMurtray, Aaron M.
Sultzer, David L.
Monserratt, Lorena
Yeo, Tuty
Mendez, Mario F.
TI Content-specific delusions from right caudate lacunar stroke:
Association with prefrontal hypometabolism
SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES
LA English
DT Article
ID NEURO-BEHAVIORAL CHANGES; BASAL GANGLIA; COGNITIVE IMPAIRMENT;
ALZHEIMERS-DISEASE; LESIONS; INFARCTS; DEMENTIA; CIRCUITS; NUCLEUS;
CORTEX
AB Patients with caudate lesions can present with content-specific delusions, possibly due to disruption of frontosubcortical circuits connecting the frontal lobes with the basal ganglia. This study included eight patients who presented with content-specific delusions after right caudate stroke and an equal number of matched controls, without stroke or delusions. Compared to controls, patients with caudate lesions performed less well on tests of memory, abstract reasoning, and frontal executive functions, and had significantly reduced metabolism in the inferior prefrontal cortex. These patients suggest an etiological relationship between alterations in inferior prefrontal functions and the development of content-specific delusions.
C1 [McMurtray, Aaron M.; Sultzer, David L.; Monserratt, Lorena; Mendez, Mario F.] VA Greater Los Angeles Healthcare Syst, Neurobehav Unit 116AF, Neurol Serv, Los Angeles, CA 90073 USA.
[McMurtray, Aaron M.; Sultzer, David L.; Monserratt, Lorena; Mendez, Mario F.] VA Greater Los Angeles Healthcare Syst, Neurobehav Unit 116AF, Psychiat & Mental Hlth Serv, Los Angeles, CA 90073 USA.
[McMurtray, Aaron M.; Sultzer, David L.; Monserratt, Lorena; Yeo, Tuty; Mendez, Mario F.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA.
[McMurtray, Aaron M.; Sultzer, David L.; Monserratt, Lorena; Yeo, Tuty; Mendez, Mario F.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA.
RP Mendez, MF (reprint author), VA Greater Los Angeles Healthcare Syst, Neurobehav Unit 116AF, Neurol Serv, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM mmendez@ucla.edu
FU PHS HHS [R01 56031]
NR 31
TC 11
Z9 11
U1 0
U2 0
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0895-0172
J9 J NEUROPSYCH CLIN N
JI J. Neuropsychiatr. Clin. Neurosci.
PD WIN
PY 2008
VL 20
IS 1
BP 62
EP 67
DI 10.1176/appi.neuropsych.20.1.62
PG 6
WC Clinical Neurology; Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 264SP
UT WOS:000253311000006
PM 18305285
ER
PT J
AU McQueen, M
MacCollin, M
Gusella, J
Plotkin, SR
AF McQueen, Mary
MacCollin, Mia
Gusella, James
Plotkin, Scott R.
TI Patient and Physician Attitudes Regarding Clinical Trials in
Neurofibromatosis 1
SO JOURNAL OF NEUROSCIENCE NURSING
LA English
DT Article
AB Neurofibromatosis 1 (NF1) is a multisystem genetic disorder that primarily affects the skin (freckling and cafe-au-lait macules), nervous system (neurofibromas, optic gliomas, and learning disabilities), and skeletal system (pseudoarthroses). The interest in pharmacological intervention for patients with NF1 has grown in recent years. However, little is known about the attitudes and priorities of patients, families, and physicians regarding participation in clinical trials. We surveyed 74 adult patients or parents of patients with NF1 and 69 care providers participating in a neurofibromatosis clinic to assess their willingness to participate in clinical trials and their opinions about which conditions they thought were most important to treat. Both patients and care providers are willing to participate in clinical trials for NF1 and both groups rate malignant peripheral nerve sheath tumors as the most urgent for new treatments. There are concordant views among patients and physicians concerning clinical trials for NF1, and patients do not dismiss participation in placebo-controlled trials. Neuroscience nurses are poised to facilitate the research process from conception through implementation as they take the viewpoints of our study populations into consideration.
C1 [MacCollin, Mia; Plotkin, Scott R.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[McQueen, Mary] Univ Colorado, Wardenburg Hlth Ctr, Boulder, CO 80309 USA.
[Gusella, James] Harvard Univ, Sch Med, Ctr Neurofibromatosis & Allied Disorders, Boston, MA USA.
[Gusella, James] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
RP Plotkin, SR (reprint author), Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
EM splotkin@partners.org
FU Neurofibromatosis Inc., New England; Alsam Foundation
FX This work was supported by grants to James Gusella, PhD, from
Neurofibromatosis Inc., New England, and from the Alsam Foundation.
NR 10
TC 4
Z9 4
U1 1
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0888-0395
J9 J NEUROSCI NURS
JI J. Neurosci. Nurs.
PD DEC
PY 2008
VL 40
IS 6
BP 341
EP 345
PG 5
WC Clinical Neurology; Nursing
SC Neurosciences & Neurology; Nursing
GA V13AM
UT WOS:000207639700005
PM 19170300
ER
PT J
AU Ahmad, M
Rose, ME
Vagni, V
Griffith, RP
Dixon, CE
Kochanek, PM
Hickey, RW
Graham, SH
AF Ahmad, Muzamil
Rose, Marie E.
Vagni, Vincent
Griffith, Raymond P.
Dixon, C. Edward
Kochanek, Patrick M.
Hickey, Robert W.
Graham, Steven H.
TI Genetic Disruption of Cyclooxygenase-2 Does Not Improve Histological or
Behavioral Outcome After Traumatic Brain Injury in Mice
SO JOURNAL OF NEUROSCIENCE RESEARCH
LA English
DT Article
DE cyclooxygenase; prostaglandin E(2); TUNEL staining; behavior; Morris
water maze
ID CELL-DEATH; INHIBITOR ROFECOXIB; COX-2 INHIBITORS; IN-SITU; RATS;
EXPRESSION; CELECOXIB; INFLAMMATION; NEURONS; EDEMA
AB Increasing evidence suggests a role for cyclooxygenase-2 (COX-2) in traumatic brain injury (TBI). In the present study, the role of COX-2 in TBI was investigated using COX-2 gene-disrupted (COX-2 null) mice and wild-type (WT) controls that were subjected to the controlled cortical impact (CCI) model of TBI. There was increased expression of COX-2 in ipsilateral hippocampus in WT mice subjected to CCI. CCI resulted in a significant increase in prostaglandin E(2) concentrations in WT compared with COX-2 null hippocampi. There was a significant increase in TUNEL staining of CA1 neurons 24 hr after CCI in WT, but not in COX-2 null mice, compared with sham-operated controls, which is consistent with a protective role for COX-2 in the early phase of injury after TBI. However, there was no difference in lesion volume 21 days after CCI in COX-2 null and WT mice. COX-2 gene disruption did not alter Morris water maze performance. Taken together, these results suggest only a minor role for COX-2 activity in determining outcome after TBI in mouse. (c) 2008 Wiley-Liss, Inc.
C1 [Ahmad, Muzamil; Rose, Marie E.; Graham, Steven H.] VA Pittsburgh Healthcare Syst, Ctr Geriatr Res Educ & Clin, Pittsburgh, PA 15206 USA.
[Ahmad, Muzamil; Rose, Marie E.; Graham, Steven H.] Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15261 USA.
[Vagni, Vincent; Kochanek, Patrick M.] Univ Pittsburgh, Sch Med, Dept Crit Care Med, Pittsburgh, PA USA.
[Griffith, Raymond P.; Dixon, C. Edward] Univ Pittsburgh, Sch Med, Dept Neurosurg, Pittsburgh, PA 15261 USA.
[Kochanek, Patrick M.; Hickey, Robert W.] Univ Pittsburgh, Sch Med, Dept Pediat, Pittsburgh, PA 15261 USA.
RP Graham, SH (reprint author), VA Pittsburgh Healthcare Syst, Ctr Geriatr Res Educ & Clin, 151-UH,7108 Highland Dr, Pittsburgh, PA 15206 USA.
EM sgra@pitt.edu
RI Kochanek, Patrick/D-2371-2015
OI Kochanek, Patrick/0000-0002-2627-913X
FU Department of Veterans Affairs/Department of Defense; Traumatic Brain
Injury Initiative Merit Review Program; NIH [R01 NS37459]
FX Contract grant sponsor: Department of Veterans Affairs/Department of
Defense, Traumatic Brain Injury Initiative Merit Review Program (to
S.H.G.); Contract grant sponsor: NIH; Contract grant number: R01 NS37459
(to S.H.G.).
NR 48
TC 17
Z9 17
U1 0
U2 1
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0360-4012
J9 J NEUROSCI RES
JI J. Neurosci. Res.
PD DEC
PY 2008
VL 86
IS 16
BP 3605
EP 3612
DI 10.1002/jnr.21809
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 383CO
UT WOS:000261651900012
PM 18711748
ER
PT J
AU Susarla, SM
Dodson, TB
Kaban, LB
AF Susarla, Srinivas M.
Dodson, Thomas B.
Kaban, Leonard B.
TI Measurement and Interpretation of a Maxillary Occlusal Cant in the
Frontal Plane
SO JOURNAL OF ORAL AND MAXILLOFACIAL SURGERY
LA English
DT Article
ID ASYMMETRY; EXPANSION
AB Purpose: A cant of the maxillary intermolar (M1-M1) plane is a reflection of facial asymmetry and can be measured on an anterior-posterior cephalogram in degrees relative to the true horizontal or directly on the patient as the difference in millimeters between the right and left medial canthi to canine distances. The purpose of this study is to measure the correlation between the maxillary cant measured in degrees and measured in millimeters.
Materials and Methods: We hypothesize that the number of degrees of maxillary cant equals the millimeter difference between the lengths of the 2 sides of the maxilla, based upon the trigonometric relationship between the degree of cant, vertical length, and M1-M1 distance. To confirm this hypothesis, we evaluated a range of M1-M1 distances and Computed the predicted vertical discrepancy between the 2 sides of the maxilla. Bivariate correlations were used to evaluate the association between the degree of cant and predicted vertical discrepancy.
Results: In the range of M1-M1 distances (47.5-61.1 mm) evaluated, cants ranging from 3 to 10 degrees are highly correlated with the vertical difference in millimeters (r = 0.96 P < .01). The mean error between the degree of cant and vertical difference was 9%.
Conclusion: The degrees Of occlusal cant relative to the true horizontal measured cephalometrically in the frontal plane is equal to the linear millimeter difference between the right and left medial canthi to the right and left canine tips. (C) 2008 American Association of Oral and Maxillofacial Surgeons
C1 [Susarla, Srinivas M.; Kaban, Leonard B.] Massachusetts Gen Hosp, Dept Oral & Maxillofacial Surg, Boston, MA 02114 USA.
[Dodson, Thomas B.] Harvard Univ, Sch Dent Med, Dept Oral & Maxillofacial Surg, Boston, MA 02115 USA.
[Dodson, Thomas B.] Massachusetts Gen Hosp, Ctr Appl Clin Invest, Boston, MA 02114 USA.
RP Susarla, SM (reprint author), Massachusetts Gen Hosp, Dept Oral & Maxillofacial Surg, 55 Fruit St,Warren 1201, Boston, MA 02114 USA.
EM smsusarla@gmail.com
OI Susarla, Srinivas/0000-0003-0155-8260
FU Oral and Maxillofacial Surgery Foundation Fellowship in Clinical
Investigation; Massachusetts General Hospital Department of Oral and
Maxillofacial Surgery Education and Research Fund
FX This study was made possible by Support from the Oral and Maxillofacial
Surgery Foundation Fellowship in Clinical Investigation (S.M.S.) and the
Massachusetts General Hospital Department of Oral and Maxillofacial
Surgery Education and Research Fund (T.B.D., S.M.S.).
NR 7
TC 7
Z9 7
U1 1
U2 3
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0278-2391
J9 J ORAL MAXIL SURG
JI J. Oral Maxillofac. Surg.
PD DEC
PY 2008
VL 66
IS 12
BP 2498
EP 2502
DI 10.1016/j.joms.2008.06.072
PG 5
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 378VB
UT WOS:000261351400013
PM 19022130
ER
PT J
AU Peritz, DC
Duncan, C
Kurek, K
Perez-Atayde, AR
Lehmann, LE
AF Peritz, David C.
Duncan, Christine
Kurek, Kyle
Perez-Atayde, Antonio R.
Lehmann, Leslie E.
TI Visceral Varicella Zoster Virus (VZV) After Allogeneic Hematopoietic
Stem Cell Transplant (HSCT) in Pediatric Patients With Chronic
Graft-Versus-Host Disease (cGVHD)
SO JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY
LA English
DT Article
DE hematopoietic stem cell transplant; reactivation of varicella zoster
virus; allogeneic; chronic graft-versus-host disease; hyponatremia
ID BONE-MARROW-TRANSPLANTATION; HERPES-ZOSTER; RISK-FACTORS; INFECTION;
ACYCLOVIR; CHILDREN; INVOLVEMENT
AB Reactivation of latent varicella zoster virus is one infectious complication associated with the extensive immuno-suppression necessary for hematopoietic stein cell transplant. Most cases are limited to skin and mortality is low. Isolated visceral zoster is rare, presenting with ileus/abdominal pain, hepatitis, and/or hyponatremia. We present 2 cases of visceral varicella zoster virus in adolescents with chronic graft-versus-host disease after hematopoietic stein cell transplant. Both presented with elevated liver enzymes, severe abdominal pain, and hyponatremia but lacked cutaneous involvement. Both received high-dose acyclovir and showed improvement, but eventually expired from hepatic failure. The diagnosis of visceral zoster can be difficult especially without cutaneous manifestations. Vigilance is necessary in patients with chronic graft-versus-host disease, abdominal pain, and/or hepatitis and antiviral therapy should be initiated promptly.
C1 [Peritz, David C.; Duncan, Christine; Lehmann, Leslie E.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Kurek, Kyle; Perez-Atayde, Antonio R.] Childrens Hosp, Boston, MA 02115 USA.
RP Peritz, DC (reprint author), 44 Binney St, Boston, MA 02115 USA.
EM David_Peritz@dfci.harvard.edu
NR 18
TC 10
Z9 10
U1 2
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1077-4114
J9 J PEDIAT HEMATOL ONC
JI J. Pediatr. Hematol. Oncol.
PD DEC
PY 2008
VL 30
IS 12
BP 931
EP 934
PG 4
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA 381DW
UT WOS:000261516800016
PM 19131784
ER
PT J
AU Lovejoy, FH
Nathan, DG
Zuckerman, BS
Pizzo, PA
Fleisher, GR
Vinci, RJ
AF Lovejoy, Frederick H., Jr.
Nathan, David G.
Zuckerman, Barry S.
Pizzo, Philip A.
Fleisher, Gary R.
Vinci, Robert J.
TI The Merger of Two Pediatric Residency Programs: Lessons Learned
SO JOURNAL OF PEDIATRICS
LA English
DT Editorial Material
C1 [Lovejoy, Frederick H., Jr.; Pizzo, Philip A.; Fleisher, Gary R.] Childrens Hosp, Dept Med, Boston, MA 02115 USA.
[Nathan, David G.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Zuckerman, Barry S.; Vinci, Robert J.] Boston Med Ctr, Dept Pediat, Boston, MA USA.
[Pizzo, Philip A.] Stanford Med Sch, Palo Alto, CA USA.
RP Lovejoy, FH (reprint author), Childrens Hosp, Dept Med, 300 Longwood Ave,Hunnewell 2, Boston, MA 02115 USA.
EM lovejoy@tch.harvard.edu
OI Vinci, Robert/0000-0002-2616-1879; Zuckerman, Barry/0000-0002-0044-2592
NR 0
TC 2
Z9 2
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
JI J. Pediatr.
PD DEC
PY 2008
VL 153
IS 6
BP 731
EP 732
DI 10.1016/j.jpeds.2008.07.036
PG 2
WC Pediatrics
SC Pediatrics
GA 383FK
UT WOS:000261659300001
PM 19014810
ER
PT J
AU Cole, CM
Sundararaj, KP
Leite, RS
Nareika, A
Slate, EH
Sanders, JJ
Lopes-Virella, MF
Huang, Y
AF Cole, C. M.
Sundararaj, K. P.
Leite, R. S.
Nareika, A.
Slate, E. H.
Sanders, J. J.
Lopes-Virella, M. F.
Huang, Y.
TI A trend of increase in periodontal interleukin-6 expression across
patients with neither diabetes nor periodontal disease, patients with
periodontal disease alone, and patients with both diseases
SO JOURNAL OF PERIODONTAL RESEARCH
LA English
DT Article
DE periodontal diseases; diabetes mellitus; interleukin-6; gene expression
ID INFLAMMATION; MEDIATOR
AB Epidemiological studies have established that patients with diabetes have increased prevalence and severity of periodontal disease. However, the periodontal expression of inflammatory cytokines and matrix metalloproteinases (MMPs) in diabetic patients has not been well characterized. The objective of this study was to determine the difference in the periodontal expression of MMP-1, MMP-8, interleukin-6, tumor necrosis factor-alpha and interleukin-1 beta between diabetic and nondiabetic patients.
Periodontal tissue specimens were collected from nine nondiabetic patients without periodontal disease (group 1), from 11 nondiabetic patients with periodontal disease (group 2) and from seven diabetic patients with periodontal disease (group 3). The expression of MMP-1, MMP-8, interleukin-6, tumor necrosis factor-alpha and interleukin-1 beta was quantified using real-time polymerase chain reaction.
The nonparametric Kruskal-Wallis test showed that the difference in interleukin-6 expression among the groups was statistically significant (p = 0.04). Furthermore, the generalized Kruskal-Wallis nonparametric linear-by-linear association test showed a statistically significant trend of increase in the expression of interleukin-6 from group 1 to group 2 to group 3 (p = 0.02) and a suggestion of such a trend for MMP-1 (p = 0.05). No increase in MMP-8 expression was observed in patients in group 3 compared to patients in groups 1 and 2. Although the average expression levels of MMP-1, interleukin-1 beta and tumor necrosis factor-alpha were increased from group 1 to group 3, the differences were not statistically significant.
A trend of increased interleukin-6 expression in periodontal tissues was observed across patients with neither diabetes nor periodontal disease, patients with periodontal disease alone, and patients with both diseases.
C1 [Cole, C. M.; Leite, R. S.; Sanders, J. J.] Med Univ S Carolina, Div Periodont, Dept Stomatol, Coll Dent Med, Charleston, SC 29403 USA.
[Sundararaj, K. P.; Nareika, A.; Lopes-Virella, M. F.; Huang, Y.] Med Univ S Carolina, Div Endocrinol Diabet & Med Genet, Dept Med, Charleston, SC 29403 USA.
[Slate, E. H.] Med Univ S Carolina, Dept Biostat Bioinformat & Epidemiol, Charleston, SC 29403 USA.
[Lopes-Virella, M. F.; Huang, Y.] Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC USA.
RP Huang, Y (reprint author), Med Univ S Carolina, Vet Affairs Med Ctr, 114 Doughty St, Charleston, SC 29403 USA.
EM huangyan@musc.edu
FU NIH [DE16353]; NIH/NCRR COBRE [P20 RR017696]
FX This work was supported by NIH grant DE16353 and a Merit Review Grant
from the Department of Veterans Affairs (to YH). EHS, JJS, SDL and MFL-V
additionally acknowledge partial support from the NIH/NCRR COBRE project
P20 RR017696.
NR 28
TC 15
Z9 15
U1 0
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-3484
J9 J PERIODONTAL RES
JI J. Periodont. Res.
PD DEC
PY 2008
VL 43
IS 6
BP 717
EP 722
DI 10.1111/j.1600-0765.2008.01082.x
PG 6
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 374TZ
UT WOS:000261067900016
PM 18627438
ER
PT J
AU Claude, O
Picard, A
O'Sullivan, N
Baccache, S
Momtchilova, M
Enjolras, O
Vazquez, MP
Diner, PA
AF Claude, O.
Picard, A.
O'Sullivan, N.
Baccache, S.
Momtchilova, M.
Enjolras, O.
Vazquez, M. P.
Diner, P. A.
TI Use of ultrasonic dissection in the early surgical management of
periorbital haemangiomas
SO JOURNAL OF PLASTIC RECONSTRUCTIVE AND AESTHETIC SURGERY
LA English
DT Article
DE Haemangioma; Periorbital; Ultrasonic scalpel; Dissectron (R); Amblyopia
ID INTRALESIONAL CORTICOSTEROID INJECTION; CAPILLARY HEMANGIOMAS; VASCULAR
MALFORMATIONS; CUTANEOUS HEMANGIOMAS; INFANTILE HEMANGIOMA; ADRENAL
SUPPRESSION; ARTERY-OCCLUSION; LASER TREATMENT; THERAPY; INFANCY
AB Purpose: To evaluate the efficacy and safety of the early surgical excision of periorbital haemangiomas with an ultrasonic scalpel in infants at risk of visual impairment.
Study: A retrospective analysis of 67 infants diagnosed to be at risk of amblyopia from periorbital haemangiomas, treated consecutively with the Dissectron (R) between 1994 and 2005. Ophthalmic outcome parameters included the pre- and postoperative measurement of visual axis occlusion, strabismus, astigmatism, and degree of amblyopia.
Results: Visual performance showed an overall improvement of 30% following treatment. Seventy-six patients were found to have abnormal ophthalmic examinations preoperatively, compared to 46 following surgery. After surgery, visual axis occlusion decreased from 73 to 6%; amblyopia decreased from 67 to 22%, strabismus decreased from 26 to 18% and astigmatism (>one dioptre) decreased from 66 to 31 %. Mean astigmatism values decreased from 3.5 to 1.9 dioptres. No new cases of astigmatism, strabismus or amblyopia were diagnosed postoperativeiy. Three minor complications resolved with conservative treatment. All patients were satisfied with the outcome of their surgery.
Conclusion: Early surgical excision of periorbital haemangiomas using the Dissectron (R) in infants with an established risk of visual impairment is a safe and effective alternative to pharmacological therapy. The use of the Dissectron (R) is associated with reduced operative times and a shorter hospital stay. (C) 2007 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved.
C1 [Claude, O.; Picard, A.; Baccache, S.; Enjolras, O.; Vazquez, M. P.; Diner, P. A.] Univ Paris 06, Children Hosp Armand Trousseau, INSERM, U714,Dept Plast & Maxillofacial Surg, F-75012 Paris, France.
[O'Sullivan, N.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Plast Surg Res Lab, Boston, MA 02114 USA.
[Momtchilova, M.] Univ Paris 06, Children Hosp Armand Trousseau, Dept Ophthalmol, F-75012 Paris, France.
RP Claude, O (reprint author), Univ Paris 06, Children Hosp Armand Trousseau, INSERM, U714,Dept Plast & Maxillofacial Surg, 26 Rue Docteur Arnold Netter, F-75012 Paris, France.
EM olivier_claude@hotmail.com
NR 35
TC 4
Z9 4
U1 0
U2 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1748-6815
J9 J PLAST RECONSTR AES
JI J. Plast. Reconstr. Aesthet. Surg.
PD DEC
PY 2008
VL 61
IS 12
BP 1479
EP 1485
DI 10.1016/j.bjps.2007.09.027
PG 7
WC Surgery
SC Surgery
GA 381EI
UT WOS:000261518000009
PM 18037085
ER
PT J
AU Greer, JA
Pirl, WF
Park, ER
Lynch, TJ
Ternel, JS
AF Greer, Joseph A.
Pirl, William F.
Park, Elyse R.
Lynch, Thomas J.
Ternel, Jennifer S.
TI Behavioral and psychological predictors of chemotherapy adherence in
patients with advanced non-small cell lung cancer
SO JOURNAL OF PSYCHOSOMATIC RESEARCH
LA English
DT Article
DE Non-small cell lung cancer; Chemotherapy; Adherence
ID QUALITY-OF-LIFE; DEPRESSION; SURVIVAL; DISTRESS; SMOKING; ANXIETY; SCALE
AB Objective: Dose delays and reductions in chemotherapy due to hematologic toxicities are common among patients with advanced non-small cell lung cancer (NSCLC). However, limited data on behavioral or psychological predictors of chemotherapy adherence exist. The goal of this study was to explore the frequency and clinical predictors of infusion dose delays and reductions in this patient population. Methods: Fifty patients newly diagnosed with advanced NSCLC of high performance status (Eastern Cooperative Oncology Group Performance Status=0-1) completed baseline assessments on quality of life (Functional Assessment of Cancer Therapy - Lung) and mood (Hospital Anxiety and Depression Scale) within 8 weeks of diagnosis. Participants were followed prospectively for 6 months. Chemotherapy dosing data came from medical chart review. Results: All patients received chemotherapy during the course of the study, beginning with a platinum-based doublet (74%), an oral epidermal growth factor receptor-tyrosine kinase inhibitor (14%), or a parenteral single agent (12%). Forty percent (n=20) of patients had a dose delay (39%) and/or reduction (16%) in their scheduled infusions. Fisher's Exact Tests and regression analyses showed that patients who experienced neutropenia, smoked at the time of diagnosis, or reported heightened baseline anxiety were significantly more likely to experience dose delays or reductions. There were no associations between chemotherapy adherence and patient demographics, performance status, or quality of life. Conclusion: In this sample, more than one third of patients with advanced NSCLC experienced either a dose delay or reduction in prescribed chemotherapy regimens. Behavioral and psychological factors, such as tobacco use and anxiety symptoms, appear to play an important role in chemotherapy adherence, though further study is required to confirm these findings. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Greer, Joseph A.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
RP Greer, JA (reprint author), Massachusetts Gen Hosp, Dept Psychiat, WACC 812,15 Parkman St, Boston, MA 02114 USA.
EM jgreer2@partners.org
FU NIH/NCI [R03 CA129478, K23 CA115908]; Amgen (Temel)
FX This work was supported by NIH/NCI R03 CA129478 (Greer), NIH/NCI K23
CA115908 (Pirl), and an investigator-initiated research grant from Amgen
(Temel).
NR 16
TC 41
Z9 41
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0022-3999
J9 J PSYCHOSOM RES
JI J. Psychosomat. Res.
PD DEC
PY 2008
VL 65
IS 6
BP 549
EP 552
DI 10.1016/j.jpsychores.2008.03.005
PG 4
WC Psychiatry
SC Psychiatry
GA 382RK
UT WOS:000261622900006
PM 19027443
ER
PT J
AU Huffman, JC
Smith, FA
Blais, MA
Januzzi, JL
Fricchione, GL
AF Huffman, Jeff C.
Smith, Felicia A.
Blais, Mark A.
Januzzi, James L.
Fricchione, Gregory L.
TI Anxiety, independent of depressive symptoms, is associated with
in-hospital cardiac complications after acute myocardial infarction
SO JOURNAL OF PSYCHOSOMATIC RESEARCH
LA English
DT Article
DE Anxiety; Depression; Depressive disorder, major; Myocardial infarction
ID CORONARY-ARTERY-DISEASE; PRIMARY-CARE PATIENTS; HEART-DISEASE;
CARDIOVASCULAR-DISEASE; MAJOR DEPRESSION; CHEST-PAIN; TASK-FORCE;
EVENTS; IMPACT; DISORDERS
AB Objective: Post-myocardial infarction (MI) anxiety, independent of demographic and medical variables, has been linked to in-hospital cardiac complications in prior studies, but such studies have not included a concomitant assessment of depressive symptoms. The aim of this exploratory study was to determine whether post-MI anxiety was associated with in-hospital cardiac complications, independent of depressive symptoms. Methods: Subjects within 72 hours of acute MI (n=110) were prospectively assessed for anxiety [using the Beck Anxiety Inventory (BAI)] and depressive symptoms (using the Beck Depression Inventory-II and structured interview diagnoses of major depressive disorder). Individual in-hospital complications and pooled serious cardiac complications (defined as recurrent ischemia, reinfarction, congestive heart failure, and ventricular arrhythmia requiring intervention) were recorded via chart review. Results: On hierarchical multiple logistic regression analysis that accounted for demographic variables, cardiac illness, and depressive symptoms, post-MI anxiety was significantly associated with pooled serious in-hospital cardiac complications (P=.003). In addition, when the anxiety measure was limited to only the psychological symptoms of anxiety ("BAI-P"), post-MI anxiety remained an independent predictor of cardiac complications (P=.015). Conclusions: These findings suggest that the association of post-MI anxiety with in-hospital cardiac complications exists above and beyond the effects of depression. Larger studies are needed to confirm these findings, and treatment studies are needed to determine the impact of anxiety treatment on in-hospital cardiac outcomes. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Huffman, Jeff C.; Smith, Felicia A.; Blais, Mark A.; Fricchione, Gregory L.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Januzzi, James L.] Massachusetts Gen Hosp, Dept Cardiol, Boston, MA 02114 USA.
[Huffman, Jeff C.; Smith, Felicia A.; Blais, Mark A.; Januzzi, James L.; Fricchione, Gregory L.] Harvard Univ, Sch Med, Boston, MA USA.
RP Huffman, JC (reprint author), Massachusetts Gen Hosp, Dept Psychiat, 55 Fruit St Warren 1220C, Boston, MA 02114 USA.
EM jhuffman@partners.org
FU Kaplen Fellowship Award; Livingston Fellowship Award; Harvard Medical
School, Boston, MA, USA
FX The authors would like to thank Sara Nadelman for her editorial
assistance. This study was supported by the Kaplen Fellowship Award
Grant and the Livingston Fellowship Award Grant, both through Harvard
Medical School, Boston, MA, USA.
NR 43
TC 37
Z9 42
U1 0
U2 5
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0022-3999
J9 J PSYCHOSOM RES
JI J. Psychosomat. Res.
PD DEC
PY 2008
VL 65
IS 6
BP 557
EP 563
DI 10.1016/j.jpsychores.2008.08.001
PG 7
WC Psychiatry
SC Psychiatry
GA 382RK
UT WOS:000261622900008
PM 19027445
ER
PT J
AU Maserejian, NN
Tavares, MA
Hayes, C
Soncini, JA
Trachtenberg, FL
AF Maserejian, Nancy Nairi
Tavares, Mary A.
Hayes, Catherine
Soncini, Jennifer A.
Trachtenberg, Felicia L.
TI Rural and urban disparities in caries prevalence in children with unmet
dental needs: The New England Children's Amalgam Trial
SO JOURNAL OF PUBLIC HEALTH DENTISTRY
LA English
DT Article
DE dental caries; child; rural health; urban health; oral health; New
England; zero-inflated models
ID ZERO-INFLATED POISSON; ORAL-HEALTH-STATUS; EPIDEMIOLOGY; DETERMINANTS;
CONSUMPTION; ADOLESCENTS; ADULTS
AB Objectives: To compare the prevalence of caries between rural and urban children with unmet dental health needs who participated in the New England Children's Amalgam Trial. Methods: Baseline tooth and surface caries were clinically assessed in children from rural Maine (n = 243) and urban Boston (n = 291), who were aged 6 to 10 years, with two or more posterior carious teeth and no previous amalgam restorations. Statistical analyses used negative binomial models for primary dentition caries and zero-inflated models for permanent dentition caries. Results: Urban children had a higher mean number of carious primary surfaces (8.5 versus 7.4) and teeth (4.5 versus 3.9) than rural children. The difference remained statistically significant after adjusting for sociodemographic factors and toothbrushing frequency. In permanent dentition, urban children were approximately three times as likely to have any carious surfaces or teeth. However, rural/urban dwelling was not statistically significant in the linear analysis of caries prevalence among children with any permanent dentition caries. Covariates that were statistically significant in all models were age and number of teeth. Toothbrushing frequency was also important for permanent teeth. Conclusions: Within this population of New England children with unmet oral health needs, significant differences were apparent between rural and urban children in the extent of untreated dental decay. Results indicate that families who agree to participate in programs offering reduced cost or free dental care may present with varying amounts of dental need based on geographic location.
C1 [Maserejian, Nancy Nairi; Trachtenberg, Felicia L.] New England Res Inst, Watertown, MA 02472 USA.
[Tavares, Mary A.; Soncini, Jennifer A.] Forsyth Inst, Boston, MA USA.
[Hayes, Catherine] Tufts Univ, Sch Med, Dept Publ Hlth, Boston, MA 02111 USA.
[Hayes, Catherine] Tufts Univ, Sch Med, Community Serv, Boston, MA 02111 USA.
[Soncini, Jennifer A.] Boston Univ, Sch Dent Med, Dept Pediat Dent, Boston, MA 02215 USA.
RP Maserejian, NN (reprint author), New England Res Inst, 9 Galen St, Watertown, MA 02472 USA.
EM nmaserejian@neriscience.com
FU NIDCR NIH HHS [U01 DE11886]
NR 31
TC 8
Z9 8
U1 0
U2 3
PU AAPHD NATIONAL OFFICE
PI PORTLAND
PA 3760 SW LYLE COURT, PORTLAND, OR 97221 USA
SN 0022-4006
J9 J PUBLIC HEALTH DENT
JI J. Public Health Dent.
PD WIN
PY 2008
VL 68
IS 1
BP 7
EP 13
DI 10.1111/j.1752-7325.2007.00057.x
PG 7
WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
GA 275TR
UT WOS:000254095000002
PM 18179469
ER
PT J
AU Maserejian, NN
Trachtenberg, F
Hayes, C
Tavares, M
AF Maserejian, Nancy Nairi
Trachtenberg, Felicia
Hayes, Catherine
Tavares, Mary
TI Oral health disparities in children of immigrants: Dental caries
experience at enrollment and during follow-up in the New England
Children's Amalgam Trial
SO JOURNAL OF PUBLIC HEALTH DENTISTRY
LA English
DT Article
DE immigrants; dental care for children; pediatric dentistry; health
services delivery; public health dentistry; caries; incidence;
disparities
ID SWEDEN; ACCULTURATION; PREVALENCE; FAMILIES; SERVICE; AGE
AB Objectives: Previous research shows increased dental decay among immigrants, but little is known about the oral health of the growing population of children of immigrants. We compared the children of immigrants to the children of US-born caregivers in their caries experience at enrollment and their new caries increments during the 5-year New England Children's Amalgam Trial (NECAT). Methods: NECAT recruited 283 Boston-area children aged 6 to 10 with untreated caries and offered free semiannual preventive and restorative dental care during the trial. Sociodemographic factors and caregiver immigrant status were assessed through interviews. Multivariate negative binomial models evaluated the association between caregiver immigrant status and clinically assessed carious surfaces. Results: Forty percent of these Boston-area children had immigrant caregivers. At baseline, the children of immigrants had more carious surfaces (11.5 versus 9.4, adjusted for race/ethnicity, age, gender, and caregiver smoking status). Caregiver language preference explained some of this association. Immigrant status and language preference were not associated with 5-year caries increments. Conclusions: Prevalent disparities in the unmet dental needs of the immigrants' children were quickly ameliorated during participation in NECAT. Dental initiatives that target neighborhoods and are sensitive to acculturation levels may help improve and maintain the oral health of immigrant families.
C1 [Maserejian, Nancy Nairi; Trachtenberg, Felicia] New England Res Inst, Watertown, MA 02472 USA.
[Hayes, Catherine] Tufts Univ, Sch Dent Med, Dept Publ Hlth, Boston, MA 02111 USA.
[Hayes, Catherine] Tufts Univ, Sch Dent Med, Community Serv, Boston, MA 02111 USA.
[Tavares, Mary] Forsyth Inst, Boston, MA USA.
RP Maserejian, NN (reprint author), New England Res Inst, 9 Galen St, Watertown, MA 02472 USA.
EM nmaserejian@neriscience.com
FU NIDCR NIH HHS [U01 DE11886]
NR 25
TC 14
Z9 15
U1 0
U2 2
PU AAPHD NATIONAL OFFICE
PI PORTLAND
PA 3760 SW LYLE COURT, PORTLAND, OR 97221 USA
SN 0022-4006
J9 J PUBLIC HEALTH DENT
JI J. Public Health Dent.
PD WIN
PY 2008
VL 68
IS 1
BP 14
EP 21
DI 10.1111/j.1752-7325.2007.00060.x
PG 8
WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
GA 275TR
UT WOS:000254095000003
PM 18179466
ER
PT J
AU Pumbwe, L
Curzon, M
Wexler, HM
AF Pumbwe, Lilian
Curzon, Matthew
Wexler, Hannah M.
TI RAPID MULTIPLEX PCR ASSAY FOR SIMULTANEOUS DETECTION OF MAJOR ANTIBIOTIC
RESISTANCE DETERMINANTS IN CLINICAL ISOLATES OF BACTEROIDES FRAGILIS
SO JOURNAL OF RAPID METHODS AND AUTOMATION IN MICROBIOLOGY
LA English
DT Article
ID INDUCIBLE METRONIDAZOLE RESISTANCE; ANAEROBIC-BACTERIA; CONJUGATIVE
TRANSPOSON; NIM GENES; SUSCEPTIBILITY; CLINDAMYCIN; PREVALENCE; SPP.;
ERMF; CFIA
AB This study developed a rapid and cost-effective multiplex polymerase chain reaction assay (M-PCR) for simultaneous detection of major clinically relevant antibiotic resistance genes in Bacteroides fragilis. The M-PCR optimized amplification conditions with primers designed for detection of five resistance genes: carbapenems (cfiA) and cephalosporins (cepA), clindamycin (ermF), metronidazole (nimA-F) and tetracycline (tetQ), plus a set of primers for the B. fragilis 16S rRNA gene (positive control). An initial single PCR was performed for each gene, followed by a gradient PCR to determine the optimal PCR conditions for each primer set. This was followed by several test M-PCRs using the Qiagen multiplex PCR kit (Valencia, CA) with 60 ng of a template DNA mastermix containing all genes of interest and 0.2 mu M of each primer set. Multiplex PCR products were detectable at annealing temperatures ranging from 53-57C for 30-35 cycles. The final optimized M-PCR was then used to evaluate 21 different B. fragilis isolates from various patients. Eleven different M-PCR genotypes were obtained, which correlated with phenotypic antibiograms and nitrocefin beta-lactamase production assays. This M-PCR provides an accurate, rapid, sensitive and cost-effective tool for detecting clinically relevant antibiotic resistance genes in B. fragilis, and owing to its high sensitivity, it could also be used to investigate the prevalence of such genetic determinants in mixed bacterial specimens.
C1 [Pumbwe, Lilian; Wexler, Hannah M.] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
[Pumbwe, Lilian; Curzon, Matthew; Wexler, Hannah M.] Greater Los Angeles Vet Adm Healthcare Syst, Los Angeles, CA USA.
RP Pumbwe, L (reprint author), Wadsworth Anaerobe Lab, Bldg 304,Room E3-226, Los Angeles, CA 90073 USA.
EM lilskil@ucla.edu
FU Department of Veterans Affairs
FX This study was supported by Merit Review Funds from the Department of
Veterans Affairs.
NR 28
TC 2
Z9 2
U1 1
U2 4
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1060-3999
J9 J RAPID METH AUT MIC
JI J Rapid Methods Autom. Microbiol.
PD DEC
PY 2008
VL 16
IS 4
BP 381
EP 393
DI 10.1111/j.1745-4581.2008.00143.x
PG 13
WC Biotechnology & Applied Microbiology; Food Science & Technology
SC Biotechnology & Applied Microbiology; Food Science & Technology
GA 378ZZ
UT WOS:000261365100010
ER
PT J
AU Petri, M
Naqibuddin, M
Carson, KA
Wallace, DJ
Weisman, MH
Holliday, SL
Sampedro, M
Narayana, S
Fox, PT
Franklin, C
Padilla, PA
Brey, RL
AF Petri, Michelle
Naqibuddin, Mohammad
Carson, Kathryn A.
Wallace, Daniel J.
Weisman, Michael H.
Holliday, Stephen L.
Sampedro, Margaret
Narayana, Shalini
Fox, Peter T.
Franklin, Crystal
Padilla, Patricia A.
Brey, Robin L.
TI Brain Magnetic Resonance Imaging in Newly Diagnosed Systemic Lupus
Erythematosus
SO JOURNAL OF RHEUMATOLOGY
LA English
DT Article
DE SYSTEMIC LUPUS ERYTHEMATOSUS; MAGNETIC RESONANCE IMAGING;
CEREBRALATROPHY
ID OVERT NEUROPSYCHIATRIC MANIFESTATIONS; MULTIPLE-SCLEROSIS;
ANTIPHOSPHOLIPID ANTIBODIES; ANTICARDIOLIPIN ANTIBODIES; REVISED
CRITERIA; CEREBRAL ATROPHY; DISEASE-ACTIVITY; RATING-SCALE; MRI;
CLASSIFICATION
AB Objective. We wished to determine the prevalence of cerebral atrophy and focal lesions in a cohort of patients with newly diagnosed systemic lupus erythematosus (SLE) and the association of these brain abnormalities with clinical characteristics.
Methods. A total of 97 patients with SLE, within 9 months of diagnosis, with 4 or more American College of Rheumatology classification criteria, were enrolled. Brain magnetic resonance imaging was performed.
Results. The patients were 97% female. mean age 38.1 (SD 12.2) years, education 15.1 (2.8) years; 59 Caucasian, I I African American, 19 Hispanic, 5 Asian, and 3 other ethnicity. Cerebral atrophy was prevalent in 18% (95% Cl 11%-27%): mild in 12%, moderate in 5%. Focal lesions were prevalent in 8% (95% Cl 4%-16%): mild in 2%, moderate in 5%. severe in 1%. Patients with cerebral atrophy were more likely to have anxiety disorder (p = 0.04). Patients with focal lesions were more likely to be African American (p = 0.045) and had higher Safety of Estrogens in Lupus Erythematosus National Assessment SLEDAI scores (p = 0.02) and anti-dsDNA (p = 0.05).
Conclusion. In this population with newly diagnosed SLE, brain abnormalities were prevalent in 25% of patients. These findings suggest that the brain may be affected extremely early in the course of SLE, even before the clinical diagnosis of SLE is made. Followup of these patients is planned. to determine the reversibility or progression of these abnormalities and their association with and potential predictive value for subsequent neuropsychiatric SLE manifestations. (First Release Sept 15 2008 J Rheumatol 200835:2348-54: doi: 10.3899/jrheum.071010)
C1 [Petri, Michelle; Naqibuddin, Mohammad; Sampedro, Margaret] Johns Hopkins Univ, Baltimore, MD 21205 USA.
[Carson, Kathryn A.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Wallace, Daniel J.; Weisman, Michael H.] Univ Calif Los Angeles, David Geffen Sch Med, Cedars Sinai Med Ctr, Los Angeles, CA 90095 USA.
[Holliday, Stephen L.] S Texas Vet Hlth Care Syst, Psychol Serv, San Antonio, TX USA.
[Narayana, Shalini; Fox, Peter T.; Franklin, Crystal] Univ Texas Hlth Sci Ctr San Antonio, Res Imaging Ctr, San Antonio, TX 78229 USA.
[Narayana, Shalini] Univ Texas Hlth Sci Ctr San Antonio, Dept Radiol, San Antonio, TX 78229 USA.
[Padilla, Patricia A.; Brey, Robin L.] Univ Texas Hlth Sci Ctr San Antonio, Dept Neurol, San Antonio, TX 78229 USA.
RP Petri, M (reprint author), Johns Hopkins Univ, 1830 E Monument St,Suite 7500, Baltimore, MD 21205 USA.
EM mpetri@jhmi.edu
RI Fox, Peter/B-4725-2010; Narayana, Shalini/F-3031-2010
OI Fox, Peter/0000-0002-0465-2028;
FU NIH [RO1-AR049125, AR043727]; Johns Hopkins University General Clinical
Research Center [M01-RR00052]; University of Texas Health Science Center
at San Antonio Frederic C. Bartter General Clinical Research Center
[MOI-RR01346]
FX The Brain CONECTIONS study is supported by NIH RO1-AR049125. AR043727.
and the Johns Hopkins University General Clinical Research Center (K.
Carson is supported by M01-RR00052) and the University of Texas Health
Science Center at San Antonio Frederic C. Bartter General Clinical
Research Center (MOI-RR01346).
NR 53
TC 33
Z9 35
U1 0
U2 1
PU J RHEUMATOL PUBL CO
PI TORONTO
PA 920 YONGE ST, SUITE 115, TORONTO, ONTARIO M4W 3C7, CANADA
SN 0315-162X
J9 J RHEUMATOL
JI J. Rheumatol.
PD DEC
PY 2008
VL 35
IS 12
BP 2348
EP 2354
DI 10.3899/jrehum.071010
PG 7
WC Rheumatology
SC Rheumatology
GA 379XA
UT WOS:000261428400013
PM 18793003
ER
PT J
AU Christie, M
Mckenna, JT
Connolly, NP
Bolortuya, Y
Mccarley, RW
Strecker, RE
AF Christie, M.
Mckenna, J. T.
Connolly, N. P.
Bolortuya, Y.
Mccarley, R. W.
Strecker, R. E.
TI The rat-psychomotor vigilance task: sleep disruption and basal forebrain
adenosine dialysis
SO JOURNAL OF SLEEP RESEARCH
LA English
DT Meeting Abstract
CT 19th Congress of the European-Sleep-Research-Society
CY SEP 09-13, 2008
CL Glasgow, SCOTLAND
SP European Sleep Res Soc
C1 VA Boston Healthcare Syst, Brockton, MA USA.
Harvard Univ, Sch Med, Brockton, MA 02401 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0962-1105
J9 J SLEEP RES
JI J. Sleep Res.
PD DEC
PY 2008
VL 17
BP 67
EP 67
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 400EH
UT WOS:000262850300161
ER
PT J
AU Fuller, CA
Fuller, PM
Robinson, EL
AF Fuller, C. A.
Fuller, P. M.
Robinson, E. L.
TI Blue light affects timing of sleep in rhesus monkeys but not sleep
homeostasis
SO JOURNAL OF SLEEP RESEARCH
LA English
DT Meeting Abstract
CT 19th Congress of the European-Sleep-Research-Society
CY SEP 09-13, 2008
CL Glasgow, SCOTLAND
SP European Sleep Res Soc
C1 [Fuller, C. A.; Robinson, E. L.] Univ Calif Davis, Sect NPB, Davis, CA 95616 USA.
[Fuller, P. M.] Harvard Univ, Sch Med, Dept Neurol, BIDMC, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0962-1105
J9 J SLEEP RES
JI J. Sleep Res.
PD DEC
PY 2008
VL 17
BP 79
EP 79
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 400EH
UT WOS:000262850300192
ER
PT J
AU Roth, T
Mccall, W
Wessel, T
Amato, D
Paska, W
Fava, M
AF Roth, T.
Mccall, W.
Wessel, T.
Amato, D.
Paska, W.
Fava, M.
TI Eszopiclone co-administered with fluoxetine for insomnia co-existing
with major depressive disorder (MDD): a subgroup analysis
SO JOURNAL OF SLEEP RESEARCH
LA English
DT Meeting Abstract
CT 19th Congress of the European-Sleep-Research-Society
CY SEP 09-13, 2008
CL Glasgow, SCOTLAND
SP European Sleep Res Soc
C1 [Roth, T.] Henry Ford Sleep Disorders Ctr, Detroit, MI USA.
[Mccall, W.] Wake Forest Univ Hlth Sci, Winston Salem, NC 27109 USA.
[Wessel, T.; Amato, D.] Sepracor Inc, Marlborough, MA USA.
[Paska, W.] GlaxoSmithKline Inc, Greenford, Middx, England.
[Fava, M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0962-1105
J9 J SLEEP RES
JI J. Sleep Res.
PD DEC
PY 2008
VL 17
BP 191
EP 192
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 400EH
UT WOS:000262850300534
ER
PT J
AU Fava, M
Schaefer, K
Rockett, CB
Amato, D
Roth, T
AF Fava, M.
Schaefer, K.
Rockett, C. B.
Amato, D.
Roth, T.
TI Differential sleep effects of eszopiclone treatment and discontinuation
in patients with primary insomnia and insomnia co-existing with major
depressive disorder (MDD) or generalized anxiety disorder (GAD)
SO JOURNAL OF SLEEP RESEARCH
LA English
DT Meeting Abstract
CT 19th Congress of the European-Sleep-Research-Society
CY SEP 09-13, 2008
CL Glasgow, SCOTLAND
SP European Sleep Res Soc
C1 [Fava, M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Roth, T.] Henry Ford Sleep Disorders Ctr, Detroit, MI USA.
[Schaefer, K.; Amato, D.] Sepracor Inc, Marlborough, MA USA.
[Rockett, C. B.] GlaxoSmithKline Inc, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0962-1105
J9 J SLEEP RES
JI J. Sleep Res.
PD DEC
PY 2008
VL 17
BP 192
EP 192
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 400EH
UT WOS:000262850300536
ER
PT J
AU Partinen, M
Leger, D
Hirshkowitz, M
Chokroverty, S
Hedner, J
AF Partinen, M.
Leger, D.
Hirshkowitz, M.
Chokroverty, S.
Hedner, J.
TI Frequency of insomnia symptoms in PCPS patients: results of the EQUINOX
international survey
SO JOURNAL OF SLEEP RESEARCH
LA English
DT Meeting Abstract
CT 19th Congress of the European-Sleep-Research-Society
CY SEP 09-13, 2008
CL Glasgow, SCOTLAND
SP European Sleep Res Soc
C1 [Leger, D.] Physiol Explorat Fonct Ctr Sommeil, Hotel Dieu, Paris, France.
[Hirshkowitz, M.] VA Med Ctr, Sleep Disorders & Res Ctr, Houston, TX USA.
[Chokroverty, S.] New Jersey Neurosci Inst, JFK Med Ctr, Edison, NJ USA.
[Hedner, J.] Sahlgrens Univ Hosp, Sleep Lab Unit, Dept Resp Med & Allergol, Gothenburg, Sweden.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0962-1105
J9 J SLEEP RES
JI J. Sleep Res.
PD DEC
PY 2008
VL 17
BP 196
EP 197
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 400EH
UT WOS:000262850300550
ER
PT J
AU Gass, N
Kalinchuk, A
Stenberg, T
AF Gass, N.
Kalinchuk, A.
Stenberg, T.
TI Basal forebrain adenosine receptors and REM sleep recovery in rats
SO JOURNAL OF SLEEP RESEARCH
LA English
DT Meeting Abstract
CT 19th Congress of the European-Sleep-Research-Society
CY SEP 09-13, 2008
CL Glasgow, SCOTLAND
SP European Sleep Res Soc
C1 [Gass, N.; Stenberg, T.] Univ Helsinki, Helsinki, Finland.
[Kalinchuk, A.] Harvard Univ, Sch Med, Boston VA Healthcare Syst, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0962-1105
J9 J SLEEP RES
JI J. Sleep Res.
PD DEC
PY 2008
VL 17
BP 202
EP 202
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 400EH
UT WOS:000262850300566
ER
PT J
AU McKenna, JT
Cordeira, JW
Christie, MA
Tartar, JL
McCoy, JG
Lee, E
McCarley, RW
Strecker, RE
AF McKenna, James T.
Cordeira, Joshua W.
Christie, Michael A.
Tartar, Jaime L.
McCoy, John G.
Lee, Eunho
McCarley, Robert W.
Strecker, Robert E.
TI Assessing sleepiness in the rat: a multiple sleep latencies test
compared to polysomnographic measures of sleepiness
SO JOURNAL OF SLEEP RESEARCH
LA English
DT Article
DE electroencephalogram; non-rapid eye movement; rat; sleep; sleep latency
ID LIGHT-DARK CYCLES; ANOVA DESIGNS; DEPRIVATION; EEG; INTENSITY; SPECTRA;
VALUES; MEMORY; MICE
AB Sleepiness following 6 h of sleep deprivation (SD) was evaluated with a rat multiple sleep latencies test (rMSLT), and the findings were compared to conventional polysomnographic measures of sleepiness. The 6 h of SD was produced by automated activity wheels, and was terminated at either the end of the light period or at the beginning of the dark period. The rMSLT consisted of 5 min wakefulness induced by sensory stimulation followed by 25 min of freedom to sleep. This procedure was repeated every 30 min for 3 h and was designed to minimize the amount of sleep lost due to the testing procedure. In separate rats, 6 h SD was followed by undisturbed recovery, allowing evaluation of conventional polysomnographic measures of sleepiness. Sleep onset latencies were reduced following SD, with recovery in the light (baseline = 8 min, 3 s versus post-SD = 1 min, 17 s) and dark period (baseline = 14 min, 17 s versus 7 min, 7 s). Sleep onset latencies were not altered by varying the duration criterion for the first sleep bout (i.e., sleep bout length criteria of 10, 20, 30, or 60 s were compared). Polysomnographic variables (non-rapid eye movement sleep episode duration, delta power, and number of awakenings) also provided reliable indirect measures of sleepiness, regardless of whether the recovery sleep occurred in the light or dark period. Evaluation of effect size indicated that the rMSLT was a strong measure of sleepiness, and was influenced by homeostatic, circadian, and illumination factors. The rMSLT provided a simple, objective, robust and direct measure of sleepiness that was as effective as conventional polysomnographic measures of sleepiness.
C1 [McKenna, James T.; Cordeira, Joshua W.; Christie, Michael A.; Tartar, Jaime L.; McCoy, John G.; Lee, Eunho; McCarley, Robert W.; Strecker, Robert E.] Harvard Univ, Sch Med, Brockton, MA 02301 USA.
[McKenna, James T.; Christie, Michael A.; McCarley, Robert W.; Strecker, Robert E.] VA Boston Healthcare Syst, Dept Psychiat, Brockton, MA 02301 USA.
[Cordeira, Joshua W.] Tufts Univ, Sch Med, Dept Neurosci, Boston, MA 02111 USA.
[Tartar, Jaime L.] Nova SE Univ, Dept Social & Behav Sci, Ft Lauderdale, FL 33314 USA.
[McCoy, John G.] Univ So Mississippi, Dept Psychol, Hattiesburg, MS 39406 USA.
[Lee, Eunho] SK Holdings, Discovery Lab, Taejon, South Korea.
RP McKenna, JT (reprint author), Harvard Univ, Sch Med, VAMC Res 151-C,940 Belmont St,Bldg 44,Rm 111, Brockton, MA 02301 USA.
EM james_mckenna@hms.harvard.edu
RI McCarley, Robert/N-5562-2014;
OI McCarley, Robert/0000-0001-5705-7495; Tartar, Jaime/0000-0002-3452-0579
FU US Department of Veterans; Medical Research Awards; NIH [HL060292,
MH039683, HL07901, MH070156]
FX We thank Y. Bolortuya and B. Jeffrey for technical assistance, Margaret
Niznikiewicz for statistical advice, and Ritchie Brown for editorial
review. This research was supported by US Department of Veterans A. airs
Medical Research Awards to RWM and RES, NIH HL060292, NIH MH039683, NIH
HL07901 to JLT and JTM, and NIH MH070156 to JTM.
NR 38
TC 6
Z9 6
U1 1
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0962-1105
J9 J SLEEP RES
JI J. Sleep Res.
PD DEC
PY 2008
VL 17
IS 4
BP 365
EP 375
DI 10.1111/j.1365-2869.2008.00686.x
PG 11
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 377PO
UT WOS:000261263300002
PM 18823428
ER
PT J
AU Christie, MA
McKenna, JT
Connolly, NP
McCarley, RW
Strecker, RE
AF Christie, Michael A.
McKenna, James T.
Connolly, Nina P.
McCarley, Robert W.
Strecker, Robert E.
TI 24 hours of sleep deprivation in the rat increases sleepiness and
decreases vigilance: introduction of the rat-psychomotor vigilance task
SO JOURNAL OF SLEEP RESEARCH
LA English
DT Article
DE mean sleep latency test; psychomotor vigilance task; rat; sleep; sleep
deprivation; sleep latency; vigilance
ID SUSTAINED ATTENTION PERFORMANCE; SLOW-WAVE ACTIVITY; LATENCY TEST;
EXCESSIVE SLEEPINESS; DOSE-RESPONSE; TIME-COURSE; REM-SLEEP;
RESTRICTION; EEG; HOMEOSTASIS
AB A novel animal-analog of the human psychomotor vigilance task (PVT) was validated by subjecting rats to 24 h of sleep deprivation (SD) and examining the effect on performance in the rat-PVT (rPVT), and a rat multiple sleep latency test (rMSLT). During a three-phase (separate cohorts) crossover design, vigilance performance in the rPVT was compared with 24 h SD-induced changes in sleepiness assessed by polysomnographic evaluation and the rMSLT. Twenty-four hours of SD was produced by brief rotation of activity wheels at regular intervals in which the animals resided throughout the experiment. In the rPVT experiment, exercise controls (EC) experienced the same overall amount of locomotor activity as during SD, but allowed long periods of undisturbed sleep. After 24 h SD response latencies slowed, and lapses increased significantly during rPVT performance when compared with baseline and EC conditions. During the first 3 h of the recovery period following 24 h SD, polysomnographic measures indicated sleepiness. Latency to fall asleep after 24 h SD was assessed six times during the first 3 h after SD. Rats fell asleep significantly faster immediately after SD, than after non-SD baseline sessions. In conclusion, 24 h of SD in rats increased sleepiness, as indicated by polysomnography and the rMSLT, and impaired vigilance as measured by the rPVT. The rPVT closely resembles the human PVT test widely used in human sleep research and will assist investigation of the neurobiologic mechanisms that produce vigilance impairments after sleep disruption.
C1 VA Boston Healthcare Syst, Brockton, MA USA.
Harvard Univ, Sch Med, Brockton, MA 02401 USA.
RP Strecker, RE (reprint author), 940 Belmont St,Res 151-C, Brockton, MA 02301 USA.
EM michael_christie@hms.harvard.edu; robert_strecker@hms.harvard.edu
RI McCarley, Robert/N-5562-2014
OI McCarley, Robert/0000-0001-5705-7495
FU Department of Veterans Affairs Medical Research Service Award; NHLBI
[P50 HL060292, T32 HL07901]; NIMH [R37 MH039683, F32 MH070156]
FX We thank Lauren Kane, Stephanie Cummings, Jeremy Beech, and Courtney
Foster for technical assistance. This research was supported by the
Department of Veterans Affairs Medical Research Service Award to RES,
NHLBI - P50 HL060292 (RES & RWM), NIMH - R37 MH039683 (RWM), NHLBI T32
HL07901 (MAC & JTM), NIMH - F32 MH070156 (JTM).
NR 37
TC 17
Z9 17
U1 1
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0962-1105
J9 J SLEEP RES
JI J. Sleep Res.
PD DEC
PY 2008
VL 17
IS 4
BP 376
EP 384
DI 10.1111/j.1365-2869.2008.00698.x
PG 9
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 377PO
UT WOS:000261263300003
PM 19021853
ER
PT J
AU Horn, JH
Pratt, SR
Durrant, JD
AF Horn, Jennifer H.
Pratt, Sheila R.
Durrant, John D.
TI Parameters to Maximize 2f2-f1 Distortion Product Otoacoustic Emission
Levels
SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH
LA English
DT Article
DE distortion product otoacoustic emissions (DPOAEs); parameters; 2f2-f1;
input-output functions
ID NORMALLY HEARING SUBJECTS; PRIMARY FREQUENCIES RATIO; HUMAN NEWBORNS;
HUMAN EARS; AMPLITUDE; HUMANS; 2F1-F2; ADULTS; PHASE; INTERRELATIONS
AB Purpose: Past research has established parameters for the 2f1-f2 distortion product otoacoustic emissions (DPOAEs) that enhance response levels ( e. g., L1-L2 = 10 dB; f2/f1 = 1.22; L1, L2 = 65, 55 dB SPL). These same parameters do not optimize 2f2-f1 DPOAEs. Therefore, this study was conducted to evaluate more completely those parameters that produce the most robust 2f2-f1 output.
Method: Input-output functions of the 2f2-f1 component were obtained from 20 normal-hearing adults ( with f2 = 2000 Hz and 4000 Hz). Frequency ratios, level differences, and overall sound levels were manipulated with parameter combinations chosen to expand on information established in previous studies. The DPOAE signal-to-noise ratio (SNR), response presence, and output levels were measured.
Results: In general, mean SNRs and 2f2-f1 levels were greater, and DPOAEs were present more often for 2000 than for 4000 Hz across all parameter combinations. No single parameter combination resulted in pronounced maxima for 2f2-f1, which is consistent with past studies but is in sharp contrast to results for the more familiar 2f1-f2.
Conclusions: Overall, the results suggest that to maximize the 2f2-f1 level, lower test frequencies, low frequency ratio, essentially equal levels of primary tones, and moderate stimulus levels are best, and such parameters might be important for applying DPOAE measurement to assessment of normal and impaired auditory function.
C1 [Horn, Jennifer H.] Univ Pittsburgh, Dept Commun Sci & Disorders, Pittsburgh, PA 15260 USA.
[Horn, Jennifer H.; Pratt, Sheila R.] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
RP Horn, JH (reprint author), Univ Pittsburgh, Dept Commun Sci & Disorders, 4033 Forbes Tower, Pittsburgh, PA 15260 USA.
EM jhhst15@pitt.edu
RI Pratt, Sheila/H-7139-2013
NR 35
TC 3
Z9 4
U1 0
U2 2
PU AMER SPEECH-LANGUAGE-HEARING ASSOC
PI ROCKVILLE
PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA
SN 1092-4388
J9 J SPEECH LANG HEAR R
JI J. Speech Lang. Hear. Res.
PD DEC 1
PY 2008
VL 51
IS 6
BP 1620
EP 1629
DI 10.1044/1092-4388(2008/07-0179)
PG 10
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA 376PS
UT WOS:000261196100019
PM 18664689
ER
PT J
AU Campbell, DA
Henderson, WG
Englesbe, MJ
Hall, BL
O'Reilly, M
Bratzler, D
Dellinger, EP
Neumayer, L
Bass, BL
Hutter, MM
Schwartz, J
Ko, C
Itani, K
Steinberg, SM
Siperstein, A
Sawyer, RG
Turner, DJ
Khuri, SF
AF Campbell, Darrell A., Jr.
Henderson, William G.
Englesbe, Michael J.
Hall, Bruce L.
O'Reilly, Michael
Bratzler, Dale
Dellinger, E. Patchen
Neumayer, Leigh
Bass, Barbara L.
Hutter, Matthew M.
Schwartz, James
Ko, Clifford
Itani, Kamal
Steinberg, Steven M.
Siperstein, Allan
Sawyer, Robert G.
Turner, Douglas J.
Khuri, Shukri F.
TI Surgical Site Infection Prevention: The Importance of Operative Duration
and Blood Transfusion-Results of the First American College of
Surgeons-National Surgical Quality Improvement Program Best Practices
Initiative
SO JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS
LA English
DT Article
ID RISK ADJUSTMENT; HOSPITALS; CARE; COMPLICATIONS; MORTALITY; INCREASE;
NSQIP; TRIAL
AB BACKGROUND: Surgical site infections (SSI) continue to be a significant problem in surgery. The American College of Surgeons-National Surgical Quality Improvement Program (ACS-NSQIP) Best Practices Initiative compared process and structural characteristics among 117 private sector hospitals in an effort to define best practices aimed at preventing SSI.
STUDY DESIGN: Using standard NSQIP methodologies, we identified 20 low outlier and 13 high outlier hospitals for SSI using data from the ACS-NSQIP in 2006. Each hospital was administered a process of care survey, and site visits were conducted to five hospitals. Comparisons between the low and high outlier hospitals were made with regard to patient characteristics, operative variables, structural variables, and processes of care.
RESULTS: Hospitals that were high outliers for SSI had higher trainee-to-bed ratios (0.61 versus 0.25, p < 0.0001), and the operations took significantly longer (128.3 +/- 104.3 minutes versus 102.7 +/- 83.9 minutes, p < 0.001). Patients operated on at low outlier hospitals were less likely to present to the operating room anemic (4.9% versus 9.7%, p = 0.007) or to receive a transfusion (5.1% versus 8.0%, p = 0.03). In general, perioperative policies and practices were very similar between the low and high outlier hospitals, although low outlier hospitals were readily identified by site visitors. Overall, low outlier hospitals were smaller, efficient in the delivery of care, and experienced little operative staff turnover.
CONCLUSIONS: Our findings suggest that evidence-based SSI prevention practices do not easily distinguish well from poorly performing hospitals. But structural and process of care characteristics of hospitals were found to have a significant association with good results. (J Am Coll Surg 2008;207: 810-820. (C) 2008 by the American College of Surgeons)
C1 [Campbell, Darrell A., Jr.; Englesbe, Michael J.] Univ Michigan, Dept Surg, Ann Arbor, MI 48109 USA.
[O'Reilly, Michael] Univ Michigan, Dept Anesthesiol, Ann Arbor, MI 48109 USA.
[Henderson, William G.] VA NSQIP, Aurora, CO USA.
[Bratzler, Dale] Washington Univ, Oklahoma Fdn Med Qual, St Louis, MO USA.
[Hall, Bruce L.] Washington Univ, Dept Surg, St Louis, MO USA.
[Dellinger, E. Patchen] Univ Washington, Dept Surg, Seattle, WA 98195 USA.
[Neumayer, Leigh] Univ Utah, Salt Lake City, UT USA.
[Bass, Barbara L.] Methodist Hosp, Houston, TX 77030 USA.
[Itani, Kamal; Khuri, Shukri F.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Hutter, Matthew M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Steinberg, Steven M.] Ohio State Univ, Columbus, OH 43210 USA.
[Siperstein, Allan] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Sawyer, Robert G.] Univ Virginia, Charlottesville, VA USA.
[Turner, Douglas J.] Univ Maryland, Baltimore, MD 21201 USA.
[Schwartz, James] Kaiser Sunnyside Med Ctr, Sunnyside, CA USA.
[Ko, Clifford] Amer Coll Surg, Chicago, IL USA.
RP Englesbe, MJ (reprint author), Univ Michigan, Dept Surg, 1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA.
RI Steinberg, Steven/E-4142-2011;
OI Englesbe, Michael/0000-0001-8691-9111
NR 33
TC 109
Z9 109
U1 4
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1072-7515
J9 J AM COLL SURGEONS
JI J. Am. Coll. Surg.
PD DEC
PY 2008
VL 207
IS 6
BP 810
EP 820
DI 10.1016/j.jamcollsurg.2008.08.018
PG 11
WC Surgery
SC Surgery
GA 382GE
UT WOS:000261592800003
PM 19183526
ER
PT J
AU Boyd, CM
Landefeld, CS
Counsell, SR
Palmer, RM
Fortinsky, RH
Kresevic, D
Burant, C
Covinsky, KE
AF Boyd, Cynthia M.
Landefeld, C. Seth
Counsell, Steven R.
Palmer, Robert M.
Fortinsky, Richard H.
Kresevic, Denise
Burant, Christopher
Covinsky, Kenneth E.
TI Recovery of Activities of Daily Living in Older Adults After
Hospitalization for Acute Medical Illness
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE hospitalization; functional decline; recovery
ID HOME HEALTH-CARE; PROSPECTIVE-PAYMENT SYSTEM; HIP FRACTURE PATIENTS;
POST-ACUTE CARE; FUNCTIONAL OUTCOMES; THERAPY INTENSITY; REHABILITATION;
DISABILITY; COMMUNITY; INDEPENDENCE
AB To compare functional outcomes in the year after discharge for older adults discharged from the hospital after an acute medical illness with a new or additional disability in their basic self-care activities of daily living (ADL) (compared with preadmission baseline 2 weeks before admission) with those of older adults discharged with baseline ADL function and identify predictors of failure to recover to baseline function 1 year after discharge.
Observational.
Tertiary care hospital, community teaching hospital.
Older (aged >= 70) patients nonelectively admitted to general medical services (1993-1998).
Number of ADL disabilities at preadmission baseline and 1, 3, 6, and 12 months after discharge. Outcomes were death, sustained decline in ADL function, and recovery to baseline ADL function at each time point.
By 12 months after discharge, of those discharged with new or additional ADL disability, 41.3% died, 28.6% were alive but had not recovered to baseline function, and 30.1% were at baseline function. Of those discharged at baseline function, 17.8% died, 15.2% were alive but with worse than baseline function, and 67% were at their baseline function (P <.001). Of those discharged with new or additional ADL disability, the presence or absence of recovery by 1 month was associated with long-term outcomes. Age, cardiovascular disease, dementia, cancer, low albumin, and greater number of dependencies in instrumental ADLs independently predicted failure to recover.
For older adults discharged with new or additional disability in ADL after hospitalization for medical illness, prognosis for functional recovery is poor. Rehabilitation interventions of longer duration and timing than current reimbursement allows, caregiver support, and palliative care should be evaluated.
C1 [Boyd, Cynthia M.] Johns Hopkins Univ, Sch Med, Div Geriatr Med & Gerontol, Baltimore, MD 21224 USA.
[Boyd, Cynthia M.] Johns Hopkins Univ, Sch Med, Dept Med, Ctr Aging & Hlth, Baltimore, MD 21224 USA.
[Boyd, Cynthia M.] Johns Hopkins Univ, Dept Hlth Policy & Management, Ctr Aging & Hlth, Baltimore, MD 21224 USA.
[Boyd, Cynthia M.] Johns Hopkins Univ, Roger C Lipitz Ctr Integrated Hlth Care, Bloomberg Sch Publ Hlth, Baltimore, MD 21224 USA.
[Landefeld, C. Seth; Covinsky, Kenneth E.] Univ Calif San Francisco, Dept Med, Div Geriatr, San Francisco, CA USA.
[Landefeld, C. Seth; Covinsky, Kenneth E.] San Francisco VA Med Ctr, Interdisciplinary Res Program Improve Care Older, San Francisco, CA USA.
[Landefeld, C. Seth; Covinsky, Kenneth E.] San Francisco VA Med Ctr, Qual Scholars Program, San Francisco, CA USA.
[Counsell, Steven R.] Indiana Univ, Ctr Aging Res, Indianapolis, IN 46204 USA.
[Palmer, Robert M.] Univ Pittsburgh, Sch Med Ctr, Div Geriatr Med, Pittsburgh, PA USA.
[Fortinsky, Richard H.] Univ Connecticut, Ctr Hlth, Ctr Aging, Farmington, CT USA.
[Fortinsky, Richard H.] Univ Connecticut, Ctr Hlth, Div Geriatr, Farmington, CT USA.
[Kresevic, Denise] Case Western Reserve Univ, Sch Nursing, Dept Sociol & Bioeth,Univ Hosp Case Med Ctr, Louis Stokes Cleveland Vet Affairs Med Ctr,GRE, Cleveland, OH 44106 USA.
RP Boyd, CM (reprint author), Johns Hopkins Univ, Sch Med, Div Geriatr Med & Gerontol, Mason F Lord Bldg,Ctr Tower,7th Floor,5200 Easter, Baltimore, MD 21224 USA.
EM cboyd1@jhmi.edu
FU National Institute on Aging [AG029233, AG00912, AG10418, K24AG029812];
Johns Hopkins University (CMB); Summa Health System Foundation to Akron
City Hospital; John A. Hartford Foundation, Inc. [2003-0455]
FX Conflict of Interest: Drs. Landefeld, Covinsky, Palmer, Counsell
Fortinsky, Burant, and Kresevic have all received funding from the NIA.
Dr Kresevic has received funding from the Department of Veterans
Affairs. Drs. Landefeld and Boyd have received funding from the John A.
Hartford Foundation. Dr. Boyd was a Pfizer/American Geriatrics Society
Junior Faculty Scholar for Research on Health Outcomes during the
conduct of this study. Dr. Boyd is a Johns Hopkins Bayview Scholar in
the Center for Innovative Medicine. This work was supported by grants
from the National Institute on Aging to the Claude Pepper Older
Americans Independence Center at Case Western Reserve University and
Johns Hopkins University (CMB), National Institute on Aging Grants
AG029233, AG00912, AG10418, and K24AG029812. The Summa Health System
Foundation to Akron City Hospital, and the John A. Hartford Foundation,
Inc. 2003-0455 to the University of California, San Francisco.; Author
Contributions: Dr. Boyd conceptualized the manuscript, obtained funding,
developed the design of the analysis with Dr. Covinsky and wrote the
manuscript. Dr. Landefeld and Dr. Counsell were responsible for
collaborating in study design and implementation, obtaining funding,
analysis and interpretation of data and critical revision of the
manuscript for important intellectual content. Dr. Palmer was a
co-investigator responsible for collaborating in design and
implementation, interpretation of data, and critical revision of the
manuscript for important intellectual content. Dr. Fortinsky was a
co-investigator responsible for collaborating in the analysis and
interpretation of data and critical revision of the manuscript for
important intellectual content. Dr. Kresevic was a co-investigator
responsible for collaborating in design and implementation,
interpretation of data, and critical revision of the manuscript for
important intellectual content. Dr. Covinsky was responsible for
supervision of the entire project and manuscript and collaborated on the
design and implementation and analysis and interpretation of data and
undertook critical revision of this manuscript for important
intellectual content.; Sponsors' Role: The funding sources had no role
in the design and conduct of the study; collection, management, analysis
or interpretation of the data; or the preparation, review, or approval
of the manuscript.
NR 50
TC 166
Z9 171
U1 2
U2 25
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0002-8614
EI 1532-5415
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD DEC
PY 2008
VL 56
IS 12
BP 2171
EP 2179
DI 10.1111/j.1532-5415.2008.02023.x
PG 9
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 378ZP
UT WOS:000261364100001
PM 19093915
ER
PT J
AU Sarkisian, CA
Gruenewald, TL
Boscardin, WJ
Seeman, TE
AF Sarkisian, Catherine A.
Gruenewald, Tara L.
Boscardin, W. John
Seeman, Teresa E.
TI Preliminary Evidence for Subdimensions of Geriatric Frailty: The
MacArthur Study of Successful Aging
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE frailty; disability; aged; comorbidity
ID OLDER-ADULTS; FUNCTIONAL DECLINE; PHYSICAL-ACTIVITY; ELDERLY-PEOPLE;
WOMENS HEALTH; DISABILITY; MORTALITY; COAGULATION; ACTIVATION; PHENOTYPE
AB To identify frailty subdimensions.
Longitudinal cohort (MacArthur Study).
Three U.S. urban centers.
One thousand one hundred eighteen high-functioning subjects aged 70 to 79 in 1988.
Participants with three or more of five Cardiovascular Health Study (CHS) frailty criteria (weight loss, weak grip, exhaustion, slow gait, and low physical activity) in 1991 were classified as having the CHS frailty phenotype. To identify frailty subdimensions, factor analysis was conducted using the CHS variables and an expanded set including the CHS variables, cognitive impairment, interleukin-6 (IL-6), C-reactive protein (CRP), subjective weakness, and anorexia. Participants with four or more of 10 criteria were classified as having an expanded frailty phenotype. Predictive validity of each identified frailty subdimension was assessed using regression models for 4-year disability and 9-year mortality.
Two subdimensions of the CHS phenotype and four subdimensions of the expanded frailty phenotype were identified. Cognitive function was consistently part of a subdimension including slower gait, weaker grip, and lower physical activity. The CHS subdimension of slower gait, weaker grip, and lower physical activity predicted disability (adjusted odds ratio (AOR)=1.7, 95% confidence interval (CI)=1.3-2.2) and mortality (AOR=1.5, 95% CI=1.3-1.8). Subdimensions of the expanded model with predictive validity were higher IL-6 and CRP (AOR=1.2 for mortality); slower gait, weaker grip, lower physical activity, and lower cognitive function (AOR=1.8 for disability; AOR=1.5 for mortality), and anorexia and weight loss (AOR=1.2 for disability).
This study provides preliminary empirical support for subdimensions of geriatric frailty, suggesting that pathways to frailty differ and that subdimension-adapted care might enhance care of frail seniors.
C1 [Sarkisian, Catherine A.] GRECC, VA Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA.
[Sarkisian, Catherine A.; Gruenewald, Tara L.; Seeman, Teresa E.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Geriatr, Los Angeles, CA 90095 USA.
[Boscardin, W. John] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
RP Sarkisian, CA (reprint author), GRECC, VA Greater Los Angeles Healthcare Syst, Bldg 220,Room 315 11G,11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM csarkisian@mednet.ucla.edu
FU Paul B. Beeson Career Development Award in Aging; National Institute on
Aging [1K23AG0 24811-03, R21, 5 R21 AG025764-02, 5 P30 AG017265-08];
University of Southern California/University of California at Los
Angeles Center for the Study of Biodemography and Population Health;
MacArthur Research Network on Successful Aging; John D. and Catherine T.
MacArthur Foundation
FX The authors want to express their appreciation to Ms. Constance Gewa,
Ms. Sungjin Kim, and Ms. Diana Liao for carefully carrying out the
computer programming necessary for this manuscript.; Conflict of
Interest: The editor in chief has reviewed the conflict of interest
checklist provided by the authors and has determined that the authors
have no financial or any other kind of personal conflicts with this
manuscript. This work was supported by a Paul B. Beeson Career
Development Award in Aging, National Institute on Aging (1K23AG0
24811-03), an R21 from the National Institute on Aging (5 R21
AG025764-02), the University of Southern California/University of
California at Los Angeles Center for the Study of Biodemography and
Population Health, National Institute on Aging (5 P30 AG017265-08), and
by the MacArthur Research Network on Successful Aging and the MacArthur
Research Network on SES and Health through grants from the John D. and
Catherine T. MacArthur Foundation.; Author Contributions: All four
authors contributed to the study concept and design, analysis and
interpretation of data, and preparation of the manuscript. Dr. Seeman
also contributed to subject enrollment and data collection. Sponsor's
Role: The funders had no role in this investigation's design, conduct,
or reporting.
NR 29
TC 48
Z9 49
U1 4
U2 7
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD DEC
PY 2008
VL 56
IS 12
BP 2292
EP 2297
DI 10.1111/j.1532-5415.2008.02041.x
PG 6
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 378ZP
UT WOS:000261364100017
PM 19016933
ER
PT J
AU Shay, K
Burris, JF
AF Shay, Kenneth
Burris, James F.
CA State Art Planning Comm
TI Setting the Stage for a New Strategic Plan for Geriatrics and Extended
Care in the Veterans Health Administration: Summary of the 2008 VA State
of the Art Conference, "The Changing Faces of Geriatrics and Extended
Care: Meeting the Needs of Veterans in the Next Decade"
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
ID RANDOMIZED CONTROLLED-TRIAL; INTEGRATED CARE; PRISM-E; DEPRESSION;
OUTCOMES; PARTICIPATE; MANAGEMENT; PROGRAM; MODELS
AB The Department of Veterans Affairs (VA) assumed an early leadership role in focusing on care of elderly adults. In 1998, the Federal Advisory Committee on the Future of VA Long-Term Care, appointed by the VA Undersecretary for Health, recommended redirection of VA's extended care programs toward noninstitutional forms. A decade later, VA's Office of Geriatrics and Extended Care (GEC) initiated a strategic planning process by convening experts in geriatrics and health care, policy, and finance in Virginia on March 25 to 27, 2008, to present to VA clinicians and clinical managers the "State of the Art" of VA GEC.
Recurring clinical themes included rising numbers and complexity of aging veterans, recent addition of younger veterans to VA's extended care mix, challenges that dementia and mental illness exert throughout GEC, and need for seamlessness in delivery of care across multiple venues. Ongoing research efforts quantifying demand and resources and validating models of care will remain indispensible for meeting clinical challenges.
Serious undersupply of clinicians of all disciplines with general or specialty geriatrics knowledge persists. Much of VA's healthcare workforce and leadership are approaching retirement age, driving the need for new educational approaches, recruitment and retention strategies, and innovative delivery systems. Growing dependence on informal caregivers highlights the need for supporting these partners.
VA's healthcare budget allocation illustrates how national policy dictates systemic, regional, and local clinical decisions. Rehabilitation of the newest veterans is resulting in systemwide efficiencies. Educating and empowering patients and families results in optimized utilization of health resources.
C1 [Shay, Kenneth; Burris, James F.] US Dept Vet Affairs, Off Geriatr & Extended Care, Washington, DC USA.
RP Shay, K (reprint author), VA Cent Off 114, 810 Vermont Ave NW, Washington, DC 20420 USA.
EM Kenneth.shay@va.gov
NR 20
TC 12
Z9 12
U1 0
U2 5
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD DEC
PY 2008
VL 56
IS 12
BP 2330
EP 2339
DI 10.1111/j.1532-5415.2008.02079.x
PG 10
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 378ZP
UT WOS:000261364100023
PM 19093933
ER
PT J
AU Luks, AM
Johnson, RJ
Swenson, ER
AF Luks, Andrew M.
Johnson, Richard J.
Swenson, Erik R.
TI Chronic Kidney Disease at High Altitude
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Review
ID ENDOTHELIAL GROWTH-FACTOR; MODERATELY HIGH-ALTITUDE; RIGHT
PULMONARY-ARTERY; STAGE RENAL-DISEASE; CHRONIC HYPOXIA; RAT-KIDNEY;
SEA-LEVEL; TUBULOINTERSTITIAL INJURY; RESPIRATORY ALKALOSIS; IMPAIRED
ANGIOGENESIS
AB With a prevalence of 10 to 11% in the general population, it is likely that many patients with chronic kidney disease will visit or reside in mountainous areas. Little is known, however, about whether short- or long-duration, high-altitude exposure poses a risk in this patient population. Given that many areas of the kidney are marginally oxygenated even at sea level and that kidney disease may result in further renal hypoxia and hypoxia-associated renal injury, there is concern that high altitude may accelerate the progression of chronic kidney disease. In this review, we address how chronic kidney disease and its management is affected at high altitude. We postulate that arterial hypoxemia at high altitude poses a risk of faster disease progression in those with preexisting kidney disease. In addition, we consider the risks of developing acute altitude illness in patients with chronic kidney disease and the appropriate use of medications for the prevention and treatment of these problems.
C1 [Swenson, Erik R.] Univ Washington, VA Puget Sound Hlth Care Syst, Div Pulm & Crit Care Med, Seattle, WA 98108 USA.
[Johnson, Richard J.] Univ Colorado, Div Renal Dis & Hypertens, Denver, CO 80202 USA.
RP Swenson, ER (reprint author), Univ Washington, VA Puget Sound Hlth Care Syst, Div Pulm & Crit Care Med, 1660 S Columbian Way, Seattle, WA 98108 USA.
EM eswenson@u.washington.edu
FU NHLBI NIH HHS [R01 HL068607, R01 HL068607-07A2]; NIDDK NIH HHS [R01
DK052121-12, R01 DK052121]
NR 105
TC 21
Z9 22
U1 0
U2 3
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1046-6673
J9 J AM SOC NEPHROL
JI J. Am. Soc. Nephrol.
PD DEC
PY 2008
VL 19
IS 12
BP 2262
EP 2271
DI 10.1681/ASN.2007111199
PG 10
WC Urology & Nephrology
SC Urology & Nephrology
GA 381MC
UT WOS:000261539300007
PM 18842990
ER
PT J
AU Stelfox, HT
Goverman, J
AF Stelfox, Henry Thomas
Goverman, Jeremy
TI The Number, Content, and Quality of Randomized Controlled Trials in the
Prevention and Care of Injuries
SO JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE
LA English
DT Article
DE Injury; Trauma; Randomized controlled trial; Systematic review; Research
design
ID GLOBAL BURDEN; METHODOLOGIC QUALITY; CLINICAL-TRIALS; DISEASE;
DISABILITY; MORTALITY; JOURNALS
AB Background: Injuries represent an important and growing global burden of disease. The availability of evidence-based injury control interventions is unknown. We aimed to assess trends with respect to the number, content, and methodologic quality of reports of randomized controlled trials (RCTs) in the prevention and care of injuries.
Methods: We searched MEDLINE and the Cochrane Central Register of Controlled Trials for reports of RCTs of interventions in the prevention and care of injuries published between January 1, 1966 and January 1, 2006. Ten percent of reports, stratified by year, were randomly sampled. Studies were abstracted using a standardized form for nature of intervention, sample size, patients studied, and methodologic quality.
Results: The rate of publication of injury-related RCTs increased from 1.2 to 5.3 articles per 100 RCTs published in MEDLINE (p < 0.001) during the study period. A total of 308 reports were included in the analysis of content and methodologic quality. Poisonings (31 [10%]) were the single most common isolated mechanism of patient injury studied, whereas only 12 reports (4%) focused on road traffic injuries. The majority of interventions were hospital based (211 [68%]) and half (45%) were judged to be only available in high-income countries. Allocation concealment was deemed adequate in 73 articles (24%). One quarter of reports documented blinding of participants (77 [25%]), investigators (68 [22%]), and outcome assessors (83 [27%]). Only 44 articles (14%) reported intention-to-treat analyses.
Conclusions: The number of RCTs specific to the prevention and care of injuries is small, but increasing. The reporting of injury-related RCTs has important deficiencies including inadequate allocation concealment; failure to blind patients, investigators, and assessors; and per protocol analyses. In addition, many interventions studied are not available in low-income countries where the majority of the world's population resides and injury rates are highest.
C1 [Stelfox, Henry Thomas] Univ Calgary, Foothills Med Ctr, Dept Crit Care Med, Calgary, AB T2N 2T9, Canada.
[Goverman, Jeremy] Massachusetts Gen Hosp, Dept Surg, Burns Serv, Boston, MA 02114 USA.
RP Stelfox, HT (reprint author), Univ Calgary, Foothills Med Ctr, Dept Crit Care Med, EG23A,1403-29 St NW, Calgary, AB T2N 2T9, Canada.
EM tom.stelfox@calgaryhealthregion.ca
FU Canadian Institutes of Health Research
FX H.T.S. was supported by a Postdoctoral Fellowship award from the
Canadian Institutes of Health Research.
NR 26
TC 4
Z9 4
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-5282
J9 J TRAUMA
JI J. Trauma-Injury Infect. Crit. Care
PD DEC
PY 2008
VL 65
IS 6
BP 1488
EP 1493
DI 10.1097/TA.0b013e3181568cfc
PG 6
WC Critical Care Medicine; Surgery
SC General & Internal Medicine; Surgery
GA 383WV
UT WOS:000261706000054
PM 19077647
ER
PT J
AU Litz, BT
AF Litz, Brett T.
TI Early Intervention for Trauma: Where Are We and Where Do We Need to Go?
A Commentary
SO JOURNAL OF TRAUMATIC STRESS
LA English
DT Article; Proceedings Paper
CT 23rd Annual Conference of the International-Society-of-Traumatic-Studies
CY NOV, 2007
CL Baltimore, MD
SP Int Soc Traumat Studies
ID POSTTRAUMATIC-STRESS-DISORDER; MANAGEMENT
AB In this commentary, the author underscores the importance of early intervention for trauma and describes the challenges that lie ahead for researchers, decision makers, and care providers. The author also provides a review of where things stand, briefly reviews psychological first aid strategies, and underscores where we need to go from here. Although the field has advanced considerably in the last decade or so, and there are compelling trials underway, there is much work that needs to be done, especially in terms of effectiveness and the task of integrating early intervention into various work cultures, such as the military.
C1 [Litz, Brett T.] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Litz, Brett T.] Massachusetts Vet Epidemiol Res & Informat Ctr, Natl Ctr PTSD, VA Boston Healthcare Syst, Boston, MA 02130 USA.
RP Litz, BT (reprint author), NCPTSD 116B4, 150 S Huntington Ave, Boston, MA 02130 USA.
EM brett.litz@va.gov
NR 9
TC 24
Z9 24
U1 2
U2 4
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0894-9867
J9 J TRAUMA STRESS
JI J. Trauma Stress
PD DEC
PY 2008
VL 21
IS 6
BP 503
EP 506
DI 10.1002/jts.20373
PG 4
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 391ZD
UT WOS:000262271800002
PM 19107726
ER
PT J
AU Ricci, P
Cantisani, V
D'Onotrip, M
Sahani, D
Pagliara, E
Calliada, F
Mehmet, E
Sanjeva, K
Faccioli, N
Pozzi-Mucelli, R
D'Ambrosio, U
Passariello, R
AF Ricci, Paolo
Cantisani, Vito
D'Onotrip, Mirko
Sahani, Dushyant
Pagliara, Elisa
Calliada, Fabrizio
Mehmet, Erturk
Sanjeva, Kalva
Faccioli, Nicola
Pozzi-Mucelli, Roberto
D'Ambrosio, Ugo
Passariello, Roberto
TI Behavior of Hepatocellular Adenoma on Real-time Low-Mechanical Index
Contrast-Enhanced Ultrasonography With a Second-Generation Contrast
Agent
SO JOURNAL OF ULTRASOUND IN MEDICINE
LA English
DT Article
DE contrast-enhanced ultrasonography; hepatocellular adenoma;
second-generation ultrasound contrast media; ultrasonography
ID FOCAL NODULAR HYPERPLASIA; LIVER-SPECIFIC MICROBUBBLES; COLOR DOPPLER
SONOGRAPHY; PROSPECTIVE MULTICENTER; HEPATIC ADENOMAS; LESIONS;
DIFFERENTIATION; ULTRASOUND; BENIGN; TUMORS
AB Objective. The purpose of this study was to describe the behavior of histologically proven hepatocellular adenoma (HCA) on low-mechanical index (MI) contrast-enhanced ultrasonography (CEUS). Methods. A review of the databases from 4 academic hospitals revealed 18 patients (15 female and 3 male; mean age, 40 years; range, 25-71 years) with 25 histologically proven HCA lesions who were studied with CEUS at a low MI (0.04-0.1). Results. Twenty-four of 25 lesions (96%; 95% confidence interval [CI], 80.5%-99.3%) showed high-intensity enhancement, scored as 3 on a scale of 0 to 3, whereas only 1 lesion (4%; 95% CI, 0.7%-19.5%) was scored as 2. The time of peak enhancement ranged between 10 and 19 seconds (average, 13 seconds). All but 1 of the 25 lesions (96%; 95% CI, 80.5%-99.3%) showed early homogeneous and centripetal enhancement during the hepatic arterial phase. No portal venous phase enhancement was observed in any lesion because all showed rapid wash-out (100%; 95% CI, 86.7%-100%). Twenty lesions (80%; 95% CI, 60.9%-91.1 %) were found to be isoechoic to slightly hypoechoic during the portal phase, and 19 (76%; 95% CI, 56.6%-88.5%) were isoechoic to mildly hypoechoic, whereas 7 (24%; 95% CI, 11.5%-43.4%) were hypoechoic during the late phase. Conclusions. Contrast-enhanced ultrasonography is an effective technique for identifying the microvascular and macrovascular characteristics of HCA. Typically, HCA shows early (10-19 seconds) and centripetal enhancement during the arterial phase and isoechogenicity or mild hypoechogenicity during the portal phase, remaining slightly hypoechoic or isoechoic during the late phase in most cases.
C1 [Ricci, Paolo; Cantisani, Vito; Pagliara, Elisa; D'Ambrosio, Ugo; Passariello, Roberto] Univ Roma La Sapienza, Dept Radiol, Rome, Italy.
[D'Onotrip, Mirko; Faccioli, Nicola; Pozzi-Mucelli, Roberto] Univ Verona, Dept Radiol, I-37100 Verona, Italy.
[Sahani, Dushyant; Sanjeva, Kalva] Harvard Univ, Sch Med, Dept Radiol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Calliada, Fabrizio] Univ Pavia, Dept Radiol, Policlin San Matteo, I-27100 Pavia, Italy.
[Mehmet, Erturk] Sisli Etfal Training & Res Hosp, Dept Radiol, Istanbul, Turkey.
RP Ricci, P (reprint author), Azienda Policlin Umberto 1, Dipartimento Sci Radiol, Viale Regina Elena 324, I-00161 Rome, Italy.
EM paolo.ricci@uniroma1.it
RI D'Onofrio, Mirko/S-6828-2016;
OI D'Onofrio, Mirko/0000-0003-3229-9329; CANTISANI,
VITO/0000-0003-1525-214X
NR 20
TC 10
Z9 11
U1 0
U2 2
PU AMER INST ULTRASOUND MEDICINE
PI LAUREL
PA SUBSCRIPTION DEPT, 14750 SWEITZER LANE, STE 100, LAUREL, MD 20707-5906
USA
SN 0278-4297
J9 J ULTRAS MED
JI J. Ultrasound Med.
PD DEC
PY 2008
VL 27
IS 12
BP 1719
EP 1726
PG 8
WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
GA 377WQ
UT WOS:000261283200006
PM 19022997
ER
PT J
AU Spencer, JK
Adler, RS
AF Spencer, Jacqueline K.
Adler, Ronald S.
TI Utility of Portable Ultrasound in a Community in Ghana
SO JOURNAL OF ULTRASOUND IN MEDICINE
LA English
DT Article
DE developing countries; Ghana; portable ultrasound
ID DEVELOPING-COUNTRIES; DEVELOPING-WORLD; ULTRASONOGRAPHY
AB Objective. in many developing countries, access to medical imaging is limited by availability of resources. Portable ultrasound shows great promise to meet the needs in these countries because it is transportable and relatively inexpensive, and it has a wide range of applications. As part of the Ghana Health Mission, Sekondi-Takoradi, Ghana, we explored the utility of ultrasound in primary care and hospital settings during March 2004. Our objective was to evaluate the clinical utility of a portable ultrasound machine in a variety of physical conditions and multiple clinical scenarios. Methods. Ultrasound examinations were performed at 2 primary care sites and 2 hospitals using a portable ultrasound machine with linear and curved linear phased array transducers. Most ultrasound examinations were musculoskeletal, with the remainder being obstetric, pelvic, breast, vascular, abdominal, and genitourinary examinations. Results. In clinic settings, musculoskeletal ultrasound represented 46% (16) of the ultrasound examinations performed, and 29% (10) of the cases were a combination of abdominal, pelvic, and genitourinary examinations. In hospital settings, abdominal, pelvic, and genitourinary ultrasound examinations combined were 56% (18), and musculoskeletal was 41 % (13). Of the 67 ultrasound examinations performed, 81 % (54) showed abnormal findings, 81 % (54) were considered to add to the clinical diagnosis, and 40% (27) influenced medical care for the patients. Conclusions. This experience shows the usefulness of portable ultrasound examinations performed by a skilled radiologist in a clinical setting in Ghana; the challenge is to address how to best incorporate ultrasound into the current practice of medical professionals in developing countries.
C1 [Adler, Ronald S.] Hosp Special Surg, Div Ultrasound & Body Imaging, Dept Radiol & Imaging, New York, NY 10021 USA.
[Spencer, Jacqueline K.] VA Boston Healthcare Syst, Dept Primary & Ambulatory Care, Boston, MA USA.
RP Adler, RS (reprint author), Hosp Special Surg, Div Ultrasound & Body Imaging, Dept Radiol & Imaging, 535 E 70th St, New York, NY 10021 USA.
EM adlerr@hss.edu
NR 13
TC 32
Z9 32
U1 0
U2 0
PU AMER INST ULTRASOUND MEDICINE
PI LAUREL
PA SUBSCRIPTION DEPT, 14750 SWEITZER LANE, STE 100, LAUREL, MD 20707-5906
USA
SN 0278-4297
J9 J ULTRAS MED
JI J. Ultrasound Med.
PD DEC
PY 2008
VL 27
IS 12
BP 1735
EP 1743
PG 9
WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
GA 377WQ
UT WOS:000261283200008
PM 19022999
ER
PT J
AU McDougal, WS
AF McDougal, W. Scott
TI Factors Predicting Renal Functional Outcome After Partial Nephrectomy
COMMENT
SO JOURNAL OF UROLOGY
LA English
DT Editorial Material
C1 Massachusetts Gen Hosp, Dept Urol, Boston, MA 02114 USA.
RP McDougal, WS (reprint author), Massachusetts Gen Hosp, Dept Urol, 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 0022-5347
J9 J UROLOGY
JI J. Urol.
PD DEC
PY 2008
VL 180
IS 6
BP 2368
EP 2368
DI 10.1016/j.juro.2008.08.112
PG 1
WC Urology & Nephrology
SC Urology & Nephrology
GA 373OT
UT WOS:000260982200025
ER
PT J
AU Schanzer, A
Mega, J
Meadows, J
Samson, RH
Bandyk, DF
Conte, MS
AF Schanzer, Andres
Mega, Jessica
Meadows, Judith
Samson, Russell H.
Bandyk, Dennis F.
Conte, Michael S.
TI Risk stratification in critical limb ischemia: Derivation and validation
of a model to predict amputation-free survival using multicenter
surgical outcomes data
SO JOURNAL OF VASCULAR SURGERY
LA English
DT Article; Proceedings Paper
CT 62nd Annual Meeting of the Society-for-Vascular-Surgery
CY JUN 05-08, 2008
CL San Diego, CA
SP Soc Vasc Surg
ID PERIPHERAL-ARTERIAL-DISEASE; EXTREMITY BYPASS-SURGERY; C-REACTIVE
PROTEIN; QUALITY-OF-LIFE; VEIN BYPASS; INFRAINGUINAL BYPASS;
VASCULAR-DISEASE; CONTROLLED-TRIAL; HIGH PREVALENCE; MORTALITY
AB Background: Patients with critical limb ischemia (CLI) are a heterogeneous population with respect to risk for mortality and limb loss, complicating clinical decision-making. Endovascular options, compared with bypass, offer a tradeoff between reduced procedural risk and inferior durability. Risk stratified data predictive of amputation-free survival (AFS) may improve clinical decision making and allow for better assessment of new technology in the CLI population.
Methods. This was a retrospective analysis of prospectively collected data from patients who underwent infrainguinal vein by ass surgery for CLI. Two datasets were used: the PREVENT III randomized trial (n = 1404) and a multicenter. P registry (n = 716) from three distinct vascular centers (two academic, one community-based). The PREVENT III cohort was randomly assigned to a derivation set (n = 953) and to a validation set (11 = 451). The primary endpoint was AFS. Predictors of AFS identified on univariate screen (inclusion threshold, P < .20) were included in a stepwise selection Cox model. The resulting five significant predictors were assigned an integer score to stratify, patients into three risk groups. The prediction rule was internally validated in the PREVENT III validation set and externally validated in the multicenter cohort.
Results: The estimated 1-year AFS in the derivation, internal validation, and external validation sets were 76.3%, 72.5%, and 77.0%, respectively. In the derivation set, dialysis (hazard ratio [HR] 2.81, P < .0001), tissue loss (HR 2.22, P = .0004), age 2:75 (HR 1.64, P = .001), hematocrit <= 30 (HR 1.61, P = .012), and advanced CAD (HR 1.41, P = .021) were significant predictors for ATS in the multivariable model. An integer score, derived from the 9 coefficients, was used to generate three risk categories (low <= 3 [44.4% of cohort], medium 4-7 [46.7% of cohort], high >= 8 [8.8% of cohort]). Stratification of the patients, in each dataset, according to risk category yielded three significantly different Kaplan-Meier estimates for 1-year AFS (86%, 73%, and 45% for low, medium, and high risk groups, respectively). For a given risk category, the ATS estimate was consistent between the derivation and validation sets.
Conclusion: Among patients selected to undergo surgical bypass for infrainguinal disease, this parsimonious risk stratification model reliably identified a category of CLI patients with a >50% chance of death or major amputation at 1 year. Calculation of a "PIII risk score" may be useful for surgical decision making and for clinical trial designs in the CLI population. (J Vasc Surg 2008;48:1464-71.)
C1 [Schanzer, Andres] Univ Massachusetts, Mem Med Ctr, Div Vasc & Endovasc Surg, Worcester, MA 01655 USA.
[Mega, Jessica] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Meadows, Judith; Conte, Michael S.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Samson, Russell H.] Florida State Univ, Sarasota, FL USA.
[Bandyk, Dennis F.] Univ S Florida, Tampa, FL USA.
RP Schanzer, A (reprint author), Univ Massachusetts, Mem Med Ctr, Div Vasc & Endovasc Surg, 55 Lake Ave N, Worcester, MA 01655 USA.
EM schanzea@ummhc.org
FU NHLBI NIH HHS [T32 HL007575-17, T32 HL007575-23, T32 HL007575-20, T32
HL007575-22, T32 HL007575-16, T32 HL007575-19, T32 HL007575-24, T32
HL007575, T32 HL007575-21, T32 HL007575-18]
NR 38
TC 110
Z9 111
U1 2
U2 6
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0741-5214
J9 J VASC SURG
JI J. Vasc. Surg.
PD DEC
PY 2008
VL 48
IS 6
BP 1464
EP 1471
DI 10.1016/j.jvs.2008.07.062
PG 8
WC Surgery; Peripheral Vascular Disease
SC Surgery; Cardiovascular System & Cardiology
GA 388FX
UT WOS:000262006800017
PM 19118735
ER
PT J
AU Li, X
Sodroski, J
AF Li, Xing
Sodroski, Joseph
TI The TRIM5 alpha B-Box 2 Domain Promotes Cooperative Binding to the
Retroviral Capsid by Mediating Higher-Order Self-Association
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; PROTEIN-PROTEIN INTERACTIONS; MURINE
LEUKEMIA-VIRUS; RESTRICTION FACTOR; TRIPARTITE MOTIF; MONKEY
TRIM5-ALPHA; CYTOPLASMIC BODIES; RHESUS TRIM5-ALPHA; CYCLOPHILIN-A;
HIV-1
AB The retroviral restriction factor, TRIM5 alpha, blocks infection of a spectrum of retroviruses soon after virus entry into the cell. TRIM5 alpha consists of RING, B-box 2, coiled-coil, and B30.2(SPRY) domains. The B-box 2 domain is essential for retrovirus restriction by TRIM5 alpha, but its specific function is unknown. We show here that the B-box 2 domain mediates higher-order self-association of TRIM5 alpha rh oligomers. This self-association increases the efficiency of TRIM5 alpha binding to the retroviral capsid, thus potentiating restriction of retroviral infection. The contribution of the B-box 2 domain to cooperative TRIM5 alpha association with the retroviral capsid explains the conditional nature of the restriction phenotype exhibited by some B-box 2 TRIM5 alpha mutants; the potentiation of capsid binding that results from B-box 2-mediated self-association is essential for restriction when B30.2(SPRY) domain-mediated interactions with the retroviral capsid are weak. Thus, B-box 2-dependent higher-order self-association and B30.2(SPRY)-dependent capsid binding represent complementary mechanisms whereby sufficiently dense arrays of capsid-bound TRIM5 alpha proteins can be achieved.
C1 [Li, Xing] Harvard Univ, Dept Canc Immunol & AIDS, Dana Farber Canc Inst, Div Aids,Med Sch, Boston, MA 02115 USA.
[Sodroski, Joseph] Harvard Univ, Dept Immunol & Infect Dis, Sch Publ Hlth, Boston, MA 02115 USA.
RP Sodroski, J (reprint author), Harvard Univ, Dept Canc Immunol & AIDS, Dana Farber Canc Inst, Div Aids,Med Sch, 44 Binney St JFB 824, Boston, MA 02115 USA.
EM joseph_sodroski@dfci.harvard.edu
RI Li, Xing/D-3852-2009
FU National Institutes of Health [AI063987, AI076094, AI06354];
International AIDS Vaccine Initiative
FX We thank Yvette McLaughlin and Elizabeth Carpelan for manuscript
preparation.; This study was supported by the National Institutes of
Health (grants AI063987 and AI076094 and a Center for AIDS Research
Award AI06354), the International AIDS Vaccine Initiative, and the late
William F. McCarty-Cooper.
NR 49
TC 76
Z9 79
U1 0
U2 9
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 DEC
PY 2008
VL 82
IS 23
BP 11495
EP 11502
DI 10.1128/JVI.01548-08
PG 8
WC Virology
SC Virology
GA 370UX
UT WOS:000260789700002
PM 18799578
ER
PT J
AU Shun, MC
Botbol, Y
Li, X
Di Nunzio, F
Daigle, JE
Yan, N
Lieberman, J
Lavigne, M
Engelman, A
AF Shun, Ming-Chieh
Botbol, Yair
Li, Xiang
Di Nunzio, Francesca
Daigle, Janet E.
Yan, Nan
Lieberman, Judy
Lavigne, Marc
Engelman, Alan
TI Identification and Characterization of PWWP Domain Residues Critical for
LEDGF/p75 Chromatin Binding and Human Immunodeficiency Virus Type 1
Infectivity
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID INTEGRASE INTERACTOR LEDGF/P75; NUCLEAR-LOCALIZATION SIGNAL; HIV-1
INTEGRASE; GROWTH-FACTOR; DNA INTEGRATION; IN-VITRO; COACTIVATOR P75;
HUMAN GENOME; HUMAN-CELLS; PREINTEGRATION COMPLEXES
AB Lens epithelium-derived growth factor (LEDGF)/p75 functions as a bimodal tether during lentiviral DNA integration: its C-terminal integrase-binding domain interacts with the viral preintegration complex, whereas the N-terminal PWWP domain can bind to cellular chromatin. The molecular basis for the integrase-LEDGF/p75 interaction is understood, while the mechanism of chromatin binding is unknown. The PWWP domain is homologous to other protein interaction modules that together comprise the Tudor clan. Based on primary amino acid sequence and three-dimensional structural similarities, 24 residues of the LEDGF/p75 PWWP domain were mutagenized to garner essential details of its function during human immunodeficiency virus type 1 (HIV-1) infection. Mutating either Trp-21 or Ala-51, which line the inner wall of a hydrophobic cavity that is common to Tudor clan members, disrupts chromatin binding and virus infectivity. Consistent with a role for chromatin-associated LEDGF/p75 in stimulating integrase activity during infection, recombinant W21A protein is preferentially defective for enhancing integration into chromatinized target DNA in vitro. The A51P mutation corresponds to the S270P change in DNA methyltransferase 3B that causes human immunodeficiency, centromeric instability, and facial anomaly syndrome, revealing a critical role for this amino acid position in the chromatin binding functions of varied PWWP domains. Our results furthermore highlight the requirement for a conserved Glu in the hydrophobic core that mediates interactions between other Tudor clan members and their substrates. This initial systematic mutagenesis of a PWWP domain identifies amino acid residues critical for chromatin binding function and the consequences of their changes on HIV-1 integration and infection.
C1 [Shun, Ming-Chieh; Li, Xiang; Di Nunzio, Francesca; Daigle, Janet E.; Engelman, Alan] Harvard Univ, Dept Canc Immunol & AIDS, Dana Farber Canc Inst, Sch Med, Boston, MA 02115 USA.
[Shun, Ming-Chieh; Li, Xiang; Di Nunzio, Francesca; Daigle, Janet E.; Engelman, Alan] Harvard Univ, Div Aids, Sch Med, Boston, MA 02115 USA.
[Botbol, Yair; Lavigne, Marc] Inst Pasteur, Dept Virol, Unit Struct Biol, F-75724 Paris, France.
[Yan, Nan; Lieberman, Judy] Harvard Univ, Immune Dis Inst, Sch Med, Boston, MA 02115 USA.
[Yan, Nan; Lieberman, Judy] Harvard Univ, Dept Pediat, Sch Med, Boston, MA 02115 USA.
RP Engelman, A (reprint author), Harvard Univ, Dept Canc Immunol & AIDS, Dana Farber Canc Inst, Sch Med, 44 Binney St, Boston, MA 02115 USA.
EM alan_engelman@dfci.harvard.edu
RI Li, Xiang/C-4588-2011; Lieberman, Judy/A-2717-2015; Di Nunzio,
Francesca/A-6153-2014
OI Di Nunzio, Francesca/0000-0003-2879-3164
FU National Institutes of Health (NIH) [AI39394, AI70042, AI45587, AI60354,
AI07245]; Agence Nationale de Recherche sur le SIDA; HMS CFAR Scholar
Award
FX HeLa TZM-b1 cells were obtained through the NIH AIDS Research and
Reference Reagent Program from John Kappes, Xiaoyun Wu, and Tranzyme,
Inc. We thank Manuel Llano for advice with the fractionation technique
used for chromatin binding analyses, Peter Cherepanov and Lavanya
Krishnan for their comments on the manuscript, and L. Krishnan for
advice with figure preparation.; This study was supported by grants from
the National Institutes of Health (NIH) (AI39394 and AI70042 [A.E.],
AI45587 [J.L.], and AI60354 [Harvard Medical School Center for AIDS
Research]) and the Agence Nationale de Recherche sur le SIDA (2005/004
and 2006/124 [M. L.]). N.Y. was supported by a HMS CFAR Scholar Award,
and M.-C. S. was supported by NIH Training Grant AI07245.
NR 71
TC 45
Z9 46
U1 1
U2 4
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 DEC
PY 2008
VL 82
IS 23
BP 11555
EP 11567
DI 10.1128/JVI.01561-08
PG 13
WC Virology
SC Virology
GA 370UX
UT WOS:000260789700008
PM 18799576
ER
PT J
AU Zahn, RC
Rett, MD
Korioth-Schmitz, B
Sun, Y
Buzby, AP
Goldstein, S
Brown, CR
Byrum, RA
Freeman, GJ
Letvin, NL
Hirsch, VM
Schmitz, JE
AF Zahn, Roland C.
Rett, Melisa D.
Korioth-Schmitz, Birgit
Sun, Yue
Buzby, Adam P.
Goldstein, Simoy
Brown, Charles R.
Byrum, Russell A.
Freeman, Gordon J.
Letvin, Norman L.
Hirsch, Vanessa M.
Schmitz, Joern E.
TI Simian Immunodeficiency Virus (SIV)-Specific CD8(+) T-Cell Responses in
Vervet African Green Monkeys Chronically Infected with SIVagm
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID NEUTRALIZING ANTIBODY-RESPONSES; I-ASSOCIATED MYELOPATHY; HIV-1
INFECTION; NATURAL HOSTS; GRANZYME-B; VIRAL LOAD; PROLIFERATIVE
CAPACITY; PROGRAMMED DEATH-1; IMMUNE-RESPONSES; TYPE-1 INFECTION
AB African green monkeys (AGM) do not develop overt signs of disease following simian immunodeficiency virus (SIV) infection. While it is still unknown how natural hosts like AGM can cope with this lentivirus infection, a large number of investigations have shown that CD8(+) T-cell responses are critical for the containment of AIDS viruses in humans and Asian nonhuman primates. Here we have compared the phenotypes of T-cell subsets and magnitudes of SIV-specific CD8(+) T-cell responses in vervet AGM chronically infected with SIVagm and rhesus monkeys (RM) infected with SIVmac. In comparison to RM, vervet AGM exhibited weaker signs of immune activation and associated proliferation of CD8(+) T cells as detected by granzyme B, Ki-67, and programmed death 1 staining. By gamma interferon enzyme-linked immunospot assay and intracellular cytokine staining, SIV Gag- and Env-specific immune responses were detectable at variable but lower levels in vervet AGM than in RM. These observations demonstrate that natural hosts like SIV-infected vervet AGM develop SIV-specific T-cell responses, but the disease-free course of infection does not depend on the generation of robust CD8(+) T-cell responses.
C1 [Zahn, Roland C.; Rett, Melisa D.; Korioth-Schmitz, Birgit; Sun, Yue; Buzby, Adam P.; Letvin, Norman L.; Schmitz, Joern E.] Harvard Univ, Div Viral Pathogenesis, Beth Israel Deaconess Med Ctr, Sch Med,Ctr Life Sci, Boston, MA 02115 USA.
[Goldstein, Simoy; Brown, Charles R.; Hirsch, Vanessa M.] NIAID, Mol Microbiol Lab, Natl Inst Hlth, Bethesda, MD 20892 USA.
[Byrum, Russell A.] Bioqual Inc, Rockville, MD 20852 USA.
[Freeman, Gordon J.] Harvard Univ, Dept Med Oncol, Dana Farber Canc Inst, Dept Med,Sch Med, Boston, MA 02115 USA.
RP Schmitz, JE (reprint author), Harvard Univ, Div Viral Pathogenesis, Beth Israel Deaconess Med Ctr, Sch Med,Ctr Life Sci, ECLS 1037,3 Blackfan Circle, Boston, MA 02115 USA.
EM jschmitz@bidmc.harvard.edu
RI Korioth-Schmitz, Birgit/M-7816-2015
OI Korioth-Schmitz, Birgit/0000-0002-5271-9223
FU NIH [AI065335, AI56299]; NIAID Center for HIV/AIDS Vaccine Immunology
(CHAVI) [AI067854]; Harvard Medical School Center for AIDS Research
(CFAR) [AI060354]; Foundation for the NIH through the Grand Challenges
in Global Health initiative; Division of Intramural Research
FX This work was supported by the NIH grants AI065335 (to J.E.S.) and
AI56299 (to G.J.F.), NIAID Center for HIV/AIDS Vaccine Immunology
(CHAVI) grant AI067854 (to N.L.L.), Harvard Medical School Center for
AIDS Research (CFAR) grant AI060354, the Foundation for the NIH through
the Grand Challenges in Global Health initiative (G.J.F.), and the
Division of Intramural Research, NIAID, NIH (V. M. H., S. G., and C. R.
B.).
NR 76
TC 28
Z9 28
U1 0
U2 1
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 DEC
PY 2008
VL 82
IS 23
BP 11577
EP 11588
DI 10.1128/JVI.01779-08
PG 12
WC Virology
SC Virology
GA 370UX
UT WOS:000260789700010
PM 18829748
ER
PT J
AU Kar, AK
Diaz-Griffero, F
Li, Y
Li, X
Sodroski, J
AF Kar, Alak Kanti
Diaz-Griffero, Felipe
Li, Yuan
Li, Xing
Sodroski, Joseph
TI Biochemical and Biophysical Characterization of a Chimeric TRIM21-TRIM5
alpha Protein
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID TRIM5-ALPHA RESTRICTION FACTOR; RETROVIRAL RESTRICTION; B30.2 DOMAIN;
SIMIAN IMMUNODEFICIENCY; B30.2(SPRY) DOMAIN; MONKEY TRIM5-ALPHA;
CYTOPLASMIC BODIES; VIRUS RESTRICTION; UBIQUITIN LIGASE; HIV-1 INFECTION
AB The tripartite motif (TRIM) protein, TRIM5 alpha, is an endogenous factor in primates that recognizes the capsids of certain retroviruses after virus entry into the host cell. TRIM5 alpha promotes premature uncoating of the capsid, thus blocking virus infection. Low levels of expression and tendencies to aggregate have hindered the biochemical, biophysical, and structural characterization of TRIM proteins. Here, a chimeric TRIM5 alpha protein (TRIM5Rh-21R) with a RING domain derived from TRIM21 was expressed in baculovirus-infected insect cells and purified. Although a fraction of the TRIM5Rh-21R protein formed large aggregates, soluble fractions of the protein formed oligomers (mainly dimers), exhibited a protease-resistant core, and contained a high percentage of helical secondary structure. Cross-linking followed by negative staining and electron microscopy suggested a globular structure. The purified TRIM5Rh-21R protein displayed E3-ligase activity in vitro and also self-ubiquitylated in the presence of ubiquitin-activating and -conjugating enzymes. The purified TRIM5Rh-21R protein specifically associated with human immunodeficiency virus type 1 capsid-like complexes; a deletion within the V1 variable region of the B30.2(SPRY) domain decreased capsid binding. Thus, the TRIM5Rh-21R restriction factor can directly recognize retroviral capsid-like complexes in the absence of other mammalian proteins.
C1 [Kar, Alak Kanti; Diaz-Griffero, Felipe; Li, Yuan; Li, Xing; Sodroski, Joseph] Harvard Univ, Sch Med, Dana Farber Canc Inst,Div AIDS, Dept Canc Immunol & AIDS, Boston, MA 02115 USA.
[Sodroski, Joseph] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
RP Sodroski, J (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst,Div AIDS, Dept Canc Immunol & AIDS, 44 Binney St,JFB 824, Boston, MA 02115 USA.
EM joseph_sodroski@dfci.harvard.edu
RI Li, Xing/D-3852-2009; Li, Yuan/B-4098-2013
FU National Institutes of Health [AI063987, AI076094]; Center for AIDS
Research Award [AI06354]; International AIDS Vaccine Initiative
FX We thank Charles Langelier and Wesley Sundquist for the plasmids
expressing the OSF-FL and OSF-Delta V1 proteins and for helpful
discussions. We thank Yvette McLaughlin and Elizabeth Carpelan for
manuscript preparation.; This study was supported by grants from the
National Institutes of Health (AI063987 and AI076094) and a Center for
AIDS Research Award (AI06354), the International AIDS Vaccine
Initiative, and the late William F. McCarty-Cooper.
NR 52
TC 56
Z9 56
U1 1
U2 10
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 DEC
PY 2008
VL 82
IS 23
BP 11669
EP 11681
DI 10.1128/JVI.01559-08
PG 13
WC Virology
SC Virology
GA 370UX
UT WOS:000260789700018
PM 18799572
ER
PT J
AU Langelier, CR
Sandrin, V
Eckert, DM
Christensen, DE
Chandrasekaran, V
Alam, SL
Aiken, C
Olsen, JC
Kar, AK
Sodroski, JG
Sundquist, WI
AF Langelier, Charles R.
Sandrin, Virginie
Eckert, Debra M.
Christensen, Devin E.
Chandrasekaran, Viswanathan
Alam, Steven L.
Aiken, Christopher
Olsen, John C.
Kar, Alak Kanti
Sodroski, Joseph G.
Sundquist, Wesley I.
TI Biochemical Characterization of a Recombinant TRIM5 alpha Protein That
Restricts Human Immunodeficiency Virus Type 1 Replication
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID MURINE LEUKEMIA-VIRUS; E3 UBIQUITIN LIGASE; RETROVIRAL RESTRICTION;
HIV-1 INFECTION; CYCLOPHILIN-A; B30.2(SPRY) DOMAIN; MONKEY TRIM5-ALPHA;
CYTOPLASMIC BODIES; RHESUS TRIM5-ALPHA; STRUCTURAL BASIS
AB The rhesus monkey intrinsic immunity factor TRIM5 alpha(rh) recognizes incoming capsids from a variety of retroviruses, including human immunodeficiency virus type 1 (HIV-1) and equine infectious anemia virus (EIAV), and inhibits the accumulation of viral reverse transcripts. However, direct interactions between restricting TRIM5 alpha proteins and retroviral capsids have not previously been demonstrated using pure recombinant proteins. To facilitate structural and mechanistic studies of retroviral restriction, we have developed methods for expressing and purifying an active chimeric TRIM5 alpha(rh) protein containing the RING domain from the related human TRIM21 protein. This recombinant TRIM5-21R protein was expressed in SF-21 insect cells and purified through three chromatographic steps. Two distinct TRIM5-21R species were purified and shown to correspond to monomers and dimers, as analyzed by analytical ultracentrifugation. Chemically cross-linked recombinant TRIM5-21R dimers and mammalian-expressed TRIM5-21R and TRIM5 alpha proteins exhibited similar sodium dodecyl sulfate-polyacrylamide gel electrophoresis mobilities,indicating that mammalian TRIM5 alpha proteins are predominantly dimeric. Purified TRIM5-21R had ubiquitin ligase activity and could autoubquitylate with different E2 ubiquitin conjugating enzymes in vitro. TRIM5-21R bound directly to synthetic capsids composed of recombinant HIV-1 CA-NC proteins and to authentic EIAV core particles. HIV-1 CA-NC assemblies bound dimeric TRIM5-21R better than either monomeric TRIM5-21R or TRIM5-21R constructs that lacked the SPRY domain or its V1 loop. Thus, our studies indicate that TRIM5 alpha proteins are dimeric ubiquitin E3 ligases that recognize retroviral capsids through direct interactions mediated by the SPRY domain and demonstrate that these activities can be recapitulated in vitro using pure recombinant proteins.
C1 [Langelier, Charles R.; Sandrin, Virginie; Eckert, Debra M.; Christensen, Devin E.; Chandrasekaran, Viswanathan; Alam, Steven L.; Sundquist, Wesley I.] Univ Utah, Dept Biochem, Salt Lake City, UT 84112 USA.
[Aiken, Christopher] Vanderbilt Univ, Sch Med, Dept Microbiol & Immunol, Nashville, TN 37232 USA.
[Olsen, John C.] Univ N Carolina, Cyst Fibrosis Pulm Res & Treatment Ctr, Dept Med, Chapel Hill, NC 27599 USA.
[Kar, Alak Kanti; Sodroski, Joseph G.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS,Div AIDS, Boston, MA 02115 USA.
RP Sundquist, WI (reprint author), Univ Utah, Dept Biochem, Salt Lake City, UT 84112 USA.
EM wes@biochem.utah.edu
FU National Institutes of Health [AI076121, AI063978, AI076094, AI045405,
GM082545]
FX We are grateful to Chad Nelson and the University of Utah Mass
Spectrometry facility for ESI and LC mass spectral analyses, Rachel
Klevit for the gift of expression vectors for E1 and E2 enzymes, and
Chris Hill for critical review of the manuscript.; This research was
supported by National Institutes of Health grants AI076121 (to C. A.),
AI063978 and AI076094 (to J. G. S.), and AI045405 and GM082545 (to W. I.
S.).
NR 74
TC 93
Z9 94
U1 1
U2 5
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD DEC
PY 2008
VL 82
IS 23
BP 11682
EP 11694
DI 10.1128/JVI.01562-08
PG 13
WC Virology
SC Virology
GA 370UX
UT WOS:000260789700019
PM 18799573
ER
PT J
AU Salloum, S
Oniangue-Ndza, C
Neumann-Haefelin, C
Hudson, L
Giugliano, S
Siepen, MAD
Nattermann, J
Spengler, U
Lauer, GM
Wiese, M
Klenerman, P
Bright, H
Scherbaum, N
Thimme, R
Roggendorf, M
Viazov, S
Timm, J
AF Salloum, Shadi
Oniangue-Ndza, Cesar
Neumann-Haefelin, Christoph
Hudson, Laura
Giugliano, Silvia
Siepen, Marc Aus Dem
Nattermann, Jacob
Spengler, Ulrich
Lauer, Georg M.
Wiese, Manfred
Klenerman, Paul
Bright, Helen
Scherbaum, Norbert
Thimme, Robert
Roggendorf, Michael
Viazov, Sergei
Timm, Joerg
TI Escape from HLA-B*08-Restricted CD8 T Cells by Hepatitis C Virus Is
Associated with Fitness Costs
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID RNA HELICASE DOMAIN; LYMPHOCYTE RESPONSE; CHRONIC INFECTION; SOURCE
OUTBREAK; SINGLE-SOURCE; IN-VIVO; TYPE-1; REPLICATION; PROTEASE; GAG
AB The inherent sequence diversity of the hepatitis C virus (HCV) represents a major hurdle for the adaptive immune system to control viral replication. Mutational escape within targeted CD8 epitopes during acute HCV infection has been well documented and is one possible mechanism for T-cell failure. HLA-B*08 was recently identified as one HLA class I allele associated with spontaneous clearance of HCV replication. Selection of escape mutations in the immunodominant HLA-B*08-restricted epitope HSKKKCDEL(1395-1403) was observed during acute infection. However, little is known about the impact of escape mutations in this epitope on viral replication capacity. Their previously reported reversion back toward the consensus residue in patients who do not possess the B*08 allele suggests that the consensus sequence in this epitope is advantageous for viral replication in the absence of immune pressure. The aim of this study was to determine the impact of mutational escape from this immunodominant epitope on viral replication. We analyzed it with a patient cohort with chronic HCV genotype 1b infection and in a single-source outbreak (genotype 1b). Sequence changes in this highly conserved region are rare and selected almost exclusively in the presence of the HLA-B*08 allele. When tested in the subgenomic replicon (Con1), the observed mutations reduce viral replication compared with the prototype sequence. The results provide direct evidence that escape mutations in this epitope are associated with fitness costs and that the antiviral effect of HLA-B*08-restricted T cells is sufficiently strong to force the virus to adopt a relatively unfavorable sequence.
C1 [Salloum, Shadi; Oniangue-Ndza, Cesar; Giugliano, Silvia; Siepen, Marc Aus Dem; Roggendorf, Michael; Viazov, Sergei; Timm, Joerg] Univ Essen Gesamthsch, Dept Virol, D-45147 Essen, Germany.
[Neumann-Haefelin, Christoph; Thimme, Robert] Univ Freiburg, Dept Med 2, D-79106 Freiburg, Germany.
[Hudson, Laura; Bright, Helen] GlaxoSmithKline Inc, Dept Virol, Stevenage SG1 2NY, Herts, England.
[Nattermann, Jacob; Spengler, Ulrich] Univ Bonn, Dept Med 1, D-53105 Bonn, Germany.
[Lauer, Georg M.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02129 USA.
[Wiese, Manfred] St Georg Hosp, Dept Med 2, D-04129 Leipzig, Germany.
[Klenerman, Paul] John Radcliffe Hosp, Oxford Biomed Res Ctr, Oxford OX3 9DU, England.
[Scherbaum, Norbert] Hosp Univ Duisburg Essen, Rhine State Hosp, Dept Psychiat & Psychotherapy, Addict Res Grp, D-45147 Essen, Germany.
RP Timm, J (reprint author), Univ Essen Gesamthsch, Dept Virol, Virchowstr 179, D-45147 Essen, Germany.
EM joerg.timm@uni-due.de
RI Neumann-Haefelin, Christoph/E-5550-2011
FU Deutsche Forschungsgemeinschaft DFG [TI 323/3-1]; Wellcome Trust, James
Martin School; NIHR Biomedical Research Centre Programme; Federal
Ministry of Education and Research (German Hepatitis Network)
FX We thank the East German Study Group e.V. for contributing samples of
the East German Anti-D cohort.; J.T. was supported by the Deutsche
Forschungsgemeinschaft DFG (TI 323/3-1). P. K. was supported by the
Wellcome Trust, James Martin School for the 21st Century, and NIHR
Biomedical Research Centre Programme. This work was supported by the
Federal Ministry of Education and Research (German Hepatitis Network).
NR 33
TC 34
Z9 34
U1 0
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 DEC
PY 2008
VL 82
IS 23
BP 11803
EP 11812
DI 10.1128/JVI.00997-08
PG 10
WC Virology
SC Virology
GA 370UX
UT WOS:000260789700032
PM 18815309
ER
PT J
AU Accortt, EE
Freeman, MP
Allen, JJB
AF Accortt, Eynav Elgavish
Freeman, Marlene P.
Allen, John J. B.
TI Women and Major Depressive Disorder: Clinical Perspectives on Causal
Pathways
SO JOURNAL OF WOMENS HEALTH
LA English
DT Review
ID PREMENSTRUAL DYSPHORIC DISORDER; FRONTAL EEG ASYMMETRY;
NATIONAL-COMORBIDITY-SURVEY; SEX-DIFFERENCES; POSTPARTUM DEPRESSION;
LIFE STRESS; GENDER DIFFERENCES; MENSTRUAL-CYCLE;
ELECTROENCEPHALOGRAPHIC ASYMMETRY; PSYCHIATRIC-DISORDERS
AB Background and aims: Epidemiological data on the prevalence of mood disorders demonstrate that major depressive disorder (MDD) is approximately twice as common in women as in men and that its first onset peaks during the reproductive years. We aimed to review key social, psychological, and biological factors that seem strongly implicated in the etiology of major depression and to focus on sex-specific aspects of depression, such as the role of a woman's reproductive life cycle in depressive symptomatology.
Methods: A review of the literature, from 1965 to present, was conducted.
Results: An integrated etiological model best explains gender and sex differences in depression. Social, psychological, and biological variables must be simultaneously taken into account. These vulnerabilities include ( but are not limited to) gender-specific roles in society, life stress such as trauma, a tendency toward ruminative coping strategies, and the effects of sex hormones and genetic factors.
Conclusions: To effectively treat MDD in women and to prevent the recurrence of illness in vulnerable women, clinicians must understand the sex-specific aspects of mood disorders over the longitudinal course of women's reproductive lives. A biopsychosocial approach should, therefore, be the main focus of future research and practice, to eventually result in an integrated etiological model of depression in women. Based on the prevalence of MDD in women, timely screening, diagnosis, and intervention should be public health priorities.
C1 [Accortt, Eynav Elgavish; Allen, John J. B.] Univ Arizona, Dept Psychol, Tucson, AZ 85721 USA.
[Freeman, Marlene P.] Massachusetts Gen Hosp, Dept Psychiat, Ctr Womens Mental Hlth, Boston, MA 02114 USA.
RP Accortt, EE (reprint author), Univ Arizona, Dept Psychol, POB 210068, Tucson, AZ 85721 USA.
EM eynav@email.arizona.edu
FU National Institute for Mental Health; U. S. Food and Drug
Administration; GlaxoSmithKline; Meadows Foundation; Chatham Institute
(KV Pharmaceuticals), Lilly, Forest; National Institutes of Health;
National Alliance for Research on Schizophrenia and Depression;
Institute for Mental Health Research
FX E. E. A. has nothing to disclose. M. P. F. received research support
from the National Institute for Mental Health, U. S. Food and Drug
Administration, GlaxoSmithKline, The Meadows Foundation, Honorarium from
CME program from the Chatham Institute (KV Pharmaceuticals), Lilly,
Forest. J.B.A. received funding from the National Institutes of Health,
the National Alliance for Research on Schizophrenia and Depression, and
the Institute for Mental Health Research.
NR 122
TC 46
Z9 49
U1 6
U2 22
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
J9 J WOMENS HEALTH
JI J. Womens Health
PD DEC
PY 2008
VL 17
IS 10
BP 1583
EP 1590
DI 10.1089/jwh.2007.0592
PG 8
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA 378OG
UT WOS:000261331500008
PM 19049352
ER
PT J
AU Bartels, C
Goetz, S
Ward, E
Carnes, M
AF Bartels, Christie
Goetz, Sarah
Ward, Earlise
Carnes, Molly
TI Internal Medicine Residents' Perceived Ability to Direct Patient Care:
Impact of Gender and Experience
SO JOURNAL OF WOMENS HEALTH
LA English
DT Article
ID SEX-ROLE INVENTORY; WOMEN; STEREOTYPES; LEADERSHIP; METAANALYSIS
AB Background: Physicians are expected to effect patient care by giving orders to members of a healthcare team. Because women are socialized to be less directive than men, the assertive behavior required of new physicians may be experienced differently by male and female residents. We sought to explore the effects of gender and year of training on residents' experiences and perceived ability to direct patient care.
Methods: This was a mixed-methods, cross-sectional, descriptive study employing a quantitative written survey and qualitative interviews among internal medicine residents at an academic health center. Measurements included questionnaires and interviews about stress, assertiveness, and personal factors that influence their effectiveness in directing patient care. Analyses examined differences by gender and year of training.
Results: One hundred residents were invited to participate; 65 returned questionnaires, and 16 of these residents were interviewed. Compared with male residents, female residents selected less assertive behaviors for clinical scenarios ( p = 0.047) and were more likely to perceive gender as inhibiting their ability to influence patient care ( p = 0.01). Stress associated with being assertive varied more with experience than gender. Interviews corroborated these findings and supported the complexity of gender norms for behavior for female residents in a directive leadership position.
Conclusions: When compared with male peers, female residents reported more gender issues in residency and chose less assertive behaviors in clinical scenarios. Experience mitigated some gender differences. Our findings suggest that discussion of the existing research on prescriptive gender norms for behavior and leadership may be warranted in resident orientation.
C1 [Bartels, Christie; Carnes, Molly] Univ Wisconsin, Dept Med, Madison, WI 53715 USA.
[Carnes, Molly] William S Middleton Mem Vet Adm Med Ctr, Ctr Geriatr Res Educ & Clin, Madison, WI USA.
RP Carnes, M (reprint author), Univ Wisconsin, Dept Med Psychiat & Ind & Syst Engn, Ctr Womens Hlth Res, 700 Regent St,Suite 101, Madison, WI 53715 USA.
EM mlcarnes@wisc.edu
FU University of Wisconsin-Madison School of Medicine and Public Health;
Jean Manchester Biddick-Bascom Endowed Professorship; Meriter Hospital
FX This work was supported by a Shapiro Grant from the University of
Wisconsin-Madison School of Medicine and Public Health, the Jean
Manchester Biddick-Bascom Endowed Professorship, and Meriter Hospital.
We thank Tim Hess for statistical support and Linda Baier for reviewing
the manuscript.
NR 27
TC 16
Z9 16
U1 1
U2 7
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
J9 J WOMENS HEALTH
JI J. Womens Health
PD DEC
PY 2008
VL 17
IS 10
BP 1615
EP 1621
DI 10.1089/jwh.2008.0798
PG 7
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA 378OG
UT WOS:000261331500012
PM 19049356
ER
PT J
AU Martin, JL
Alam, T
Harker, JO
Josephson, KR
Alessi, CA
AF Martin, Jennifer L.
Alam, Tarannum
Harker, Judith O.
Josephson, Karen R.
Alessi, Cathy A.
TI Sleep in Assisted Living Facility Residents Versus Home-Dwelling Older
Adults
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Sleep; Aging; Circadian rhythms; Assisted living
ID ACTIVITY RHYTHMS; INDEX; WAKE
AB Background. Sleep problems among assisted living facility (ALF) residents are not well understood, and sleep-related differences between ALF residents and home-dwelling older adults have not been examined.
Methods. We compared sleep patterns in 19 ALF residents to sleep patterns in 19 matched home-dwelling older people (age >= 65 years). All were participating in the follow-up portion of a longitudinal study of sleep and functional outcomes following post-acute rehabilitation. Sleep was assessed with the Pittsburgh Sleep Quality Index and l week of wrist actigraphy.
Results. By actigraphy, ALF residents awoke earlier in the morning and exhibited more nighttime awakenings compared to home-dwelling participants (06:50 hours +/- 1:29 hours vs 07:51 hours +/- 1:19 hours and 19.5 +/- 8.5 vs 12.9 +/- 11.4 awakenings, respectively).
Conclusions. Larger studies are needed to confirm these initial findings that ALF residents have more disrupted sleep than do home-dwelling older persons, and to examine the functional and health consequences of poor sleep among ALF residents.
C1 [Martin, Jennifer L.; Alam, Tarannum; Harker, Judith O.; Josephson, Karen R.; Alessi, Cathy A.] VA Greater Los Angeles Healthcare Syst, Ctr Geriatr Res Educ & Clin, Los Angeles, CA USA.
[Martin, Jennifer L.; Alessi, Cathy A.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
RP Martin, JL (reprint author), VA Sepulveda GRECC 11E, 16111 Plummer St, North Hills, CA 91343 USA.
EM jennifer.martin@va.gov
FU National Institute on Aging (NIA) [K23AG028452]; VA Special Fellowship
Program in Advanced Geriatrics; VA Health Services Research and
Development Service [IIR01-053-1, AlA03-047]; UCLA Older Americans
Independence Center (OAIC) [5-P60-AG010415]; VA Greater Los Angeles
Healthcare System Geriatric Research, Education and Clinical Center
FX This work was supported by National Institute on Aging (NIA) grant
K23AG028452, the VA Special Fellowship Program in Advanced Geriatrics,
VA Health Services Research and Development Service grants IIR01-053-1
and AlA03-047. UCLA Older Americans Independence Center (OAIC) grant
5-P60-AG010415, and by the VA Greater Los Angeles Healthcare System
Geriatric Research, Education and Clinical Center.; Portions of this
article were presented at the 2005 American Geriatrics Society meeting,
Orlando, Florida.
NR 17
TC 6
Z9 6
U1 0
U2 1
PU GERONTOLOGICAL SOC AMER
PI WASHINGTON
PA 1030 15TH ST NW, STE 250, WASHINGTON, DC 20005202-842 USA
SN 1079-5006
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD DEC
PY 2008
VL 63
IS 12
BP 1407
EP 1409
PG 3
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 395PG
UT WOS:000262535400018
PM 19126856
ER
PT J
AU Isshiki, K
He, ZH
Maeno, Y
Ma, RC
Yasuda, Y
Kuroki, T
White, GS
Patti, ME
Weir, GC
King, GL
AF Isshiki, Keiji
He, Zhiheng
Maeno, Yasuhiro
Ma, Ronald C.
Yasuda, Yutaka
Kuroki, Tatsuya
White, Gregory S.
Patti, Mary E.
Weir, Gordon C.
King, George L.
TI Insulin regulates SOCS2 expression and the mitogenic effect of IGF-1 in
mesangial cells
SO KIDNEY INTERNATIONAL
LA English
DT Article
DE diabetes; insulin; SOCS2; STAT; signaling; nephropathy
ID GROWTH-FACTOR-I; DIABETIC-NEPHROPATHY; CYTOKINE SIGNALING-2;
SKELETAL-MUSCLE; SUPPRESSOR; RECEPTOR; MICE; COMPLICATIONS; PROTEINS;
MELLITUS
AB Renal hypertrophy and deposition of extracellular matrix proteins are consistent findings in diabetic nephropathy and these processes can be halted or reversed by euglycemic control. Using DNA microarray analysis of glomerular RNA from control and diabetic rats we found that the expression levels of insulin-like growth factor 1 receptor (IGF-1R) were increased while those of suppressor of cytokine signaling 2 (SOCS2) and STAT5 were decreased. All of these changes were normalized by islet cell transplantation. Overexpression of SOCS2 in rat mesangial cells inhibited IGF-1-induced activation of extracellular signal-regulated kinase, which subsequently reduced type IV collagen and DNA synthesis, an effect due to interaction of SOCS2 with IGF-1R. Inhibition of SOCS2 overexpression by small interfering RNA suppressed IGF-1R-mediated actions by preventing phosphorylation of tyrosine 317 in the p66Shc adaptor protein; however, overexpression of either SOCS1 or SOCS3 did not affect IGF-1R signaling. Insulin directly increased STAT5 and SOCS2 expression in mesangial cells. This study shows that insulin can inhibit the mitogenic action of IGF-1 in mesangial cells by regulating STAT5/SOCS2 expression. Insulin deficiency may contribute to the mesangial expansion found in diabetes through reduced STAT5/SOCS2 expression.
C1 [Isshiki, Keiji; He, Zhiheng; Maeno, Yasuhiro; Ma, Ronald C.; Yasuda, Yutaka; Kuroki, Tatsuya; White, Gregory S.; Patti, Mary E.; Weir, Gordon C.; King, George L.] Harvard Univ, Sch Med, Joslin Diabet Ctr, Div Res, Boston, MA 02215 USA.
RP King, GL (reprint author), Harvard Univ, Sch Med, Joslin Diabet Ctr, Div Res, 1 Joslin Pl, Boston, MA 02215 USA.
EM george.king@joslin.harvard.edu
RI Ma, Ronald/C-2788-2009
OI Ma, Ronald/0000-0002-1227-803X
FU National Institute of Health [DK53105]; Joslin's Diabetes and
Endocrinology Research Center [DK36836]; American Diabetes Association;
Juvenile Diabetes Research Foundation
FX This work is supported by a grant from National Institute of Health
(DK53105) to GLK, and DK36836 (Joslin's Diabetes and Endocrinology
Research Center Grant). KI and YY are recipients of American Diabetes
Association mentor-based fellowship. ZH is a recipient of Juvenile
Diabetes Research Foundation fellowship.
NR 37
TC 8
Z9 9
U1 1
U2 2
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 DEC
PY 2008
VL 74
IS 11
BP 1434
EP 1443
DI 10.1038/ki.2008.403
PG 10
WC Urology & Nephrology
SC Urology & Nephrology
GA 372CQ
UT WOS:000260879600011
PM 19008912
ER
PT J
AU Zalyapin, EA
Bouley, R
Hasler, U
Vilardaga, JP
Lin, HY
Brown, D
Ausiello, DA
AF Zalyapin, Elena A.
Bouley, Richard
Hasler, Udo
Vilardaga, Jean-Pierre
Lin, Herbert Y.
Brown, Dennis
Ausiello, Dennis A.
TI Effects of the renal medullary pH and ionic environment on vasopressin
binding and signaling
SO KIDNEY INTERNATIONAL
LA English
DT Article
DE G-protein-coupled receptor signaling; vasopressin; hypertonicity
ID THICK ASCENDING LIMB; DUCT PRINCIPAL CELLS; ARGININE-VASOPRESSIN;
COLLECTING DUCT; MOLECULAR-CLONING; CAMP PRODUCTION; ANGIOTENSIN-II;
WATER CHANNEL; V2 RECEPTOR; RAT-KIDNEY
AB The kidney has a cortico-medullary interstitial gradient of decreasing pH and increasing concentrations of sodium chloride and urea, but the influence of these gradients on receptor signaling is largely unknown. Here, we measured G-protein coupled receptor function in LLC-PK1 cells acutely exposed to conditions mimicking different kidney regions. Signaling through the parathyroid hormone receptor, normally expressed in the cortex, was greatly reduced at an acidic pH similar to that of the inner medulla. Parathyroid hormone receptor, tagged with green fluorescent protein, showed no ligand-induced internalization. In contrast, under both acidic and hyperosmotic conditions, vasopressin increased intracellular cAMP, and upon binding to its type 2 receptor (V2R) was internalized and degraded. Dosedisplacement binding assays with selective vasopressin/oxytocin receptor ligands under inner medullary conditions indicated a shift in the V2R pharmacological profile. Oxytocin did not bind to the V2R, as it does under normal conditions and the vasopressin type 1 receptor (V1R) had reduced affinity for vasopressin compared to the V2R in low pH and high osmolality. We suggest that the cortico-medullary gradient causes a receptor-specific selectivity in ligand binding that is of functional significance to the kidney. While the gradient is important for urinary concentration, it may also play a substantial role in fine-tuning of the vasopressin response through the V2R.
C1 [Bouley, Richard] Massachusetts Gen Hosp, Div Nephrol, MGH Ctr Syst Biol, Program Membrane Biol,Simches Res Ctr, Boston, MA 02114 USA.
[Vilardaga, Jean-Pierre] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
[Vilardaga, Jean-Pierre] Harvard Univ, Sch Med, Boston, MA USA.
RP Bouley, R (reprint author), Massachusetts Gen Hosp, Div Nephrol, MGH Ctr Syst Biol, Program Membrane Biol,Simches Res Ctr, 185 Cambridge St, Boston, MA 02114 USA.
EM bouley.richard@mgh.harvard.edu
FU NIH [PO1DK38452, DK071837]; National Kidney Foundation; Swiss FSBMB
Fellowship; ECOR Fellowship; Boston Area Diabetes and Endocrinology
Research Center [DK57521]; Study of Inflammatory Bowel Disease [DK43341]
FX This work was supported by NIH grants PO1DK38452 (DB and DAA). H. Y. Lin
was supported by an NIH RO1award (DK071837). R. Bouley received an
investigator award from the National Kidney Foundation. U. Hasler is
supported by a Swiss FSBMB Fellowship as well as an ECOR Fellowship
awarded by MGH. The Microscopy Core facility of the MGH Program in
Membrane Biology receives additional support from the Boston Area
Diabetes and Endocrinology Research Center (DK57521) and the Center for
the Study of Inflammatory Bowel Disease (DK43341).
NR 78
TC 10
Z9 10
U1 1
U2 3
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 DEC
PY 2008
VL 74
IS 12
BP 1557
EP 1567
DI 10.1038/ki.2008.412
PG 11
WC Urology & Nephrology
SC Urology & Nephrology
GA 382TJ
UT WOS:000261628000010
PM 18813286
ER
PT J
AU Fiorentino, M
Zadra, G
Palescandolo, E
Fedele, G
Bailey, D
Fiore, C
Nguyen, PL
Migita, T
Zamponi, R
Di Vizio, D
Priolo, C
Sharma, C
Xie, W
Hemler, ME
Mucci, L
Giovannucci, E
Finn, S
Loda, M
AF Fiorentino, Michelangelo
Zadra, Giorgia
Palescandolo, Emanuele
Fedele, Giuseppe
Bailey, Dyane
Fiore, Christopher
Nguyen, Paul L.
Migita, Toshiro
Zamponi, Raffaella
Di Vizio, Dolores
Priolo, Carmen
Sharma, Chandan
Xie, Wanling
Hemler, Martin E.
Mucci, Lorelei
Giovannucci, Edward
Finn, Stephen
Loda, Massimo
TI Overexpression of fatty acid synthase is associated with palmitoylation
of Wnt1 and cytoplasmic stabilization of beta-catenin in prostate cancer
SO LABORATORY INVESTIGATION
LA English
DT Article
DE beta-catenin; fatty acid synthase; prostate cancer;
immunohistochemistry; palmitoylation; Wnt1
ID EXPRESSION; CELLS; CARCINOMA; APOPTOSIS; GROWTH; ADENOCARCINOMA;
LOCALIZATION; PREDICTOR; INHIBITOR; MORTALITY
AB Fatty acid synthase (FASN), a key metabolic enzyme for liponeogenesis highly expressed in several human cancers, displays oncogenic properties such as resistance to apoptosis and induction of proliferation when overexpressed. To date, no mechanism has been identified to explain the oncogenicity of FASN in prostate cancer. We generated immortalized prostate epithelial cells (iPrECs) overexpressing FASN, and found that (14)C-acetate incorporation into palmitate synthesized de novo by FASN was significantly elevated in immunoprecipitated Wnt-1 when compared to isogenic cells not overexpressing FASN. Overexpression of FASN caused membranous and cytoplasmic beta-catenin protein accumulation and activation, whereas FASN knockdown by short-hairpin RNA resulted in a reduction in the extent of beta-catenin activation. Orthotopic transplantation of iPrECs overexpressing FASN in nude mice resulted in invasive tumors that overexpressed beta-catenin. A strong significant association between FASN and cytoplasmic ( stabilized) beta-catenin immunostaining was found in 862 cases of human prostate cancer after computerized subtraction of the membranous beta-catenin signal (P < 0.001, Spearman's rho = 0.33). We propose that cytoplasmic stabilization of beta-catenin through palmitoylation of Wnt-1 and subsequent activation of the pathway is a potential mechanism of FASN oncogenicity in prostate cancer.
C1 [Fiorentino, Michelangelo; Zadra, Giorgia; Palescandolo, Emanuele; Fedele, Giuseppe; Bailey, Dyane; Fiore, Christopher; Nguyen, Paul L.; Migita, Toshiro; Zamponi, Raffaella; Priolo, Carmen; Finn, Stephen; Loda, Massimo] Brigham & Womens Hosp, Dana Farber Canc Inst, Ctr Mol Oncol Pathol, Dept Med Oncol, Boston, MA 02115 USA.
[Di Vizio, Dolores; Hemler, Martin E.] Harvard Univ, Sch Med, Childrens Hosp, Dept Urol, Boston, MA USA.
[Sharma, Chandan] Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA.
[Xie, Wanling] Dana Farber Canc Inst, Dept Biostat, Boston, MA 02115 USA.
[Mucci, Lorelei; Giovannucci, Edward] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Brigham & Womens Hosp,Channing Lab, Boston, MA 02115 USA.
RP Loda, M (reprint author), Dana Farber Canc Inst, Dept Canc Immunol & AIDS, D1536,44 Binney St, Boston, MA 02115 USA.
EM massimo_loda@dfci.harvard.edu
FU National Cancer Institute [RO1CA131945, PO1CA89021, P50 CA90381, P50
CA55075]; Prostate Cancer Foundation, DFCI-Novartis Drug Development
Program; Linda and Arthur Gelb Center for Translational Research; Jimmy
Fund; Loda laboratory; Samuel Waxman Foundation [SPA P01-Waxman-CS01];
NIH [GM38903]; American-Italian Cancer Foundation
FX This work (to ML) was supported from the National Cancer Institute
(RO1CA131945, PO1CA89021, P50 CA90381 and CA55075), the Prostate Cancer
Foundation, DFCI-Novartis Drug Development Program, the Linda and Arthur
Gelb Center for Translational Research, a gift from Nuclea Biomarkers to
the Jimmy Fund and the Loda laboratory, and the Samuel Waxman Foundation
(SPA P01-Waxman-CS01). This study was also support to MEH from NIH grant
GM38903. GZ and EP are supported by grants from the American-Italian
Cancer Foundation. We are grateful to Dr William C Hahn for the
engineering of the immortalized human prostate epithelial cell lines and
to Dr Phillip Febbo and Dr Ramesh A Shivdasani for helpful suggestions.
NR 43
TC 60
Z9 64
U1 0
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD DEC
PY 2008
VL 88
IS 12
BP 1340
EP 1348
DI 10.1038/labinvest.2008.97
PG 9
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 375JD
UT WOS:000261109100008
PM 18838960
ER
PT J
AU Norden, AD
Drappatz, J
Wen, PY
AF Norden, Andrew D.
Drappatz, Jan
Wen, Patrick Y.
TI Novel anti-angiogenic therapies for malignant gliomas
SO LANCET NEUROLOGY
LA English
DT Review
ID ENDOTHELIAL GROWTH-FACTOR; PHASE-II TRIAL; HIGH-GRADE GLIOMAS;
NEWLY-DIAGNOSED GLIOBLASTOMA; TUMOR ANGIOGENESIS; IN-VIVO; ANAPLASTIC
ASTROCYTOMA; METRONOMIC CHEMOTHERAPY; EUROPEAN ORGANIZATION;
RADIATION-THERAPY
AB Background Despite optimum treatment with surgery, radiation therapy, and chemotherapy, most patients with malignant glioma have a poor prognosis. Malignant gliomas are vascular tumours that produce vascular endothelial growth factor (VEGF), which is an important mediator of angiogenesis. Preclinical data indicate that angiogenesis is essential for the proliferation and survival of malignant glioma cells, which suggests that inhibition of angiogenesis might be an effective therapeutic strategy. Anti-angiogenic therapies that target VEGF and the VEGF receptor (VEGFR) are effective adjuncts to the treatment of solid tumours. Normalisation of dilated and leaky tumour vasculature might also enable anti-angiogenic therapy to increase the efficacy of radiation therapy and cytotoxic chemotherapy.
Recent developments Several studies have investigated the use of bevacizumab-a humanised monoclonal antibody against VEGF-for patients with recurrent malignant glioma. Treatment with bevacizumab is commonly combined with cytotoxic chemotherapy and results in dramatic responses seen on radiographs, prolongation of progression-free survival, and less need for corticosteroids. Similar results have been shown with small-molecule inhibitors of VEGFR, such as cediranib. Anti-angiogenic treatment is generally well tolerated but common adverse effects include hypertension and proteinuria, whereas the potentially more serious adverse effects, such as thromboembolic disease and haemorrhage, occur infrequently. At least half of patients fail to respond to anti-angiogenic treatment and the response duration is variable. Resistance to anti-angiogenic therapy might implicate alternative pro-angiogenic factors, such as basic fibroblast growth factor, stromal-derived factor-la, the angiopoietin receptor Tie2, and placental growth factor. Anti-angiogenic therapy might also lead to mobilisation of circulating endothelial cells towards the turnout, which supports angiogenesis. Another possible mechanism of resistance of malignant glioma cells might be upregulation of pro-invasive molecules, which would result in increased infiltrative turnout growth along the blood vessels.
Where next? Although anti-angiogenic therapies are promising, the duration of response with available regimens is modest. Continuing investigations will determine whether these drugs are best used for newly diagnosed or recurrent tumours and will establish the optimum combinations with radiation, cytotoxic chemotherapy, and other targeted molecular compounds. As yet, there are no effective treatments for patients on anti-angiogenic therapies whose tumours progress. Further understanding of the mechanisms of resistance to anti-angiogenic therapies and better selection of patients will be crucial to improve outcomes for patients with malignant glioma.
C1 [Norden, Andrew D.; Drappatz, Jan; Wen, Patrick Y.] Brigham & Womens Hosp, Dept Neurol, Div Neurooncol, Boston, MA 02115 USA.
[Norden, Andrew D.; Drappatz, Jan; Wen, Patrick Y.] Dana Farber Brigham & Womens Canc Ctr, Dept Med Oncol, Ctr Neurooncol, Boston, MA USA.
[Norden, Andrew D.; Drappatz, Jan; Wen, Patrick Y.] Harvard Univ, Sch Med, Boston, MA USA.
RP Norden, AD (reprint author), Dana Farber Canc Inst, Ctr Neurooncol, 44 Binney St, Boston, MA 02115 USA.
EM anorden@partners.org
FU Cure Brain Tumor research funds
FX The authors thank the Amos E Wasgatt, Neil Harrington, Christopher S
Elliott, and Par Fore The Cure Brain Tumor research funds for their
financial support.
NR 84
TC 126
Z9 135
U1 0
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1474-4422
J9 LANCET NEUROL
JI Lancet Neurol.
PD DEC
PY 2008
VL 7
IS 12
BP 1152
EP 1160
DI 10.1016/S1474-4422(08)70260-6
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA 379KV
UT WOS:000261396000020
PM 19007739
ER
PT J
AU Platt, MP
Cunnane, ME
Curtin, HD
Metson, R
AF Platt, Michael P.
Cunnane, Mary E.
Curtin, Hugh D.
Metson, Ralph
TI Anatomical Changes of the Ethmoid Cavity After Endoscopic Sinus Surgery
SO LARYNGOSCOPE
LA English
DT Article; Proceedings Paper
CT 111th Annual Meeting of the Triological-Society
CY MAY 03-04, 2008
CL Orlando, FL
SP Triol Soc
DE Endoscopic sinus surgery; ethmoid sinus; sinusitis
ID PARANASAL SINUSES; CYSTIC-FIBROSIS; FACIAL GROWTH; CT
AB Objective: Alteration of the bony architecture of the sinus cavities has been observed in chronic sinusitis. Plasticity of the ethmoid sinus framework after endoscopic surgery, however, is a newly described entity. The objective of this study was to determine the incidence and extent of changes in ethmoid size after ethmoidectomy.
Study Design: Retrospective review performed at an academic medical center.
Methods: Computed tomography scans performed from 2006 through 2007 at the Massachusetts Eye and Ear Infirmary (n = 5,131) were reviewed to identify 100 consecutive patients who underwent sinus surgery and met inclusion criteria. Seven dimensions were measured for each pre- and postoperative scan (n = 200) using Voxar 3D software.
Results: Computed tomography scans performed before and 2 to 37 months after ethmoidectomy demonstrated a decrease of 1.1 +/- 1.6 mm in mean ethmoid cavity width at the level of the cribriform plate and posterior globe after surgery (P < .0001). Twenty-five patients (25%) had > 1 mm decrease in mean ethmoid width, and six patients (6%) had a decrease of >2 mm (mean 3.1 +/- 0.9 mm). These findings seemed to be the result of postoperative bowing of the medial ethmoid walls with a corresponding increase in orbital volume. These volumetric changes resulted in a postoperative subclinical retrodisplacement (enophthalmos) of the globes (mean 0.2 +/- 0.8 mm, P = .008). The extent of surgery, including performance of frontal recess dissection (P = .007) and total ethmoidectomy (P = .021) were found to be independent predictors of the observed changes in sinus dimensions.
Conclusions: Postsurgical plasticity of the ethmoid cavity is a new concept supported by observed changes in sinus dimensions after ethmoidectomy. These changes
C1 [Platt, Michael P.] Massachusetts Eye & Ear Infirm, Dept Otolaryngol Head & Neck Surg, Boston, MA 02114 USA.
[Cunnane, Mary E.] Massachusetts Eye & Ear Infirm, Dept Radiol, Boston, MA 02114 USA.
[Curtin, Hugh D.] Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02115 USA.
[Metson, Ralph] Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA.
RP Metson, R (reprint author), Zero Emerson Pl, Boston, MA 02114 USA.
EM Ralph_metson@meei.harvard.edu
NR 10
TC 5
Z9 5
U1 0
U2 2
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0023-852X
J9 LARYNGOSCOPE
JI Laryngoscope
PD DEC
PY 2008
VL 118
IS 12
BP 2240
EP 2244
DI 10.1097/MLG.0b013e31818379cd
PG 5
WC Medicine, Research & Experimental; Otorhinolaryngology
SC Research & Experimental Medicine; Otorhinolaryngology
GA 405CV
UT WOS:000263200900029
PM 19029868
ER
PT J
AU Cavo, M
Attal, M
Gertz, MA
Giralt, S
Ludwig, H
Morgan, GJ
Anderson, KC
AF Cavo, Michele
Attal, Michel
Gertz, Morie A.
Giralt, Sergio
Ludwig, Heinz
Morgan, Gareth J.
Anderson, Kenneth C.
TI Proceedings of an educational symposium at the 34th Annual Meeting of
the European Group for Blood and Marrow Transplantation 30 March 2008
Florence, Italy Lenalidomide in multiple myeloma: in pursuit of optimal
treatment
SO LEUKEMIA RESEARCH
LA English
DT Article; Proceedings Paper
CT 34th Annual Meeting of the
European-Group-for-Blood-and-Marrow-Transplantation/24nd Meeting of the
EBMT-Nurses-Group/7th Meeting of the EBMT-Data-Management-Group
CY MAR 30-APR 02, 2008
CL Florence, ITALY
SP European Grp Blood & Marrow Transplantat, EBMT Nurses Grp, EBMT Data Management Grp
ID NEWLY-DIAGNOSED MYELOMA; ELDERLY UNTREATED PATIENTS; BORTEZOMIB PLUS
MELPHALAN; AUTOLOGOUS TRANSPLANTATION; COMBINATION THERAPY;
RANDOMIZED-TRIAL; DEXAMETHASONE; THALIDOMIDE; CHEMOTHERAPY; PREDNISONE
C1 [Cavo, Michele] Univ Bologna, Sch Med, Seragnoli Inst Hematol & Med Oncol, Bologna, Italy.
[Attal, Michel] Univ Toulouse 3, Dept Haematol, F-31062 Toulouse, France.
[Attal, Michel] Purpan Hosp, Dept Haematol, Toulouse, France.
[Gertz, Morie A.] Mayo Clin, Dept Internal Med, Div Hematol, Rochester, MN USA.
[Giralt, Sergio] Univ Texas Houston, MD Anderson Canc Ctr, Dept Stem Cell Transplantat & Cellular Therapy, Houston, TX 77030 USA.
[Ludwig, Heinz] Wilhelminenspital Stadt Wien, Ctr Oncol & Haematol, Dept Med 1, Vienna, Austria.
[Morgan, Gareth J.] Inst Canc Res, Sutton, Surrey, England.
[Morgan, Gareth J.] Royal Marsden NHS Fdn Trust, Sutton, Surrey, England.
[Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Cavo, M (reprint author), Univ Bologna, Sch Med, Seragnoli Inst Hematol & Med Oncol, Bologna, Italy.
OI CAVO, MICHELE/0000-0003-4514-3227
NR 69
TC 1
Z9 1
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0145-2126
J9 LEUKEMIA RES
JI Leuk. Res.
PD DEC
PY 2008
VL 32
SU 1
BP S1
EP S24
DI 10.1016/S0145-2126(08)70002-X
PG 24
WC Oncology; Hematology
SC Oncology; Hematology
GA 369UY
UT WOS:000260720600001
PM 18954677
ER
PT J
AU Kozak, KR
Hong, TS
Sluss, PM
Lewandrowski, EL
Aleryani, SL
MacDonald, SM
Choi, NC
Yock, TI
AF Kozak, Kevin R.
Hong, Theodore S.
Sluss, Patrick M.
Lewandrowski, Elizabeth L.
Aleryani, Samir L.
MacDonald, Shannon M.
Choi, Noah C.
Yock, Torunn I.
TI Cardiac blood biomarkers in patients receiving thoracic (chemo)radiation
SO LUNG CANCER
LA English
DT Article
DE Cardiotoxicity; Troponin; CK-MB; BNP; Radiation; Lung cancer
ID BREAST-CANCER; ADJUVANT RADIOTHERAPY; LUNG-CANCER; POSTOPERATIVE
RADIOTHERAPY; HODGKINS-DISEASE; SURVIVORS; CHILDREN; SOCIETY; MARKERS;
RISK
AB Cardiotoxicity is a known consequence of thoracic irradiation and there are multiple overlapping risk factors for cardiac disease and thoracic malignancies. In this study, we quantified the impact of thoracic (chemo) radiation on cardiac troponin T (TnT), creatine kinase-myocardial. band (CK-MB) and aminoterminal. pro-brain natriuretic peptide (NT-proBNP). Thirty patients receiving radiation therapy to the thorax with or without concurrent chemotherapy were evaluated. Serum was collected at baseline, 2 weeks into treatment and at the completion of radiation therapy. TnT, CK-MB and NT-proBNP were quantified using commercially available immunoassays. Cardiac dosimetric parameters and clinical. risk factors were examined. In 29 of 30 patients, serum TnT remained undetectable (<0.01 ng/mL) throughout (chemo) radiation. In the one patient with detectable serum TnT, levels did not change significantly with treatment. Similarly, thoracic (chemo)radiation did not cause statistically significant elevations in serum CK-MB and NT-proBNP. Thus, contemporary thoracic (chemo) radiation does not commonly result in elevations of serum TnT, CK-MB or NT-proBNP. Elevations in these markers during treatment merit further evaluation. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
C1 [Kozak, Kevin R.; Hong, Theodore S.; MacDonald, Shannon M.; Choi, Noah C.; Yock, Torunn I.] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
[Kozak, Kevin R.] Massachusetts Gen Hosp, Harvard Radiat Oncol Program, Boston, MA 02114 USA.
[Sluss, Patrick M.; Lewandrowski, Elizabeth L.; Aleryani, Samir L.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
RP Kozak, KR (reprint author), Massachusetts Gen Hosp, Dept Radiat Oncol, 100 Blossom St,Cox 3, Boston, MA 02114 USA.
EM kkozak@partners.org
NR 20
TC 17
Z9 18
U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0169-5002
J9 LUNG CANCER
JI Lung Cancer
PD DEC
PY 2008
VL 62
IS 3
BP 351
EP 355
DI 10.1016/j.lungcan.2008.03.024
PG 5
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA 391EX
UT WOS:000262217700011
PM 18462828
ER
PT J
AU Setsompop, K
Alagappan, V
Gagoski, B
Witzel, T
Polimeni, J
Potthast, A
Hebrank, F
Fontius, U
Schmitt, F
Wald, LL
Adalsteinsson, E
AF Setsompop, Kawin
Alagappan, Vijayanand
Gagoski, Borjan
Witzel, Thomas
Polimeni, Jonathan
Potthast, Andreas
Hebrank, Franz
Fontius, Ulrich
Schmitt, Franz
Wald, Lawrence L.
Adalsteinsson, Elfar
TI Slice-Selective RF Pulses for In Vivo B(1)(+) Inhomogeneity Mitigation
at 7 Tesla Using Parallel RF Excitation With a 16-Element Coil
SO MAGNETIC RESONANCE IN MEDICINE
LA English
DT Article
DE parallel excitation; slice-selective excitation; RF inhomogeneity
mitigation; multidimensional RF pulse; RF coil array
ID TRANSMIT SENSE; 8 CHANNELS; DESIGN; MRI
AB Slice-selective RF waveforms that mitigate severe B dagger inhomogeneity at 7 Tesla using parallel excitation were designed and validated in a water phantom and human studies on six subjects using a 16-element degenerate stripline array coil driven with a butler matrix to utilize the eight most favorable birdcage modes. The parallel RF waveform design applied magnitude least-squares (MLS) criteria with an optimized k-space excitation trajectory to significantly improve profile uniformity compared to conventional least-squares (LS) designs. Parallel excitation RF pulses designed to excite a uniform in-plane flip angle (FA) with slice selection in the z-direction were demonstrated and compared with conventional sinc-pulse excitation and RF shimming. In all cases, the parallel RF excitation significantly mitigated the effects of inhomogeneous B dagger on the excitation FA. The optimized parallel RF pulses for human B dagger mitigation were only 67% longer than a conventional sinc-based excitation, but significantly outperformed RF shimming. For example the standard deviations (SDs) of the in-plane FA (averaged over six human studies) were 16.7% for conventional sinc excitation, 13.3% for RF shimming, and 7.6% for parallel excitation. This work demonstrates that excitations with parallel RF systems can provide slice selection with spatially uniform FAs at high field strengths with only a small pulse-duration penalty. Magn Reson Med 60:1422-1432, 2008. (C) 2008 Wiley-Liss, Inc.
C1 [Setsompop, Kawin; Gagoski, Borjan; Adalsteinsson, Elfar] MIT, Dept Elect Engn & Comp Sci, Cambridge, MA 02139 USA.
[Alagappan, Vijayanand; Witzel, Thomas; Polimeni, Jonathan; Wald, Lawrence L.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Radiol,AA Martinos Ctr Biomed Imaging, Charlestown, MA USA.
[Witzel, Thomas; Wald, Lawrence L.; Adalsteinsson, Elfar] Harvard Univ, MIT, Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
[Potthast, Andreas; Hebrank, Franz] Siemens Med Solut, Charlestown, MA USA.
[Fontius, Ulrich; Schmitt, Franz] Siemens Med Solut, Erlangen, Germany.
RP Setsompop, K (reprint author), Room 776A,Bldg 36,77 Massachusetts Ave, Cambridge, MA 02139 USA.
EM kawin@mit.edu
RI Adalsteinsson, Elfar/F-2477-2010; Setsompop, Kawin/P-1464-2014; Witzel,
Thomas/P-1402-2014; Polimeni, Jonathan/P-1395-2014; Wald,
Lawrence/D-4151-2009
OI Setsompop, Kawin/0000-0003-0455-7634; Polimeni,
Jonathan/0000-0002-1348-1179;
FU National Institute of Biomedical Imaging and Boengineering (NIBIB);
National Institutes of Health (NIH) [R01EB006847, R01EB007942,
R01EB000790]; National Center for Research Resources (NCRR), NIH
[P41RR14075]; Siemens Medical Solutions; R.J. Shillman Career
Development Award; MIND Institute
FX Grant sponsor: National Institute of Biomedical Imaging and
Boengineering (NIBIB), National Institutes of Health (NIH); Grant
numbers: R01EB006847, R01EB007942, R01EB000790; National Center for
Research Resources (NCRR), NIH; Grant number: P41RR14075; Grant
sponsors: Siemens Medical Solutions; R.J. Shillman Career Development
Award; MIND Institute.
NR 30
TC 71
Z9 71
U1 0
U2 5
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0740-3194
J9 MAGN RESON MED
JI Magn. Reson. Med.
PD DEC
PY 2008
VL 60
IS 6
BP 1422
EP 1432
DI 10.1002/mrm.21739
PG 11
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 377AW
UT WOS:000261225100018
PM 19025908
ER
PT J
AU Cao, HH
Ackerman, JL
Hrovat, MI
Graham, L
Glimcher, MJ
Wu, YT
AF Cao, Haihui
Ackerman, Jerome L.
Hrovat, Mirko I.
Graham, Lila
Glimcher, Melvin J.
Wu, Yaotang
TI Quantitative Bone Matrix Density Measurement by Water- and
Fat-Suppressed Proton Projection MRI (WASPI) With Polymer Calibration
Phantoms
SO MAGNETIC RESONANCE IN MEDICINE
LA English
DT Article
DE bone; MRI; WASPI; LITE ultrashort T-2 imaging
ID IN-VIVO; POLY(METHYL METHACRYLATE); CONTRAST AGENTS; PEO/PMMA BLENDS;
DYNAMICS; OSTEOMALACIA; SEQUENCES; PEO
AB The density of the organic matrix of bone substance is a critical parameter necessary to clinically evaluate and distinguish structural and metabolic pathological conditions such as osteornalacia in adults and rickets in growing children. Water- and fat-suppressed proton projection MRI (WASPI) was developed as a noninvasive means to obtain this information. In this study, a density calibration phantom was developed to convert WASPI intensity to true bone matrix density. The phantom contained a specifically designed poly(ethylene oxide)/poly(m ethyl methacrylate) (PEO/PMMA) blend, whose IVIRI properties (T-1, T-2, and resonance linewidth) were similar to those of solid bone matrix (collagen, tightly bound water, and other immobile molecules), minimizing the need to correct for differences in T-1 and/or T-2 relaxation between the phantom and the subject. Cortical and trabecular porcine bone specimens were imaged using WASPI with the calibration phantom in the field of view (FOV) as a stable intensity reference. Gravimetric and amino acid analyses were carried out on the same specimens after WASPI, and the chemical results were found to be highly correlated (r(2) = 0.98 and 0.95, respectively) to the WASPI intensity. By this procedure the WASPI intensity can be used to obtain the true bone matrix mass density Ing cm(-3). Magn Reson Med 60:1433-1443,2008. (C) 2008 Wiley-Liss, Inc.
C1 [Cao, Haihui; Ackerman, Jerome L.; Graham, Lila; Glimcher, Melvin J.; Wu, Yaotang] Childrens Hosp, Dept Orthoped Surg, Lab Study Skeletal Disorders & Rehabil, Boston, MA 02115 USA.
[Cao, Haihui; Ackerman, Jerome L.; Wu, Yaotang] Massachusetts Gen Hosp, Dept Radiol, Martinos Ctr, Biomat Lab, Charlestown, MA USA.
[Ackerman, Jerome L.] Harvard Univ, MIT, Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
[Hrovat, Mirko I.] Mirtech Inc, Brockton, MA USA.
[Ackerman, Jerome L.; Graham, Lila; Glimcher, Melvin J.; Wu, Yaotang] Harvard Univ, Sch Med, Boston, MA USA.
RP Wu, YT (reprint author), Childrens Hosp, Dept Orthoped Surg, Lab Study Skeletal Disorders & Rehabil, 300 Longwood Ave, Boston, MA 02115 USA.
EM yaotang.wu@childrens.harvard.edu
RI Ackerman, Jerome/E-2646-2015
OI Ackerman, Jerome/0000-0001-5176-7496
FU National Institute of Biomedical Imaging and Bioengineering, NIH
[R01-EB004012]; National Institute of Aging, NIH [R01-AG014701]; NIH
Division of Research Resources [S10-RR16811, P41-RR14075]; Peabody
Foundation; MIND Institute; Athinoula A. Martinos Center for Biomedical
Imaging
FX Grant sponsor: National Institute of Biomedical Imaging and
Bioengineering, NIH; Grant number: R01-EB004012; Grant sponsor: National
Institute of Aging, NIH; Grant number: R01-AG014701; NIH Division of
Research Resources; Grant numbers: S10-RR16811, P41-RR14075; Grant
sponsors: Peabody Foundation; MIND Institute; Athinoula A. Martinos
Center for Biomedical Imaging.
NR 26
TC 29
Z9 32
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0740-3194
EI 1522-2594
J9 MAGN RESON MED
JI Magn. Reson. Med.
PD DEC
PY 2008
VL 60
IS 6
BP 1433
EP 1443
DI 10.1002/mrm.21771
PG 11
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 377AW
UT WOS:000261225100019
PM 19025909
ER
PT J
AU Makris, N
Angelone, L
Tulloch, S
Sorg, S
Kaiser, J
Kennedy, D
Bonmassar, G
AF Makris, Nikos
Angelone, Leonardo
Tulloch, Seann
Sorg, Scott
Kaiser, Jonathan
Kennedy, David
Bonmassar, Giorgio
TI MRI-based anatomical model of the human head for specific absorption
rate mapping
SO MEDICAL & BIOLOGICAL ENGINEERING & COMPUTING
LA English
DT Article
DE Head; Morphometry; Segmentation; Volumetry; Specific absorption rate;
Bioelectromagnetic computation
ID DIGITAL BRAIN PHANTOM; DIELECTRIC-PROPERTIES; BIOLOGICAL TISSUES; SAR
CALCULATIONS; FREQUENCY-RANGE; FIELD; RESONANCE; EXPOSURE; MHZ; VOLUME
AB In this study, we present a magnetic resonance imaging (MRI)-based, high-resolution, numerical model of the head of a healthy human subject. In order to formulate the model, we performed quantitative volumetric segmentation on the human head, using T1-weighted MRI. The high spatial resolution used (1 x 1 x 1 mm3), allowed for the precise computation and visualization of a higher number of anatomical structures than provided by previous models. Furthermore, the high spatial resolution allowed us to study individual thin anatomical structures of clinical relevance not visible by the standard model currently adopted in computational bioelectromagnetics. When we computed the electromagnetic field and specific absorption rate (SAR) at 7 Tesla MRI using this high-resolution model, we were able to obtain a detailed visualization of such fine anatomical structures as the epidermis/dermis, bone structures, bone-marrow, white matter and nasal and eye structures.
C1 [Makris, Nikos; Angelone, Leonardo; Kennedy, David; Bonmassar, Giorgio] Massachusetts Gen Hosp, HST Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Makris, Nikos; Tulloch, Seann; Sorg, Scott; Kaiser, Jonathan; Kennedy, David] Harvard Univ, Massachusetts Gen Hosp, Sch Med,Dept Psychiat, HST Athinoula A Martinos Ctr,Ctr Morphomet Anal, Boston, MA 02129 USA.
[Makris, Nikos; Tulloch, Seann; Sorg, Scott; Kaiser, Jonathan; Kennedy, David] Harvard Univ, Massachusetts Gen Hosp, Sch Med,Dept Neurol, HST Athinoula A Martinos Ctr,Ctr Morphomet Anal, Boston, MA 02129 USA.
[Makris, Nikos; Tulloch, Seann; Sorg, Scott; Kaiser, Jonathan; Kennedy, David] Harvard Univ, Massachusetts Gen Hosp, Sch Med,Dept Radiol Serv, HST Athinoula A Martinos Ctr,Ctr Morphomet Anal, Boston, MA 02129 USA.
[Makris, Nikos] Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA.
[Angelone, Leonardo] Tufts Univ, Dept Biomed Engn, Medford, MA 02155 USA.
RP Bonmassar, G (reprint author), Massachusetts Gen Hosp, HST Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
EM giorgio@nmr.mgh.harvard.edu
RI Kennedy, David/H-3627-2012;
OI Angelone, Leonardo/0000-0002-1105-021X
FU National Association for Research in Schizophrenia and Depression
(NARSAD); National Institutes of Health National Center for
Complementary and Alternative Medicine NCAM; Fairway Trust; NIH
[NS34189, EB005149, R01 EB002459, P41 RR014075]; MIND institute
FX Preparation of this article was supported in part by grants from: The
National Association for Research in Schizophrenia and Depression
(NARSAD) and the National Institutes of Health National Center for
Complementary and Alternative Medicine NCAM (NM); the Fairway Trust and
NIH grants NS34189 & EB005149 (DK); R01 EB002459 and P41 RR014075 (GB),
and the MIND institute. The authors would like to thank the many people
that kindly contributed to this project with discussions and useful
insights, including Franz Schmitt, Franz Hebrank and Andreas Potthast
(Siemens Medical Systems), CK Chou and Goga Bit Babik (Motorola
Corporate EME), Chris Collins (Penn State), David Kaplan, Sergio
Fantini, Peter Wong, and Mark Cronin- Golomb (Tufts University). We
would like also to thank the colleagues at the A. Martinos Center,
including Martjin Cloos, Graham Wiggins, Mary Foley, and Larry Wald for
their help with the MRI images, and Mr. George Papadimitriou and Mr.
James Howard and for their contributions to this study.
NR 63
TC 25
Z9 26
U1 1
U2 6
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0140-0118
EI 1741-0444
J9 MED BIOL ENG COMPUT
JI Med. Biol. Eng. Comput.
PD DEC
PY 2008
VL 46
IS 12
BP 1239
EP 1251
DI 10.1007/s11517-008-0414-z
PG 13
WC Computer Science, Interdisciplinary Applications; Engineering,
Biomedical; Mathematical & Computational Biology; Medical Informatics
SC Computer Science; Engineering; Mathematical & Computational Biology;
Medical Informatics
GA 376JY
UT WOS:000261181100008
PM 18985401
ER
PT J
AU Bailey, FA
AF Bailey, F. Amos
TI "I Am Not Afraid of Dying. I Just Don't Want To Be There When it
Happens"
SO MEDICAL CARE
LA English
DT Editorial Material
ID PHYSICIAN-ASSISTED SUICIDE; OF-LIFE DECISIONS; PALLIATIVE CARE;
MEDICAL-PRACTICE; END; EUTHANASIA; OUTCOMES; CANCER; DEATH
C1 Birmingham VAMC, Birmingham, AL 35233 USA.
RP Bailey, FA (reprint author), Birmingham VAMC, 700 S 19th St, Birmingham, AL 35233 USA.
EM amos-bailey@va.gov
NR 23
TC 0
Z9 0
U1 3
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD DEC
PY 2008
VL 46
IS 12
BP 1195
EP 1197
DI 10.1097/MLR.0b013e3181904fd8
PG 3
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 379UC
UT WOS:000261420700001
PM 19300307
ER
PT J
AU Keyhani, S
Hebert, PL
Ross, JS
Federman, A
Zhu, CW
Siu, AL
AF Keyhani, Salomeh
Hebert, Paul L.
Ross, Joseph S.
Federman, Alex
Zhu, Carolyn W.
Siu, Albert L.
TI Electronic Health Record Components and the Quality of Care
SO MEDICAL CARE
LA English
DT Article
DE quality of health care; personal health record; hypertension; ambulatory
care
ID RANDOMIZED CONTROLLED-TRIAL; CLINICAL REMINDERS; MEDICAL-RECORD;
UNITED-STATES; ORDER ENTRY; ERRORS; SYSTEM; IMPACT; TRANSFORMATION;
PRESCRIPTION
AB Background: Electronic health records (EHRs) have been promoted as an important tool to improve quality of care. We examined the association between EHR components, a complete EHR, and the quality of care.
Methods: Using data from the 2005 National Ambulatory Medical Care Survey and the National Hospital Ambulatory Medical Care Survey, we conducted a cross-sectional analysis of all visits with an established primary care provider and examined the association between presence of EHR components and: (1) blood pressure control; and (2) receipt of appropriate therapy for chronic conditions. We examined similar associations for complete EHRs which we defined as one that includes physician and nursing notes, electronic reminder system, computerized prescription order entry, test results, and computerized test order entry. We constructed multivariate models to examine the association between EHR components and each outcome controlling for patient sociodemographic, health, physician practice, and geographic factors.
Results: We found no association between electronic physician notes and blood pressure control or receipt of appropriate therapies, with the exception of inhaled steroids among asthmatics (adjusted odds ratio 2.86; 95% confidence interval, 1.12-7.32). We found no association between electronic reminder systems and blood pressure control or receipt of appropriate therapies, with the exception of angiotensin converting enzyme inhibitors or angiotensin receptor blockers in patients with diabetes with hypertension (odds ratio 2.58; 95% confidence interval, 1.22-5.42). We found no association between electronic physician notes and any measure of quality. We found no relationship between having a complete EHR and any of the quality measures investigated.
Conclusions: We found no consistent association between blood pressure control, management of chronic conditions, and specific EHR components. Future research focusing on how an EHR is implemented and used and how care is integrated through an EHR will improve our understanding of the impact of EHRs on the quality of care.
C1 [Keyhani, Salomeh; Hebert, Paul L.] Mt Sinai Sch Med, Dept Hlth Policy, New York, NY 10029 USA.
[Keyhani, Salomeh; Ross, Joseph S.; Zhu, Carolyn W.; Siu, Albert L.] James J Peters Vet Adm Med Ctr, Geriatr Res Educ & Clin Ctr, Bronx, NY USA.
[Ross, Joseph S.; Zhu, Carolyn W.; Siu, Albert L.] Mt Sinai Sch Med, Dept Geriatr & Adult Dev, New York, NY 10029 USA.
[Federman, Alex] Mt Sinai Sch Med, Dept Gen Internal Med, New York, NY 10029 USA.
RP Keyhani, S (reprint author), Mt Sinai Sch Med, Dept Hlth Policy, Box 1077,1 Gustave L Levy Pl, New York, NY 10029 USA.
EM salomeh.keyhani@mountsinai.org
FU Department of Veterans Affairs Health Services Research and Development
Service [TRP-02-149]; Hartford Foundation; Robert Wood Johnson
Foundation
FX Supported by Department of Veterans Affairs Health Services Research and
Development Service project #TRP-02-149 (to S.K., J.S.R., and A.L.S.);
the Hartford Foundation (to J.S.R.); and the Robert Wood Johnson
Foundation (to A.R).
NR 33
TC 50
Z9 51
U1 4
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD DEC
PY 2008
VL 46
IS 12
BP 1267
EP 1272
DI 10.1097/MLR.0b013e31817e18ae
PG 6
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 379UC
UT WOS:000261420700011
PM 19300317
ER
PT J
AU Cannon, CP
Kumar, A
AF Cannon, Christopher P.
Kumar, Amit
TI Management of hypertension in the presence of other cardiometabolic risk
factors
SO MEDICAL CLINICS OF NORTH AMERICA
LA English
DT Article
ID RENIN-ANGIOTENSIN SYSTEM; CARDIAC OUTCOMES TRIAL; PRESSURE LOWERING ARM;
NORMAL BLOOD-PRESSURE; METABOLIC SYNDROME; INSULIN-RESISTANCE;
OVERWEIGHT/OBESE PATIENTS; DIABETES-MELLITUS; FACTOR CLUSTERS;
UNITED-STATES
C1 [Cannon, Christopher P.] Harvard Univ, Sch Med, TIMI Study Grp, Div Cardiovasc,Brigham & Womens Hosp, Boston, MA 02115 USA.
[Kumar, Amit] Univ Massachusetts, Sch Med, Dept Hosp Med, Worcester, MA USA.
RP Cannon, CP (reprint author), Harvard Univ, Sch Med, TIMI Study Grp, Div Cardiovasc,Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 54
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 0025-7125
J9 MED CLIN N AM
JI Med. Clin. N. Am.
PD DEC
PY 2008
VL 92
BP 49
EP 57
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 402SX
UT WOS:000263034500005
ER
PT J
AU Cooper, RA
Dicianno, BE
Brewer, B
LoPresti, E
Ding, D
Simpson, R
Grindle, G
Wang, HW
AF Cooper, Rory A.
Dicianno, Brad E.
Brewer, Bambi
LoPresti, Edmund
Ding, Dan
Simpson, Richard
Grindle, Garrett
Wang, Hongwu
TI A perspective on intelligent devices and environments in medical
rehabilitation
SO MEDICAL ENGINEERING & PHYSICS
LA English
DT Review
DE Rehabilitation; Intelligent systems; Machine learning; Physical
impairment; Wheelchairs; Cognitive impairment
ID INDUCED MOVEMENT THERAPY; TRAUMATIC BRAIN-INJURY; UPPER-LIMB FUNCTION;
OF-THE-ART; UPPER EXTREMITY; STROKE REHABILITATION; RANDOMIZED
CROSSOVER; ASSISTIVE-TECHNOLOGY; INTERFACE PRESSURE; CARE COORDINATION
AB Globally, the number of people older than 65 years is anticipated to double between 1997 and 2025, while at the same time the number of people with disabilities is growing at it similar rate, which makes technical advances and social policies critical to attain, prolong, and preserve quality of life. Recent advancements in technology, including computation, robotics, machine learning, communication, and miniaturization of sensors have been used primarily in manufacturing, military, space exploration, and entertainment. However, few efforts have been made to utilize these technologies to enhance the quality of life of people with disabilities. This article offers a perspective of future development in seven emerging areas: translation of research into clinical practice, pervasive assistive technology, cognitive assistive technologies, rehabilitation monitoring and coaching technologies, robotic assisted therapy, and personal mobility and manipulation technology. Published by Elsevier Ltd on behalf of IPEM
C1 [Cooper, Rory A.; Dicianno, Brad E.; Brewer, Bambi; Ding, Dan; Simpson, Richard; Grindle, Garrett; Wang, Hongwu] VA Pittsburgh Healthcare Syst, Human Engn Res Labs, Dept Vet Affairs, Rehabil Res & Dev Serv, Pittsburgh, PA 15206 USA.
[Cooper, Rory A.; Dicianno, Brad E.; Brewer, Bambi; LoPresti, Edmund; Ding, Dan; Simpson, Richard; Grindle, Garrett; Wang, Hongwu] Univ Pittsburgh, Dept Rehabil Sci & Technol, Pittsburgh, PA 15260 USA.
[Cooper, Rory A.; Dicianno, Brad E.; Brewer, Bambi; LoPresti, Edmund; Ding, Dan; Simpson, Richard; Grindle, Garrett; Wang, Hongwu] Univ Pittsburgh, Dept Bioengn, Pittsburgh, PA 15260 USA.
[Cooper, Rory A.; Dicianno, Brad E.; Brewer, Bambi; LoPresti, Edmund; Ding, Dan; Simpson, Richard; Grindle, Garrett; Wang, Hongwu] Univ Pittsburgh, Dept Phys Med & Rehabil, Pittsburgh, PA 15260 USA.
[Dicianno, Brad E.; Simpson, Richard] Univ Pittsburgh, Med Ctr, Ctr Assist Technol, Pittsburgh, PA 15260 USA.
RP Cooper, RA (reprint author), VA Pittsburgh Healthcare Syst, Human Engn Res Labs, Dept Vet Affairs, Rehabil Res & Dev Serv, 151-R1,7180 Highland Dr, Pittsburgh, PA 15206 USA.
EM rcooper@pitt.edu
RI Wang, Hongwu/J-6133-2013; Simpson, Richard/G-5683-2015;
OI Wang, Hongwu/0000-0002-6567-9144; Simpson, Richard/0000-0002-6306-9393;
Dicianno, Brad/0000-0003-0738-0192
FU National Science Foundation [EEC-0540865]; Office of Research and
Development, Rehabilitation Research & Development Service, Department
of Veterans Affairs [B3142C]
FX This material is based upon work supported by the National Science
Foundation under Cooperative Agreement EEC-0540865. This material is
also based upon work supported by the Office of Research and
Development, Rehabilitation Research & Development Service, Department
of Veterans Affairs, Grant# B3142C.
NR 122
TC 21
Z9 21
U1 1
U2 18
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1350-4533
J9 MED ENG PHYS
JI Med. Eng. Phys.
PD DEC
PY 2008
VL 30
IS 10
BP 1387
EP 1398
DI 10.1016/j.medengphy.2008.09.003
PG 12
WC Engineering, Biomedical
SC Engineering
GA 386WX
UT WOS:000261914400014
PM 18993108
ER
PT J
AU Xu, QY
Hamilton, RJ
Schowengerdt, RA
Alexander, B
Jiang, SB
AF Xu, Qianyi
Hamilton, Russell J.
Schowengerdt, Robert A.
Alexander, Brian
Jiang, Steve B.
TI Lung tumor tracking in fluoroscopic video based on optical flow
SO MEDICAL PHYSICS
LA English
DT Article
DE biomedical optical imaging; collimators; diagnostic radiography; image
sequences; lung; medical image processing; pneumodynamics; tumours
ID DYNAMIC MULTILEAF COLLIMATORS; MODULATED RADIATION-THERAPY;
RESPIRATION-GATED RADIOTHERAPY; IMPLANTED FIDUCIAL MARKERS; INSPIRATION
BREATH-HOLD; DMLC TECHNIQUE; TARGET VOLUME; ORGAN MOTION; DELIVERY;
FEASIBILITY
AB Respiratory gating and tumor tracking for dynamic multileaf collimator delivery require accurate and real-time localization of the lung tumor position during treatment. Deriving tumor position from external surrogates such as abdominal surface motion may have large uncertainties due to the intra- and interfraction variations of the correlation between the external surrogates and internal tumor motion. Implanted fiducial markers can be used to track tumors fluoroscopically in real time with sufficient accuracy. However, it may not be a practical procedure when implanting fiducials bronchoscopically. In this work, a method is presented to track the lung tumor mass or relevant anatomic features projected in fluoroscopic images without implanted fiducial markers based on an optical flow algorithm. The algorithm generates the centroid position of the tracked target and ignores shape changes of the tumor mass shadow. The tracking starts with a segmented tumor projection in an initial image frame. Then, the optical flow between this and all incoming frames acquired during treatment delivery is computed as initial estimations of tumor centroid displacements. The tumor contour in the initial frame is transferred to the incoming frames based on the average of the motion vectors, and its positions in the incoming frames are determined by fine-tuning the contour positions using a template matching algorithm with a small search range. The tracking results were validated by comparing with clinician determined contours on each frame. The position difference in 95% of the frames was found to be less than 1.4 pixels (similar to 0.7 mm) in the best case and 2.8 pixels (similar to 1.4 mm) in the worst case for the five patients studied.
C1 [Xu, Qianyi] Fox Chase Canc Ctr, Dept Radiat Oncol, Philadelphia, PA 19111 USA.
[Xu, Qianyi; Schowengerdt, Robert A.] Univ Arizona, Dept Elect & Comp Engn, Tucson, AZ 85721 USA.
[Hamilton, Russell J.] Univ Arizona, Dept Radiat Oncol, Tucson, AZ 85721 USA.
[Alexander, Brian] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
[Alexander, Brian] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Jiang, Steve B.] Univ Calif San Diego, Dept Radiat Oncol, La Jolla, CA 92093 USA.
RP Xu, QY (reprint author), Fox Chase Canc Ctr, Dept Radiat Oncol, 7701 Burholme Ave, Philadelphia, PA 19111 USA.
FU NIH [1 R21 CA110177-01A1]; Varian Medical Systems, Inc.
FX This work was partially supported by research grants from NIH (1 R21
CA110177-01A1) and Varian Medical Systems, Inc.
NR 61
TC 36
Z9 36
U1 2
U2 5
PU AMER ASSOC PHYSICISTS MEDICINE AMER INST PHYSICS
PI MELVILLE
PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA
SN 0094-2405
J9 MED PHYS
JI Med. Phys.
PD DEC
PY 2008
VL 35
IS 12
BP 5351
EP 5359
DI 10.1118/1.3002323
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 376VB
UT WOS:000261210000016
PM 19175094
ER
PT J
AU Pfeiffer, D
Sutlief, S
Feng, WZ
Pierce, HM
Kofler, J
AF Pfeiffer, Douglas
Sutlief, Steven
Feng, Wenzheng
Pierce, Heather M.
Kofler, Jim
TI AAPM Task Group 128: Quality assurance tests for prostate brachytherapy
ultrasound systems
SO MEDICAL PHYSICS
LA English
DT Article
DE biological organs; biomedical ultrasonics; brachytherapy; cancer;
dosimetry; image resolution; quality assurance; tumours
ID CANCER; SPEED; SOUND
AB While ultrasound guided prostate brachytherapy has gained wide acceptance as a primary treatment tool for prostate cancer, quality assurance of the ultrasound guidance system has received very little attention. Task Group 128 of the American Association of Physicists in Medicine was created to address quality assurance requirements specific to transrectal ultrasound used for guidance of prostate brachytherapy. Accurate imaging guidance and dosimetry calculation depend upon the quality and accuracy of the ultrasound image. Therefore, a robust quality assurance program for the ultrasound system is essential. A brief review of prostate brachytherapy and ultrasound physics is provided, followed by a recommendation for elements to be included in a comprehensive test phantom. Specific test recommendations are presented, covering grayscale visibility, depth of penetration, axial and lateral resolution, distance measurement, area measurement, volume measurement, needle template/electronic grid alignment, and geometric consistency with the treatment planning computer.
C1 [Pfeiffer, Douglas] Boulder Community Foothills Hosp, Dept Imaging, Boulder, CO 80301 USA.
[Sutlief, Steven] VA Puget Sound Hlth Care Syst, VA Med Ctr, Seattle, WA 98108 USA.
[Feng, Wenzheng] William Beaumont Hosp, Royal Oak, MI 48073 USA.
[Pierce, Heather M.] CIRS Inc, Norfolk, VA 23513 USA.
[Kofler, Jim] Mayo Clin, Rochester, MN 55905 USA.
RP Pfeiffer, D (reprint author), Boulder Community Foothills Hosp, Dept Imaging, Boulder, CO 80301 USA.
EM dpfeiffer@bch.org
NR 19
TC 19
Z9 20
U1 0
U2 3
PU AMER ASSOC PHYSICISTS MEDICINE AMER INST PHYSICS
PI MELVILLE
PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA
SN 0094-2405
J9 MED PHYS
JI Med. Phys.
PD DEC
PY 2008
VL 35
IS 12
BP 5471
EP 5489
DI 10.1118/1.3006337
PG 19
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 376VB
UT WOS:000261210000029
PM 19175107
ER
PT J
AU Anderson, KL
Casey, MB
Thompson, WL
Burrage, MS
Pezaris, E
Kosslyn, SM
AF Anderson, Karen L.
Casey, M. Beth
Thompson, William L.
Burrage, Marie S.
Pezaris, Elizabeth
Kosslyn, Stephen M.
TI Performance on Middle School Geometry Problems With Geometry Clues
Matched to Three Different Cognitive Styles
SO MIND BRAIN AND EDUCATION
LA English
DT Article
AB This study investigated the relationship between 3 ability-based cognitive styles (verbal deductive, spatial imagery, and object imagery) and performance on geometry problems that provided different types of clues. The purpose was to determine whether students with a specific cognitive style outperformed other students, when the geometry problems provided clues compatible with their cognitive style. Students were identified as having a particular cognitive style when they scored equal to or above the median on the measure assessing this ability. A geometry test was developed in which each problem could be solved on the basis of verbal reasoning clues (matching verbal deductive cognitive style), mental rotation clues (matching spatial imagery cognitive style), or shape memory clues (matching object imagery cognitive style). Straightforward cognitive style-clue-compatibility relationships were not supported. Instead, for the geometry problems with either mental rotation or shape memory clues, students with a combination of both verbal and spatial cognitive styles tended to do the best. For the problems with verbal reasoning clues, students with either a verbal or a spatial cognitive style did well, with each cognitive style contributing separately to success. Thus, both spatial imagery and verbal deductive cognitive styles were important for solving geometry problems, whereas object imagery was not. For girls, a spatial imagery cognitive style was advantageous for geometry problem solving, regardless of type of clues provided.
C1 [Casey, M. Beth] Boston Coll, Lynch Sch Educ, Program Appl Dev & Educ Psychol, Chestnut Hill, MA 02492 USA.
[Anderson, Karen L.] Stonehill Coll, Dept Educ Studies, Easton, MA USA.
[Thompson, William L.; Burrage, Marie S.; Kosslyn, Stephen M.] Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA.
[Pezaris, Elizabeth] Northeastern Univ, Dept Counseling & Appl Educ Psychol, Boston, MA USA.
[Kosslyn, Stephen M.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
RP Casey, MB (reprint author), Boston Coll, Lynch Sch Educ, Program Appl Dev & Educ Psychol, 201 Campion Hall, Chestnut Hill, MA 02492 USA.
EM caseyb@bc.edu
NR 48
TC 7
Z9 7
U1 1
U2 7
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1751-2271
J9 MIND BRAIN EDUC
JI Mind Brain Educ.
PD DEC
PY 2008
VL 2
IS 4
BP 188
EP 197
DI 10.1111/j.1751-228X.2008.00053.x
PG 10
WC Education & Educational Research; Psychology, Developmental
SC Education & Educational Research; Psychology
GA V15NW
UT WOS:000207809700006
ER
PT J
AU Chen, G
Jingbo, A
Wang, M
Farley, S
Lee, LY
Lee, LC
Sawicki, MP
AF Chen, Gao
Jingbo, A.
Wang, Min
Farley, Steven
Lee, Lung-Yi
Lee, Lung-Ching
Sawicki, Mark P.
TI Menin Promotes the Wnt Signaling Pathway in Pancreatic Endocrine Cells
SO MOLECULAR CANCER RESEARCH
LA English
DT Article
ID HISTONE METHYLTRANSFERASE COMPLEX; TUMOR-SUPPRESSOR PROTEIN;
BETA-CATENIN; NEOPLASIA TYPE-1; WNT/BETA-CATENIN; GENE-EXPRESSION;
STEM-CELLS; TRANSCRIPTION; OSTEOBLAST; GROWTH
AB Menin is a tumor suppressor protein mutated in patients with multiple endocrine neoplasia type 1. We show that menin is essential for canonical Wnt/beta-catenin signaling in cultured rodent islet tumor cells. In these cells, overexpression of menin significantly enhances TCF gene assay reporter activity in response to beta-catenin activation. Contrastingly, inhibition of menin expression with Men1 siRNA decreases TCF reporter gene activity. Likewise, multiple endocrine neoplasia type 1 disease associated missense mutations of menin abrogate the ability to increase TCF reporter gene activity. We show that menin physically interacts with proteins involved in the canonical Wnt signaling pathway, including beta-catenin, TCF3 (TCFL1), and weakly with TCF4 (TCFL2). Menin overexpression increases expression of the Wnt/beta-catenin downstream target gene Axing, which is associated with increased H3K4 trimethylation of the Axing gene promoter. Moreover, inhibition of menin expression by siRNA abrogates H3K4 trimethylation and Axing gene expression. Based on these studies, we hypothesized that Wnt signaling could inhibit islet cell proliferation because loss of menin function is thought to increase endocrine tumor cell proliferation. TGP61 rodent islet tumor cells treated with a glycogen synthase kinase 3 beta inhibitor that increases Writ pathway signaling had decreased cell proliferation compared with vehicle-treated cells. Collectively, these data suggest that menin has an essential role in Wnt/beta-catenin signaling through a mechanism that eventually affects histone trimethylation of the downstream target gene Axing, and activation of Wnt/beta-catenin signaling inhibits islet tumor cell proliferation. (Mol Cancer Res 2008;6(12):1894-907)
C1 [Sawicki, Mark P.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
Greater Los Angeles VA Med Ctr, Los Angeles, CA USA.
RP Sawicki, MP (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, CHS 72-215, Los Angeles, CA 90095 USA.
EM msawicki@ucla.edu
FU NIH [R01CA095148]; VA Merit
FX Grant support: NIH grant R01CA095148 and VA Merit grants (M.P. Sawicki).
The costs of publication of this article were defrayed in part by the
payment of page charges. This article must therefore be hereby marked
advertisement in accordance with 18 U.S.C. Section 1734 solely to
indicate this fact.
NR 49
TC 23
Z9 25
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1541-7786
J9 MOL CANCER RES
JI Mol. Cancer Res.
PD DEC
PY 2008
VL 6
IS 12
BP 1894
EP 1907
DI 10.1158/1541-7786.MCR-07-2206
PG 14
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 385OZ
UT WOS:000261824800010
PM 19074834
ER
PT J
AU Gao, BB
Stuart, L
Feener, EP
AF Gao, Ben-Bo
Stuart, Lisa
Feener, Edward P.
TI Label-free Quantitative Analysis of One-dimensional PAGE LC/MS/MS
Proteome
SO MOLECULAR & CELLULAR PROTEOMICS
LA English
DT Article
ID SMOOTH-MUSCLE-CELLS; DIFFERENTIAL MASS-SPECTROMETRY; COMPLEX PEPTIDE
MIXTURES; RESOLUTION LC-MS; ANGIOTENSIN-II; LIQUID-CHROMATOGRAPHY;
IN-VIVO; SHOTGUN PROTEOMICS; EXPRESSION; PROTEINS
AB A widely used method for protein identification couples prefractionation of protein samples by one-dimensional (1D) PAGE with LC/MS/MS. We developed a new label-free quantitative algorithm by combining measurements of spectral counting, ion intensity, and peak area on 1D PAGE-based proteomics. This algorithm has several improvements over other label-free quantitative algorithms: (i) Errors in peak detection are reduced because the retention time is based on each LC/MS/MS run and actual precursor m/z. (ii) Detection sensitivity is increased because protein quantification is based on the combination of peptide count, ion intensity, and peak area. (iii) Peak intensity and peak area are calculated in each LC/MS/MS run for all slices from 1D PAGE for every single identified protein and visualized as a Western blot image. The sensitivity and accuracy of this algorithm were demonstrated by using standard curves (17.4 fmol to 8.7 pmol), complex protein mixtures (30 fmol to 1.16 pmol) of known composition, and spiked protein (34.8 fmol to 17.4 pmol) in complex proteins. We studied the feasibility of this approach using the secretome of angiotensin II (Ang II)-stimulated vascular smooth muscle cells (VSMCs). From the VSMC-conditioned medium, 629 proteins were identified including 212 putative secreted proteins. 26 proteins were differently expressed in control and Ang II-stimulated VSMCs, including 18 proteins not previously reported. Proteins related to cell growth (CYR61, protein NOV, and clusterin) were increased, whereas growth arrest-specific 6 (GAS6) and growth/differentiation factor 6 were decreased by Ang II stimulation. Ang II-stimulated changes of plasminogen activator inhibitor-1, GAS6, cathepsin B, and periostin were validated by Western blot. In conclusion, a novel label-free quantitative analysis of 1D PAGELC/MS/MS-based proteomics has been successfully applied to the identification of new potential mediators of Ang II action and may provide an alternative to traditional protein staining methods. Molecular & Cellular Proteomics 7:2399-2409,2008.
C1 [Gao, Ben-Bo; Stuart, Lisa; Feener, Edward P.] Harvard Univ, Sch Med, Joslin Diabet Ctr, Div Res, Boston, MA 02215 USA.
RP Gao, BB (reprint author), Harvard Univ, Sch Med, Joslin Diabet Ctr, Div Res, 1 Joslin Pl, Boston, MA 02215 USA.
EM benbo.gao@joslin.harvard.edu
FU National Institutes of Health [DK60165, DK36836]; Adler Foundation
FX This work was supported, in whole or in part, by National Institutes of
Health Grants DK60165 and DK36836. This work was also supported by the
Adler Foundation. The costs of publication of this article were defrayed
in part by the payment of page charges. This article must therefore be
hereby marked "advertisement" in accordance with 18 U. S. C. Section
1734 solely to indicate this fact.
NR 43
TC 55
Z9 57
U1 0
U2 12
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 1535-9476
J9 MOL CELL PROTEOMICS
JI Mol. Cell. Proteomics
PD DEC
PY 2008
VL 7
IS 12
BP 2399
EP 2409
DI 10.1074/mcp.M800104-MCP200
PG 11
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 378NK
UT WOS:000261328200009
PM 18676994
ER
PT J
AU Parra, LA
Baust, T
El Mestikawy, S
Quiroz, M
Hoffman, B
Haflett, JM
Yao, JK
Torres, GE
AF Parra, Leonardo A.
Baust, Tracy
El Mestikawy, Salah
Quiroz, Marisol
Hoffman, Beth
Haflett, Jack M.
Yao, Jeffrey K.
Torres, Gonzalo E.
TI The Orphan Transporter Rxt1/NTT4 (SLC6A17) Functions as a Synaptic
Vesicle Amino Acid Transporter Selective for Proline, Glycine, Leucine,
and Alanine
SO MOLECULAR PHARMACOLOGY
LA English
DT Article
ID VESICULAR GLUTAMATE TRANSPORTER; CENTRAL-NERVOUS-SYSTEM;
INORGANIC-PHOSPHATE COTRANSPORTER; NEUROTRANSMITTER TRANSPORTER;
MOLECULAR-CLONING; NMDA RECEPTOR; RAT-BRAIN; ACETYLCHOLINE TRANSPORTER;
DEPENDENT TRANSPORTER; EXPRESSION PATTERN
AB Rxt1/NTT4 (SLC6A17) belongs to a gene family of "orphan transporters" whose substrates and consequently functions remain unidentified. Although Rxt1/NTT4 was previously thought to function as a sodium-dependent plasma membrane transporter, recent studies localized the protein to synaptic vesicles of glutamatergic and GABAergic neurons. Here, we provide evidence indicating that Rxt1/NTT4 functions as a vesicular transporter selective for proline, glycine, leucine, and alanine. Using Western blot, immunoprecipitation, immunocytochemistry, and polymerase chain reaction approaches, we demonstrate that PC12 cells express the Rxt1/NTT4 gene and protein. Small interfering RNA (siRNA)- mediated knockdown of Rxt1/NTT4 in PC12 cells resulted in selective reductions in uptake levels for proline, glycine, leucine, and alanine. Likewise, gas chromatography analysis of amino acid content in an enriched synaptic vesicle fraction from wild-type and siRNA-Rxt1/NTT4 PC12 cells revealed that proline, glycine, leucine, and alanine levels were decreased in siRNA-treated cells compared with wild-type cells. Furthermore, Rxt1/NTT4-transfected Chinese hamster ovary (CHO) cells exhibited significant uptake increases of these amino acids compared with mock-transfected CHO cells. Finally, proline uptake in both PC12 cells and Rxt1/NTT4-transfected CHO cells was dependent on the electrochemical gradient maintained by the vacuolar-type H+-ATPase. These data indicate that the orphan Rxt1/NTT4 protein functions as a vesicular transporter for proline, glycine, leucine, and alanine, further suggesting its important role in synaptic transmission.
C1 [Parra, Leonardo A.; Baust, Tracy; Quiroz, Marisol; Torres, Gonzalo E.] Univ Pittsburgh, Sch Med, Dept Neurobiol, Pittsburgh, PA 15261 USA.
[Parra, Leonardo A.; Baust, Tracy; Quiroz, Marisol; Torres, Gonzalo E.] Univ Pittsburgh, Sch Med, Dept Pharmacol, Pittsburgh, PA 15261 USA.
[El Mestikawy, Salah] Univ Paris 06, INSERM, U513, Paris, France.
[El Mestikawy, Salah] McGill Univ, Dept Psychiat, Douglas Hosp, Res Ctr, Montreal, PQ, Canada.
[Hoffman, Beth] Amgen Inc, Dept Neurosci, Thousand Oaks, CA 91320 USA.
[Haflett, Jack M.; Yao, Jeffrey K.] VA Pittsburgh Healthcare Syst, Med Res Serv, Pittsburgh, PA USA.
[Yao, Jeffrey K.] Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, Dept Psychiat, Pittsburgh, PA 15261 USA.
[Yao, Jeffrey K.] Univ Pittsburgh, Sch Pharm, Dept Pharmaceut Sci, Pittsburgh, PA 15261 USA.
RP Torres, GE (reprint author), Univ Pittsburgh, Sch Med, Dept Neurobiol, Room 6061,BST3,3501 5th Ave, Pittsburgh, PA 15261 USA.
EM gtorres@pitt.edu
FU Amgen research [200620123]
FX This work was funded in part by Amgen research agreement 200620123.
NR 66
TC 18
Z9 19
U1 0
U2 3
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0026-895X
J9 MOL PHARMACOL
JI Mol. Pharmacol.
PD DEC
PY 2008
VL 74
IS 6
BP 1521
EP 1532
DI 10.1124/mol.108.050005
PG 12
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 373WG
UT WOS:000261003600004
PM 18768736
ER
PT J
AU Stewart, D
Desai, R
Cheng, Q
Liu, AP
Forman, SA
AF Stewart, Deirdre
Desai, Rooma
Cheng, Qi
Liu, Aiping
Forman, Stuart A.
TI Tryptophan Mutations at Azi-Etomidate Photo-Incorporation Sites on
alpha(1) or beta(2) Subunits Enhance GABA(A) Receptor Gating and Reduce
Etomidate Modulation
SO MOLECULAR PHARMACOLOGY
LA English
DT Article
ID GENERAL ANESTHETIC ETOMIDATE; A-RECEPTOR; DIRECT ACTIVATION; BETA-3
SUBUNIT; BINDING CAVITY; PROPOFOL; BENZODIAZEPINES; DESENSITIZATION;
INCREASES; RESIDUES
AB The potent general anesthetic etomidate produces its effects by enhancing GABA(A) receptor activation. Its photolabel analog [H-3]azi-etomidate labels residues within transmembrane domains on alpha and beta subunits: alpha Met236 and beta Met286. We hypothesized that these methionines contribute to etomidate sites formed at alpha-beta subunit interfaces and that increasing side-chain bulk and hydrophobicity at either locus would mimic etomidate binding and block etomidate effects. Channel activity was electrophysiologically quantified in alpha(1)beta(2)gamma(2L) receptors with alpha(1)M236W or beta(2)M286W mutations, in both the absence and the presence of etomidate. Measurements included spontaneous activation, GABA EC50, etomidate agonist potentiation, etomidate direct activation, and rapid macrocurrent kinetics. Both alpha(1)M236W and beta(2)M286W mutations induced spontaneous channel opening, lowered GABA EC50, increased maximal GABA efficacy, and slowed current deactivation, mimicking effects of etomidate on alpha(1)beta(2)gamma(2L) channels. These changes were larger with alpha(1)M236W than with beta(2)M286W. Etomidate (3.2 mu M) reduced GABA EC50 much less in alpha(1)M236W beta(2)gamma(2L) receptors (2-fold) than in wild type (23-fold). However, etomidate was more potent and efficacious in directly activating alpha(1)M236W beta(2)gamma(2L) compared with wild type. In alpha(1)beta(2)M286W gamma(2L) receptors, etomidate induced neither agonist-potentiation nor direct channel activation. These results support the hypothesis that alpha(1)Met236 and beta(2)Met286 are within etomidate sites that allosterically link to channel gating. Although alpha(1)M236W produced the larger impact on channel gating, beta(2)M286W produced more profound changes in etomidate sensitivity, suggesting a dominant role in drug binding. Furthermore, quantitative mechanistic analysis demonstrated that wild-type and mutant results are consistent with the presence of only one class of etomidate sites mediating both agonist potentiation and direct activation.
C1 [Stewart, Deirdre; Desai, Rooma; Cheng, Qi; Liu, Aiping; Forman, Stuart A.] Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Beecher Mallincrodt Labs, Boston, MA 02114 USA.
RP Forman, SA (reprint author), Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Beecher Mallincrodt Labs, Gray Jackson 4,55 Fruit St, Boston, MA 02114 USA.
EM saforman@partners.org
FU National Institutes of General Medical Sciences [R01-GM66724,
P01-GM58448]
FX This research was supported by grants from the National Institutes of
General Medical Sciences (R01-GM66724 and P01-GM58448).
NR 33
TC 44
Z9 44
U1 0
U2 4
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0026-895X
J9 MOL PHARMACOL
JI Mol. Pharmacol.
PD DEC
PY 2008
VL 74
IS 6
BP 1687
EP 1695
DI 10.1124/mol.108.050500
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 373WG
UT WOS:000261003600020
PM 18805938
ER
PT J
AU Ergenc, AF
Li, MW
Toner, M
Biggers, JD
Lloyd, KCK
Olgac, N
AF Ergenc, Ali Fuat
Li, Ming-Wen
Toner, Mehmet
Biggers, John D.
Lloyd, K. C. Kent
Olgac, Nejat
TI Rotationally Oscillating Drill (Ros-Drill (c)) for Mouse ICSI Without
Using Mercury
SO MOLECULAR REPRODUCTION AND DEVELOPMENT
LA English
DT Article
DE ICSI; microinjection; assisted reproduction; micromanipulation
ID INTRACYTOPLASMIC SPERM INJECTION; PIEZO-DRIVEN PIPETTES; SPERMATOZOA;
OOCYTES; MICRODYNAMICS; FERTILIZATION; TERM; MICE
AB Intracytoplasmic sperm injection (ICSI) is an important assisted reproductive technology (ART). Due to deployment difficulties and low efficiency of the earlier (conventional) version of ICSI, especially in the mouse, a piezo-assisted ICSI technique had evolved as a popular ART methodology in recent years. An important and remaining problem with this technique, however, is that it requires small amounts of mercury to stabilize the pipette tip when piezoelectric force pulses are applied. To eliminate this problem we developed and tested a completely different and mercury-free technology, called the "Ros-Drill (c)" (rotationally oscillating drill). The technique uses microprocessor-control led rotational oscillations on a spiked micropipette without mercury or piezo. Preliminary experimental results show that this new microinjection technology gives high survival rate (> 70% of the injected oocytes) and fertilization rate (> 80% of the survived oocytes), and blastocyst formation rates in early trials (similar to 50% of the survived oocytes). Blastocysts created by Ros-Drill (c) ICSI were transferred into the uteruses of pseudopregnant surrogate mothers and healthy pups were born and weaned. The Ros-Drill (c) ICSI technique is automated and therefore; it requires a very short preliminary training for the specialists, as evidenced in many successful biological trials. These advantages of Ros-Drill (c) ICSI over conventional and piezo-assisted ICSI are clearly demonstrated and it appears to have resolved an important problem in reproductive biology. Mol. Reprod. Dev. 75: 1744-1751, 2008. (c) 2008 Wiley-Liss, Inc.
C1 [Ergenc, Ali Fuat; Olgac, Nejat] Univ Connecticut, Dept Mech Engn, Storrs, CT 06269 USA.
[Li, Ming-Wen; Lloyd, K. C. Kent] Univ Calif Davis, Sch Vet Med, Ctr Comparat Med, Davis, CA 95616 USA.
[Toner, Mehmet; Biggers, John D.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Engn Med, Boston, MA USA.
[Toner, Mehmet; Biggers, John D.] Shriners Hosp Children, Boston, MA USA.
[Biggers, John D.] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA USA.
RP Ergenc, AF (reprint author), Univ Connecticut, Dept Mech Engn, 191 Auditorium Rd,EII Build Unit 3139, Storrs, CT 06269 USA.
EM ergenc@engr.uconn.edu
FU NIH [R24RR018934-01]; UC Davis Mouse Biology Program
FX NIH; Grant number: R24RR018934-01; Grant sponsor: UC Davis Mouse Biology
Program.
NR 17
TC 8
Z9 8
U1 1
U2 1
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1040-452X
J9 MOL REPROD DEV
JI Mol. Reprod. Dev.
PD DEC
PY 2008
VL 75
IS 12
BP 1744
EP 1751
DI 10.1002/mrd.20919
PG 8
WC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology;
Reproductive Biology
SC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology;
Reproductive Biology
GA 372AG
UT WOS:000260873200007
PM 18437690
ER
PT J
AU Skog, J
Wurdinger, T
van Rijn, S
Meijer, DH
Gainche, L
Sena-Esteves, M
Curry, WT
Carter, BS
Krichevsky, AM
Breakefield, XO
AF Skog, Johan
Wuerdinger, Tom
van Rijn, Sjoerd
Meijer, Dimphna H.
Gainche, Laura
Sena-Esteves, Miguel
Curry, William T., Jr.
Carter, Bob S.
Krichevsky, Anna M.
Breakefield, Xandra O.
TI Glioblastoma microvesicles transport RNA and proteins that promote
tumour growth and provide diagnostic biomarkers
SO NATURE CELL BIOLOGY
LA English
DT Article
ID GENE-EXPRESSION; MESSENGER-RNA; CELLS; EXOSOMES; CANCER; ANGIOGENESIS;
RECEPTOR; MEMBRANE; DETERMINANTS; SUPPRESSION
AB Glioblastoma tumour cells release microvesicles (exosomes) containing mRNA, miRNA and angiogenic proteins. These microvesicles are taken up by normal host cells, such as brain microvascular endothelial cells. By incorporating an mRNA for a reporter protein into these microvesicles, we demonstrate that messages delivered by microvesicles are translated by recipient cells. These microvesicles are also enriched in angiogenic proteins and stimulate tubule formation by endothelial cells. Tumour-derived microvesicles therefore serve as a means of delivering genetic information and proteins to recipient cells in the tumour environment. Glioblastoma microvesicles also stimulated proliferation of a human glioma cell line, indicating a self-promoting aspect. Messenger RNA mutant/variants and miRNAs characteristic of gliomas could be detected in serum microvesicles of glioblastoma patients. The tumour-specific EGFRvIII was detected in serum microvesicles from 7 out of 25 glioblastoma patients. Thus, tumour-derived microvesicles may provide diagnostic information and aid in therapeutic decisions for cancer patients through a blood test.
C1 [Skog, Johan; Wuerdinger, Tom; van Rijn, Sjoerd; Meijer, Dimphna H.; Gainche, Laura; Sena-Esteves, Miguel; Breakefield, Xandra O.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, Charlestown, MA 02129 USA.
[Skog, Johan; Wuerdinger, Tom; van Rijn, Sjoerd; Meijer, Dimphna H.; Gainche, Laura; Sena-Esteves, Miguel; Breakefield, Xandra O.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Charlestown, MA 02129 USA.
[Skog, Johan; Wuerdinger, Tom; van Rijn, Sjoerd; Meijer, Dimphna H.; Gainche, Laura; Sena-Esteves, Miguel; Breakefield, Xandra O.] Harvard Univ, Sch Med, Neurosci Program, Charlestown, MA 02129 USA.
[Wuerdinger, Tom] VU Med Ctr, Dept Neurosurg, Neurooncol Res Grp, Canc Ctr Amsterdam, NL-1007 MB Amsterdam, Netherlands.
[Curry, William T., Jr.; Carter, Bob S.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurosurg, Boston, MA 02114 USA.
[Krichevsky, Anna M.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Neurol, Boston, MA 02115 USA.
RP Breakefield, XO (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, 149 13th St, Charlestown, MA 02129 USA.
EM breakefield@hms.harvard.edu
RI leng, xianwei/F-9073-2011
FU Wenner-Gren Foundation [NCI CA86355, NCI CA69246]; Goldhirs Foundation;
Brain Tumor Society; American Brain Tumor Association
FX We wish to express our gratitude to B. Tannous for supplying the Gluc
lentivirus construct, C. Maguire, M. Broekman, K. Miranda, L. Russo and
O. Saydam for fruitful discussions. We also would like to thank Applied
Biosystems for supplying the miRNA qRT-PCR primers and S. Idema
(Neuro-oncology Research Group, Cancer Center Amsterdam) for supplying
some of the serum/biopsy samples. This work was supported by the
Wenner-Gren Foundation (J.S.) Stiftelsen Olle Engkvist Byggmastare
(J.S.), NCI CA86355 (X. O. B. and M. S. E.), NCI CA69246 (X. O. B., M.
S. E. and B. S. C.), The Goldhirs Foundation (B. S. C.) the Brain Tumor
Society (A. M. K.) and the American Brain Tumor Association (T. W.).
NR 37
TC 1486
Z9 1571
U1 44
U2 209
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1465-7392
J9 NAT CELL BIOL
JI Nat. Cell Biol.
PD DEC
PY 2008
VL 10
IS 12
BP 1470
EP U209
DI 10.1038/ncb1800
PG 12
WC Cell Biology
SC Cell Biology
GA 377OZ
UT WOS:000261261800019
PM 19011622
ER
PT J
AU Gadhoum, SZ
Sackstein, R
AF Gadhoum, Samah Zeineb
Sackstein, Robert
TI CD15 expression in human myeloid cell differentiation is regulated by
sialidase activity
SO NATURE CHEMICAL BIOLOGY
LA English
DT Article
ID HUMAN HEMATOPOIETIC PROGENITORS; ANTI-CD44 MONOCLONAL-ANTIBODIES; HUMAN
T-CELLS; E-SELECTIN; ADHESION MOLECULES; LYMPHOCYTE MIGRATION;
PLASMA-MEMBRANE; DENDRITIC CELLS; LEUKEMIA CELLS; BONE-MARROW
AB The glycan determinant CD15 (also known as Lewis x, or Le(x)) is a distinguishing marker for human myeloid cells and mediates neutrophil adhesion to dendritic cells. Despite broad interest in this structure, the mechanisms underlying CD15 expression remain relatively uncharacterized. Accordingly, we investigated the molecular basis of increasing CD15 expression associated with human myeloid cell differentiation. Flow cytometric analysis of differentiating cells together with biochemical studies using inhibitors of glycan synthesis and of sialidases showed that increased CD15 expression is not due to de novo biosynthesis of CD15, but results predominantly from induction of alpha(2- 3)-sialidase activity, which yields CD15 from cell-surface sialyl-CD15 (also known as sialyl-Lewis x, sLe(x) or CD15s). This differentiation-associated conversion of surface CD15s to CD15 occurs mainly on glycoproteins. Until now, modulation of post-translational glycan modifications has been attributed solely to dynamic variations in glycosyltransferase expression. Our results unveil a new paradigm by demonstrating a critical role for post-Golgi membrane glycosidase activity in the 'biosynthesis' of a key glycan determinant.
C1 [Gadhoum, Samah Zeineb; Sackstein, Robert] Brigham & Womens Hosp, Dept Dermatol, Boston, MA 02115 USA.
[Gadhoum, Samah Zeineb; Sackstein, Robert] Harvard Univ, Sch Med, Harvard Skin Dis Res Ctr, Boston, MA 02115 USA.
[Sackstein, Robert] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Sackstein, Robert] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Sackstein, R (reprint author), Brigham & Womens Hosp, Dept Dermatol, 75 Francis St, Boston, MA 02115 USA.
EM rsackstein@rics.bwh.harvard.edu
FU US National Heart, Lung, and Blood Institute [RO1 HL60528]; US National
Institute of Diabetes and Digestive and Kidney Diseases [R21 DK075012];
Team Jobie Leukemia Research fund
FX We are grateful to D. Floyd, S. Hamdan, C. Silvescu and C. Knoblauch for
technical support, to J. Merzaban, N. Stamatos, C. Dimitroff and M.
Burdick for helpful discussions of the manuscript, and to I. Galinsky,
R. Stone, D. DeAngelo, M. Wadleigh and A. Sirulnik for assistance in
procuring leukemia samples. This work was supported by US National
Heart, Lung, and Blood Institute grant RO1 HL60528 (R.S.), US National
Institute of Diabetes and Digestive and Kidney Diseases grant R21
DK075012 (R.S.) and the Team Jobie Leukemia Research fund (R.S.).
NR 44
TC 40
Z9 43
U1 2
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 1552-4450
J9 NAT CHEM BIOL
JI Nat. Chem. Biol.
PD DEC
PY 2008
VL 4
IS 12
BP 751
EP 757
DI 10.1038/nchembio.116
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 373FH
UT WOS:000260955900011
PM 18953356
ER
PT J
AU Burnett-Bowie, SAM
AF Burnett-Bowie, Sherri-Ann M.
TI Is twice-yearly denosumab beneficial in postmenopausal women with
osteopenia but no history of fracture?
SO NATURE CLINICAL PRACTICE ENDOCRINOLOGY & METABOLISM
LA English
DT Editorial Material
DE BMD; bone turnover marker; denosumab; osteoporosis; women
ID OSTEOPOROSIS; RECEPTOR
AB This Practice Point commentary discusses the findings and limitations of the first randomized, placebo-controlled trial of twice-yearly denosumab to be performed in postmenopausal women with low BMD but no previous fracture. Bone et al. found that treatment with denosumab significantly increased BMD at all sites measured and reduced the levels of bone turnover markers when compared with placebo. Despite these beneficial effects, denosumab was associated with increased rates of sore throat, rash and infections requiring hospitalization. Furthermore, the study was limited by lack of information on antifracture efficacy, although such information will presumably be forthcoming in the near future. Here, I highlight how denosumab therapy differs from other antiresorptive agents with respect to mechanism of action and effects on BMD. The findings of Bone et al. suggest that denosumab might represent a novel anti-osteoporosis agent. Nonetheless, further investigations of efficacy and long-term safety are needed before denosumab can be adopted into routine clinical practice.
C1 [Burnett-Bowie, Sherri-Ann M.] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
[Burnett-Bowie, Sherri-Ann M.] Harvard Univ, Sch Med, Boston, MA USA.
RP Burnett-Bowie, SAM (reprint author), Massachusetts Gen Hosp, Endocrine Unit, Thier 1051,50 Blossom St, Boston, MA 02114 USA.
EM sburnett-bowie@partners.org
OI Burnett-Bowie, Sherri-Ann/0000-0002-0064-096X
NR 7
TC 1
Z9 1
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1745-8366
J9 NAT CLIN PRACT ENDOC
JI Nat. Clin. Pract. Endocrinol. Metab.
PD DEC
PY 2008
VL 4
IS 12
BP 660
EP 661
DI 10.1038/ncpendmet0981
PG 2
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 375JB
UT WOS:000261108900007
PM 18981994
ER
PT J
AU Jain, SH
Sadow, PM
Nose, V
Dluhy, RG
AF Jain, Shilpa H.
Sadow, Peter M.
Nose, Vania
Dluhy, Robert G.
TI A patient with ectopic cortisol production derived from malignant
testicular masses
SO NATURE CLINICAL PRACTICE ENDOCRINOLOGY & METABOLISM
LA English
DT Article
DE adrenal rest cells; adrenocortical carcinoma; Cushing syndrome; Leydig
cell tumor
ID CUSHINGS-SYNDROME; ADRENOGENITAL SYNDROME; TUMORS
AB Background A 65-year-old man presented to an oncology clinic with bilateral testicular masses, lower extremity edema, and cushingoid appearance.
Investigations Measurements of serum cortisol and adrenocorticotropic hormone levels, testicular ultrasound and abdominal CT scans, and review of histopathology to identify the cellular origin of the ectopic cortisol production.
Diagnosis Cushing syndrome was diagnosed on the basis of a markedly elevated 24-hour urine free cortisol level and classic cushingoid features. The etiology of Cushing syndrome was determined to be an adrenocortical carcinoma arising from testicular adrenal rest cells. Nevertheless, the possibility of a malignant Leydig cell tumor with ectopic cortisol production could not be excluded.
Management Mitotane and metyrapone were used to decrease cortisol production. Excess mineralocorticoid activity was blocked with spironolactone; sodium retention was also managed with sodium restriction and diuretics. Despite initial success with this regimen, the patient died as a result of tumor progression and complications of poorly controlled hypercortisolism.
C1 [Dluhy, Robert G.] Brigham & Womens Hosp, Div Endocrinol Diabet & Hypertens, Boston, MA 02115 USA.
[Sadow, Peter M.; Dluhy, Robert G.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Nose, Vania] Harvard Univ, Sch Med, Boston, MA USA.
[Sadow, Peter M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
EM shjain@partners.org
NR 12
TC 6
Z9 7
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1745-8366
J9 NAT CLIN PRACT ENDOC
JI Nat. Clin. Pract. Endocrinol. Metab.
PD DEC
PY 2008
VL 4
IS 12
BP 695
EP 700
DI 10.1038/ncpendmet0985
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 375JB
UT WOS:000261108900013
PM 18941436
ER
PT J
AU Brugge, WR
AF Brugge, William R.
TI Contrast-enhanced endoscopic ultrasound for diagnosis of pancreatic
malignancy-a visual aid or a distraction?
SO NATURE CLINICAL PRACTICE GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Editorial Material
DE contrast-enhanced EUS; diagnosis; EUS; pancreatic adenocarcinoma;
pancreatic lesions
ID EUS-GUIDED FNA; FOCAL PANCREATITIS; TUMORS; ULTRASONOGRAPHY; DISEASES;
CANCER
AB Endoscopic ultrasound with fine-needle aspiration (EUS-FNA) is the gold standard for diagnosis of pancreatic malignancy. This commentary discusses the findings and limitations of a study by Dietrich and colleagues that examined the operative characteristics of contrast-enhanced EUS (CE-EUS) in patients with a solitary, solid, pancreatic mass of less than 4 cm in diameter. The authors compared the vascularity of adenocarcinomas with that of neuroendocrine tumors and other lesions of the pancreas. The finding of decreased vascularity on CE-EUS had a sensitivity of 92% and a specificity of 100% for the differentiation of adenocarcinomas from neuroendocrine tumors. It seems unlikely that CE-EUS will replace EUS-FNA for the diagnosis of pancreatic malignancy, but CE-EUS might have a role in differentiating adenocarcinomas from neuroendocrine tumors. It might be possible to use CE-EUS to assist in confirming the diagnosis of neuroendocrine tumors and perhaps in directing EUS-FNA.
C1 [Brugge, William R.] Massachusetts Gen Hosp, GI Unit, GI Endoscopy, Boston, MA 02114 USA.
[Brugge, William R.] Harvard Univ, Sch Med, Boston, MA USA.
RP Brugge, WR (reprint author), Massachusetts Gen Hosp, GI Unit, GI Endoscopy, Blake 452C, Boston, MA 02114 USA.
EM wbrugge@partners.org
NR 13
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1743-4378
J9 NAT CLIN PRACT GASTR
JI Nat. Clin. Pract. Gastroenterol. Hepatol.
PD DEC
PY 2008
VL 5
IS 12
BP 662
EP 663
DI 10.1038/ncpgasthep1285
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 376PY
UT WOS:000261196700002
PM 18852727
ER
PT J
AU Hodi, FS
Fisher, DE
AF Hodi, F. Stephen
Fisher, David E.
TI Adoptive transfer of antigen-specific CD4(+) T cells in the treatment of
metastatic melanoma
SO NATURE CLINICAL PRACTICE ONCOLOGY
LA English
DT Editorial Material
DE antigen-specific; CD4+T cells; cancer; metastatic melanoma
ID CANCER; THERAPY; IMMUNOTHERAPY
AB Clinical investigations of adoptive therapy in solid tumors have primarily focused on CD8(+) cells. A study by Hunder et al. is the first to demonstrate the significance of antigen-specific CD4(+) T cells. An in vitro method was used to treat a patient with metastatic melanoma using autologous CD4(+) cells against NY-ESO-1 (cancer and/or testis antigen 1). The successful adoptive transfer of antigen-specific CD4(+) cells to a patient with metastatic melanoma is not only an important technical accomplishment but also provides increased understanding of tumor immunity. This report demonstrates an impressive persistence of adoptively transferred cells together with durability of clinical response. CD4(+) T cells that target a particular antigen can augment T-cell responses to other tumor-associated targets. These observations underline the importance of ongoing research for effective, non-toxic immune therapies for cancer.
C1 [Fisher, David E.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Dermatol,Melanoma Program, Boston, MA 02114 USA.
[Fisher, David E.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Boston, MA 02114 USA.
[Hodi, F. Stephen] Harvard Univ, Sch Med, Dana Farber Canc Inst, Melanoma Program, Boston, MA 02114 USA.
RP Fisher, DE (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Dermatol,Melanoma Program, 55 Fruit St, Boston, MA 02114 USA.
EM dfisher3@partners.org
NR 7
TC 9
Z9 9
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1743-4254
J9 NAT CLIN PRACT ONCOL
JI Nat. Clin. Pract. Oncol.
PD DEC
PY 2008
VL 5
IS 12
BP 696
EP 697
DI 10.1038/ncponc1259
PG 2
WC Oncology
SC Oncology
GA 376QE
UT WOS:000261197300006
PM 18852719
ER
PT J
AU Rosenberg, JE
Oh, WK
AF Rosenberg, Jonathan E.
Oh, William K.
TI What is the current status of second-line chemotherapy for
castration-resistant prostate cancer?
SO NATURE CLINICAL PRACTICE UROLOGY
LA English
DT Editorial Material
DE chemotherapy; chemotherapy resistance; mitoxantrone; prostate cancer;
salvage treatment
ID MITOXANTRONE; DOCETAXEL; PREDNISONE; SURVIVAL; TAX-327; PHASE-2
AB Patients with castration-resistant prostate cancer (CRPC) who show progression of disease after first-line chemotherapy with docetaxel have few proven treatment options. Mitoxantrone plus prednisone is frequently used in this setting. The retrospective analysis by Berthold et al. of mitoxantrone after first-line docetaxel in patients with CRPC suggests that mitoxantrone has a modest level of activity in this setting, with a second-line PSA response rate of 15% and a median time to PSA progression of 3.2 months. Patients with CRPC treated with docetaxel after progression on first-line mitoxantrone had a PSA response rate of 28% and a median time to PSA progression of 5.9 months. In this analysis, median survival of patients was 10 months and did not differ according to choice of first-line agent. Mitoxantrone therapy can be considered in select patients after failure of first-line docetaxel, and vice versa. Other cytotoxic agents such as carboplatin might have a limited role in this patient population. In general, patients with CRPC should be directed towards clinical trials, when available.
C1 [Rosenberg, Jonathan E.; Oh, William K.] Dana Farber Canc Inst, Lank Ctr Genitourinary Oncol, Boston, MA 02446 USA.
[Rosenberg, Jonathan E.; Oh, William K.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
RP Rosenberg, JE (reprint author), Dana Farber Canc Inst, Lank Ctr Genitourinary Oncol, 44 Binney St,D1230, Boston, MA 02446 USA.
EM jonathan_rosenberg@dfci.harvard.edu
RI Oh, William/B-9163-2012
OI Oh, William/0000-0001-5113-8147
NR 8
TC 1
Z9 1
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1743-4270
J9 NAT CLIN PRACT UROL
JI Nat. Clin. Pract. Urol.
PD DEC
PY 2008
VL 5
IS 12
BP 650
EP 651
DI 10.1038/ncpuro1232
PG 2
WC Urology & Nephrology
SC Urology & Nephrology
GA 379GF
UT WOS:000261384000006
PM 18936787
ER
PT J
AU Cooper, JD
Smyth, DJ
Smiles, AM
Plagnol, V
Walker, NM
Allen, JE
Downes, K
Barrett, JC
Healy, BC
Mychaleckyj, JC
Warram, JH
Todd, JA
AF Cooper, Jason D.
Smyth, Deborah J.
Smiles, Adam M.
Plagnol, Vincent
Walker, Neil M.
Allen, James E.
Downes, Kate
Barrett, Jeffrey C.
Healy, Barry C.
Mychaleckyj, Josyf C.
Warram, James H.
Todd, John A.
TI Meta-analysis of genome-wide association study data identifies
additional type 1 diabetes risk loci
SO NATURE GENETICS
LA English
DT Article
ID LARGE-SCALE; PKC-THETA; DISEASES; REGION; BACH2
AB We carried out a meta-analysis of data from three genome-wide association (GWA) studies of type 1 diabetes (T1D), testing 305,090 SNPs in 3,561 T1D cases and 4,646 controls of European ancestry. We obtained further support for 4q27 (IL2-IL21, P = 1.9 x 10(-8)) and, after genotyping an additional 6,225 cases, 6,946 controls and 2,828 families, convincing evidence for four previously unknown and distinct risk loci in chromosome regions 6q15 (BACH2, P = 4.7 x 10(-12)), 10p15 (PRKCQ, P = 3.7 x 10(-9)), 15q24 (CTSH, P = 3.2 x 10(-15)) and 22q13 (C1QTNF6, P = 2.0 x 10(-8)).
C1 [Cooper, Jason D.; Smyth, Deborah J.; Plagnol, Vincent; Walker, Neil M.; Allen, James E.; Downes, Kate; Barrett, Jeffrey C.; Healy, Barry C.; Todd, John A.] Univ Cambridge, Addenbrookes Hosp, Juvenile Diabet Res Fdn,Cambridge Inst Med Res, Wellcome Trust Diabet & Inflammat Lab,Dept Med Ge, Cambridge CB2 0XY, England.
[Smiles, Adam M.; Warram, James H.] Joslin Diabet Ctr, Div Res, Boston, MA 02215 USA.
[Mychaleckyj, Josyf C.] Univ Virginia, Ctr Publ Hlth Genom, Charlottesville, VA 22908 USA.
RP Cooper, JD (reprint author), Univ Cambridge, Addenbrookes Hosp, Juvenile Diabet Res Fdn,Cambridge Inst Med Res, Wellcome Trust Diabet & Inflammat Lab,Dept Med Ge, Cambridge CB2 0XY, England.
EM jason.cooper@cimr.cam.ac.uk
RI Allen, James/B-2457-2009; Plagnol, Vincent/A-5667-2011; Todd,
John/A-3542-2010;
OI Allen, James/0000-0002-3894-4854; Walker, Neil/0000-0001-9796-7688;
smyth, deborah/0000-0002-6330-2669; Plagnol, Vincent/0000-0002-5597-9215
FU Juvenile Diabetes Research Foundation International; Wellcome Trust;
National Institute for Health Research Cambridge Biomedical Centre;
Wellcome Trust Strategic Award [079895]; Wellcome Trust [076113]
FX This work was funded by the Juvenile Diabetes Research Foundation
International, the Wellcome Trust and the National Institute for Health
Research Cambridge Biomedical Centre. The Cambridge Institute for
Medical Research (CIMR) is in receipt of a Wellcome Trust Strategic
Award (079895). We thank all study participants and family members. We
gratefully acknowledge D. Clayton for methodology advice and comments on
the manuscript. We acknowledge use of DNA from the British 1958 Birth
Cohort collection, funded by the Medical Research Council and the
Wellcome Trust. We thank The Avon Longitudinal Study of Parents and
Children laboratory in Bristol and the British 1958 Birth Cohort team,
including S. Ring, R. Jones, M. Pembrey, W. McArdle, D. Strachan and P.
Burton, for preparing and providing the control DNA samples. We also
thank H. Stevens, P. Clarke, G. Coleman, S. Duley, D. Harrison, S.
Hawkins, M. Maisuria, T. Mistry and N. Taylor for preparation of DNA
samples. We acknowledge use of DNA from the Human Biological Data
Interchange and Diabetes UK for the USA and UK multiplex families,
respectively; the Norwegian Study Group for Childhood Diabetes (D.
Undlien and K. Ronningen) for the Norwegian families; D. Savage, C.
Patterson, D. Carson and P. Maxwell for the Northern Irish families; the
Genetics of Type 1 Diabetes in Finland (GET1FIN); J. Tuomilehto, L.
Kinnunen, E. Tuomilehto-Wolf, V. Harjutsalo and T. Valle for the Finnish
families; and C. Guja and C. Ionescu-Tirgoviste for the Romanian
families. WTCCC: This study makes use of data generated by the Wellcome
Trust Case Control Consortium. A full list of the investigators who
contributed to the generation of the data are available from
http://www.wtccc.org.uk/. Funding for the project was provided by the
Wellcome Trust under award 076113 (see ref. 1). NIMH: We gratefully
acknowledge the National Institute of Mental Health for generously
allowing the use of their control CEL and genotype data. Control
subjects from the National Institute of Mental Health Schizophrenia
Genetics Initiative (NIMH-GI), data and biomaterials are being collected
by the "Molecular Genetics of Schizophrenia II'' (MGS-2) collaboration.
The investigators and co-investigators are as follows: P.V. Gejman
(Collaboration coordinator) and A. R. Sanders (ENH/Northwestern
University, MH059571); F. Amin (Emory University School of Medicine,
MH59587); N. Buccola (Louisiana State University Health Sciences Center,
MH067257); W. Byerley (University of California-Irvine, MH60870); C. R.
Cloninger (Washington University, St. Louis, U01, MH060879); R. Crowe
(PI) and D. Black (University of Iowa, MH59566); R. Freedman (University
of Colorado, MH059565); D. Levinson (University of Pennsylvania,
MH061675); B. Mowry (University of Queensland, MH059588); and J.
Silverman (Mt. Sinai School of Medicine, MH59586). The samples were
collected by V.L. Nimgaonkar's group at the University of Pittsburgh as
part of a multi-institutional collaborative research project with J.
Smoller and P. Sklar (Massachusetts General Hospital) (grant MH 63420).
GoKinD: We acknowledge the National Institutes of Health for allowing
the use of their control allele signal intensity and genotype data. The
dataset(s) used for the analyses described in this manuscript were
obtained from the GAIN Database, controlled through dbGaP accession
number phs000018.v1.p1.
NR 15
TC 261
Z9 265
U1 0
U2 7
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD DEC
PY 2008
VL 40
IS 12
BP 1399
EP 1401
DI 10.1038/ng.249
PG 3
WC Genetics & Heredity
SC Genetics & Heredity
GA 376XI
UT WOS:000261215900012
PM 18978792
ER
PT J
AU Dengler, HS
Baracho, GV
Omori, SA
Bruckner, S
Arden, KC
Castrillon, DH
DePinho, RA
Rickert, RC
AF Dengler, Hart S.
Baracho, Gisele V.
Omori, Sidne A.
Bruckner, Shane
Arden, Karen C.
Castrillon, Diego H.
DePinho, Ronald A.
Rickert, Robert C.
TI Distinct functions for the transcription factor Foxo1 at various stages
of B cell differentiation
SO NATURE IMMUNOLOGY
LA English
DT Article
ID CLASS-SWITCH RECOMBINATION; IMMUNOGLOBULIN GENE REARRANGEMENTS;
INTERLEUKIN-7 RECEPTOR; REGULATORY FACTOR-4; IMMUNE-SYSTEM; MICE
LACKING; EXPRESSION; ACTIVATION; LINEAGE; PROLIFERATION
AB The transcription factors Foxo1, Foxo3 and Foxo4 modulate cell fate 'decisions' in diverse systems. Here we show that Foxo1-dependent gene expression was critical at many stages of B cell differentiation. Early deletion of Foxo1 caused a substantial block at the pro-B cell stage due to a failure to express interleukin 7 receptor-alpha. Foxo1 inactivation in late pro-B cells resulted in an arrest at the pre-B cell stage due to lower expression of the recombination-activating genes Rag1 and Rag2. Deletion of Foxo1 in peripheral B cells led to fewer lymph node B cells due to lower expression of L-selectin and failed class-switch recombination due to impaired upregulation of the gene encoding activation-induced cytidine deaminase. Thus, Foxo1 regulates a transcriptional program that is essential for early B cell development and peripheral B cell function.
C1 [Dengler, Hart S.; Baracho, Gisele V.; Omori, Sidne A.; Bruckner, Shane; Rickert, Robert C.] Burnham Inst Med Res, Program Inflammatory Dis Res, La Jolla, CA 92037 USA.
[Arden, Karen C.] Univ Calif San Diego, Ludwig Inst Canc Res, La Jolla, CA 92093 USA.
[Castrillon, Diego H.] Univ Texas SW Med Ctr Dallas, Dept Pathol, Dallas, TX 75390 USA.
[DePinho, Ronald A.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Belfer Inst Innovat Canc Sci,Ctr Appl Canc Sci, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Dept Med & Genet, Boston, MA 02115 USA.
RP Rickert, RC (reprint author), Burnham Inst Med Res, Program Inflammatory Dis Res, La Jolla, CA 92037 USA.
EM robert@burnham.org
FU US National Institutes of Health [AI059447]; American Cancer Society;
Robert A. and Renee E. Befler Foundation Institute for Innovative Cancer
Science
FX We thank K. Rajewsky (Harvard University) and M. Reth (Max-Planck
Institute) for Cd21Cre and mb1Cre mice,
respectively; B. Finlay (Burnham Institute for Medical Research) and K.
Mowen (The Scripps Research Institute) for retroviruses expressing
Bcl-xL and Cre, respectively; and S. Hedrick and members of
the Rickert laboratory for discussions and reading of the manuscript.
Supported by the US National Institutes of Health (AI059447 to R. C.
R.), the American Cancer Society (R. A. D.) and the Robert A. and Renee
E. Befler Foundation Institute for Innovative Cancer Science (R. A. D.).
NR 50
TC 145
Z9 148
U1 1
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA
SN 1529-2908
J9 NAT IMMUNOL
JI Nat. Immunol.
PD DEC
PY 2008
VL 9
IS 12
BP 1388
EP 1398
DI 10.1038/ni.1667
PG 11
WC Immunology
SC Immunology
GA 372FY
UT WOS:000260888700014
PM 18978794
ER
PT J
AU Engelman, JA
Chen, L
Tan, XH
Crosby, K
Guimaraes, AR
Upadhyay, R
Maira, M
McNamara, K
Perera, SA
Song, YC
Chirieac, LR
Kaur, R
Lightbown, A
Simendinger, J
Li, T
Padera, RF
Garcia-Echeverria, C
Weissleder, R
Mahmood, U
Cantley, LC
Wong, KK
AF Engelman, Jeffrey A.
Chen, Liang
Tan, Xiaohong
Crosby, Katherine
Guimaraes, Alexander R.
Upadhyay, Rabi
Maira, Michel
McNamara, Kate
Perera, Samanthi A.
Song, Youngchul
Chirieac, Lucian R.
Kaur, Ramneet
Lightbown, Angela
Simendinger, Jessica
Li, Timothy
Padera, Robert F.
Garcia-Echeverria, Carlos
Weissleder, Ralph
Mahmood, Umar
Cantley, Lewis C.
Wong, Kwok-Kin
TI Effective use of PI3K and MEK inhibitors to treat mutant Kras G12D and
PIK3CA H1047R murine lung cancers
SO NATURE MEDICINE
LA English
DT Article
ID PHOSPHOINOSITIDE 3-KINASE; REGULATORY SUBUNIT; CATALYTIC SUBUNIT; MICE;
MUTATIONS; RAS; TUMORIGENESIS; SENSITIVITY; EXPRESSION; P110-ALPHA
AB Somatic mutations that activate phosphoinositide 3-kinase (PI3K) have been identified in the p110-alpha catalytic subunit (encoded by PIK3CA)(1). They are most frequently observed in two hotspots: the helical domain (E545K and E542K) and the kinase domain (H1047R). Although the p110-alpha mutants are transforming in vitro, their oncogenic potential has not been assessed in genetically engineered mouse models. Furthermore, clinical trials with PI3K inhibitors have recently been initiated, and it is unknown if their efficacy will be restricted to specific, genetically defined malignancies. In this study, we engineered a mouse model of lung adenocarcinomas initiated and maintained by expression of p110-alpha H1047R. Treatment of these tumors with NVP-BEZ235, a dual pan-PI3K and mammalian target of rapamycin (mTOR) inhibitor in clinical development, led to marked tumor regression as shown by positron emission tomography-computed tomography, magnetic resonance imaging and microscopic examination. In contrast, mouse lung cancers driven by mutant Kras did not substantially respond to single-agent NVP-BEZ235. However, when NVP-BEZ235 was combined with a mitogen-activated protein kinase kinase (MEK) inhibitor, ARRY-142886, there was marked synergy in shrinking these Kras-mutant cancers. These in vivo studies suggest that inhibitors of the PI3K-mTOR pathway may be active in cancers with PIK3CA mutations and, when combined with MEK inhibitors, may effectively treat KRAS mutated lung cancers.
C1 Beth Israel Hosp, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA.
[Engelman, Jeffrey A.; Song, Youngchul; Kaur, Ramneet] Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA 02129 USA.
[Engelman, Jeffrey A.; Kaur, Ramneet; Cantley, Lewis C.; Wong, Kwok-Kin] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[Chen, Liang; Tan, Xiaohong; McNamara, Kate; Perera, Samanthi A.; Wong, Kwok-Kin] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Chen, Liang; Tan, Xiaohong; McNamara, Kate; Perera, Samanthi A.; Wong, Kwok-Kin] Dana Farber Harvard Canc Ctr, Ludwig Ctr, Boston, MA 02115 USA.
[Crosby, Katherine; Lightbown, Angela; Simendinger, Jessica] Cell Signaling Technol, Danvers, MA 01923 USA.
[Guimaraes, Alexander R.; Upadhyay, Rabi; Weissleder, Ralph; Mahmood, Umar] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Mol Imaging Res, Charlestown, MA 02129 USA.
[Guimaraes, Alexander R.; Upadhyay, Rabi; Weissleder, Ralph; Mahmood, Umar] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Maira, Michel; Garcia-Echeverria, Carlos] Novartis Inst Biomed Res, Oncol Dis Area, CH-4057 Basel, Switzerland.
[Chirieac, Lucian R.; Padera, Robert F.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Weissleder, Ralph; Cantley, Lewis C.] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA.
RP Cantley, LC (reprint author), Beth Israel Hosp, Beth Israel Deaconess Med Ctr, 77 Ave Louis Pasteur, Boston, MA 02115 USA.
EM lewis_cantley@hms.harvard.edu; KWONG1@PARTNERS.ORG
RI Cantley, Lewis/D-1800-2014;
OI Cantley, Lewis/0000-0002-1298-7653; wong, kwok kin/0000-0001-6323-235X
FU US National Institutes of Health (NIH) [CA120060-01]; American
Association for Cancer Research; International Association for the Study
of Lung Cancer; NIH [CA089021, P01 CA117969, R01 GM41890, K08 AG024004,
R01 CA122794, R01 AG2400401]; Dana-Farber-Harvard Cancer Center Lung
Cancer Specialized Program of Research Excellence (SPORE) [P50
CA090578]; Dana-Farber-Harvard Cancer Center Gastrointestinal Cancer
SPORE [P50 CA127003, U24-CA092782]; Joan Scarangello Foundation to
Conquer Lung Cancer; Cecily and Robert Harris Foundation; Flight
Attendant Medical Research Institute
FX CCSP-rtTA mice were generously provided by J. Whitsett at the University
of Cincinnati. Tet-op-Kras mice were generously provided by H. Varmus
(Memorial Sloan-Kettering Cancer Center). LSL-Kras G12D mice were kindly
provided by T. Jacks (Massachusetts Institute of Technology). This work
was supported by US National Institutes of Health (NIH) K08 grant
CA120060-01 (J. A. E.), the American Association for Cancer Research (J.
A. E.), the International Association for the Study of Lung Cancer (J.
A. E.), NIH prostate cancer grant P01 CA089021 (L. C. C.), NIH
pancreatic cancer grant P01 CA117969 (L. C. C.), NIH grant R01 GM41890
(L. C. C.), a Dana-Farber-Harvard Cancer Center Lung Cancer Specialized
Program of Research Excellence (SPORE) grant P50 CA090578 (J. A. E. and
K.-K.W.) and Dana-Farber-Harvard Cancer Center Gastrointestinal Cancer
SPORE grants P50 CA127003 (J. A. E., R. W., U. M. and L. C. C.) and
U24-CA092782 (R. W., U. M., A. R. G.). K.-K.W. was supported by NIH
grants K08 AG024004, R01 CA122794 and R01 AG2400401; the Joan
Scarangello Foundation to Conquer Lung Cancer; the Cecily and Robert
Harris Foundation; and the Flight Attendant Medical Research Institute.
NR 21
TC 754
Z9 776
U1 3
U2 38
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
J9 NAT MED
JI Nat. Med.
PD DEC
PY 2008
VL 14
IS 12
BP 1351
EP 1356
DI 10.1038/nm.1890
PG 6
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 379JX
UT WOS:000261393600019
PM 19029981
ER
PT J
AU Yu, PB
Deng, DY
Lai, CS
Hong, CC
Cuny, GD
Bouxsein, ML
Hong, DW
McManus, PM
Katagiri, T
Sachidanandan, C
Kamiya, N
Fukuda, T
Mishina, Y
Peterson, RT
Bloch, KD
AF Yu, Paul B.
Deng, Donna Y.
Lai, Carol S.
Hong, Charles C.
Cuny, Gregory D.
Bouxsein, Mary L.
Hong, Deborah W.
McManus, Patrick M.
Katagiri, Takenobu
Sachidanandan, Chetana
Kamiya, Nobuhiro
Fukuda, Tomokazu
Mishina, Yuji
Peterson, Randall T.
Bloch, Kenneth D.
TI BMP type I receptor inhibition reduces heterotopic ossification
SO NATURE MEDICINE
LA English
DT Article
ID SMOOTH-MUSCLE-CELLS; PROGRESSIVA FOP; BONE-FORMATION; SMAD PROTEINS;
DIFFERENTIATION; MOUSE; ACVR1; ALK2; MUTATION; ARREST
AB Fibrodysplasia ossificans progressiva (FOP) is a congenital disorder of progressive and widespread postnatal ossification of soft tissues(1-4) and is without known effective treatments. Affected individuals harbor conserved mutations in the ACVR1 gene that are thought to cause constitutive activation of the bone morphogenetic protein (BMP) type I receptor, activin receptor-like kinase-2 (ALK2)(5). Here we show that intramuscular expression in the mouse of an inducible transgene encoding constitutively active ALK2 (caALK2), resulting from a glutamine to aspartic acid change at amino acid position 207, leads to ectopic endochondral bone formation, joint fusion and functional impairment, thus phenocopying key aspects of human FOP. A selective inhibitor of BMP type I receptor kinases, LDN-193189 (ref. 6), inhibits activation of the BMP signaling effectors SMAD1, SMAD5 and SMAD8 in tissues expressing caALK2 induced by adenovirus specifying Cre (Ad. Cre). This treatment resulted in a reduction in ectopic ossification and functional impairment. In contrast to localized induction of caALK2 by Ad. Cre (which entails inflammation), global postnatal expression of caALK2 (induced without the use of Ad. Cre and thus without inflammation) does not lead to ectopic ossification. However, if in this context an inflammatory stimulus was provided with a control adenovirus, ectopic bone formation was induced. Like LDN-193189, corticosteroid treatment inhibits ossification in Ad.Cre-injected mutant mice, suggesting caALK2 expression and an inflammatory milieu are both required for the development of ectopic ossification in this model. These results support the role of dysregulated ALK2 kinase activity in the pathogenesis of FOP and suggest that small molecule inhibition of BMP type I receptor activity may be useful in treating FOP and heterotopic ossification syndromes associated with excessive BMP signaling.
C1 [Yu, Paul B.; Deng, Donna Y.; Lai, Carol S.; Hong, Deborah W.; McManus, Patrick M.; Sachidanandan, Chetana; Peterson, Randall T.; Bloch, Kenneth D.] Massachusetts Gen Hosp, Div Cardiol, Dept Med, Boston, MA 02114 USA.
[Yu, Paul B.; Bloch, Kenneth D.] Massachusetts Gen Hosp, Anesthesia Ctr Crit Care Res, Boston, MA 02114 USA.
[Yu, Paul B.; Bloch, Kenneth D.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Hong, Charles C.] Vanderbilt Univ, Sch Med, Div Cardiovasc Med, Nashville, TN 37232 USA.
[Hong, Charles C.] Vanderbilt Univ, Sch Med, Dept Pharmacol, Nashville, TN 37232 USA.
[Cuny, Gregory D.] Brigham & Womens Hosp, Lab Drug Discovery Neurodegenerat, Harvard NeuroDiscovery Ctr, Cambridge, MA 02139 USA.
[Cuny, Gregory D.] Harvard Univ, Sch Med, Cambridge, MA 02139 USA.
[Bouxsein, Mary L.] Beth Israel Deaconess Med Ctr, Orthopaed Biomech Lab, Boston, MA 02215 USA.
[Bouxsein, Mary L.] Harvard Univ, Sch Med, Boston, MA 02215 USA.
[Katagiri, Takenobu] Saitama Med Univ, Div Pathophysiol, Res Ctr Genom Med, Hidaka, Saitama 3501241, Japan.
[Kamiya, Nobuhiro; Fukuda, Tomokazu; Mishina, Yuji] NIEHS, Mol Dev Biol Sect, Lab Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC 27709 USA.
RP Yu, PB (reprint author), Massachusetts Gen Hosp, Div Cardiol, Dept Med, Thier 505,50 Blossom St, Boston, MA 02114 USA.
EM pbyu@partners.org
RI Hong, Charles/C-9989-2010
FU US National Institutes of Health [HL079943, HL074352]; US National
Institute of Environmental Health Sciences Intramural Research Program
[ES071003-10]; Howard Hughes Medical Institute Early Career Award;
GlaxoSmithKline Research & Education Foundation for Cardiovascular
Disease; Center for Research in Fibrodysplasia Ossificans Progressiva
and Related Disorders at the University of Pennsylvania
FX We thank P. ten Dijke (Leiden University Medical Center) for providing
BRE-Luc and CAGA-Luc and K. Miyazono (University of Tokyo) for providing
caALK2, caALK3, caALK4, caALK5, caALK6 and caALK7. We are grateful to H.
Beppu, E. Schipani, H. Kronenberg, A. Wagers, J. Groppe, W. Zapol and F.
Kaplan for insightful discussions and technical expertise, A. Graveline
and D. Panus for technical assistance and E. Buys for technical
expertise. This work was supported by US National Institutes of Health
grants HL079943 (P.B.Y.) and HL074352 (K. D. B.), the US National
Institute of Environmental Health Sciences Intramural Research Program
grant ES071003-10 (Y.M.) and Partners Healthcare. This work was also
supported by a Howard Hughes Medical Institute Early Career Award
(P.B.Y.), a Pulmonary Hypertension Association Mentored Clinical
Scientist Award (P.B.Y.), a grant from the GlaxoSmithKline Research &
Education Foundation for Cardiovascular Disease (P.B.Y.) and a
Developmental Grant from the Center for Research in Fibrodysplasia
Ossificans Progressiva and Related Disorders at the University of
Pennsylvania (C. C. H.).
NR 33
TC 269
Z9 279
U1 5
U2 28
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
J9 NAT MED
JI Nat. Med.
PD DEC
PY 2008
VL 14
IS 12
BP 1363
EP 1369
DI 10.1038/nm.1888
PG 7
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 379JX
UT WOS:000261393600021
PM 19029982
ER
PT J
AU Hartley, JL
Salehi-Ashtiani, K
Hill, DE
AF Hartley, James L.
Salehi-Ashtiani, Kourosh
Hill, David E.
TI Proteome expression moves in vitro: resources and tools for harnessing
the human proteome
SO NATURE METHODS
LA English
DT Editorial Material
ID OPEN READING FRAMES; ORFEOME VERSION 1.1; COLLECTION; GENOME
AB Comprehensive sets of clones and improved high-throughput methods for production of functional proteins now allow proteome-scale in vitro experiments on nearly 15,000 human genes.
C1 [Hartley, James L.] NCI, SAIC Frederick, Frederick, MD 21702 USA.
[Salehi-Ashtiani, Kourosh; Hill, David E.] Dana Farber Canc Inst, Ctr Canc Syst Biol, Boston, MA 02115 USA.
[Salehi-Ashtiani, Kourosh; Hill, David E.] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
RP Hartley, JL (reprint author), NCI, SAIC Frederick, Frederick, MD 21702 USA.
EM hartley@ncifcrf.gov; kourosh_salehi-ashtiani@dfci.harvard.edu;
david_hill@dfci.harvard.edu
RI Hill, David/B-6617-2011;
OI Salehi-Ashtiani, Kourosh/0000-0002-6521-5243
NR 12
TC 3
Z9 3
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1548-7091
J9 NAT METHODS
JI Nat. Methods
PD DEC
PY 2008
VL 5
IS 12
BP 1001
EP 1002
DI 10.1038/nmeth1208-1001
PG 2
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 376WC
UT WOS:000261212700009
PM 19034266
ER
PT J
AU Fernandez-Suarez, M
Ting, AY
AF Fernandez-Suarez, Marta
Ting, Alice Y.
TI Fluorescent probes for super-resolution imaging in living cells
SO NATURE REVIEWS MOLECULAR CELL BIOLOGY
LA English
DT Review
ID PHOTOACTIVATED LOCALIZATION MICROSCOPY; OPTICAL RECONSTRUCTION
MICROSCOPY; DIFFRACTION RESOLUTION BARRIER; SMALL-MOLECULE PROBES; LIVE
CELLS; STIMULATED-EMISSION; QUANTUM DOTS; IN-VIVO; STED MICROSCOPY;
NEAR-FIELD
AB In 1873, Ernst Abbe discovered that features closer than similar to 200 nm cannot be resolved by lens-based light microscopy. In recent years, however, several new far-field super-resolution imaging techniques have broken this diffraction limit, producing, for example, video-rate movies of synaptic vesicles in living neurons with 62 nm spatial resolution. Current research is focused on further improving spatial resolution in an effort to reach the goal of video-rate imaging of live cells with molecular (1-5 nm) resolution. Here, we describe the contributions of fluorescent probes to far-field super-resolution imaging, focusing on fluorescent proteins and organic small-molecule fluorophores. We describe the features of existing super-resolution fluorophores and highlight areas of importance for future research and development.
C1 [Fernandez-Suarez, Marta; Ting, Alice Y.] MIT, Dept Chem, Cambridge, MA 02139 USA.
[Fernandez-Suarez, Marta] Massachusetts Gen Hosp, Ctr Engn Med, Charlestown, MA 02129 USA.
RP Fernandez-Suarez, M (reprint author), MIT, Dept Chem, 77 Massachusetts Ave, Cambridge, MA 02139 USA.
EM martafs@alum.mit.edu; ating@mit.edu
NR 120
TC 601
Z9 614
U1 64
U2 441
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-0072
J9 NAT REV MOL CELL BIO
JI Nat. Rev. Mol. Cell Biol.
PD DEC
PY 2008
VL 9
IS 12
BP 929
EP 943
DI 10.1038/nrm2531
PG 15
WC Cell Biology
SC Cell Biology
GA 375PW
UT WOS:000261126800013
PM 19002208
ER
PT J
AU Dresemann, G
Sorenson, G
Reardon, DA
Hosius, C
Parker, R
Nikolova, Z
AF Dresemann, G.
Sorenson, G.
Reardon, D. A.
Hosius, C.
Parker, R.
Nikolova, Z.
TI QUANTIFYING ASSESSMENTS FOR GLIOBLASTOMA MULTIFORME (GBM) FOR CLINICAL
TRIALS - AN ALTERNATIVE APPROACH
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
CT 8th Congress of the European-Association-for-Neuro-Oncology (EANO)
CY SEP 12-14, 2008
CL Barcelona, SPAIN
SP European Assoc Neuro Oncol
C1 [Dresemann, G.] CTC Standort Franz Hosp, Dulmen, Germany.
[Sorenson, G.] Massachusetts Gen Hosp, Charlestown, MA USA.
[Reardon, D. A.] Duke Univ, Med Ctr, Durham, NC USA.
[Hosius, C.] Novartis Pharma Oncol, Nurnberg, Germany.
[Parker, R.; Nikolova, Z.] Novartis Pharma Oncol, Basel, Switzerland.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU DUKE UNIV PRESS
PI DURHAM
PA 905 W MAIN ST, STE 18-B, DURHAM, NC 27701 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD DEC
PY 2008
VL 10
IS 6
BP 1139
EP 1139
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 383TG
UT WOS:000261695800318
ER
PT J
AU Helt, M
Kelley, E
Kinsbourne, M
Pandey, J
Boorstein, H
Herbert, M
Fein, D
AF Helt, Molly
Kelley, Elizabeth
Kinsbourne, Marcel
Pandey, Juhi
Boorstein, Hilary
Herbert, Martha
Fein, Deborah
TI Can Children with Autism Recover? If So, How?
SO NEUROPSYCHOLOGY REVIEW
LA English
DT Review
DE Autism spectrum disorders; Language development; Recovery; Stereotyped
motor behavior
ID PERVASIVE DEVELOPMENTAL DISORDER; INTENSIVE BEHAVIORAL INTERVENTION;
FUSIFORM FACE AREA; FOLLOW-UP; SPECTRUM DISORDERS; YOUNG-CHILDREN;
REPETITIVE BEHAVIORS; JOINT ATTENTION; 1ST YEAR; COMMUNICATION
INTERVENTION
AB Although Autism Spectrum Disorders (ASD) are generally assumed to be lifelong, we review evidence that between 3% and 25% of children reportedly lose their ASD diagnosis and enter the normal range of cognitive, adaptive and social skills. Predictors of recovery include relatively high intelligence, receptive language, verbal and motor imitation, and motor development, but not overall symptom severity. Earlier age of diagnosis and treatment, and a diagnosis of Pervasive Developmental Disorder-Not Otherwise Specified are also favorable signs. The presence of seizures, mental retardation and genetic syndromes are unfavorable signs, whereas head growth does not predict outcome. Controlled studies that report the most recovery came about after the use of behavioral techniques. Residual vulnerabilities affect higher-order communication and attention. Tics, depression and phobias are frequent residual co-morbidities after recovery. Possible mechanisms of recovery include: normalizing input by forcing attention outward or enriching the environment; promoting the reinforcement value of social stimuli; preventing interfering behaviors; mass practice of weak skills; reducing stress and stabilizing arousal. Improving nutrition and sleep quality is non-specifically beneficial.
C1 [Helt, Molly; Boorstein, Hilary; Fein, Deborah] Univ Connecticut, Dept Psychol, Storrs, CT 06268 USA.
[Kelley, Elizabeth] Queens Univ, Dept Psychol, Kingston, ON K7L 3N6, Canada.
[Kinsbourne, Marcel] New Sch, Dept Psychol, New York, NY USA.
[Pandey, Juhi] Childrens Hosp Philadelphia, Ctr Autism Res, Philadelphia, PA 19104 USA.
[Herbert, Martha] Massachusetts Gen Hosp, Dept Neurol, Charlestown, MA USA.
[Herbert, Martha] Massachusetts Gen Hosp, TRANSCEND Res Program, Charlestown, MA USA.
RP Helt, M (reprint author), Univ Connecticut, Dept Psychol, Storrs, CT 06268 USA.
EM molly.helt@uconn.edu
NR 180
TC 110
Z9 113
U1 10
U2 42
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1040-7308
EI 1573-6660
J9 NEUROPSYCHOL REV
JI Neuropsychol. Rev.
PD DEC
PY 2008
VL 18
IS 4
BP 339
EP 366
DI 10.1007/s11065-008-9075-9
PG 28
WC Psychology, Clinical; Neurosciences
SC Psychology; Neurosciences & Neurology
GA 400HJ
UT WOS:000262858300007
PM 19009353
ER
PT J
AU Owens, MJ
Krulewicz, S
Simon, JS
Sheehan, DV
Thase, ME
Carpenter, DJ
Plott, SJ
Nemeroff, CB
AF Owens, Michael J.
Krulewicz, Stan
Simon, Jeffrey S.
Sheehan, David V.
Thase, Michael E.
Carpenter, David J.
Plott, Susan J.
Nemeroff, Charles B.
TI Estimates of Serotonin and Norepinephrine Transporter Inhibition in
Depressed Patients Treated with Paroxetine or Venlafaxine
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE antidepressant; transporters; reuptake; occupancy; depression; SSRI
ID REUPTAKE INHIBITORS; CEREBROSPINAL-FLUID; DOUBLE-BLIND; RESISTANT
DEPRESSION; CLINICAL-RESPONSE; MAJOR DEPRESSION; BINDING PROFILE;
PLASMA-LEVELS; ANTIDEPRESSANTS; METABOLITES
AB Paroxetine and venlafaxine are potent serotonin transporter (SERT) antagonists and weaker norepinephrine transporter ( NET) antagonists. However, the relative magnitude of effect at each of these sites during treatment is unknown. Using a novel blood assay that estimates CNS transporter occupancy we estimated the relative SERT and NET occupancy of paroxetine and venlafaxine in human subjects to assess the relative magnitude of SERT and NET inhibition. Outpatient subjects (N = 86) meeting criteria for major depression were enrolled in a multicenter, 8 week, randomized, double-blind, parallel group, antidepressant treatment study. Subjects were treated by forced-titration of paroxetine CR (12.5-75 mg/day) or venlafaxine XR (75-375 mg/day) over 8 weeks. Blood samples were collected weekly to estimate transporter inhibition. Both medications produced dose-dependent inhibition of the SERT and NET. Maximal SERT inhibition at week 8 for paroxetine and venlafaxine was 90% (SD 7) and 85% ( SD 10), respectively. Maximal NET inhibition for paroxetine and venlafaxine at week 8 was 36% ( SD 19) and 60% ( SD 13), respectively. The adjusted mean change from baseline ( mean 28.6) at week 8 LOCF in MADRS total score was -16.7 ( SE 8.59) and -17.3 ( SE 8.99) for the paroxetine and venlafaxine-treated patients, respectively. The magnitudes of the antidepressant effects were not significantly different from each other (95% CI - 3.42, 4.54, p = 0.784). The results clearly demonstrate that paroxetine and venlafaxine are potent SERT antagonists and less potent NET antagonists in vivo. NET antagonism has been posited to contribute to the antidepressant effects of these compounds. The clinical significance of the magnitude of NET antagonism by both medications remains unclear at present.
C1 [Owens, Michael J.; Plott, Susan J.; Nemeroff, Charles B.] Emory Univ, Dept Psychiat & Behav Sci, Sch Med, Lab Neuropsychopharmacol, Atlanta, GA 30322 USA.
[Krulewicz, Stan; Carpenter, David J.] GlaxoSmithKline Inc, Neurosci Med Dev Ctr, Clin Psychiat N Amer, King Of Prussia, PA USA.
[Simon, Jeffrey S.] Northbrooke Res Ctr, Brown Deer, WI USA.
[Sheehan, David V.] Univ S Florida, Dept Psychiat, Tampa, FL USA.
[Thase, Michael E.] Univ Penn, Philadelphia Vet Affairs Med Ctr, Dept Psychiat, Philadelphia, PA 19104 USA.
RP Owens, MJ (reprint author), Emory Univ, Dept Psychiat & Behav Sci, Sch Med, Lab Neuropsychopharmacol, 101 Woodruff Circle,Suite 4000, Atlanta, GA 30322 USA.
EM mowens@emory.edu
RI Owens, Michael/G-5191-2012
FU GlaxoSmithKline; NIH [MH-77083, MH-69056, MH-58922, MH-42088, MH-39415,
MH-68036]
FX We thank Drs Raj Rajani, Murray Rosenthal, and Nicholas Vatakis for
their contribution to this study. We also acknowledge Peter Gething, B.
S. at INC Research and Mary Kelley, Ph. D ( Departments of Psychiatry
and Behavioral Sciences and Biostatistics, Emory University) for
performing the statistical analyses and Kathy Sheehan, Ph. D. (
Department of Psychiatry, University of South Florida) for the post hoc
MADRS response and remission analyses. This work was supported by a
collaborative research grant to MJO from GlaxoSmithKline. The authors
are also supported by NIH MH-77083, MH-69056, MH-58922, MH-42088,
MH-39415, and MH-68036.
NR 43
TC 32
Z9 33
U1 1
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD DEC
PY 2008
VL 33
IS 13
BP 3201
EP 3212
DI 10.1038/npp.2008.47
PG 12
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 370GP
UT WOS:000260751000021
PM 18418363
ER
PT J
AU Forghani, R
Farb, RI
AF Forghani, R.
Farb, R. I.
TI Diagnosis and temporal evolution of signs of intracranial hypotension on
MRI of the brain
SO NEURORADIOLOGY
LA English
DT Article
DE Intracranial hypotension; Intracranial hypovolemia; MRI; FLAIR
ID CEREBROSPINAL-FLUID LEAKS; CERVICAL EPIDURAL VEINS; THUNDERCLAP
HEADACHE; POSTURAL HEADACHE; MANAGEMENT; PRESSURE; HYPOVOLEMIA; FEATURES
AB Introduction A comprehensive evaluation of cranial magnetic resonance imagings (MRIs) of 23 patients with intracranial hypotension (IH) was performed, and the evolution of the abnormalities on follow-up MRIs was correlated with the clinical outcome.
Materials and methods The MRI report database at the University Health Network in Toronto was searched, and 23 cases of IH were identified between 2001 and 2007. A retrospective review of the MRIs of the brain and the electronic patient chart was performed. A control group of 40 subjects was also selected to complement the analysis of the pituitary gland.
Results A positive venous distention sign (VDS) was observed in 23 out of 23 patients and was the first sign to disappear on early follow-up scans following successful treatment. Pachymeningeal enhancement was seen in 23 out of 23 patients, and pachymeningeal thickening was detectable on unenhanced fluid attenuation inversion recovery (FLAIR) sequences in 17 out of 23 patients (74%). An increase in pituitary size in IH was also demonstrated based on the measured pituitary height and was qualitatively detectable in 12 out of 21 (57%) patients as the protrusion of the pituitary gland above the sella turica (two postpartum patients were excluded from this analysis). Overall, there was good correlation between the imaging findings and clinical outcome following treatment.
Conclusion Accurate diagnosis and follow-up of IH should be possible is some patients on unenhanced MRI of the brain by combining the signs on FLAIR and sagittal T1W images, enabling timely diagnosis in unsuspected cases and avoiding unnecessary administration of gadolinium compounds. In addition, VDS might be useful for early assessment of response to treatment.
C1 [Forghani, R.] McGill Univ, Ctr Hlth, Dept Radiol, Montreal, PQ, Canada.
[Farb, R. I.] Univ Toronto, Toronto Western Hosp, Dept Med Imaging, Div Neuroradiol, Toronto, ON M5T 2S8, Canada.
RP Forghani, R (reprint author), Massachusetts Gen Hosp, Div Neuroradiol, Gray 273A-55 Fruit St, Boston, MA 02114 USA.
EM rforghani@partners.org
NR 34
TC 23
Z9 23
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0028-3940
J9 NEURORADIOLOGY
JI Neuroradiology
PD DEC
PY 2008
VL 50
IS 12
BP 1025
EP 1034
DI 10.1007/s00234-008-0445-z
PG 10
WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 385CS
UT WOS:000261791300005
PM 18795275
ER
PT J
AU McInerney, PA
Ncama, BP
Wantland, D
Bhengu, BR
McGibbon, C
Davis, SM
Corless, IB
Nicholas, PK
AF McInerney, Patricia A.
Ncama, Busisiwe P.
Wantland, Dean
Bhengu, Busisiwe R.
McGibbon, Chris
Davis, Sheila M.
Corless, Inge B.
Nicholas, Patrice K.
TI Quality of life and physical functioning in HIV-infected individuals
receiving antiretroviral therapy in KwaZulu-Natal, South Africa
SO NURSING & HEALTH SCIENCES
LA English
DT Article
DE adherence; HIV; AIDS; quality of life
ID HEALTH SURVEY SF-36; SUB-SAHARAN AFRICA; MEDICATION ADHERENCE;
DRUG-RESISTANCE; TUBERCULOSIS; METAANALYSIS; OUTCOMES; PROGRAM
AB KwaZulu-Natal province, South Africa, accounts for 28.7% of the HIV infection total and one-third of infections among youth and children in South Africa. The purpose of this study was to examine the variables of HIV/AIDS symptoms, social support, influence of comorbid medical problems, length of time adhering to antiretroviral therapy medications, quality of life, adherence to antiretroviral medications, and physical functioning in HIV-infected individuals. Based on our model, the combination of these variables was found to determine physical functioning outcomes and adherence to HIV medications. Significant relationships were observed between physical functioning and the dependent variables of length of time on medications, comorbid health problems, and social support. A linear regression model was built to determine the degree to which these variables predicted physical functioning. In total, these predictor variables explained 29% of the variance in physical functioning. These results indicate that those individuals who reported a greater length of time on medications, fewer comorbid health problems, and greater social support had better physical functioning.
C1 [McInerney, Patricia A.; Ncama, Busisiwe P.; Bhengu, Busisiwe R.] Univ KwaZulu Natal, Sch Nursing, Durban, South Africa.
[Wantland, Dean] Univ Calif San Francisco, Sch Nursing, San Francisco, CA 94143 USA.
[Davis, Sheila M.] Massachusetts Gen Hosp, MGH Inst Hlth Profess, Dept Infect Dis, Boston, MA 02114 USA.
[Corless, Inge B.; Nicholas, Patrice K.] Massachusetts Gen Hosp, MGH Inst Hlth Profess, Grad Program Nursing, Boston, MA 02114 USA.
[Nicholas, Patrice K.] Brigham & Womens Hosp, Ctr Nursing Excellence, Div Social Med & Hlth Inequal, Boston, MA 02115 USA.
[McGibbon, Chris] Univ New Brunswick, Dept Kinesiol, Fredericton, NB, Canada.
RP Nicholas, PK (reprint author), 1 Brigham Circle,4th Floor,Suite 6, Boston, MA USA.
EM pnicholas@partners.org
OI Corless, Inge/0000-0003-0438-2037
NR 23
TC 12
Z9 12
U1 1
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1441-0745
J9 NURS HEALTH SCI
JI Nurs. Health Sci.
PD DEC
PY 2008
VL 10
IS 4
BP 266
EP 272
DI 10.1111/j.1442-2018.2008.00410.x
PG 7
WC Nursing
SC Nursing
GA 369CW
UT WOS:000260672100007
PM 19128302
ER
PT J
AU Aguirre, V
Stylopoulos, N
Grinbaum, R
Kaplan, LM
AF Aguirre, Vincent
Stylopoulos, Nicholas
Grinbaum, Ronit
Kaplan, Lee M.
TI An Endoluminal Sleeve Induces Substantial Weight Loss and Normalizes
Glucose Homeostasis in Rats with Diet-Induced Obesity
SO OBESITY
LA English
DT Article
ID JEJUNAL BYPASS SLEEVE; BETA-CELL FUNCTION; Y GASTRIC BYPASS;
FOOD-INTAKE; BARIATRIC SURGERY; BODY-WEIGHT; ILEAL TRANSPOSITION;
PORCINE MODEL; ELECTRICAL-STIMULATION; ENERGY-BALANCE
AB To investigate the contributions of two surgical gut manipulations-exclusion of the proximal intestine from alimentary flow and exposure of the jejunum to partially digested nutrients-to body weight regulation and metabolism, we have developed a rat model of an investigational device, the endoluminal sleeve (ELS). The ELS is a 10 cm, nutrient-impermeable, flexible tube designed for endoluminal implantation. ELS devices were surgically implanted in the duodenal bulb of rats with diet-induced obesity. Body weight, food intake, stool caloric content, and glucose homeostasis were subsequently evaluated. ELS-implanted rats demonstrated a 20% reduction of body weight compared to sham-operated (SO) controls. ELS-treated animals consumed an average of 27% fewer kcal/day than SO, and there was no evidence of malabsorption. ELS treatment improved fasting glycemia and glucose tolerance after oral and intraperitoneal (IP) administration. ELS treatment enhanced insulin sensitivity, as demonstrated by decreased fasting and glucose-stimulated insulin levels and confirmed by calculation of homeostasis model assessment of insulin resistance (IR). These data suggest that selective bypass of the proximal intestine by ELS, with enhanced delivery of partially digested nutrients to the jejunum, mimics many of the effects of Roux-en-Y gastric bypass (RYGB) on body weight and glucose metabolism. Thus, ELS implantation may be an effective treatment for obesity and diabetes. Since the ELS device is amenable to endoscopic placement, it may offer a valuable alternative to more invasive surgical approaches in selected patients with obesity and its metabolic complications.
C1 [Aguirre, Vincent; Stylopoulos, Nicholas; Grinbaum, Ronit; Kaplan, Lee M.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[Aguirre, Vincent; Stylopoulos, Nicholas; Grinbaum, Ronit; Kaplan, Lee M.] Massachusetts Gen Hosp, MGH Weight Ctr, Boston, MA 02114 USA.
[Aguirre, Vincent; Stylopoulos, Nicholas; Grinbaum, Ronit; Kaplan, Lee M.] Harvard Univ, Sch Med, Boston, MA USA.
RP Kaplan, LM (reprint author), Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
EM lmkaplan@partners.org
FU National Institutes of Health [DK057478, DK046200, DK043351]; GI
Dynamics (Watertown, MA); [DK007191]; [HD052961]
FX We thank Andy Levine for invaluable help in the development of the rat
ELS model and Philip Davis and Lynn Wartschaw for excellent technical
assistance. We also thank Morris White and Daniel Podolsky for their
helpful review of the manuscript. These studies were supported by
National Institutes of Health grants DK057478, DK046200, DK043351 (to
L.M.K.); training awards DK007191 (to V.A.) and HD052961 (to N.S.); and
a research grant from GI Dynamics (Watertown, MA).
NR 39
TC 56
Z9 60
U1 1
U2 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD DEC
PY 2008
VL 16
IS 12
BP 2585
EP 2592
DI 10.1038/oby.2008.502
PG 8
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 379OJ
UT WOS:000261405800004
PM 19279655
ER
PT J
AU Lara-Castro, C
Doud, EC
Tapia, PC
Munoz, AJ
Fernandez, JR
Hunter, GR
Gower, BA
Garvey, WT
AF Lara-Castro, Cristina
Doud, Erin C.
Tapia, Patrick C.
Munoz, Andres J.
Fernandez, Jose R.
Hunter, Gary R.
Gower, Barbara A.
Garvey, W. Timothy
TI Adiponectin Multimers and Metabolic Syndrome Traits: Relative
Adiponectin Resistance in African Americans
SO OBESITY
LA English
DT Article
ID HIGH-MOLECULAR-WEIGHT; INSULIN SENSITIVITY; GENETIC ADMIXTURE; WAIST
CIRCUMFERENCE; SERUM ADIPONECTIN; FAT DISTRIBUTION; RISK-FACTORS;
PLASMA; PIOGLITAZONE; ASSOCIATIONS
AB African Americans (AAs) tend to have lower total adiponectin levels compared to European Americans (EA); however, it is not known whether race affects adiponectin multimer distribution and their relationships to metabolic traits. We measured total adiponectin, high molecular weight (HMW), low molecular weight (LMW) (i.e., hexamer), and trimer adiponectin in 132 normoglycemic premenopausal women (75 AAs, 57 EAs), together with measures of total and abdominal fat, plasma lipids, insulin sensitivity (S(i)), and genetic admixture estimates. We found that lower total adiponectin in AAs was explained by reduced LMW, and trimer forms because levels of HMW did not differ between races. In EAs, HMW was highly correlated with multiple metabolic syndrome traits. In contrast, the LMW and trimer forms were most highly correlated with metabolic traits in AAs, including abdominal adiposity, lipids, and S(i). At similar levels of visceral adiposity, AAs exhibited significantly lower LMW adiponectin than EAs. Similarly, at comparable levels of HMW and LMW adiponectin, AAs were more insulin resistant than their EA counterparts. In conclusion, (i) serum adiponectin is lower in AAs predominantly as a result of reduced concentrations of LMW and trimers multimeric forms; (ii) LMW and trimer, not HMW, are most broadly correlated with metabolic traits in AAs. Thus, HMW adiponectin may exert less bioactivity in explaining the metabolic syndrome trait cluster in populations of predominant African genetic background.
C1 [Lara-Castro, Cristina; Doud, Erin C.; Tapia, Patrick C.; Munoz, Andres J.; Fernandez, Jose R.; Hunter, Gary R.; Gower, Barbara A.; Garvey, W. Timothy] Univ Alabama, Dept Nutr Sci, Birmingham, AL 35294 USA.
[Garvey, W. Timothy] Birmingham Vet Affairs Med Ctr, Birmingham, AL USA.
RP Lara-Castro, C (reprint author), Univ Alabama, Dept Nutr Sci, Birmingham, AL 35294 USA.
EM larac@uab.edu
FU NIH [DK 49779, DK51684, DK-38764, PO1 HL-55782]; UAB GCRC [M01-RR00032];
CNRU [P30-DK56336]; T32 grant [HL-007457]; Merit Review program of the
Department of Veterans Affairs; Nestle Food Co
FX We thank our sources of support: the NIH grants DK 49779, DK51684,
DK-38764, and PO1 HL-55782, the UAB GCRC M01-RR00032, the CNRU
(P30-DK56336), the T32 grant (HL-007457) (PI: S. Oparil), and the Merit
Review program of the Department of Veterans Affairs. We also
acknowledge support from Nestle Food Co. for providing Stouffer's Lean
Cuisine entrees.
NR 44
TC 23
Z9 24
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD DEC
PY 2008
VL 16
IS 12
BP 2616
EP 2623
DI 10.1038/oby.2008.411
PG 8
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 379OJ
UT WOS:000261405800008
PM 18820653
ER
PT J
AU Chonghaile, TN
Letai, A
AF Chonghaile, T. Ni
Letai, A.
TI Mimicking the BH3 domain to kill cancer cells
SO ONCOGENE
LA English
DT Review
DE BH3 mimetic; Bcl-2; apoptosis; cancer; drug resistance and ABT-737
ID OUTER MITOCHONDRIAL-MEMBRANE; CHRONIC LYMPHOCYTIC-LEUKEMIA;
SMALL-MOLECULE INHIBITOR; BCL-2 FAMILY PROTEINS; SURVIVAL-PROMOTING
PROTEINS; MIMETIC ABT-737; CYTOCHROME-C; X-L; PROAPOPTOTIC ACTIVITY;
ANTIAPOPTOTIC BCL-2
AB Cancer cells show deviant behavior that induces apoptotic signaling. To survive, cancer cells typically acquire changes enabling evasion of death signals. One way they do this is by increasing the expression of anti- apoptotic BCL-2 proteins. Anti-apoptotic BCL-2 family proteins antagonize death signaling by forming heterodimers with pro-death proteins. Heterodimer formation occurs through binding of the pro-apoptotic protein's BH3 domain into the hydrophobic cleft of anti- apoptotic proteins. The BH3 mimetics are small molecule antagonists of the anti- apoptotic BCL-2 members that function as competitive inhibitors by binding to the hydrophobic cleft. Under certain conditions, antagonism of antiapoptotic BCL-2 family proteins can unleash pro-death molecules in cancer cells. Thus, the BH3 mimetics are a new class of cancer drugs that specifically target a mechanism of cancer cell survival to selectively kill cancer cells. Oncogene (2009) 27, S149-S157; doi: 10.1038/onc.2009.52
C1 [Chonghaile, T. Ni; Letai, A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Letai, A (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Dana 530B,44 Binney St, Boston, MA 02115 USA.
EM anthony_letai@dfci.harvard.edu
RI Ni Chonghaile, Triona/L-9418-2015
OI Ni Chonghaile, Triona/0000-0002-3041-4031
NR 93
TC 105
Z9 105
U1 2
U2 14
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD DEC
PY 2008
VL 27
SU 1
BP S149
EP S157
DI 10.1038/onc.2009.52
PG 9
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA 478DA
UT WOS:000268566800013
ER
PT J
AU Danial, NN
AF Danial, N. N.
TI BAD: undertaker by night, candyman by day
SO ONCOGENE
LA English
DT Review
DE BAD; apoptosis; metabolism; survival signaling
ID BCL-X-L; DEPENDENT PROTEIN-KINASE; CULTURED HIPPOCAMPAL-NEURONS; HUMAN
PANCREATIC-ISLETS; PROMOTES CELL-SURVIVAL; CYTOCHROME-C RELEASE;
DNA-DAMAGE RESPONSE; DEATH AGONIST BAD; GROWTH-FACTOR-II; BETA-CELLS
AB The BH3-only pro-apoptotic proteins are upstream sensors of cellular damage that selectively respond to specific, proximal death and survival signals. Genetic models and biochemical studies indicate that these molecules are latent killers until activated through transcriptional or post-translational mechanisms in a tissue-restricted and signal-specific manner. The large number of BH3-only proteins, their unique subcellular localization, protein-interaction network and diverse modes of activation suggest specialization of their damage-sensing function, ensuring that the core apoptotic machinery is poised to receive input from a wide range of cellular stress signals. The apoptotic response initiated by the activation of BH3-only proteins ultimately culminates in allosteric activation of pro-apoptotic BAX and BAK, the gateway proteins to the mitochondrial pathway of apoptosis. From activation of BH3-only proteins to oligomerization of BAX and BAK and mitochondrial outer membrane permeabilization, an intricate network of interactions between the pro-and anti-apoptotic members of the BCL-2 family orchestrates the decision to undergo apoptosis. Beyond regulation of apoptosis, multiple BCL-2 proteins have recently emerged as active components of select homeostatic pathways carrying other cellular functions. This review focuses on BAD, which was the first BH3-only protein linked to proximal survival signals through phosphorylation by survival kinases. In addition to findings that delineated the physiological role of BAD in apoptosis and its dynamic regulation by phosphorylation, studies pointing to new roles for this protein in other physiological pathways, such as glucose metabolism, are highlighted. By executing its 'day' and 'night' jobs in metabolism and apoptosis, respectively, BAD helps coordinate mitochondrial fuel metabolism and the apoptotic machinery. Oncogene (2009) 27, S53-S70; doi: 10.1038/onc.2009.44
C1 [Danial, N. N.] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
[Danial, N. N.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
RP Danial, NN (reprint author), Dana Farber Canc Inst, Dept Canc Biol, 3 Blackfan Circle,CLSB 11-143, Boston, MA 02115 USA.
EM nika_danial@dfci.harvard.edu
FU National Cancer Institute (NCI, Rockville, MD, USA) [5 K01 CA106596-02];
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK,
Bethesda, MD, USA) [R01 DK078081-01]; Iacocca Foundation ( Boston, MA,
USA); Juvenile Diabetes Research Foundation (JDRF, London, UK); Novartis
(Basel, Switzerland); DFCI/Novartis Drug Discovery Program
FX NN Danial iscurrent ly receiving grant support from the National Cancer
Institute (NCI, Rockville, MD, USA) (5 K01 CA106596-02), the National
Institute of Diabetes and Digestive and Kidney Diseases (NIDDK,
Bethesda, MD, USA) (R01 DK078081-01), the Iacocca Foundation ( Boston,
MA, USA) and the Juvenile Diabetes Research Foundation (JDRF, London,
UK). The author is also in receipt of a grant from Novartis ( Basel,
Switzerland) as part of the DFCI/Novartis Drug Discovery Program and has
a Career Award in the Biomedical Sciences from the Burroughs Wellcome
Fund (Durham, NC, USA). NN Danial is a consultant/an advisor for the
Novartis Institute for Biomedical Research (NIBR, Cambridge, MA, USA).
NR 176
TC 119
Z9 120
U1 0
U2 9
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD DEC
PY 2008
VL 27
BP S53
EP S70
DI 10.1038/onc.2009.44
PG 18
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA 478DA
UT WOS:000268566800005
PM 19641507
ER
PT J
AU Stipp, RN
Goncalves, RB
Hofling, JF
Smith, DJ
Mattos-Graner, RO
AF Stipp, R. N.
Goncalves, R. B.
Hofling, J. F.
Smith, D. J.
Mattos-Graner, R. O.
TI Transcriptional analysis of gtfB, gtfC, and gbpB and their putative
response regulators in several isolates of Streptococcus mutans
SO ORAL MICROBIOLOGY AND IMMUNOLOGY
LA English
DT Article
DE gene expression; genetic diversity; glucan-binding protein;
glucosyltransferase; Streptococcus mutans; two-component system
ID GLUCAN-BINDING PROTEINS; BIOFILM FORMATION; COMPETENCE DEVELOPMENT;
GENETIC COMPETENCE; GLUCOSYLTRANSFERASE; EXPRESSION; DIVERSITY; STRAINS;
SYSTEM; GROWTH
AB Background: Streptococcus mutans, a major dental caries pathogen, expresses several virulence genes that mediate its growth, accumulation on tooth surfaces, and acid-mediated tooth demineralization. GtfB and GtfC catalyze the extracellular synthesis of water-insoluble glucan matrix from sucrose, and are essential for accumulation of bacteria in the dental biofilm. GbpB, an essential protein of S. mutans, might also mediate cell-surface interaction with glucan.
Methods: In this study, we determined the transcription levels of gtfB, gtfC, and gbpB, and several putative transcriptional response regulators (rr) at different phases of planktonic growth in 11 S. mutans strains.
Aim/Methods: Activities of gtfB and gtfC were growth-phase dependent and assumed divergent patterns in several strains during specific phases of growth, while gbpB activities appeared to be under modest influence of the growth phase. Transcription patterns of the rr vicR, covR, comE, ciaR, and rr1 were growth-phase dependent and some of these genes were expressed in a highly coordinated way. Each rr, except comE, was expressed by all the strains. Patterns of virulence and regulatory genes were, however, strain-specific.
Conclusions: The findings suggest that mechanisms controlling virulence gene expression are variable among genotypes, providing the notion that the genetic diversity of S. mutans may have important implications for understanding mechanisms that regulate the expression of virulence genes in this species.
C1 [Stipp, R. N.; Goncalves, R. B.; Hofling, J. F.; Mattos-Graner, R. O.] Univ Estadual Campinas, Dept Microbiol & Immunol, Piracicaba Dent Sch, Campinas, SP, Brazil.
[Smith, D. J.] Forsyth Inst, Dept Immunol, Boston, MA USA.
RP Mattos-Graner, RO (reprint author), Univ Estadual Campinas, Dept Microbiol & Imunol, Fac Odontol Piracicaba, Av Limeira 901, BR-13414018 Piracicaba, SP, Brazil.
EM rmgraner@fop.unicamp.br
RI Mattos-Graner, Renata/C-9410-2012
OI Mattos-Graner, Renata/0000-0001-8309-8135
FU Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)
[02/07156-1, 03/01836-3, 04/03242-6]; NIH-Fogarty [TW-06324]
FX This study was supported by Fundacao de Amparo a Pesquisa do Estado de
Sao Paulo (FAPESP, grant 02/07156-1). R.O.M-G is supported by FAPESP
(proc. 03/01836-3). R.N.S. was supported by FAPESP (proc. 04/03242-6)
and NIH-Fogarty TW-06324. We thank Drs Edgard Graner and Michelle
Agostini (FOP-UNI-CAMP, SP, Brazil) for assistance with the
semi-quantitative RT-PCR analysis, and Dr Siu Mui Tsai (CENA/ESALQ-USP,
SP, Brazil) for assistance with the sequence analysis.
NR 38
TC 18
Z9 19
U1 1
U2 7
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0902-0055
J9 ORAL MICROBIOL IMMUN
JI Oral Microbiol. Immunol.
PD DEC
PY 2008
VL 23
IS 6
BP 466
EP 473
DI 10.1111/j.1399-302X.2008.00451.x
PG 8
WC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology
SC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology
GA 360JI
UT WOS:000260053400005
PM 18954352
ER
PT J
AU Isenbarger, TA
Carr, CE
Johnson, SS
Finney, M
Church, GM
Gilbert, W
Zuber, MT
Ruvkun, G
AF Isenbarger, Thomas A.
Carr, Christopher E.
Johnson, Sarah Stewart
Finney, Michael
Church, George M.
Gilbert, Walter
Zuber, Maria T.
Ruvkun, Gary
TI The Most Conserved Genome Segments for Life Detection on Earth and Other
Planets
SO ORIGINS OF LIFE AND EVOLUTION OF BIOSPHERES
LA English
DT Article
DE Polymerase chain reaction; DNA; RNA; Ribosome; Panspermia; Mars
ID WATER RESERVOIRS; COMMON ANCESTOR; MARS; METEORITE; PCR; SEQUENCES;
EVOLUTION; TRANSPORTER; DIVERSITY; PHYLOGENY
AB On Earth, very simple but powerful methods to detect and classify broad taxa of life by the polymerase chain reaction (PCR) are now standard practice. Using DNA primers corresponding to the 16S ribosomal RNA gene, one can survey a sample from any environment for its microbial inhabitants. Due to massive meteoritic exchange between Earth and Mars (as well as other planets), a reasonable case can be made for life on Mars or other planets to be related to life on Earth. In this case, the supremely sensitive technologies used to study life on Earth, including in extreme environments, can be applied to the search for life on other planets. Though the 16S gene has become the standard for life detection on Earth, no genome comparisons have established that the ribosomal genes are, in fact, the most conserved DNA segments across the kingdoms of life. We present here a computational comparison of full genomes from 13 diverse organisms from the Archaea, Bacteria, and Eucarya to identify genetic sequences conserved across the widest divisions of life. Our results identify file 16S and 23S ribosomal RNA genes as well as other universally conserved nucleotide sequences in genes encoding particular classes of transfer RNAs and within the nucleotide binding domains of ABC transporters as the most conserved DNA sequence segments across phylogeny. This set of sequences defines a core set of DNA regions that have changed the least over billions of years of evolution and provides a means to identify and classify divergent life, including ancestrally related life on other planets.
C1 [Isenbarger, Thomas A.; Finney, Michael; Ruvkun, Gary] Massachusetts Gen Hosp, Dept Mol Biol, Cambridge, MA USA.
[Isenbarger, Thomas A.; Finney, Michael; Ruvkun, Gary] Harvard Univ, Microbial Sci Initiat, Cambridge, MA 02138 USA.
[Carr, Christopher E.; Johnson, Sarah Stewart; Zuber, Maria T.] MIT, Dept Earth Atmospher & Planetary Sci, Cambridge, MA USA.
[Church, George M.] Harvard Univ, Sch Med, Dept Genet, Cambridge, MA 02138 USA.
[Gilbert, Walter] Harvard Univ, Dept Mol & Cellular Biol, Cambridge, MA 02138 USA.
RP Ruvkun, G (reprint author), Massachusetts Gen Hosp, Dept Mol Biol, Cambridge, MA USA.
EM ruvkun@molbio.mgh.harvard.edu
OI Carr, Christopher/0000-0002-7946-5622
FU National Aeronautics and Space Administration [NNG05GK27G]
FX TAI thanks Professor Jo Handelsman for support during the preparation of
this manuscript, Ilya Ruvinsky and members of the Ruvkun laboratory for
helpful comments and review of the manuscript, Lance Davidow for
assistance with computing resources, and Qinghu Ren at TIGR for helpful
discussions regarding ABC transporters. This work was funded by National
Aeronautics and Space Administration grant NNG05GK27G.
NR 55
TC 22
Z9 22
U1 4
U2 13
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0169-6149
J9 ORIGINS LIFE EVOL B
JI Orig. Life Evol. Biosph.
PD DEC
PY 2008
VL 38
IS 6
BP 517
EP 533
DI 10.1007/s11084-008-9148-z
PG 17
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA 403FD
UT WOS:000263067600005
PM 18853276
ER
PT J
AU Price, DL
Wong, RJ
Randolph, GW
AF Price, Daniel L.
Wong, Richard J.
Randolph, Gregory W.
TI Invasive Thyroid Cancer: Management of the Trachea and Esophagus
SO OTOLARYNGOLOGIC CLINICS OF NORTH AMERICA
LA English
DT Article
ID RECURRENT LARYNGEAL NERVE; EXTERNAL-BEAM RADIOTHERAPY; PAPILLARY
CARCINOMA; AIRWAY INVASION; DIFFERENTIATED CARCINOMA; LARYNGOTRACHEAL
INVASION; RESECTIONAL MANAGEMENT; SURGICAL-MANAGEMENT; RISK;
ULTRASONOGRAPHY
AB Well-differentiated thyroid cancer most commonly presents as an intrathyroidal tumor; however, extrathyroidal extension occurs in approximately 6% to 13% of patients and carries a significant negative impact on survival. Extrathyroidal disease may involve critical structures in the central neck, including the recurrent laryngeal nerves, trachea, esophagus, and larynx, requiring surgery extending significantly beyond the thyroid gland. Appropriate surgical management is of great importance and can normalize survival curves, whereas gross residual disease postoperatively may lead to recurrence and decreased survival. Adjuvant postoperative therapies for thyroid cancers with extrathyroidal extension include thyroid hormone suppression, radioactive iodine therapy, and external beam radiotherapy. This summary reviews approaches to the management of invasive thyroid cancers involving the aerodigestive tract.
C1 [Price, Daniel L.; Wong, Richard J.] Mem Sloan Kettering Canc Ctr, Dept Surg, Head & Neck Serv, New York, NY 10065 USA.
[Randolph, Gregory W.] Massachusetts Gen Hosp, Massachusetts Eye & Ear Infirm, Endocrine Surg Serv, Thyroid & Parathyroid Surg Div, Boston, MA 02114 USA.
[Randolph, Gregory W.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Price, DL (reprint author), Mem Sloan Kettering Canc Ctr, Dept Surg, Head & Neck Serv, 1275 York Ave, New York, NY 10065 USA.
EM Priced12@mskcc.org
OI Price, Daniel/0000-0003-3398-0562
FU NCI NIH HHS [T32 CA009685, T32 CA009685-17]
NR 64
TC 17
Z9 20
U1 1
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0030-6665
J9 OTOLARYNG CLIN N AM
JI Otolaryngol. Clin. N. Am.
PD DEC
PY 2008
VL 41
IS 6
BP 1155
EP +
DI 10.1016/j.otc.2008.08.002
PG 16
WC Otorhinolaryngology
SC Otorhinolaryngology
GA 390PV
UT WOS:000262177100010
PM 19040976
ER
PT J
AU Nadol, JB
Eddington, DK
Burgess, BJ
AF Nadol, Joseph B., Jr.
Eddington, Donald K.
Burgess, Barbara J.
TI Foreign Body or Hypersensitivity Granuloma of the inner Ear After
Cochlear Implantation: One Possible Cause of a Soft Failure?
SO OTOLOGY & NEUROTOLOGY
LA English
DT Article
DE Cochlear implant; Granuloma; Histopathology of ear; Soft failure
ID SILICONE ALLERGY; MALFUNCTION
AB Hypothesis: A tissue response in the form of foreign body or a hypersensitivity reaction to cochlear implantation is common and may be one possible cause of a soft failure of cochlear implantation.
Background: After a successful cochlear implantation, delayed failure may occur. The causes of a "soft" failure, that is, one in which device malfunction cannot be proven, are unknown.
Methods: The histopathology of the temporal bones of a patient who, in life, had experienced a soft failure after cochlear implantation was described. In addition, the temporal bones of 8 other subjects who, in life, had undergone cochlear implantation were studied for evidence of a foreign body or hypersensitivity reaction.
Results: In the case report, a necrotizing granulomatous giant cell reaction surrounded the cochlear implant electrode track through the mastoid and the middle ear and into the cochlea in both ears. There was osteolysis of the cribrose area, otic capsule, and bone between the facial nerve and the cochlea and destruction of the organ of Corti and spiral ganglion. In the additional 8 cases studied, a similar, although less pronounced, foreign body or hypersensitivity reaction was seen in 6 (75%) of the cases.
Conclusion: A foreign body or hypersensitivity reaction in the form of giant cells and lymphocytic cell infiltration is common after cochlear implantation and may be one possible cause of soft failure.
C1 [Nadol, Joseph B., Jr.; Eddington, Donald K.; Burgess, Barbara J.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Otol & Laryngol, Boston, MA 02114 USA.
RP Nadol, JB (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Otol & Laryngol, 243 Charles St, Boston, MA 02114 USA.
EM joseph_nadol@meei.harvard.edu
FU National Institutes of Health/National Institute on Deafness and Other
Communication [R01 DC000152]
FX This study was supported by Grant R01 DC000152 from the National
Institutes of Health/National Institute on Deafness and Other
Communication Disorders.
NR 26
TC 16
Z9 17
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1531-7129
J9 OTOL NEUROTOL
JI Otol. Neurotol.
PD DEC
PY 2008
VL 29
IS 8
BP 1076
EP 1084
DI 10.1097/MAO.0b013e31818c33cf
PG 9
WC Clinical Neurology; Otorhinolaryngology
SC Neurosciences & Neurology; Otorhinolaryngology
GA 379LH
UT WOS:000261397200005
PM 18997635
ER
PT J
AU Yang, LL
Wang, SX
Lim, G
Sung, B
Zeng, Q
Mao, JR
AF Yang, Liling
Wang, Shuxing
Lim, Grewo
Sung, Backil
Zeng, Qing
Mao, Jianren
TI Inhibition of the ubiquitin-proteasome activity prevents glutamate
transporter degradation and morphine tolerance
SO PAIN
LA English
DT Article
DE Glutamate transporter; EAAC1; GLAST; GLT-1; Morphine tolerance; MG-132
ID ABNORMAL PAIN SENSITIVITY; SPINAL-CORD; RECEPTOR ANTAGONIST; NEUROPATHIC
PAIN; CELL-DEATH; RATS; EXPRESSION; SYSTEM; HYPERALGESIA; DEPENDENCE
AB Glutamate transporters play a Crucial role in physiological glutamate homeostasis and neurotoxicity. Recently, we have shown that downregulation of glutamate transporters after chronic morphine exposure contributed to the development of morphine tolerance. In the present study, we examined whether regulation of the glutamate transporter expression with the proposed proteasome inhibitor MG-132 would contribute to the development of tolerance to repeated intrathecal (twice daily x 7 days) morphine administration in rats. The results showed that MG-132 (5 nmol) given intrathecally blocked morphine-induced glutamate transporter downregulation and the decrease in glutamate uptake activity within the spinal cord dorsal horn. Co-administration of morphine (15 nmol) with MG-132 (vehicle = 1 < 2.5 < 5 = 10 nmol) also dose-dependently prevented the development of morphine tolerance in rats. These findings suggest that prevention of spinal glutamate transporter downregulation may regulate the glutamatergic function that has been implicated in the development of morphine tolerance. The possible relationship between MG-132-mediated regulation of glutamate transporters, ubiquitin-proteasome system, and the cellular Mechanisms of morphine tolerance is discussed in light of these findings. (C) 2008 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
C1 [Yang, Liling; Wang, Shuxing; Lim, Grewo; Sung, Backil; Zeng, Qing; Mao, Jianren] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Anesthesia & Crit Care,MGH Ctr Translat Pain, Boston, MA 02114 USA.
RP Mao, JR (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Anesthesia & Crit Care,MGH Ctr Translat Pain, WACC 324,15 Parkman St, Boston, MA 02114 USA.
EM jmao@partners.org
FU US PHS RO1 [DE 18214, DE18538, NS45681]
FX This work was supported by US PHS RO1 Grants DE 18214, DE18538, and
NS45681.
NR 31
TC 15
Z9 16
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-3959
J9 PAIN
JI Pain
PD DEC
PY 2008
VL 140
IS 3
BP 472
EP 478
DI 10.1016/j.pain.2008.09.028
PG 7
WC Anesthesiology; Clinical Neurology; Neurosciences
SC Anesthesiology; Neurosciences & Neurology
GA 388BK
UT WOS:000261995100013
PM 18986766
ER
PT J
AU Sepucha, KR
Levin, CA
Uzogara, EE
Barry, MJ
O'Connor, AM
Mulley, AG
AF Sepucha, Karen R.
Levin, Carrie A.
Uzogara, Ekeorna E.
Barry, Michael J.
O'Connor, Annette M.
Mulley, Albert G.
TI Developing instruments to measure the quality of decisions: Early
results for a set of symptom-driven decisions
SO PATIENT EDUCATION AND COUNSELING
LA English
DT Article
DE Quality; Decisions; Decision making; Decision quality; Measurement
ID PATIENT; CARE; OSTEOARTHRITIS; PROGRAM; SYSTEMS; KNOWLEDGE
AB Objective: To identify a set of critical facts and key goals and concerns for five common medical conditions, benign prostate disease, hip and knee osteoarthritis, herniated disc and spinal stenosis and examine the validity of the method for identifying these items.
Methods: Investigators identified facts and goals through literature reviews and qualitative work with patients and providers. A cross-sectional survey of patients and providers was conducted to examine the accuracy, importance and completeness of the identified items.
Results: 42 facts (6-16 per condition) and 31 goals and concerns (4-13 per condition) were identified. 182 responses were obtained from patients (76.5% response rate) and 113 responses from providers (78% response rate). Overall, the facts were accurate, important and complete across all conditions. For one condition (hip osteoarthritis), the goals did not meet the criteria for completeness. There was more disagreement between patients and providers around the ranking of goals than of facts.
Conclusions: Overall, respondents found the identified facts and goals accurate, important and complete. Significant differences between patients' and providers' rankings highlight the importance of including both perspectives.
Practice implications: Instruments to measure whether or not patients are informed and the extent to which treatments reflect patients' goals must balance patients' and providers' perspectives when selecting items to include. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
C1 [Sepucha, Karen R.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Hlth Decis Res Unit, Boston, MA 02114 USA.
[O'Connor, Annette M.] Univ Ottawa, Ottawa, CA USA.
RP Sepucha, KR (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Hlth Decis Res Unit, 50 Staniford St,9th Floor, Boston, MA 02114 USA.
EM ksepucha@partners.org
RI Agaliotis, Maria/G-5334-2012
FU Foundation for Informed Medical Decision Making (FIMDM)
FX Role of the funding source: The study was funded by the Foundation for
Informed Medical Decision Making (FIMDM), a not for-profit organization.
Dr. Levin is employed by FIMDM and collaborated on the Study design,
collection of data and interpretation of the data.
NR 23
TC 30
Z9 31
U1 1
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0738-3991
J9 PATIENT EDUC COUNS
JI Patient Educ. Couns.
PD DEC
PY 2008
VL 73
IS 3
BP 504
EP 510
DI 10.1016/j.pec.2008.07.009
PG 7
WC Public, Environmental & Occupational Health; Social Sciences,
Interdisciplinary
SC Public, Environmental & Occupational Health; Social Sciences - Other
Topics
GA 382UL
UT WOS:000261630800017
PM 18718734
ER
PT J
AU Voronov, P
Tobin, MJ
Billings, K
Cote, CJ
Iyer, A
Suresh, S
AF Voronov, Polina
Tobin, Michael J.
Billings, Kathleen
Cote, Charles J.
Iyer, Aditya
Suresh, Santhanam
TI Postoperative pain relief in infants undergoing myringotomy and tube
placement: comparison of a novel regional anesthetic block to intranasal
fentanyl - a pilot analysis
SO PEDIATRIC ANESTHESIA
LA English
DT Article
DE myringotomy tube; postoperative analgesia; nerve of Arnold block;
intranasal fentanyl
ID SEVOFLURANE ANESTHESIA; CHILDREN; ACETAMINOPHEN
AB Aim: The aim of this study was to investigate the use of a novel regional anesthetic technique for the management of pain in the postoperative period in infants and children undergoing myringotomy and tube placement.
Methods: After institutional review board (IRB) approval was obtained, 200 children were randomized in this double blind, prospective, randomized controlled trial to receive either a nerve block of the auricular branch of the Vagus (Nerve of Arnold) with 0.2 ml of 0.25% bupivacaine or receive intranasal fentanyl 2 mcg.kg(-1) after induction of general anesthesia. Patients were monitored in the recovery room for analgesia, need for additional analgesia, incidence of nausea and vomiting, and time to discharge from the hospital. Additional analgesics administered in the PACU, surgical short-stay unit as well as at home were also recorded.
Results: There was no difference in the pain scores between groups (P = 0.53); there was no difference in the amount of rescue medications between groups (P = 0.86); there was no difference in the incidence of nausea and vomiting between groups (P = 0.34); there was no difference in the time to discharge between groups (P = 0.5).
Conclusions: This pilot study demonstrates the efficacy of a peripheral nerve block for management of postoperative pain in infants and children undergoing myringotomy and tube placement. This may be a viable alternative for postoperative pain control in this population. Future multi-center, randomized controlled trials may be necessary to validate the efficacy of this block in infants and children.
C1 [Voronov, Polina; Suresh, Santhanam] Northwestern Univ, Childrens Mem Hosp, Feinberg Sch Med, Chicago, IL 60611 USA.
[Tobin, Michael J.] Shriners Hosp Children, Oak Pk, IL USA.
[Billings, Kathleen] Northwestern Univ, Childrens Mem Hosp, Div Pediat Otolaryngol, Feinberg Sch Med, Chicago, IL 60611 USA.
[Cote, Charles J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02115 USA.
[Iyer, Aditya] Northwestern Univ, Childrens Mem Hosp, Feinberg Sch Med, Chicago, IL 60611 USA.
RP Suresh, S (reprint author), 2300 Childrens Plaza, Chicago, IL 60614 USA.
EM ssuresh@childrensmemorial.org
NR 7
TC 11
Z9 11
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1155-5645
J9 PEDIATR ANESTH
JI Pediatr. Anesth.
PD DEC
PY 2008
VL 18
IS 12
BP 1196
EP 1201
DI 10.1111/j.1460-9592.2008.02789.x
PG 6
WC Anesthesiology; Pediatrics
SC Anesthesiology; Pediatrics
GA 367GM
UT WOS:000260540500008
PM 19076574
ER
PT J
AU Zhang, XP
Cote, CJ
AF Zhang, Xiaopeng
Cote, Charles J.
TI Raynaud's phenomenon in a child presenting as oxygen desaturation during
transfusion with cold blood
SO PEDIATRIC ANESTHESIA
LA English
DT Article
DE transfusion; Raynaud's; blood; monitoring; pulse oximetry
ID ENDOTHELIN-1
AB We report a case of Raynaud's phenomenon (RP) triggered by transfusion of cold blood to a pediatric burn patient under general anesthesia. The child was febrile so a decision was made to not use a blood warmer. When the blood was rapidly administered the child suddenly developed 'desaturation'. The child was placed on 100% oxygen, adequate ventilation assured, and the color of his oral mucosa assessed as 'pink'. Placement of the oximeter on the opposite hand revealed 100% saturation. To our knowledge, this is the first case of apparent RP reported in a pediatric patient triggered by transfusion of cold blood.
C1 [Zhang, Xiaopeng; Cote, Charles J.] Harvard Univ, Sch Med, Div Pediat Anesthesia,Massachusetts Gen Hosp, Dept Anesthesia & Crit Care,Mass Gen Hosp Childre, Boston, MA 02115 USA.
RP Cote, CJ (reprint author), Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, 55 Fruit St, Boston, MA 02114 USA.
EM cjcote@partners.org
NR 8
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1155-5645
J9 PEDIATR ANESTH
JI Pediatr. Anesth.
PD DEC
PY 2008
VL 18
IS 12
BP 1208
EP 1210
DI 10.1111/j.1460-9592.2008.02782.x
PG 3
WC Anesthesiology; Pediatrics
SC Anesthesiology; Pediatrics
GA 367GM
UT WOS:000260540500010
PM 19076576
ER
PT J
AU Inhoff, T
Monnikes, H
Noetzel, S
Stengel, A
Goebel, M
Dinh, QT
Riedl, A
Bannert, N
Wisser, AS
Wiedenmann, B
Klapp, BF
Tache, Y
Kobelt, P
AF Inhoff, Tobias
Moennikes, Hubert
Noetzel, Steffen
Stengel, Andreas
Goebel, Miriam
Dinh, Q. Thai
Riedl, Andrea
Bannert, Norbert
Wisser, Anna-Sophia
Wiedenmann, Bertram
Klapp, Burghard F.
Tache, Yvette
Kobelt, Peter
TI Desacyl ghrelin inhibits the orexigenic effect of peripherally injected
ghrelin in rats
SO PEPTIDES
LA English
DT Article
DE Rat; Desacyl ghrelin; Ghrelin; Food intake; c-Fos; ARC
ID DES-ACYL GHRELIN; HYPOTHALAMIC ARCUATE NUCLEUS; STIMULATES FOOD-INTAKE;
FOS EXPRESSION; PARAVENTRICULAR NUCLEUS; CONSCIOUS RATS; PEPTIDE; BRAIN;
STOMACH; NEURONS
AB Studies showed that the metabolic unlike the neuroendocrine effects of ghrelin could be abrogated by co-administered unacylated ghrelin. The aim was to investigate the interaction between ghrelin and desacyl ghrelin administered intraperitoneally on food intake and neuronal activity (c-Fos) in the arcuate nucleus in non-fasted rats. Ghrelin (13 mu g/kg) significantly increased food intake within the first 30 min post-injection. Desacyl ghrelin at 64 and 127 mu g/kg injected simultaneously with ghrelin abolished the stimulatory effect of ghrelin on food intake. Desacyl ghrelin alone at both doses did not alter food intake. Both doses of desacyl ghrelin injected separately in the light phase had no effects on food intake when rats were fasted for 12 h. Ghrelin and desacyl ghrelin (64 mu g/kg) injected alone increased the number of Fos positive neurons in the arcuate nucleus compared to vehicle. The effect on neuronal activity induced by ghrelin was significantly reduced when injected simultaneously with desacyl ghrelin. Double labeling revealed that nesfatin-1 immunoreactive neurons in the arcuate nucleus are activated by simultaneous injection of ghrelin and desacyl ghrelin. These results suggest that desacyl ghrelin suppresses ghrelin-induced food intake by curbing ghrelin-induced increased neuronal activity in the arcuate nucleus and recruiting nesfatin-1 immunopositive neurons. (c) 2008 Elsevier Inc. All rights reserved.
C1 [Dinh, Q. Thai; Riedl, Andrea; Klapp, Burghard F.; Kobelt, Peter] Charite, Div Psychosomat Med & Psychotherapy, Dept Med, D-10117 Berlin, Germany.
[Inhoff, Tobias; Noetzel, Steffen; Wisser, Anna-Sophia; Wiedenmann, Bertram; Kobelt, Peter] Charite, Div Hepatol Gastroenterol & Endocrinol, Dept Med, D-10117 Berlin, Germany.
[Stengel, Andreas; Goebel, Miriam] Univ Calif Los Angeles, Dept Med, CURE Digest Dis Res Ctr, Ctr Neurobiol Stress,Digest Dis Div, Los Angeles, CA 90024 USA.
[Stengel, Andreas; Goebel, Miriam; Tache, Yvette] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Moennikes, Hubert] Martin Luther Hosp, Dept Med, Berlin, Germany.
[Moennikes, Hubert] Martin Luther Hosp, Inst Neurogastroenterol, Berlin, Germany.
[Bannert, Norbert] Robert Koch Inst, D-1000 Berlin, Germany.
RP Kobelt, P (reprint author), Charite, Div Psychosomat Med & Psychotherapy, Dept Med, Campus Mitte,Luisenstr 13A, D-10117 Berlin, Germany.
EM peter.kobelt@charite.de
FU Charite Universitatsmedizin Berlin [UFF 2008-251]; Research Career
Scientist Award; Department of Veterans Affairs; NIHDK [R01 33061]
FX This work was supported by grants from the Charite Universitatsmedizin
Berlin (UFF 2008-251), and grants to Y.T. (Research Career Scientist
Award, Department of Veterans Affairs and NIHDK R01 33061).
NR 38
TC 102
Z9 108
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0196-9781
J9 PEPTIDES
JI Peptides
PD DEC
PY 2008
VL 29
IS 12
BP 2159
EP 2168
DI 10.1016/j.peptides.2008.09.014
PG 10
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
Pharmacology & Pharmacy
GA 384BG
UT WOS:000261718000010
PM 18938204
ER
PT J
AU Abdolmaleky, HM
Zhou, JR
Thiagalingam, S
Smith, CL
AF Abdolmaleky, Hamid Mostafavi
Zhou, Jing-Rong
Thiagalingam, Sam
Smith, Cassandra L.
TI Epigenetic and pharmacoepigenomic studies of major psychoses and
potentials for therapeutics
SO PHARMACOGENOMICS
LA English
DT Review
DE bipolar disorder; brain; chromatin; DNA methylation; epigenetics;
nutrition; pharmacoepigenomics; pharmacogenomics; psychiatry;
schizophrenia
ID FRAGILE-X-SYNDROME; ADULT-MOUSE BRAIN; DNA-METHYLATION;
METHYLENETETRAHYDROFOLATE REDUCTASE; SCHIZOPHRENIC-PATIENTS; BIPOLAR
DISORDER; DOWN-REGULATION; HISTONE MODIFICATIONS; PLASMA HOMOCYSTEINE;
PREFRONTAL CORTEX
AB Individuals with neuropsychiatric diseases have epigenetic programming disturbances, both in the brain, which is the primary affected organ, and in secondary tissues. Epigenetic modulations are molecular modifications made to DNA, RNA and proteins that fine-tune genotype into phenotype and do not include DNA base changes. For instance, gene-expression modulation is linked to epigenetic codes in chromatin that consist of post-replication DNA methylation and histone protein modifications (e.g., methylation, acetylation and so on), particularly in gene-promoter regions. Epigenetic coding is modulated globally, and in a gene-specific manner by environmental exposures that include nutrition, toxins, drugs and so on. Analysis of epigenetic aberrations in diseases helps to identify dysfunctional genes and pathways, establish more robust cause-effect relationships than genetic studies alone, and identify new pharmaceutical targets and drugs, including nucleic acid reagents such as inhibitory RNAs. The emerging science of pharmacoepigenomics can impact the treatment of psychiatric and other complex diseases. In fact, some therapeutics now in use target epigenetic programming. In the near future, epigenetic interventions should help stabilize affected individuals and lead to prevention strategies.
C1 [Abdolmaleky, Hamid Mostafavi; Zhou, Jing-Rong] Harvard Univ, Sch Med, Lab Nutr & Metab, BIDMC, Boston, MA 02115 USA.
[Abdolmaleky, Hamid Mostafavi; Smith, Cassandra L.] Boston Univ, Dept Biomed Engn, Boston, MA 02215 USA.
[Abdolmaleky, Hamid Mostafavi; Thiagalingam, Sam] Boston Univ, Sch Med, Dept Med Genet & Genom, Boston, MA 02215 USA.
[Abdolmaleky, Hamid Mostafavi] Iran Univ Med Sci, Dept Psychiat, Tehran, Iran.
[Abdolmaleky, Hamid Mostafavi] Iran Univ Med Sci, Tehran Psychiat Inst, Tehran, Iran.
RP Abdolmaleky, HM (reprint author), Harvard Univ, Sch Med, Lab Nutr & Metab, BIDMC, Boston, MA 02115 USA.
EM sabdolma@bidmc.harvard.edu
OI Thiagalingam, Sam/0000-0001-5211-266X; Smith,
Cassandra/0000-0002-0346-8907
NR 154
TC 22
Z9 24
U1 0
U2 7
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1462-2416
J9 PHARMACOGENOMICS
JI Pharmacogenomics
PD DEC
PY 2008
VL 9
IS 12
BP 1809
EP 1823
DI 10.2217/14622416.9.12.1809
PG 15
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 399EK
UT WOS:000262783000012
PM 19072640
ER
PT J
AU Heitjan, DF
Asch, DA
Ray, R
Rukstalis, M
Patterson, F
Lerman, C
AF Heitjan, D. F.
Asch, D. A.
Ray, Riju
Rukstalis, Margaret
Patterson, Freda
Lerman, C.
TI Cost-effectiveness of pharmacogenetic testing to tailor
smoking-cessation treatment
SO PHARMACOGENOMICS JOURNAL
LA English
DT Article
DE addiction; genetic testing; Monte Carlo simulation; tobacco dependence
ID NICOTINE REPLACEMENT THERAPY; RECEPTOR PARTIAL AGONIST; SHORT-TERM
RESPONSE; TOBACCO DEPENDENCE; TRANSDERMAL NICOTINE; CIGARETTE-SMOKING;
SUSTAINED-RELEASE; CONTROLLED-TRIAL; FOLLOW-UP; BUPROPION
AB We evaluated the cost-effectiveness of a range of smoking cessation drug treatments, including varenicline, transdermal nicotine (TN), bupropion and the use of a genetic test to choose between TN and bupropion. We performed Monte Carlo simulation with sensitivity analysis, informing analyses with published estimates of model parameters and current prices for genetic testing and smoking-cessation therapy. The primary outcomes were discounted life-years (LY) and lifetime tobacco-cessation treatment costs. In the base case, varenicline treatment was optimal with an ICER, compared to bupropion, of $2985/LY saved. In sensitivity analyses, varenicline was in all cases (and bupropion in most cases) admissible; only under favorable assumptions was the genetically tailored approach competitive. Our data suggest that an untailored approach of treatment with either bupropion or varenicline is a cost-effective form of tobacco dependence treatment, but a tailored approach for selecting between TN and bupropion can be cost-effective under plausible assumptions.
C1 [Heitjan, D. F.] Univ Penn, Sch Med, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA.
[Heitjan, D. F.; Asch, D. A.; Lerman, C.] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Heitjan, D. F.; Asch, D. A.; Ray, Riju; Rukstalis, Margaret; Patterson, Freda; Lerman, C.] Philadelphia Vet Adm Med Ctr, Ctr Hlth Equ Res & Promot, Philadelphia, PA USA.
[Asch, D. A.; Lerman, C.] Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA.
[Asch, D. A.] Univ Penn, Transdisciplinary Tobacco Use Res Ctr, Philadelphia, PA 19104 USA.
[Ray, Riju] Univ Penn, Dept Psychiat, Philadelphia, PA 19104 USA.
[Rukstalis, Margaret; Patterson, Freda; Lerman, C.] Univ Penn, Dept Pharmacol, Philadelphia, PA 19104 USA.
RP Heitjan, DF (reprint author), Univ Penn, Sch Med, Dept Biostat & Epidemiol, 622 Blockley Hall,423 Guardian Dr, Philadelphia, PA 19104 USA.
EM dheitjan@mail.med.upenn.edu
RI Ray, Riju/D-1113-2009; Heitjan, Daniel/D-1116-2009;
OI Asch, David/0000-0002-7970-286X
FU National Cancer Institute [P50 CA084718, R01 CA063562]; National
Institutes on Drug Abuse
FX We acknowledge the contributions of the following investigators to the
pharmacogenetic studies on which this analysis was based: Wade H
Berrettini, Susan Crystal-Mansour, Leonard Epstein, Larry Hawk, Vyga
Kaufmann, David Main, Ray Niaura, Angela Pinto, Peter Shields, Susan
Ware and E Paul Wileyto. We also thank Steven Siegel for helpful
comments on an earlier draft.; Sources of funding: This study was
supported by Grants P50 CA084718 from the National Cancer Institute and
National Institutes on Drug Abuse and R01 CA063562 from the National
Cancer Institute, which had no role in its design, conduct or reporting.
NR 62
TC 21
Z9 23
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1470-269X
J9 PHARMACOGENOMICS J
JI Pharmacogenomics J.
PD DEC
PY 2008
VL 8
IS 6
BP 391
EP 399
DI 10.1038/sj.tpj.6500492
PG 9
WC Genetics & Heredity; Pharmacology & Pharmacy
SC Genetics & Heredity; Pharmacology & Pharmacy
GA 372CC
UT WOS:000260878100004
PM 18347612
ER
PT J
AU Troemel, ER
Felix, MA
Whiteman, NK
Barriere, A
Ausubel, FM
AF Troemel, Emily R.
Felix, Marie-Anne
Whiteman, Noah K.
Barriere, Antoine
Ausubel, Frederick M.
TI Microsporidia Are Natural Intracellular Parasites of the Nematode
Caenorhabditis elegans
SO PLOS BIOLOGY
LA English
DT Article
ID 16S RIBOSOMAL-RNA; INNATE IMMUNITY; BACTERIAL PATHOGENS; OLIGONUCLEOTIDE
PROBES; LISTERIA-MONOCYTOGENES; MAXIMUM-LIKELIHOOD; BIOLOGICAL-CONTROL;
MODEL; POPULATIONS; INFECTION
AB For decades the soil nematode Caenorhabditis elegans has been an important model system for biology, but little is known about its natural ecology. Recently, C. elegans has become the focus of studies of innate immunity and several pathogens have been shown to cause lethal intestinal infections in C. elegans. However none of these pathogens has been shown to invade nematode intestinal cells, and no pathogen has been isolated from wild-caught C. elegans. Here we describe an intracellular pathogen isolated from wild-caught C. elegans that we show is a new species of microsporidia. Microsporidia comprise a large class of eukaryotic intracellular parasites that are medically and agriculturally important, but poorly understood. We show that microsporidian infection of the C. elegans intestine proceeds through distinct stages and is transmitted horizontally. Disruption of a conserved cytoskeletal structure in the intestine called the terminal web correlates with the release of microsporidian spores from infected cells, and appears to be part of a novel mechanism by which intracellular pathogens exit from infected cells. Unlike in bacterial intestinal infections, the p38 MAPK and insulin/insulin-like growth factor (IGF) signaling pathways do not appear to play substantial roles in resistance to microsporidian infection in C. elegans. We found microsporidia in multiple wild-caught isolates of Caenorhabditis nematodes from diverse geographic locations. These results indicate that microsporidia are common parasites of C. elegans in the wild. In addition, the interaction between C. elegans and its natural microsporidian parasites provides a system in which to dissect intracellular intestinal infection in vivo and insight into the diversity of pathogenic mechanisms used by intracellular microbes.
C1 [Troemel, Emily R.; Ausubel, Frederick M.] Harvard Univ, Sch Med, Dept Genet, Dept Mol Biol, Boston, MA USA.
[Troemel, Emily R.; Ausubel, Frederick M.] Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Boston, MA 02114 USA.
[Felix, Marie-Anne; Barriere, Antoine] Univ Paris 06, CNRS, Inst Jacques Monod, Paris, France.
[Felix, Marie-Anne; Barriere, Antoine] Univ Paris 07, Inst Jacques Monod, CNRS, F-75251 Paris, France.
[Whiteman, Noah K.] Harvard Univ, Dept Organism & Evolutionary Biol, Cambridge, MA 02138 USA.
RP Troemel, ER (reprint author), Univ Calif San Diego, Sect Cell & Dev Biol, La Jolla, CA 92093 USA.
EM etroemel@ucsd.edu
FU Leukemia/Lymphoma Society; Kirschstein National Research Service Award
(NRSA); National Institutes of Allergy and Infectious Diseases
[F32AI069732]; National Institutes of Health (NIH) [R01 AI064332, R01
AI072508, P01 AI044220]; French Research Ministry; Centre National de la
Recherche Scientifique; Inflammatory Bowel Disease [DK43351]; Boston
Area Diabetes and Endocrinology Research Center [DK57521]
FX This work was supported by a Leukemia/Lymphoma Society Fellowship to
ERT, a Kirschstein National Research Service Award (NRSA) fellowship to
NKW from the National Institutes of Allergy and Infectious Diseases
(F32AI069732), National Institutes of Health (NIH) grants R01 AI064332,
R01 AI072508, and P01 AI044220 awarded to FMA. AB and M-AF were
supported by the French Research Ministry and the Centre National de la
Recherche Scientifique. Electron microscopy was performed in the
Microscopy Core of the Center for Systems Biology, which is supported by
an Inflammatory Bowel Disease Grant DK43351 and a Boston Area Diabetes
and Endocrinology Research Center Award DK57521.
NR 68
TC 95
Z9 101
U1 4
U2 15
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1544-9173
J9 PLOS BIOL
JI PLoS. Biol.
PD DEC
PY 2008
VL 6
IS 12
BP 2736
EP 2752
DI 10.1371/journal.pbio.0060309
PG 17
WC Biochemistry & Molecular Biology; Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics
GA 386WQ
UT WOS:000261913700015
PM 19071962
ER
PT J
AU Nishikawa, T
Gulbahce, N
Motter, AE
AF Nishikawa, Takashi
Gulbahce, Natali
Motter, Adilson E.
TI Spontaneous Reaction Silencing in Metabolic Optimization
SO PLOS COMPUTATIONAL BIOLOGY
LA English
DT Article
ID ESCHERICHIA-COLI METABOLISM; LIMITED CONTINUOUS-CULTURE; IN-SILICO
MODELS; FLUX ANALYSIS; SACCHAROMYCES-CEREVISIAE; OBJECTIVE FUNCTIONS;
GENETIC ROBUSTNESS; GROWTH PHENOTYPES; CELL BIOLOGY; NETWORKS
AB Metabolic reactions of single-cell organisms are routinely observed to become dispensable or even incapable of carrying activity under certain circumstances. Yet, the mechanisms as well as the range of conditions and phenotypes associated with this behavior remain very poorly understood. Here we predict computationally and analytically that any organism evolving to maximize growth rate, ATP production, or any other linear function of metabolic fluxes tends to significantly reduce the number of active metabolic reactions compared to typical nonoptimal states. The reduced number appears to be constant across the microbial species studied and just slightly larger than the minimum number required for the organism to grow at all. We show that this massive spontaneous reaction silencing is triggered by the irreversibility of a large fraction of the metabolic reactions and propagates through the network as a cascade of inactivity. Our results help explain existing experimental data on intracellular flux measurements and the usage of latent pathways, shedding new light on microbial evolution, robustness, and versatility for the execution of specific biochemical tasks. In particular, the identification of optimal reaction activity provides rigorous ground for an intriguing knockout-based method recently proposed for the synthetic recovery of metabolic function.
C1 [Nishikawa, Takashi; Motter, Adilson E.] Northwestern Univ, Dept Phys & Astron, Evanston, IL 60208 USA.
[Nishikawa, Takashi; Motter, Adilson E.] Northwestern Univ, NW Inst Complex Syst, Evanston, IL USA.
[Nishikawa, Takashi] Clarkson Univ, Div Math & Comp Sci, New York, NY USA.
[Gulbahce, Natali] Northeastern Univ, Dept Phys, Boston, MA 02115 USA.
[Gulbahce, Natali] Northwestern Univ, Ctr Complex Network Res, Evanston, IL USA.
[Gulbahce, Natali] Dana Farber Canc Inst, Ctr Canc Syst Biol, Boston, MA 02115 USA.
RP Motter, AE (reprint author), Northwestern Univ, Dept Phys & Astron, Evanston, IL 60208 USA.
EM motter@northwestern.edu
RI Nishikawa, Takashi/B-3752-2010
OI Nishikawa, Takashi/0000-0002-2147-0242
FU National Science Foundation (NSF) [DMR-0520513]; Materials Research
Center of Northwestern University (AEM); Department of Energy
[DE-AC52-06NA25396]; NSF [DMS-0709212]
FX This work was supported by the National Science Foundation (NSF)
Materials Research Science and Engineering Center program (Grant No.
DMR-0520513) at the Materials Research Center of Northwestern University
(AEM), Department of Energy under contract DE-AC52-06NA25396 (NG), and
NSF under Grant No. DMS-0709212 (TN and AEM).
NR 79
TC 27
Z9 27
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7358
J9 PLOS COMPUT BIOL
JI PLoS Comput. Biol.
PD DEC
PY 2008
VL 4
IS 12
AR e1000236
DI 10.1371/journal.pcbi.1000236
PG 12
WC Biochemical Research Methods; Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Mathematical & Computational Biology
GA 415HB
UT WOS:000263923800016
PM 19057639
ER
PT J
AU Hill, AS
Nishino, A
Nakajo, K
Zhang, GX
Fineman, JR
Selzer, ME
Okamura, Y
Cooper, EC
AF Hill, Alexis S.
Nishino, Atsuo
Nakajo, Koichi
Zhang, Giuxin
Fineman, Jaime R.
Selzer, Michael E.
Okamura, Yasushi
Cooper, Edward C.
TI Ion Channel Clustering at the Axon Initial Segment and Node of Ranvier
Evolved Sequentially in Early Chordates
SO PLOS GENETICS
LA English
DT Article
ID KCNQ POTASSIUM CHANNELS; K+ CHANNEL; ANKYRIN-G; NEURAL CREST;
ANTICONVULSANT RETIGABINE; MOLECULAR EVOLUTION; ANTIEPILEPTIC DRUGS;
SPIKE INITIATION; VOLTAGE SENSOR; MOTOR-NEURON
AB In many mammalian neurons, dense clusters of ion channels at the axonal initial segment and nodes of Ranvier underlie action potential generation and rapid conduction. Axonal clustering of mammalian voltage-gated sodium and KCNQ (Kv7) potassium channels is based on linkage to the actin-spectrin cytoskeleton, which is mediated by the adaptor protein ankyrin-G. We identified key steps in the evolution of this axonal channel clustering. The anchor motif for sodium channel clustering evolved early in the chordate lineage before the divergence of the wormlike cephalochordate, amphioxus. Axons of the lamprey, a very primitive vertebrate, exhibited some invertebrate features ( lack of myelin, use of giant diameter to hasten conduction), but possessed narrow initial segments bearing sodium channel clusters like in more recently evolved vertebrates. The KCNQ potassium channel anchor motif evolved after the divergence of lampreys from other vertebrates, in a common ancestor of shark and humans. Thus, clustering of voltage-gated sodium channels was a pivotal early innovation of the chordates. Sodium channel clusters at the axon initial segment serving the generation of action potentials evolved long before the node of Ranvier. KCNQ channels acquired anchors allowing their integration into pre-existing sodium channel complexes at about the same time that ancient vertebrates acquired myelin, saltatory conduction, and hinged jaws. The early chordate refinements in action potential mechanisms we have elucidated appear essential to the complex neural signaling, active behavior, and evolutionary success of vertebrates.
C1 [Hill, Alexis S.; Zhang, Giuxin; Fineman, Jaime R.; Selzer, Michael E.; Cooper, Edward C.] Univ Penn, Dept Neurol, Penn Epilepsy Ctr, Philadelphia, PA 19104 USA.
[Hill, Alexis S.; Zhang, Giuxin; Fineman, Jaime R.; Selzer, Michael E.; Cooper, Edward C.] David Mahoney Inst Neurol Sci, Philadelphia, PA 19104 USA.
[Nishino, Atsuo] Osaka Univ, Grad Sch Sci, Dept Biol, Dev Biol Lab, Osaka, Japan.
[Nakajo, Koichi] Natl Inst Physiol Sci, Okazaki, Aichi 444, Japan.
[Selzer, Michael E.] US Dept Vet Affairs, Off Res & Dev, Washington, DC USA.
[Okamura, Yasushi] Osaka Univ, Grad Sch Med, Dept Integrat Physiol, Osaka, Japan.
RP Cooper, EC (reprint author), Univ Penn, Dept Neurol, Penn Epilepsy Ctr, Philadelphia, PA 19104 USA.
EM edc@mail.med.upenn.edu
RI Nakajo, Koichi/H-4104-2011; Nishino, Atsuo/F-5393-2013
FU NIH [R01-NS14837, R01NS38537, R24-HD050838]; US-Japan Brain Research
Cooperative Program [R01 NS49119]
FX This work was supported by the Roy and Diana Vagelos Scholars Program in
the Molecular Life Sciences ( AH), NIH Grants R01-NS14837( MES),
R01NS38537 ( MES), R24-HD050838 ( MES), the Craig H. Neilsen Foundation
( MES), a Japan- U. S. Brain Research Cooperative Program Grant ( YO), a
Human Frontiers Science Program Short Term Fellowship ( ECC), a US-Japan
Brain Research Cooperative Program Supplement ( R01 NS49119, ECC), and
the Miles Family Fund ( ECC). The funders had no role in study design,
conduct, data interpretation, or manuscript preparation.
NR 107
TC 62
Z9 64
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD DEC
PY 2008
VL 4
IS 12
AR e1000317
DI 10.1371/journal.pgen.1000317
PG 15
WC Genetics & Heredity
SC Genetics & Heredity
GA 411RO
UT WOS:000263667900032
PM 19112491
ER
PT J
AU Pare, G
Chasman, DI
Parker, AN
Nathan, DM
Miletich, JP
Zee, RY
Ridker, PM
AF Pare, Guillaume
Chasman, Daniel I.
Parker, Alexander N.
Nathan, David M.
Miletich, Joseph P.
Zee, Robert Y.
Ridker, Paul M.
TI Novel Association of HK1 with Glycated Hemoglobin in a Non-Diabetic
Population: A Genome-Wide Evaluation of 14,618 Participants in the
Women's Genome Health Study
SO PLOS GENETICS
LA English
DT Article
ID RED-BLOOD-CELL; DIABETES-MELLITUS; CARDIOVASCULAR-DISEASE; ZINC
TRANSPORTER; GLUCOKINASE GENE; FASTING GLUCOSE; BIRTH-WEIGHT; RISK LOCI;
TYPE-2; HAPLOTYPE
AB Type 2 diabetes is a leading cause of morbidity and mortality. While genetic variants have been found to influence the risk of type 2 diabetes mellitus, relatively few studies have focused on genes associated with glycated hemoglobin, an index of the mean blood glucose concentration of the preceding 8-12 weeks. Epidemiologic studies and randomized clinical trials have documented the relationship between glycated hemoglobin levels and the development of long-term complications in diabetes; moreover, higher glycated hemoglobin levels in the subdiabetic range have been shown to predict type 2 diabetes risk and cardiovascular disease. To examine the common genetic determinants of glycated hemoglobin levels, we performed a genome-wide association study that evaluated 337,343 SNPs in 14,618 apparently healthy Caucasian women. The results show that glycated hemoglobin levels are associated with genetic variation at the GCK ( rs730497; P = 2.8x10(-12)), SLC30A8 ( rs13266634; P = 9.8x10(-8)), G6PC2 ( rs1402837; P = 6.8x10-(10)), and HK1 ( rs7072268; P = 6.4x10(-9)) loci. While associations at the GCK, SLC30A8, and G6PC2 loci are confirmatory, the findings at HK1 are novel. We were able to replicate this novel association in an independent validation sample of 455 additional non-diabetic men and women. HK1 encodes the enzyme hexokinase, the first step in glycolysis and a likely candidate for the control of glucose metabolism. This observed genetic association between glycated hemoglobin levels and HK1 polymorphisms paves the way for further studies of the role of HK1 in hemoglobin glycation, glucose metabolism, and diabetes.
C1 [Pare, Guillaume; Chasman, Daniel I.; Zee, Robert Y.; Ridker, Paul M.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Ctr Cardiovasc Dis Prevent, Boston, MA 02115 USA.
[Pare, Guillaume; Chasman, Daniel I.; Zee, Robert Y.; Ridker, Paul M.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Donald W Reynolds Ctr Cardiovasc Res, Boston, MA USA.
[Parker, Alexander N.; Miletich, Joseph P.] Amgen Inc, Cambridge, MA USA.
[Nathan, David M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Diabet, Boston, MA USA.
RP Pare, G (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Ctr Cardiovasc Dis Prevent, Boston, MA 02115 USA.
EM gpare@rics.bwh.harvard.edu
FU NCI NIH HHS [CA047988, R01 CA047988]; NHLBI NIH HHS [HL080467, R01
HL043851, R01 HL080467]
NR 47
TC 50
Z9 51
U1 3
U2 8
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7404
J9 PLOS GENET
JI PLoS Genet.
PD DEC
PY 2008
VL 4
IS 12
AR e1000312
DI 10.1371/journal.pgen.1000312
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 411RO
UT WOS:000263667900027
PM 19096518
ER
PT J
AU Schormann, N
Senkovich, O
Walker, K
Wright, DL
Anderson, AC
Rosowsky, A
Ananthan, S
Shinkre, B
Velu, S
Chattopadhyay, D
AF Schormann, N.
Senkovich, O.
Walker, K.
Wright, D. L.
Anderson, A. C.
Rosowsky, A.
Ananthan, S.
Shinkre, B.
Velu, S.
Chattopadhyay, D.
TI Structure-based approach to pharmacophore identification, in silico
screening, and three-dimensional quantitative structure-activity
relationship studies for inhibitors of Trypanosoma cruzi dihydrofolate
reductase function
SO PROTEINS-STRUCTURE FUNCTION AND BIOINFORMATICS
LA English
DT Article
DE Chagas' disease; antifolate; DHFR; structure-activity relationship;
HASL; eHiTS
ID SELECTIVE INHIBITORS; CHAGAS-DISEASE; PNEUMOCYSTIS-CARINII;
TOXOPLASMA-GONDII; CHEMOTHERAPY; DESIGN; DERIVATIVES; ANALOGS; POTENT;
OPTIMIZATION
AB We have employed a structure-based three-dimensional quantitative structure-activity relationship (3D-QSAR) approach to predict the biochemical activity for inhibitors of T. cruzi dihydrofolate reductase-thymidylate synthase (DHFR-TS). Crystal structures of complexes of the enzyme with eight different inhibitors of the DHFR activity together with the structure in the substrate-free state (DHFR domain) were used to validate and refine docking poses of ligands that constitute likely active conformations. Structural information from these complexes formed the basis for the structure-based alignment used as input for the QSAR study. Contrary to indirect ligand-based approaches the strategy described here employs a direct receptor-based approach. The goal is to generate a library of selective ea inhibitors for further development as antiparasitic agents. 3D-QSAR models were obtained for T cruzi DHFR-TS (30 inhibitors in learning set) and human DHFR (36 inhibitors in learning set) that show a very good agreement between experimental and predicted enzyme inhibition data. For crossvalidation of the QSAR model(s), we have used the 10% leave-one-out method. The derived 3D-QSAR models were tested against a few selected compounds (a small test set of six inhibitors for each enzyme) with known activity, which were not part of the learning set, and the quality of prediction of the initial 3D-QSAR models demonstrated that such studies are feasible. Further refinement of the models through integration of additional activity data and optimization of reliable docking poses is expected to lead to an improved predictive ability.
C1 [Schormann, N.; Senkovich, O.; Walker, K.; Shinkre, B.; Velu, S.; Chattopadhyay, D.] Univ Alabama, Dept Pharmaceut Sci, Birmingham, AL 35294 USA.
[Wright, D. L.; Anderson, A. C.] Univ Connecticut, Dept Pharmaceut Sci, Storrs, CT 06269 USA.
[Rosowsky, A.] Harvard Univ, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Ananthan, S.] So Res Inst, Dept Organ Chem, Birmingham, AL 35255 USA.
RP Chattopadhyay, D (reprint author), Univ Alabama, Dept Pharmaceut Sci, Birmingham, AL 35294 USA.
EM debasish@uab.edu
NR 36
TC 22
Z9 24
U1 1
U2 7
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0887-3585
J9 PROTEINS
JI Proteins
PD DEC
PY 2008
VL 73
IS 4
BP 889
EP 901
DI 10.1002/prot.22115
PG 13
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 375QV
UT WOS:000261129300009
PM 18536013
ER
PT J
AU Wolf, EJ
Miller, MW
Orazem, RJ
Weiefich, MR
Castillo, DT
Milford, J
Kaloupek, DG
Keane, TM
AF Wolf, Erika J.
Miller, Mark W.
Orazem, Robert J.
Weiefich, Mariann R.
Castillo, Diane T.
Milford, Jaime
Kaloupek, Danny G.
Keane, Terence M.
TI The MMPI-2 Restructured Clinical Scales in the Assessment of
Posttraumatic Stress Disorder and Comorbid Disorders
SO PSYCHOLOGICAL ASSESSMENT
LA English
DT Article
DE Minnesota Multiphasic Personality Inventory-2; Restructured Clinical
Scales; posttraumatic stress disorder; internalizing; externalizing
ID DSM-IV ANXIETY; RC SCALES; MENTAL-DISORDERS; STRUCTURAL RELATIONSHIPS;
INTERNALIZING SUBTYPES; MOOD DISORDERS; PTSD SCALE; VETERANS;
PERSONALITY; VALIDITY
AB This study examined the psychometric properties of the Minnesota Multiphasic Personality Inventory-2 (MMPI-2) Restructured Clinical Scales (RCSs) in individuals with posttraumatic stress disorder (PTSD) receiving clinical services at Department of Veterans Affairs medical centers. Study 1 included 1,098 men who completed the MMPI-2 and were assessed for a range of psychological disorders via structured clinical interview. Study 2 included 136 women who completed the MMPI-2 and were interviewed with the Clinician Administered Scale for PTSD. The utility of the RCSs was compared with that of the Clinical Scales (CSs) and the Keane PTSD (PK) scale. The RCSs demonstrated good psychometric properties and patterns of associations with other measures of psychopathology that corresponded to current theory regarding the structure of comorbidity. A notable advantage of the RCSs compared with the MMPI-2 CSs was their enhanced construct validity and clinical utility in the assessment of comorbid internalizing and externalizing psychopathology. The PK scale demonstrated incremental validity in the prediction of PTSD beyond that of the RCSs or CSs.
C1 [Wolf, Erika J.; Miller, Mark W.; Orazem, Robert J.; Weiefich, Mariann R.; Kaloupek, Danny G.; Keane, Terence M.] VA Boston Healthcare Syst, Natl Ctr PTSD, Boston, MA USA.
[Wolf, Erika J.; Orazem, Robert J.] Boston Univ, Dept Psychol, Boston, MA 02215 USA.
[Castillo, Diane T.; Milford, Jaime] VA New Mexico Healthcare Syst, Mexico City, DF, Mexico.
[Miller, Mark W.; Kaloupek, Danny G.; Keane, Terence M.] Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02215 USA.
RP Miller, MW (reprint author), VA Boston Healthcare Syst, Natl Ctr PTSD 116B2, 150 S Huntington Ave, Boston, MA 02130 USA.
EM mark.miller5@va.gov
OI Miller, Mark/0000-0001-6393-8563; Wolf, Erika/0000-0003-2666-2435
FU NIMH NIH HHS [5F31MH074267-3, F31 MH074267, F31 MH074267-01A2, F31
MH074267-02, F31 MH074267-03]
NR 55
TC 26
Z9 27
U1 8
U2 12
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 1040-3590
J9 PSYCHOL ASSESSMENT
JI Psychol. Assess.
PD DEC
PY 2008
VL 20
IS 4
BP 327
EP 340
DI 10.1037/a0012948
PG 14
WC Psychology, Clinical
SC Psychology
GA 383HD
UT WOS:000261663800002
PM 19086756
ER
PT J
AU Nieuwland, MS
Kuperberg, GR
AF Nieuwland, Mante S.
Kuperberg, Gina R.
TI When the Truth Is Not Too Hard to Handle: An Event-Related Potential
Study on the Pragmatics of Negation
SO PSYCHOLOGICAL SCIENCE
LA English
DT Article
ID BRAIN POTENTIALS; LANGUAGE COMPREHENSION; SENTENCE VERIFICATION
AB Our brains rapidly map incoming language onto what we hold to be true. Yet there are claims that such integration and verification processes are delayed in sentences containing negation words like not. However, studies have often confounded whether a statement is true and whether it is a natural thing to say during normal communication. In an event-related potential (ERP) experiment, we aimed to disentangle effects of truth value and pragmatic licensing on the comprehension of affirmative and negated real-world statements. As in affirmative sentences, false words elicited a larger N400 ERP than did true words in pragmatically licensed negated sentences (e.g., "In moderation, drinking red wine isn't bad/good..."), whereas true and false words elicited similar responses in unlicensed negated sentences (e.g., "A baby bunny's fur isn't very hard/soft..."). These results suggest that negation poses no principled obstacle for readers to immediately relate incoming words to what they hold to be true.
C1 [Nieuwland, Mante S.] Tufts Univ, Dept Psychol, Medford, MA 02155 USA.
[Nieuwland, Mante S.; Kuperberg, Gina R.] Harvard Univ, Sch Med, MIT, Massachusetts Gen Hosp,Athinoula A Martinos Ctr B, Cambridge, MA 02138 USA.
RP Nieuwland, MS (reprint author), Tufts Univ, Dept Psychol, 490 Boston Ave, Medford, MA 02155 USA.
EM mante@nmr.mgh.harvard.edu
FU NIMH NIH HHS [R01 MH071635, R01 MH071635-05, R01-MH071635]
NR 30
TC 70
Z9 71
U1 2
U2 15
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0956-7976
J9 PSYCHOL SCI
JI Psychol. Sci.
PD DEC
PY 2008
VL 19
IS 12
BP 1213
EP 1218
DI 10.1111/j.1467-9280.2008.02226.x
PG 6
WC Psychology, Multidisciplinary
SC Psychology
GA 384BH
UT WOS:000261718100003
PM 19121125
ER
PT J
AU Gray, KM
LaRowe, SD
Upadhyaya, HP
AF Gray, Kevin M.
LaRowe, Steven D.
Upadhyaya, Himanshu P.
TI Cue Reactivity in Young Marijuana Smokers: A Preliminary Investigation
SO PSYCHOLOGY OF ADDICTIVE BEHAVIORS
LA English
DT Article
DE marijuana; cannabis; craving; cue reactivity; adolescent
ID ADOLESCENT CIGARETTE SMOKERS; CRAVING QUESTIONNAIRE; CANNABIS
WITHDRAWAL; SMOKING CUES; IN-VIVO; ALCOHOL; DEPENDENCE; USERS
AB To develop and evaluate the feasibility of a cue reactivity paradigm for young marijuana smokers, the authors set up a laboratory procedure involving neutral and marijuana-related imagery, video, and in vivo cues. Fifteen adolescents and young adults with cannabis use disorders completed the procedure, which included continuous measurement of skin conductance and heart rate. Participants also completed questionnaires regarding marijuana craving before, during, and after cue presentations. Higher levels of craving and skin conductance were observed during marijuana cue presentations. The procedure appears to elicit cue reactivity among adolescents and young adults with cannabis use disorders and should be further evaluated and refined with a larger sample. Implications for future studies are discussed.
C1 [Gray, Kevin M.] Med Univ S Carolina, Dept Psychiat & Behav Sci, Youth Div, Charleston, SC 29425 USA.
[LaRowe, Steven D.] Med Univ S Carolina, Dept Psychiat & Behav Sci, Ctr Drug & Alcohol Programs, Charleston, SC 29425 USA.
[LaRowe, Steven D.] Ralph H Johnson Vet Affairs Med Ctr, Mental Hlth Serv, Subst Abuse Treatment Ctr, Charleston, SC USA.
[Upadhyaya, Himanshu P.] Med Univ S Carolina, Dept Psychiat & Behav Sci, Div Clin Neurosci, Charleston, SC 29425 USA.
RP Gray, KM (reprint author), Med Univ S Carolina, Dept Psychiat & Behav Sci, Youth Div, 67 President St,POB 250861, Charleston, SC 29425 USA.
EM graykm@musc.edu
FU NCRR NIH HHS [M01 RR001070-29, M01 RR001070, M01 RR 01070]; NIDA NIH HHS
[K12 DA000357-07, K12 DA000357, 5K12 DA 000357]
NR 28
TC 26
Z9 26
U1 3
U2 3
PU EDUCATIONAL PUBLISHING FOUNDATION
PI WASHINGTON
PA 750 FIRST ST, NE, WASHINGTON, DC 20002-4242 USA
SN 0893-164X
J9 PSYCHOL ADDICT BEHAV
JI Psychol. Addict. Behav.
PD DEC
PY 2008
VL 22
IS 4
BP 582
EP 586
DI 10.1037/a0012985
PG 5
WC Substance Abuse; Psychology, Multidisciplinary
SC Substance Abuse; Psychology
GA 380JO
UT WOS:000261462200015
PM 19071985
ER
PT J
AU Zhang, XY
Cao, LY
Song, C
Wu, GY
Chen, DC
Qi, LY
Wang, F
Xiu, MH
Chen, S
Zhang, YY
Lu, L
Kosten, TA
Kosten, TR
AF Zhang, Xiang Yang
Cao, Lian Yuan
Song, Cai
Wu, Gui Ying
Chen, Da Chun
Qi, Ling Yan
Wang, Fan
Xiu, Mei Hong
Chen, Song
Zhang, Yingyang
Lu, Lin
Kosten, Therese A.
Kosten, Thomas R.
TI Lower serum cytokine levels in smokers than nonsmokers with chronic
schizophrenia on long-term treatment with antipsychotics
SO PSYCHOPHARMACOLOGY
LA English
DT Article
DE Schizophrenia; Smoking; Nicotine; Cytokine; Immune
ID NICOTINE DEPENDENCE; CIGARETTE-SMOKING; NEUROLEPTIC TREATMENT;
INTERLEUKIN-2; PSYCHOPATHOLOGY; ASSOCIATION; RECEPTORS; IL-2; RESISTANT;
CELLS
AB Schizophrenia is associated with various abnormalities in the immune system. Suppression of inflammatory cytokines by cigarette smoke is well-established. The purpose of this study was to determine any differences in cytokine profiles in smokers and nonsmokers with schizophrenia and whether there were any relationships among altered cytokine profiles and psychopathological symptoms.
Serum interleukin (IL)-2, IL-6, IL-8, and tumor necrosis factor (TNF)-alpha levels were measured in 96 male inpatients with DSM-IV schizophrenia: 66 smokers and 30 nonsmokers. Symptoms were assessed with the Positive and Negative Syndrome Scale (PANSS).
The positive PANSS symptoms were lower in smokers than nonsmokers, while the negative symptoms were lower in those who smoked more cigarettes. Cytokine levels were positively correlated: IL-2 level with IL-6 and IL-6 with both IL-8 and TNF-alpha. Both IL-2 and IL-6, but not IL-8 or TNF-alpha, were significantly lower in smokers than nonsmokers (p < 0.002; p < 0.01). Lower IL-2 levels correlated with fewer negative symptoms and with smoking more cigarettes.
The fewer positive symptoms in smokers and fewer negative symptoms in those who smoked more cigarettes may be associated with nicotine-induced suppression of some inflammatory cytokines.
C1 [Zhang, Xiang Yang; Wu, Gui Ying; Zhang, Yingyang; Kosten, Therese A.; Kosten, Thomas R.] Baylor Coll Med, VA Med Ctr, Menninger Dept Psychiat & Behav Sci, Houston, TX 77030 USA.
[Zhang, Xiang Yang; Cao, Lian Yuan; Chen, Da Chun; Qi, Ling Yan; Wang, Fan; Xiu, Mei Hong; Chen, Song; Zhang, Yingyang] Beijing Hui Long Guan Hosp, Ctr Biol Psychiat, Beijing, Peoples R China.
[Song, Cai] Univ Prince Edward Isl, Atlantic Vet Coll, Dept Biomed Sci, Charlottetown, PE C1A 4P3, Canada.
[Song, Cai] NRC Inst Nutrisci & Hlth, Charlottetown, PE, Canada.
[Lu, Lin] Peking Univ, Natl Inst Drug Dependence, Beijing 100871, Peoples R China.
RP Kosten, TR (reprint author), Baylor Coll Med, VA Med Ctr, Menninger Dept Psychiat & Behav Sci, Res Bldg 110,2002 Holcombe Blvd, Houston, TX 77030 USA.
EM xyzhang@bcm.edu; kosten@bcm.edu
FU NIDA NIH HHS [K05-DA0454, P50-DA18827]
NR 51
TC 19
Z9 19
U1 3
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0033-3158
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD DEC
PY 2008
VL 201
IS 3
BP 383
EP 389
DI 10.1007/s00213-008-1295-4
PG 7
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 374IP
UT WOS:000261037300007
PM 18719893
ER
PT J
AU Sarna, L
Bialous, SA
Cooley, ME
Jun, HJ
Feskanich, D
AF Sarna, Linda
Bialous, Stella A.
Cooley, Mary E.
Jun, Hee-Jin
Feskanich, Diane
TI Impact of smoking and smoking cessation on health-related quality of
life in women in the Nurses' Health Study
SO QUALITY OF LIFE RESEARCH
LA English
DT Article
DE Smoking; Smoking cessation; Health-related quality of life; Quality of
life; Women; Tobacco
ID UNITED-STATES; NICOTINE DEPENDENCE; CIGARETTE-SMOKING; EX-SMOKERS;
QUESTIONNAIRE; OBESITY; ADULTS
AB To examine the relationship between smoking and health-related quality of life (HRQOL) and the impact of quitting smoking on changes in HRQOL among women in the two Nurses' Health Study (NHS) cohorts (n = 158,736) who were 29 to 71 years of age in 1992/1993 when they reported data on smoking status and completed the Short Form-36 version 1 (SF-36).
At baseline, the SF-36 physical component scores (SF-PCS) and mental component scores (SF-MCS) were examined by smoking status (never, 56%, former, 32%, and current, 13%) within 10-year age groups. Smoking characteristics were analyzed as correlates of SF-36. Changes in smoking status and SF-PCS and SF-MCS, adjusted for comorbid disease and other covariates, were reassessed at 4-year intervals among current smokers in 1992/1993 and those who either continued smoking after 4 and 8 years or reported not smoking at both intervals.
Smokers had lower HRQOL (SF-PCS and SF-MCS) as compared to never and former smokers. Current smoking, cigarettes per day and time since quitting were associated with significantly lower SF-PCS and SF-MCS. Continuing smokers and those who quit had significant declines in SF-PCS over time and significant improvements in SF-MCS at 8 years. There was minimal difference between groups, with some greater improvements in SF-MCS among those reporting non-smoking at 8 years. These findings support the lower ratings of HRQOL by smokers, but quitting alone, after an average of 21 years of smoking, did not improve HRQOL. Further study focused on the HRQOL impact of quitting smoking is needed.
C1 [Sarna, Linda] Univ Calif Los Angeles, Sch Nursing, Los Angeles, CA 90024 USA.
[Bialous, Stella A.] Tobacco Policy Int, San Francisco, CA USA.
[Cooley, Mary E.] Dana Farber Canc Inst, Phyllis E Cantor Ctr, Boston, MA 02115 USA.
[Jun, Hee-Jin; Feskanich, Diane] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Jun, Hee-Jin; Feskanich, Diane] Harvard Univ, Sch Med, Boston, MA USA.
RP Sarna, L (reprint author), Univ Calif Los Angeles, Sch Nursing, Los Angeles, CA 90024 USA.
EM lsarna@sonnet.ucla.edu
FU NCI NIH HHS [CA87979, CA50385, K07 CA095118, K07 CA92696-02, R01
CA050385]
NR 34
TC 37
Z9 39
U1 0
U2 11
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0962-9343
J9 QUAL LIFE RES
JI Qual. Life Res.
PD DEC
PY 2008
VL 17
IS 10
BP 1217
EP 1227
DI 10.1007/s11136-008-9404-8
PG 11
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 378SO
UT WOS:000261344400002
PM 18931942
ER
PT J
AU Rubenstein, LV
Hempel, S
Farmer, MM
Asch, SM
Yano, EM
Dougherty, D
Shekelle, PW
AF Rubenstein, L. V.
Hempel, S.
Farmer, M. M.
Asch, S. M.
Yano, E. M.
Dougherty, D.
Shekelle, P. W.
TI Finding order in heterogeneity: types of quality-improvement
intervention publications
SO QUALITY & SAFETY IN HEALTH CARE
LA English
DT Article
ID PATIENT-OUTCOMES-RESEARCH; RANDOMIZED CLINICAL-TRIALS; HEALTH-CARE;
ORGANIZATIONAL-CHANGE; TRANSLATING RESEARCH; SYSTEMATIC REVIEWS;
ASTHMA-CARE; DESIGN; IMPLEMENTATION; POLICY
AB Background: Stakeholders in quality improvement agree on the need for augmenting and synthesising the scientific literature supporting it. The diversity of perspectives, approaches, and contexts critical to advancing quality improvement science, however, creates challenges. The paper explores the heterogeneity in clinical quality improvement intervention (QII) publications.
Methods: A preliminary classification framework was developed for QII articles, aiming for categories homogeneous enough to support coherent scientific discussion on QII reporting standards and facilitate systematic review. QII experts were asked to identify articles important to QII science. The framework was tested and revised by applying it to the article set. The final framework screened articles into (1) empirical literature on development and testing of QIIs; (2) QII stories, theories, and frameworks; (3) QII literature syntheses and meta-analyses; or (4) development and testing of QII-related tools. To achieve homogeneity, category (1) required division into (1a) development of QIIs; 1(b) history, documentation, or description of QIIs; or (1c) success, effectiveness or impact of QIIs.
Results: By discussing unique issues and established standards relevant to each category, QII stakeholders can advance QII practice and science, including the scope and conduct of systematic literature reviews.
C1 [Rubenstein, L. V.; Farmer, M. M.; Asch, S. M.; Yano, E. M.; Shekelle, P. W.] Vet Affairs Greater Los Angeles Healthcare Syst S, North Hills, CA 91343 USA.
[Rubenstein, L. V.; Hempel, S.; Asch, S. M.; Shekelle, P. W.] RAND Corp, Santa Monica, CA USA.
[Rubenstein, L. V.; Yano, E. M.] Univ Calif Los Angeles, Sch Publ Hlth, Los Angeles, CA 90024 USA.
[Rubenstein, L. V.; Asch, S. M.; Shekelle, P. W.] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
[Dougherty, D.] Agcy Healthcare Res & Qual, Rockville, MD USA.
RP Rubenstein, LV (reprint author), Vet Affairs Greater Los Angeles Healthcare Syst S, 16111 Plummer St 152, North Hills, CA 91343 USA.
EM lisa_rubenstein@rand.org
FU Agency for Healthcare Research and Quality (AHRQ) [HHSP233200400717P];
Centers for Disease Control and Prevention
FX Agency for Healthcare Research and Quality (AHRQ) under a contract to
LVR ( contract no HHSP233200400717P) funded by an Interagency Agreement
between AHRQ and the Centers for Disease Control and Prevention.
NR 98
TC 31
Z9 31
U1 0
U2 1
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1475-3898
J9 QUAL SAF HEALTH CARE
JI Qual. Saf. Health Care
PD DEC
PY 2008
VL 17
IS 6
BP 403
EP 408
DI 10.1136/qshc.2008.028423
PG 6
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA 380YK
UT WOS:000261501800004
PM 19064654
ER
PT J
AU Boland, GWL
Blake, MA
Hahn, PF
Mayo-Smith, WW
AF Boland, Giles W. L.
Blake, Michael A.
Hahn, Peter F.
Mayo-Smith, William W.
TI Incidental Adrenal Lesions: Principles, Techniques, and Algorithms for
Imaging Characterization
SO RADIOLOGY
LA English
DT Review
ID CHEMICAL-SHIFT MR; CONTRAST-ENHANCED CT; POSITRON-EMISSION-TOMOGRAPHY;
GUIDED RADIOFREQUENCY ABLATION; NON-HODGKIN LYMPHOMA; HISTOGRAM
ANALYSIS; ADRENOCORTICAL CARCINOMA; PATHOLOGICAL CORRELATION; F-18-FDG
PET/CT; UNENHANCED CT
AB Incidental adrenal lesions are commonly detected at computed tomography, and lesion characterization is critical, particularly in the oncologic patient. Imaging tests have been developed that can accurately differentiate these lesions by using a variety of principles and techniques, and each is discussed in turn. An imaging algorithm is provided to guide radiologists toward the appropriate test to make the correct diagnosis. (C) RSNA, 2008
C1 [Boland, Giles W. L.; Blake, Michael A.; Hahn, Peter F.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02111 USA.
[Mayo-Smith, William W.] Brown Univ, Rhode Isl Hosp, Warren Alpert Med Sch, Dept Radiol, Providence, RI 02903 USA.
RP Boland, GWL (reprint author), Massachusetts Gen Hosp, Dept Radiol, White Bldg 270C,55 Fruit St, Boston, MA 02111 USA.
EM gboland@partners.org
NR 116
TC 138
Z9 147
U1 0
U2 4
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0033-8419
J9 RADIOLOGY
JI Radiology
PD DEC
PY 2008
VL 249
IS 3
BP 756
EP 775
DI 10.1148/radiol.2493070976
PG 20
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 375UP
UT WOS:000261139300006
PM 19011181
ER
PT J
AU Kopans, DB
Rusby, JE
AF Kopans, Daniel B.
Rusby, Jennifer E.
TI Cutaneous Caves and Subcutaneous Adipose Columns in the Breast:
Radiologic-Pathologic Correlation
SO RADIOLOGY
LA English
DT Article
ID SKIN THICKNESS
AB Purpose: To investigate the histologic correlations of the innumerable 2-3-mm radiolucencies that project over the breast, as seen on mammograms.
Materials and Methods: With institutional review board approval and HIPAA compliance, this work involved detailed x-ray imaging of discarded tissue from two mastectomy specimens, together with histologic examination of the skin and subcutaneous fat and evaluation of the skin during reduction mammoplasty surgery in two patients.
Results: Comparison of the histologic findings with the findings on x-ray images demonstrated that the lucencies seen by using mammography are cutaneous caves in the underside of the dermis into which insert columns of fat projecting up from the subcutaneous adipose tissue. This finding was confirmed with evaluation of the skin during reduction surgery.
Conclusion: As far as is known, this is the first description of a complex of anatomic structures that explain radiolucencies evident by using mammography. (C) RSNA, 2008
C1 [Kopans, Daniel B.] Massachusetts Gen Hosp, Avon Comprehens Breast Evaluat Ctr, Wang Ambulatory Care Ctr, Dept Radiol,Breast Imaging Div, Boston, MA 02114 USA.
[Rusby, Jennifer E.] Massachusetts Gen Hosp, Avon Comprehens Breast Evaluat Ctr, Wang Ambulatory Care Ctr, Div Surg Oncol, Boston, MA 02114 USA.
RP Kopans, DB (reprint author), Massachusetts Gen Hosp, Avon Comprehens Breast Evaluat Ctr, Wang Ambulatory Care Ctr, Dept Radiol,Breast Imaging Div, 15 Parkman St,Suite 240, Boston, MA 02114 USA.
EM dkopans@partners.org
NR 7
TC 7
Z9 7
U1 0
U2 1
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0033-8419
J9 RADIOLOGY
JI Radiology
PD DEC
PY 2008
VL 249
IS 3
BP 779
EP 784
DI 10.1148/radiol.2493080112
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 375UP
UT WOS:000261139300007
PM 18849506
ER
PT J
AU Bredella, MA
Misra, M
Miller, KK
Madisch, I
Sarwar, A
Cheung, A
Klibanski, A
Gupta, R
AF Bredella, Miriam A.
Misra, Madhusmita
Miller, Karen K.
Madisch, Ijad
Sarwar, Ammar
Cheung, Arnold
Klibanski, Anne
Gupta, Rajiv
TI Distal Radius in Adolescent Girls with Anorexia Nervosa: Trabecular
Structure Analysis with High-Resolution Flat-Panel Volume CT
SO RADIOLOGY
LA English
DT Article
ID X-RAY ABSORPTIOMETRY; BONE-STRUCTURE; COMPUTED-TOMOGRAPHY; TEMPORAL
BONE; MICRO-CT; OSTEOPOROSIS; DENSITY; WOMEN; FRACTURES; CALCANEUS
AB Purpose: To examine trabecular microarchitecture with high-resolution flat-panel volume computed tomography (CT) and bone mineral density (BMD) with dual-energy x-ray absorptiometry (DXA) in adolescent girls with anorexia nervosa (AN) and to compare these results with those in normal-weight control subjects.
Materials and Methods: The study was approved by the institutional review board and complied with HIPAA guidelines. Informed consent was obtained. Twenty adolescent girls, 10 with mild AN (mean age, 15.9 years; range, 13-18 years) and 10 age- and sex-matched normal-weight control subjects (mean age, 15.9 years; range, 12-18 years) underwent flat-panel volume CT of distal radius to determine apparent trabecular bone volume fraction (BV/TV), apparent trabecular number (TbN), apparent trabecular thickness (TbTh), and apparent trabecular separation (TbSp). All subjects underwent DXA of spine, hip, and whole body to determine BMD and body composition. The means and standard deviations (SDs) of structure parameters were calculated for AN and control groups. Groups were compared (Student t test). Linear regression analysis was performed.
Results: AN subjects compared with control subjects, respectively, showed significantly lower mean values for BV/TV (0.37% +/- 0.05 [SD] vs 0.46% +/- 0.03, P = .0002) and TbTh (0.31 mm +/- 0.03 vs 0.39 mm +/- 0.03, P < .0001) and higher mean values for TbSp (0.54 mm +/- 0.13 vs 0.44 mm +/- 0.04, P = .02). TbN was lower in AN subjects than in control subjects, but the difference was not significant (1.17 mm(-3) +/- 0.15 vs 1.22 mm(-3) +/- 0.07, P = .43). There was no significant difference in BMD between AN and control subjects. BMD parameters showed positive correlation with BV/TV and TbTh in the control group (r = 0.55-0.84, P = .05-.01) but not in AN patients.
Conclusion: Flat-panel volume CT is effective in evaluation of trabecular structure in adolescent girls with AN and demonstrates that bone structure is abnormal in these patients compared with that in normal-weight control subjects despite normal BMD. (c) RSNA, 2008
C1 [Bredella, Miriam A.; Madisch, Ijad; Sarwar, Ammar; Cheung, Arnold; Gupta, Rajiv] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Misra, Madhusmita; Miller, Karen K.; Klibanski, Anne] Massachusetts Gen Hosp, Dept Med, Neuroendocrine Unit, Boston, MA 02114 USA.
[Misra, Madhusmita] Massachusetts Gen Hosp Children, Pediat Endocrine Unit, Boston, MA USA.
RP Bredella, MA (reprint author), Massachusetts Gen Hosp, Dept Radiol, 55 Fruit St,Yawkey 6E, Boston, MA 02114 USA.
EM mbredella@partners.org
FU National Institutes of Health [R01 DK062249, K23 RR018851, M01 RR01066]
FX Supported by National Institutes of Health grants R01 DK062249, K23
RR018851, and M01 RR01066.
NR 45
TC 51
Z9 51
U1 1
U2 1
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0033-8419
J9 RADIOLOGY
JI Radiology
PD DEC
PY 2008
VL 249
IS 3
BP 938
EP 946
DI 10.1148/radiol.2492080173
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 375UP
UT WOS:000261139300026
PM 19011190
ER
PT J
AU Cantwell, CP
Pena, CS
Gervais, DA
Hahn, PF
Dawson, SL
Mueller, PR
AF Cantwell, Colin P.
Pena, Constantino S.
Gervais, Debra A.
Hahn, Peter F.
Dawson, Steven L.
Mueller, Peter R.
TI Thirty Years' Experience with Balloon Dilation of Benign Postoperative
Biliary Strictures: Long-term Outcomes
SO RADIOLOGY
LA English
DT Article
ID ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY; FOLLOW-UP;
CLINICAL-TRIAL; DILATATION; MANAGEMENT; HEPATICOJEJUNOSTOMY; SUCCESS
AB Purpose: To determine the effectiveness of percutaneous balloon dilation of benign postoperative biliary strictures.
Materials and Methods: We received approval from our institutional review board to undertake this retrospective HIPAA-compliant study, and informed consent was waived. From April 1, 1977, to April 1, 2007, percutaneous biliary balloon dilation (PBBD) was performed in 85 patients with benign biliary strictures. In the 75 patients with follow-up (31 male, 44 female; mean age, 56 years; mean follow-up, 8 years), 205 PBBD procedures were performed during 112 treatments of 84 biliary strictures. PBBD of the stricture was performed with a noncompliant balloon (8-12-mm diameter). PBBD procedures were repeated at 2- to 14-day intervals until cholangiography demonstrated free drainage of contrast material to the bowel and no residual stenosis. An internal-external biliary drain was left in situ for a mean of 14-22 days and removed after a clinical trial of catheter clamping and a normal cholangiogram.
Results: All procedures were technically successful, and 52, 11, 10, and two patients underwent a total of one, two, three, and four PBBD treatments, respectively. Four of 205 procedures (2%) led to major complications: two subphrenic abscesses, one hepatic arterial pseudoaneurysm, and one case of hematobilia treated with transfusion. Six patients died from unrelated causes and three from hepatitis C-related liver failure. The probability of a patient not developing clinically significant restenosis at 5, 10, 15, 20, and 25 years was 0.52, 0.49, 0.49, 0.41, and 0.41, respectively, after the first PBBD treatment and 0.43, 0.30, 0.20, 0.20, and 0.20, respectively, after the second PBBD treatment. No significant difference was found in the rate of clinically significant restenosis after the first PBBD between strictures at anastomotic and nonanastomotic sites (P = .75). During the follow-up period, 56 of 75 patients (75%) had successful management with PBBD.
Conclusion: PBBD of benign strictures demonstrates long-term effectiveness. No significant difference was found in the rate of clinically significant restenosis after PBBD of biliary strictures at anastomotic and nonanastomotic sites. (c) RSNA, 2008
C1 Massachusetts Gen Hosp, Div Abdominal & Intervent Radiol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Cantwell, CP (reprint author), St Vincents Hosp, Elm Pk, Dublin 4, Ireland.
EM ccanty@gofree.indigo.ie
NR 17
TC 18
Z9 21
U1 0
U2 2
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0033-8419
J9 RADIOLOGY
JI Radiology
PD DEC
PY 2008
VL 249
IS 3
BP 1050
EP 1057
DI 10.1148/radiol.2491080050
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 375UP
UT WOS:000261139300039
PM 18812559
ER
PT J
AU Roedl, JB
Colen, RR
Holalkere, NS
Fischman, AJ
Choi, NC
Blake, MA
AF Roedl, Johannes B.
Colen, Rivka R.
Holalkere, Nagaraj S.
Fischman, Alan J.
Choi, Noah C.
Blake, Michael A.
TI Adenocarcinomas of the esophagus: Response to chemoradiotherapy is
associated with decrease of metabolic tumor volume as measured on
PET-CT. Comparison to histopathologic and clinical response evaluation
SO RADIOTHERAPY AND ONCOLOGY
LA English
DT Article
DE Esophageal cancer; PET-CT; Tumor volume; Chemoradiotherapy; Response
ID POSITRON-EMISSION-TOMOGRAPHY; CELL LUNG-CANCER; NEOADJUVANT
CHEMORADIOTHERAPY; FDG-PET; ESOPHAGOGASTRIC JUNCTION; ENDOSCOPIC
ULTRASOUND; CARCINOMA; THERAPY; CHEMOTHERAPY; SURVIVAL
AB Purpose: We determined whether evaluation of treatment response is feasible by measuring metabolic tumor volume parameters on 18F-FDG (Fluorodeoxyglucose) PET-CT (Positron emission tomography-Computed tomography). We compared the response evaluation based on metabolic tumor volume parameters to a histopathologic and clinical response evaluation (clinical response criteria: RECIST criteria = Response evaluation criteria in solid tumors, and WHO criteria = World health organization). Patients and methods: A total of 51 study subjects with adenocarcinomas (Type I due to Siewert classification) of the esophagus underwent PET-CT scans before and after neoadjuvant chemoradiotherapy. Tumor volume, maximum and mean standardized uptake values (SUV) were assessed before and after chemoradiotherapy. Furthermore, the total lesion glycolysis (TLG) was calculated by multiplying the tumor volume by the mean SUV of the volume. Clinical response evaluation was performed with endoscopic ultrasound and CT using RECIST and WHO criteria. The reference standard for treatment response was the postsurgical histopathology. Results: The decrease of tumor volume between the pre- and post-treatment PET-CT scans was a better predictor of histopathologic response and survival than the decrease of the SUV and of the clinical response evaluation based on RECIST and WHO criteria. The highest accuracy, however, was achieved when using the TLG for the identification of treatment responders. A decrease of the TLG by >78% between pre- and post-therapy scans predicted histopathologic response with a sensitivity and specificity of 91% and 93%, respectively. Conclusions: Tumor volume and TLG can be used to assess treatment response and survival in patients with esophageal adenocarcinoma. (C) 2008 Elsevier Ireland Ltd. All rights reserved. Radiotherapy and Oncology 89 (2008) 278-286.
C1 [Roedl, Johannes B.; Colen, Rivka R.; Holalkere, Nagaraj S.; Fischman, Alan J.; Blake, Michael A.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Choi, Noah C.] Massachusetts Gen Hosp, Div Radiat Oncol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Roedl, JB (reprint author), Massachusetts Gen Hosp, Dept Radiol, Fruit St 55, Boston, MA 02114 USA.
EM johannes.roedl@gmail.com
OI Holalkere, Nagaraj/0000-0001-6324-7682
NR 33
TC 62
Z9 67
U1 1
U2 8
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0167-8140
J9 RADIOTHER ONCOL
JI Radiother. Oncol.
PD DEC
PY 2008
VL 89
IS 3
BP 278
EP 286
DI 10.1016/j.radonc.2008.06.014
PG 9
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 388WL
UT WOS:000262050600005
PM 18701180
ER
PT J
AU Pawlicki, T
Yoo, S
Court, LE
McMillan, SK
Rice, RK
Russell, JD
Pacyniak, JM
Woo, MK
Basran, PS
Shoales, J
Boyer, AL
AF Pawlicki, Todd
Yoo, Sua
Court, Laurence E.
McMillan, Sharon K.
Rice, Roger K.
Russell, J. Donald
Pacyniak, John M.
Woo, Milton K.
Basran, Parminder S.
Shoales, Jason
Boyer, Arthur L.
TI Moving from IMRT QA measurements toward independent computer
calculations using control charts
SO RADIOTHERAPY AND ONCOLOGY
LA English
DT Article
DE Statistical Process Control; Control charts; IMRT QA; Independent
computer calculation
ID INTENSITY-MODULATED RADIOTHERAPY; QUALITY-ASSURANCE; VERIFICATION
AB Background and purpose: In this study, we investigated IMRT QA using Statistical Process Control for the purpose of comparing the processes of patient-specific measurements and the corresponding independent computer calculations.
Materials and methods: Point dose data from the treatment planning system (TPS), independent computer calculations, and physical measurements for prostate and head and neck cases were studied. Control charts were used to analyze the IMRT QA processes from several institutions in the academic and community setting. Control charts are a method to describe the performance of a process. The width of the control chart limits (or action limits) describes the process' ability to meet clinical specifications of +/- 5%. In all, 24 process comparisons were made (112 measurement QA and 12 independent computer calculation QA).
Results: For head and neck IMRT QA, the average process ability for the measurement QA was +/- 6.9% compared to +/- 7.2% for the independent computer calculation QA. For prostate IMRT QA, the average process ability was 4.4% for both measurement QA and independent computer calculation QA. It was found that 11 of the 24 processes were in control. At none of the institutions were the processes of measurements and independent computer calculations both in control and performing within clinical specifications.
Conclusion: There is room to improve the processes of IMRT QA measurements and independent computer calculations. In situations where the improvement of the processes is such that each is in control and well within clinical specifications, it may be appropriate to suspend patient-specific IMRT QA measurements for every patient in the place of independent computer calculations. (C) 2008 Elsevier Ireland Ltd. All rights reserved. Radiotherapy and Oncology 89 (2008) 330-337.
C1 [Pawlicki, Todd; Rice, Roger K.] Univ Calif San Diego, Dept Radiat Oncol, La Jolla, CA 92093 USA.
[Yoo, Sua] Duke Univ, Dept Radiat Oncol, Durham, NC 27706 USA.
[Court, Laurence E.] Brigham & Womens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
[McMillan, Sharon K.] Decatur Mem Hosp, Dept Radiat Oncol, Decatur, IL USA.
RP Pawlicki, T (reprint author), Univ Calif San Diego, Dept Radiat Oncol, 3855 Hlth Sci Dr 0843, La Jolla, CA 92093 USA.
EM tpaw@ucsd.edu
NR 12
TC 32
Z9 34
U1 0
U2 0
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0167-8140
J9 RADIOTHER ONCOL
JI Radiother. Oncol.
PD DEC
PY 2008
VL 89
IS 3
BP 330
EP 337
DI 10.1016/j.radonc.2008.07.002
PG 8
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 388WL
UT WOS:000262050600011
PM 18701175
ER
PT J
AU Hardin, CC
Harris, RS
AF Hardin, C. Corey
Harris, R. Scott
TI Mid-Frequency Ventilation in Acute Respiratory Distress Syndrome: The
New Wave ... length?
SO RESPIRATORY CARE
LA English
DT Editorial Material
ID ACUTE LUNG INJURY; TIDAL-VOLUME VENTILATION; PRESSURE; MODEL
C1 [Harris, R. Scott] Massachusetts Gen Hosp, Pulm & Crit Care Unit, Dept Med, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Harris, RS (reprint author), Massachusetts Gen Hosp, Pulm & Crit Care Unit, Dept Med, Bulfinch 148,55 Fruit St, Boston, MA 02114 USA.
EM rharris@partners.org
NR 15
TC 1
Z9 1
U1 0
U2 0
PU DAEDALUS ENTERPRISES INC
PI IRVING
PA 9425 N MAC ARTHUR BLVD, STE 100, IRVING, TX 75063-4706 USA
SN 0020-1324
J9 RESP CARE
JI Respir. Care
PD DEC
PY 2008
VL 53
IS 12
BP 1655
EP 1656
PG 2
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 381BZ
UT WOS:000261511100002
PM 19025696
ER
PT J
AU Kasinath, BS
Mariappan, MM
Sataranatarajan, K
Lee, MJ
Choudhury, GG
Feliers, D
AF Kasinath, B. S.
Mariappan, M. M.
Sataranatarajan, K.
Lee, M. J.
Choudhury, G. Ghosh
Feliers, D.
TI Novel mechanisms of protein synthesis in diabetic nephropathy-role of
mRNA translation
SO REVIEWS IN ENDOCRINE & METABOLIC DISORDERS
LA English
DT Article
DE Protein synthesis; MicroRNA; Signaling reactions; Insulin; Glucose;
Angiotensin II; Vascular endothelial growth factor
ID RENAL EPITHELIAL-CELLS; GLYCOGEN-SYNTHASE KINASE-3; ANGIOTENSIN-II;
INITIATION-FACTOR; SIGNALING PATHWAYS; MAMMALIAN TARGET;
GENE-EXPRESSION; LET-7 MICRORNA; HIGH GLUCOSE; HNRNP-K
AB Ambient protein levels are affected by both synthesis and degradation. Synthesis of a protein is regulated by transcription and messenger RNA (mRNA) translation. Translation has emerged as an important site of regulation of protein expression during development and disease. It is under the control of distinct factors that regulate initiation, elongation and termination phases. Regulation of translation occurs via signaling reactions, guanosine diphosphate-guanosine triphosphate binding and by participation of non-coding RNA species such as microRNA. Recent work has revealed an important role for translation in hypertrophy, matrix protein synthesis, elaboration of growth factors in in vivo and in vitro models of diabetic nephropathy. Studies of translation dysregulation in diabetic nephropathy have enabled identification of novel therapeutic targets. Translation of mRNA is a fertile field for exploration in investigation of kidney disease.
C1 [Kasinath, B. S.; Mariappan, M. M.; Sataranatarajan, K.; Lee, M. J.; Choudhury, G. Ghosh; Feliers, D.] Univ Texas Hlth Sci Ctr San Antonio, Dept Med, OBrien Kidney Res Ctr, San Antonio, TX 78229 USA.
[Kasinath, B. S.; Mariappan, M. M.; Sataranatarajan, K.; Lee, M. J.; Choudhury, G. Ghosh; Feliers, D.] S Texas Vet Hlth Care Syst, San Antonio, TX USA.
RP Kasinath, BS (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Med, OBrien Kidney Res Ctr, MC 7882,7703 Floyd Curl Dr, San Antonio, TX 78229 USA.
EM kasinath@uthscsa.edu
FU O'Brien Kidney Research Center, BSK, JLB [NIH-DK061597]; BSK
[NIH-DK077295]; American Diabetes Association [7-05-RA-60]; VA Research
Service; Juvenile Diabetes Research Foundation [3-2007-245]; American
Heart Association [SDG 0630283N]; VA Research Career Scientist Award;
[NIH-DK050190]
FX Studies were supported by grants from the NIH-DK061597 (O'Brien Kidney
Research Center, BSK, JLB), NIH-DK077295 (BSK), American Diabetes
Association-7-05-RA-60 (BSK), VA Research Service (BSK, GGC, JLB),
Juvenile Diabetes Research Foundation-3-2007-245 (MMM/BSK), NIH-DK050190
(GGC), American Heart Association SDG 0630283N (DF). GGC is a recipient
of the VA Research Career Scientist Award.
NR 83
TC 7
Z9 8
U1 0
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1389-9155
J9 REV ENDOCR METAB DIS
JI Rev. Endocr. Metab. Disord.
PD DEC
PY 2008
VL 9
IS 4
BP 255
EP 266
DI 10.1007/s11154-008-9091-3
PG 12
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 365BB
UT WOS:000260379800002
PM 18654857
ER
PT J
AU Byne, W
Tatusov, A
Yiannoulos, G
Vong, GS
Marcus, S
AF Byne, William
Tatusov, Alex
Yiannoulos, Georgia
Vong, Ghe S.
Marcus, Sue
TI Effects of mental illness and aging in two thalamic nuclei
SO SCHIZOPHRENIA RESEARCH
LA English
DT Article
DE Schizophrenia; Bipolar disorder; Psychosis; Aging; Oligodendrocyte;
Myelin
ID ANTERIOR CINGULATE CORTEX; MAJOR DEPRESSIVE DISORDER; EFFERENT
CONNECTIONS; NEURON NUMBER; OLIGODENDROCYTE DYSFUNCTION; NEUROPATHOLOGY
CONSORTIUM; HIPPOCAMPAL-FORMATION; ALZHEIMERS-DISEASE; PREFRONTAL
CORTEX; BIPOLAR DISORDER
AB We previously reported a schizophrenia associated reduction of neuronal and oligodendrocyte number in the anterior principal thalamic nucleus (APN) in a cohort of severely impaired elderly subjects with schizophrenia (SZ) relative to age matched nonpsychiatric controls (NCs). The present study was undertaken to determine 1) if those findings could be replicated in an independent sample of less chronically impaired subjects with SZ and NCs stratified across a broader age range; 2) if the findings are specific to SZ or are also seen in unipolar major depressive (MDD) or bipolar disorder (BPD); and 3) if the findings are specific to the APN or also seen in another thalamic nucleus. Computer assisted stereological methods were employed to determine the number of neurons and oligodendrocytes in the APN and centromedian nucleus (CMN) of the Nissl-stained thalamic sections maintained by the Stanley Foundation Brain Bank. This collection includes specimens from NCs and age matched subjects with diagnoses of SZ, MDD, or BPD who died between the ages of 25 and 68. Data were analyzed by mixed-effects linear regressions adjusting for demographic variables and known history of exposure to psychotropic medications.
Oligodendrocyte number was decreased in both nuclei relative to NCs in subjects with SZ and in that subset of subjects with BPD who had experienced psychotic episodes. Compared to NCs both of these patient groups also exhibited an attenuation of an age-related increase in the number of oligodendrocytes. Contrary to our previous report, we did not detect a SZ-associated deficit in neuronal number in the APN. A history of exposure to neuroleptics, however, was associated with a decrease in neuronal number in both nuclei, but this decrease did not vary in relation to cumulative lifetime neuroleptic exposure in fluphenazine equivalents. Among subjects with psychiatric diagnoses, exposure to lithium was associated with an increase in the number of oligodendrocytes. No effects were detected for exposure to anticonvulsants or for abuse of alcohol or other substances. Published by Elsevier B.V.
C1 [Byne, William; Tatusov, Alex; Yiannoulos, Georgia; Vong, Ghe S.] Bronx Vet Affairs Med Ctr, Div Basic & Lab Res, Bronx, NY 10468 USA.
[Byne, William; Tatusov, Alex; Vong, Ghe S.; Marcus, Sue] Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA.
RP Byne, W (reprint author), Bronx Vet Affairs Med Ctr, Div Basic & Lab Res, Res Bldg Rm 2F37,130 W Kingsbridge Rd, Bronx, NY 10468 USA.
EM william.byne@mssm.edu
FU NIH [MH66998, MH45212]; Veterans Merit Review Award
FX Supported by the Veterans Integrated Services Network-3 Mental Illness
Research, Education and Clinical Center, NIH grants MH66998, MH45212 and
a Veterans Merit Review Award.
NR 57
TC 17
Z9 18
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0920-9964
J9 SCHIZOPHR RES
JI Schizophr. Res.
PD DEC
PY 2008
VL 106
IS 2-3
BP 172
EP 181
DI 10.1016/j.schres.2008.08.023
PG 10
WC Psychiatry
SC Psychiatry
GA 385YU
UT WOS:000261850300010
PM 18835520
ER
PT J
AU Escamilla, M
Lee, BD
Ontiveros, A
Raventos, H
Nicolini, H
Mendoza, R
Jerez, A
Munoz, R
Medina, R
Figueroa, A
Walss-Bass, C
Armas, R
Contreras, S
Ramirez, ME
Dassori, A
AF Escamilla, Michael
Lee, Byung Dae
Ontiveros, Alfonso
Raventos, Henriette
Nicolini, Humberto
Mendoza, Ricardo
Jerez, Alvaro
Munoz, Rodrigo
Medina, Rolando
Figueroa, Andres
Walss-Bass, Consuelo
Armas, Regina
Contreras, Salvador
Ramirez, Mercedes E.
Dassori, Albana
TI The epsin 4 gene is associated with psychotic disorders in families of
Latin American origin
SO SCHIZOPHRENIA RESEARCH
LA English
DT Article
DE Epsin 4 gene; Schizophrenia; Phenotype; Biobehavioral Science; Single
nucleotide polymorphisms (SNPs)
ID LINKAGE DISEQUILIBRIUM; SCHIZOPHRENIA; SUSCEPTIBILITY; CLATHRIN;
ENTHOPROTIN; SUPPORT; LOCUS
AB This study attempted to replicate evidence for association of the Epsin 4 gene (which encodes enthoprotin, a protein involved in vesicular transport) to schizophrenia in a new sample of families segregating schizophrenia drawn from the Latin American population. 1423 subjects (767 with a history of psychosis) from 337 Latino families were genotyped using three single nucleotide polymorphisms (SNPs) spanning the Epsin 4 gene. A family based association test was utilized to test for association of these SNPs to the phenotypes of psychosis and schizophrenia. Haplotypes defined by these three SNPs showed significant association to the phenotype of psychosis in this sample (global p value=0.014, bi-allelic p value=0.047). Variation in the Epsin 4 gene is significantly associated with psychotic disorder in this Latino population. This provides additional support for the involvement of enthoprotin in the pathogenesis of schizophrenia and other psychotic disorders. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Escamilla, Michael; Lee, Byung Dae; Medina, Rolando; Walss-Bass, Consuelo; Contreras, Salvador; Ramirez, Mercedes E.; Dassori, Albana] Univ Texas Hlth Sci Ctr San Antonio, Dept Psychiat, Psychiat Genet Res Center, San Antonio, TX 78229 USA.
[Ontiveros, Alfonso] Inst Informac & Invest Salud Mental, Monterrey, Mexico.
[Raventos, Henriette] Univ Costa Rica, Ctr Invest Biol & Mol, San Jose, Costa Rica.
[Medina, Rolando; Dassori, Albana] S Texas Vet Hlth Syst, Dept Psychiat, San Antonio, TX USA.
[Nicolini, Humberto] Gep Estudios Med & Familiares Carracci SC, Mexico City, DF, Mexico.
[Mendoza, Ricardo] Univ Calif Los Angeles, Harbor Med Ctr, Dept Psychiat & Biobehav Sci, Torrance, CA 90509 USA.
[Jerez, Alvaro] Ctr Invest Biomed, Guatemala City, Guatemala.
[Munoz, Rodrigo] Univ Calif San Diego, Dept Psychiat, San Diego, CA 92103 USA.
[Escamilla, Michael; Figueroa, Andres] Univ Texas Hlth Sci Ctr San Antonio, Reg Acad Hlth Ctr, S Texas Med Genet Res Group, Edinburg, TX USA.
[Armas, Regina] Univ Calif San Francisco, Langley Porter Psychiat Inst, San Francisco, CA 94143 USA.
[Figueroa, Andres] Univ Texas Pan Amer, Dept Comp Sci, Edinburg, TX 78541 USA.
RP Escamilla, M (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Psychiat, Psychiat Genet Res Center, 7703 Floyd Curl Dr MC 7789, San Antonio, TX 78229 USA.
EM escamillam@uthscsa.edu
OI Nicolini, Humberto/0000-0003-2494-0067; Raventos,
Henriette/0000-0001-9423-8308; Jerez Magana, Alvaro
Antonio/0000-0002-1208-3769
FU International Neuro-Genetics Association of Spanish America and the
United States (INGASU); NIMH; University of Texas Health Science Center
at San Antonio [MH60881]; University of California at Los Angeles-Harbor
[MH60875]
FX Additional principal investigators who participated in these grants were
Dr. Henriette Raventos (University of Costa Rica, San Jose, Costa Rica),
Dr. Alfonso Ontiveros (Instituto de Informacion de Investigacion en
Salud Mental. Monterrey, Mexico), Dr. Humberto Nicolini (Medical and
Family Research Group. Carracci S.C., Mexico City. Mexico). Dr. Rodrigo
Munoz (Family Health Centers of San Diego, California), and Dr. Alvaro
Jerez (Centro Internacional de Trastornos Afectivos y de la Conducta
Adictiva-CITACA, Guatemala). Additional investigators from the
University ofTexas Health Science Center at San Antonio included Dr.
Albana Dassori and Dr. Rolando Medina.
NR 19
TC 8
Z9 9
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0920-9964
J9 SCHIZOPHR RES
JI Schizophr. Res.
PD DEC
PY 2008
VL 106
IS 2-3
BP 253
EP 257
DI 10.1016/j.schres.2008.09.005
PG 5
WC Psychiatry
SC Psychiatry
GA 385YU
UT WOS:000261850300020
PM 18929466
ER
PT J
AU Morrow, EM
Kane, A
Goff, DC
Walsh, CA
AF Morrow, Eric M.
Kane, Anna
Goff, Donald C.
Walsh, Christopher A.
TI Sequence analysis of P21-activated kinase 3 (PAK3) in chronic
schizophrenia with cognitive impairment
SO SCHIZOPHRENIA RESEARCH
LA English
DT Article
DE Schizophrenia; Mental retardation; Pfropfschizophrenie; P21-activated
kinase PAK3; Cognitive development
ID LINKED MENTAL-RETARDATION; DISORDERS; MUTATION
AB The P27-activated kinase PAK3 is critical for cognitive development and truncating mutations cause non-syndromic mental retardation (MR). Missense mutations are also associated with psychotic disorders, most commonly with schizophrenia involving premorbid MR, namely "pfropfschizophrenie". We set out to measure the frequency of sequence variants in PAK3 in schizophrenia without premorbid MR. We conducted complete gene reseqeuncing of all coding exons and exon-intron boundaries in patients with schizophrenia with cognitive impairment but without premorbid MR. Deleterious variants in schizophrenia alone were rare (<1/ 159 or 0.6%). Thereby, while PAK3 remains a strong biological candidate in psychosis, evidence from human genetics provides strongest support for a link to pfropfschizophrenie and not to schizophrenia without premorbid intellectual disability. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Morrow, Eric M.; Kane, Anna; Walsh, Christopher A.] Harvard Univ, Childrens Hosp Boston, Sch Med, Div Genet, Boston, MA 02115 USA.
[Morrow, Eric M.; Kane, Anna; Walsh, Christopher A.] Howard Hughes Med Inst, Div Neurogenet, Chevy Chase, MD USA.
[Morrow, Eric M.; Kane, Anna; Walsh, Christopher A.] Beth Israel Deaconess Med Ctr, Dept Neurol, Boston, MA USA.
[Morrow, Eric M.; Goff, Donald C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat,Schizophrenia Res Program, Boston, MA 02114 USA.
RP Walsh, CA (reprint author), Harvard Univ, Childrens Hosp Boston, Sch Med, Div Genet, New Res Bldg 266,77 Ave Louis Pasteur, Boston, MA 02115 USA.
EM cwalsh@bidmc.harvard.edu
RI Morrow, Eric/J-2767-2013
FU NIMH [1 K23MH080954-01, K24 MH002025-06]; Burroughs Wellcome Fund;
Rappaport Research Scholarship
FX We are grateful to the patients who participated in this study. We are
grateful for support from the NIMH (1 K23MH080954-01 to E.M.M). E.M.M.
holds a Career Award for Medical Scientists from the Burroughs Wellcome
Fund and is also grateful for support from the Rappaport Research
Scholarship in Neuroscience at MGH. This work was supported by a
NARSADYoung Investigator award to E.M.M. who is the Sidney R. Baer. Jr.
Foundation Investigator. D.C.G. is supported by a mid-career development
award from the NIMH (K24 MH002025-06). CAW. is an Investigator of the
Howard Hughes Medical Institute.
NR 15
TC 6
Z9 6
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0920-9964
J9 SCHIZOPHR RES
JI Schizophr. Res.
PD DEC
PY 2008
VL 106
IS 2-3
BP 265
EP 267
DI 10.1016/j.schres.2008.08.021
PG 3
WC Psychiatry
SC Psychiatry
GA 385YU
UT WOS:000261850300022
PM 18805672
ER
PT J
AU Goff, DC
Cather, C
Gottlieb, JD
Evins, AE
Walsh, J
Raeke, L
Otto, MW
Schoenfeld, D
Green, MF
AF Goff, Donald C.
Cather, Corinne
Gottlieb, Jennifer D.
Evins, A. Eden
Walsh, Jared
Raeke, Lisa
Otto, Michael W.
Schoenfeld, David
Green, Michael F.
TI Once-weekly D-cycloserine effects on negative symptoms and cognition in
schizophrenia: An exploratory study
SO SCHIZOPHRENIA RESEARCH
LA English
DT Article
DE Schizophrenia; D-cycloserine; Negative symptoms; Cognition; Memory
consolidation
ID AGONIST D-CYCLOSERINE; PLACEBO-CONTROLLED TRIAL; D-ASPARTATE RECEPTORS;
CONVENTIONAL NEUROLEPTICS; GLYCINE RECEPTOR; D-SERINE; EXTINCTION;
MEMORY; ANTIPSYCHOTICS; EFFICACY
AB Background: Daily dosing with D-cycloserine has inconsistently improved negative symptoms in schizophrenia patients, whereas intermittent dosing significantly facilitated exposure-based therapy in two studies of patients with phobic anxiety. In animal models. single-dose administration enhances memory consolidation, but tachyphylaxis develops with repeated dosing. The objective of this exploratory study was to assess whether once-weekly dosing with D-cycloserine will produce persistent improvements in negative symptoms and cognition.
Methods: Fifty stable adult schizophrenia outpatients treated with any antipsychotic except clozapine were enrolled and 38 were randomized, double-blind, in a parallel-group, eight-week add-on trial of D-cycloserine 50 mg or placebo administered once-weekly. Symptom rating scales and a cognitive battery were administered at baseline and week 8 before the dose of study drug. As an exploratory analysis of memory consolidation, the Logical Memory Test, modified to measure recall after 7 days, was administered at baseline and after the first weekly dose of D-cycloserine. The primary outcome measures were change from baseline to week 8 on the SANS total score and on a composite cognitive score.
Results: Thirty-three subjects (87%) completed the trial. D-cycloserine significantly improved SANS total scores compared to placebo at week 8. Cognitive performance did not improve with D-cycloserine at 8 weeks. Delayed thematic recall on the Logical Memory Test was significantly improved with the first dose of D-cycloserine compared to placebo. Performance on immediate thematic recall and item recall on the Logical Memory Test did not differ between treatments.
Conclusions: Once-weekly dosing with D-cycloserine for 8 weeks produced persistent improvement of negative symptoms compared to placebo, although statistical significance was, in part, the result of worsening of negative symptoms with placebo. Consistent with animal models, a single dose of D-cycloserine facilitated memory consolidation tested after 7 days on a test of thematic recall. These results must be considered preliminary since a number of outcomes were examined without correction for multiple tests. These findings suggest that once-weekly dosing with D-cycloserine for the treatment of negative symptoms merits further study, as do D-cycloserine effects on memory consolidation. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Goff, Donald C.; Cather, Corinne; Gottlieb, Jennifer D.; Evins, A. Eden; Walsh, Jared; Raeke, Lisa] Massachusetts Gen Hosp, Dept Psychiat, Freedom Trail Clin, Boston, MA 02114 USA.
[Goff, Donald C.; Cather, Corinne; Gottlieb, Jennifer D.; Evins, A. Eden; Schoenfeld, David] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Schoenfeld, David] MGH Biostat Ctr, Boston, MA 02114 USA.
[Otto, Michael W.] Boston Univ, Ctr Anxiety & Related Disorders, Boston, MA 02215 USA.
[Green, Michael F.] Univ Calif Los Angeles, Semel Inst Neurosci & Human Behav, Los Angeles, CA 90095 USA.
[Green, Michael F.] Univ Calif Los Angeles, VA Greater Angeles Healthcare Syst, Los Angeles, CA 90095 USA.
RP Goff, DC (reprint author), Massachusetts Gen Hosp, Dept Psychiat, Freedom Trail Clin, 25 Staniford St,2nd Floor, Boston, MA 02114 USA.
EM golf@psych.mgh.harvard.edu; ccather@partners.org;
jgottlieb2@partners.org; a_eden_evins@hms.harvard.edu;
jpwalsh@partners.org; lraeke@partners.org; mwotto@bu.edu;
dschoenfeld@partners.org; mgreen@ucla.edu
FU NIMH [2 K24 MH002025-06, 2 P50 MH0060450-08A1]
FX This study was funded by NIMH 2 K24 MH002025-06 (D. Goff) and NIMH 2 P50
MH0060450-08A1 (J. Coyle). Dr. Goff had full access to all of the data
in the study and takes responsibility for the integrity of the data and
the accuracy of the data analysis.
NR 42
TC 66
Z9 66
U1 1
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0920-9964
J9 SCHIZOPHR RES
JI Schizophr. Res.
PD DEC
PY 2008
VL 106
IS 2-3
BP 320
EP 327
DI 10.1016/j.schres.2008.08.012
PG 8
WC Psychiatry
SC Psychiatry
GA 385YU
UT WOS:000261850300031
PM 18799288
ER
PT J
AU Zlotoff, DA
Schwarz, BA
Bhandoola, A
AF Zlotoff, Daniel A.
Schwarz, Benjamin A.
Bhandoola, Avinash
TI The long road to the thymus: the generation, mobilization, and
circulation of T-cell progenitors in mouse and man
SO SEMINARS IN IMMUNOPATHOLOGY
LA English
DT Review
DE Hematopoietic stem cells; Hematopoietic progenitors; Mobilization;
Thymic settling; Early thymic progenitors
ID HEMATOPOIETIC STEM-CELLS; COLONY-STIMULATING FACTOR; COMMON LYMPHOID
PROGENITORS; CHEMOKINE RECEPTOR CXCR4; UMBILICAL-CORD BLOOD; MURINE
FETAL LIVER; BONE-MARROW-CELLS; SELF-RENEWAL; PERIPHERAL-BLOOD; LINEAGE
COMMITMENT
AB The majority of T cells develop in the thymus. T-cell progenitors in the thymus do not self-renew and so progenitor cells must be continuously imported from the blood into the thymus to maintain T-cell production. Recent work has shed light on both the identity of the cells that home to the thymus and the molecular mechanisms involved. This review will discuss the cells in the bone marrow and blood that are involved in early thymopoiesis in mouse and man. Understanding the pre-thymic steps in T-cell development may translate into new therapeutics, especially in the field of hematopoietic stem cell transplantation.
C1 [Zlotoff, Daniel A.; Bhandoola, Avinash] Univ Penn, Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
[Schwarz, Benjamin A.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
RP Bhandoola, A (reprint author), Univ Penn, Sch Med, Dept Pathol & Lab Med, 264 John Morgan Bldg,3620 Hamilton Walk, Philadelphia, PA 19104 USA.
EM bhandooa@mail.med.upenn.edu
FU National Institutes of Health; Scholar of the Leukemia and Lymphoma
Society
FX We thank Taku Kambayashi, Jeremiah Bell, and Jennifer Burg for their
comments. This work was supported by grants from the National Institutes
of Health. A. B. is a Scholar of the Leukemia and Lymphoma Society.
NR 142
TC 20
Z9 20
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1863-2297
J9 SEMIN IMMUNOPATHOL
JI Semin. Immunopathol.
PD DEC
PY 2008
VL 30
IS 4
BP 371
EP 382
DI 10.1007/s00281-008-0133-4
PG 12
WC Immunology; Pathology
SC Immunology; Pathology
GA 379QX
UT WOS:000261412400002
PM 18925398
ER
PT J
AU Nuernberg, AM
Christiani, DC
AF Nuernberg, Amy M.
Christiani, David C.
TI The Future of Occupationally Related Diffuse Lung Disease
SO SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Review
DE Occupational lung disease; toxicogenomics; biomarkers; environmental
health; gene-environment interactions
ID GENE-ENVIRONMENT INTERACTIONS; WORKERS; SUSCEPTIBILITY; POLYMORPHISMS;
ASSOCIATION; BIOMARKER
AB In the last 10 years alone, several new occupational lung diseases have been described. Progress in improving measurements of exposures and risk factors for exposure-related diseases has turned to molecular epidemiology and genomics methods in recent years. There has been a dramatic increase in the number of studies investigating genetic associations and biomarkers in occupationally related diffuse lung diseases. Specifically, identifying common variant genetic polymorphisms that may have low penetrance (modest relative risk), but Impart a high population-attributable risk of disease when exposure Occurs, has been a recent research focus. Candidate gene methodology is currently the Most Popular approach, but genome-wide association studies are now more feasible for studying gene-environment interactions. The results of these studies will better define populations at particularly high risk of disease after exposure, but it is important to realize that the mainstay of prevention for occupationally related diffuse lung disease remains prevention and control of airborne exposures.
C1 [Nuernberg, Amy M.; Christiani, David C.] Massachusetts Gen Hosp, Dept Med, Div Pulm & Crit Care, Boston, MA 02115 USA.
[Nuernberg, Amy M.; Christiani, David C.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
[Nuernberg, Amy M.; Christiani, David C.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
RP Christiani, DC (reprint author), Massachusetts Gen Hosp, Div Pulm & Crit Care Med, 665 Huntington Ave,SPH I-1407, Boston, MA 02115 USA.
EM dchris@hsph.harvard.edu
NR 28
TC 1
Z9 1
U1 0
U2 0
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 1069-3424
J9 SEMIN RESP CRIT CARE
JI Semin. Respir. Crit. Care Med.
PD DEC
PY 2008
VL 29
IS 6
BP 680
EP 684
DI 10.1055/s-0028-1101278
PG 5
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 380EG
UT WOS:000261448400011
PM 19221966
ER
PT J
AU Hough, S
AF Hough, Sigmund
TI From the Editor
SO SEXUALITY AND DISABILITY
LA English
DT Editorial Material
C1 VA Boston Healthcare Syst, Spinal Cord Injury Serv SCI 128, W Roxbury, MA 02132 USA.
RP Hough, S (reprint author), VA Boston Healthcare Syst, Spinal Cord Injury Serv SCI 128, 1400 VFW Pkwy, W Roxbury, MA 02132 USA.
EM Sigmund_Hough@hms.harvard.edu
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 0146-1044
J9 SEX DISABIL
JI Sex. Disabil.
PD DEC
PY 2008
VL 26
IS 4
BP 187
EP 187
DI 10.1007/s11195-008-9095-7
PG 1
WC Rehabilitation
SC Rehabilitation
GA 373JF
UT WOS:000260967200001
ER
PT J
AU Burns, S
Mahalik, J
Hough, S
Greenwell, A
AF Burns, Shaun Michael
Mahalik, James R.
Hough, Sigmund
Greenwell, Ashley N.
TI Adjustment to Changes in Sexual Functioning Following Spinal Cord
Injury: The Contribution of Men's Adherence to Scripts for Sexual
Potency
SO SEXUALITY AND DISABILITY
LA English
DT Article
DE Adjustment; Gender scripts; Masculinity; Spinal cord injury; Sexual
functioning; Treatment interventions
ID QUALITY-OF-LIFE; ERECTILE DYSFUNCTION; HELP-SEEKING; SATISFACTION;
MASCULINITY; POPULATION; GENDER; HEALTH; IMPACT; PREDICTORS
AB Recent epidemiological statistics suggest approximately 250,000 people in the United States live with a spinal cord injury. Men constitute roughly 82% of these individuals. Following spinal cord injury, men frequently experience significant changes in their sexual functioning. As a result, men with spinal cord injuries are at an increased risk for experiencing adjustment difficulties. Unfortunately, relatively little is known about factors that promote or impede men's adjustment to these changes. In the present article, the authors highlight how men's adherence to gender scripts for sexual potency may contribute to their adjustment following a spinal cord injury. To organize the discussion, the authors review related literature and, through case examples, illustrate how men's adherence to this gender norm may influence their post-injury mental health. Directions for gender-sensitive interventions and future clinical research are provided.
C1 [Burns, Shaun Michael; Hough, Sigmund; Greenwell, Ashley N.] Boston Univ, Harvard Med Sch, Spinal Cord Injury Serv, VA Boston Healthcare Syst, Boston, MA 02215 USA.
[Mahalik, James R.] Boston Coll, Dept Counseling Dev & Educ Psychol, Chestnut Hill, MA 02167 USA.
RP Burns, S (reprint author), Boston Univ, Harvard Med Sch, Spinal Cord Injury Serv, VA Boston Healthcare Syst, Boston, MA 02215 USA.
NR 64
TC 4
Z9 4
U1 4
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0146-1044
J9 SEX DISABIL
JI Sex. Disabil.
PD DEC
PY 2008
VL 26
IS 4
BP 197
EP 205
DI 10.1007/s11195-008-9091-y
PG 9
WC Rehabilitation
SC Rehabilitation
GA 373JF
UT WOS:000260967200003
ER
PT J
AU Hough, B
AF Hough, Brian H.
TI Shriver M.: What's Wrong with Timmy?
SO SEXUALITY AND DISABILITY
LA English
DT Book Review
C1 VA Boston Healthcare Syst, Volunteer Serv Spinal Cord Injury Serv SCI 128, W Roxbury, MA 02132 USA.
RP Hough, B (reprint author), VA Boston Healthcare Syst, Volunteer Serv Spinal Cord Injury Serv SCI 128, 1400 VFW Pkwy, W Roxbury, MA 02132 USA.
EM author6698@yahoo.com
NR 1
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0146-1044
J9 SEX DISABIL
JI Sex. Disabil.
PD DEC
PY 2008
VL 26
IS 4
BP 241
EP 242
DI 10.1007/s11195-008-9102-z
PG 2
WC Rehabilitation
SC Rehabilitation
GA 373JF
UT WOS:000260967200007
ER
PT J
AU Reichardt, B
Sarwar, A
Bartling, SH
Cheung, A
Grasruck, M
Leidecker, C
Bredella, MA
Brady, TJ
Gupta, R
AF Reichardt, Benjamin
Sarwar, Ammar
Bartling, Soenke H.
Cheung, Arnold
Grasruck, Michael
Leidecker, Christianne
Bredella, Miriam A.
Brady, Thomas J.
Gupta, Rajiv
TI Musculoskeletal applications of flat-panel volume CT
SO SKELETAL RADIOLOGY
LA English
DT Review
DE Musculoskeletal applications; Flat-panel volume computed tomography;
High-resolution imaging; Trabecular imaging
ID HIGH-RESOLUTION MRI; COMPUTED-TOMOGRAPHY; STEM-CELLS; FUNDAMENTAL
PRINCIPLES; SCAPHOID FRACTURE; SPIRAL CT; BONE; RADIOGRAPHY; DETECTORS;
SCAFFOLDS
AB Flat-panel volume computed tomography (fpVCT) is a recent development in imaging. We discuss some of the musculoskeletal applications of a high-resolution flat-panel CT scanner. FpVCT has four main advantages over conventional multidetector computed tomography (MDCT): high-resolution imaging; volumetric coverage; dynamic imaging; omni-scanning. The overall effective dose of fpVCT is comparable to that of MDCT scanning. Although current fpVCT technology has higher spatial resolution, its contrast resolution is slightly lower than that of MDCT (5-10HU vs. 1-3HU respectively). We discuss the efficacy and potential utility of fpVCT in various applications related to musculoskeletal radiology and review some novel applications for pediatric bones, soft tissues, tumor perfusion, and imaging of tissue-engineered bone growth. We further discuss high-resolution CT and omni-scanning (combines fluoroscopic and tomographic imaging).
C1 [Reichardt, Benjamin; Sarwar, Ammar; Cheung, Arnold; Bredella, Miriam A.; Brady, Thomas J.; Gupta, Rajiv] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA 02114 USA.
[Bartling, Soenke H.] DKFZ, Dept Med Phys Radiol, Heidelberg, Germany.
[Grasruck, Michael; Leidecker, Christianne] Siemens Med Solut, Forchheim, Germany.
RP Gupta, R (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, 55 Fruit St,FND-216, Boston, MA 02114 USA.
EM rgupta1@partners.org
NR 23
TC 24
Z9 24
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0364-2348
J9 SKELETAL RADIOL
JI Skeletal Radiol.
PD DEC
PY 2008
VL 37
IS 12
BP 1069
EP 1076
DI 10.1007/s00256-008-0473-0
PG 8
WC Orthopedics; Radiology, Nuclear Medicine & Medical Imaging
SC Orthopedics; Radiology, Nuclear Medicine & Medical Imaging
GA 365BC
UT WOS:000260379900002
PM 18443787
ER
PT J
AU Burgess, DJ
Crowley-Matoka, M
Phelan, S
Dovidio, JF
Kerns, R
Roth, C
Saha, S
van Ryn, M
AF Burgess, Diana Jill
Crowley-Matoka, Megan
Phelan, Sean
Dovidio, John F.
Kerns, Robert
Roth, Craig
Saha, Somnath
van Ryn, Michelle
TI Patient race and physicians' decisions to prescribe opioids for chronic
low back pain
SO SOCIAL SCIENCE & MEDICINE
LA English
DT Article
DE USA; Health disparities; Chronic pain; Medical decision-making; Race;
Men; Prescribing
ID PRIMARY-CARE PHYSICIANS; CORONARY-HEART-DISEASE; CHRONIC NONCANCER PAIN;
PROVIDERS CONTRIBUTE; ETHNIC DISPARITIES; RACIAL-DIFFERENCES;
RACE/ETHNICITY; GENDER; HEALTH; COMMUNICATION
AB Nonwhite patients are less likely than white patients to have their pain adequately treated. This study examined the influence of patient race and patient verbal and nonverbal behavior on primary care physicians' treatment decisions for chronic low back pain in men. We randomly assigned physicians to receive a paper-based, clinical vignette of a chronic pain patient that differed in terms of patient race (white vs. black), verbal behavior ("challenging" vs. "non-challenging"), and nonverbal behavior (confident vs. dejected vs. angry). We employed a between-subjects factorial design and surveyed primary care physicians (N = 382), randomly selected from the American Medical Association Physician Masterfile. The primary dependent measure was the physician's decision as to whether (s)he would switch the patient to a higher dose or stronger type of opioid. Logistic regression was used to determine the effects of patient characteristics on physicians' prescribing decisions. There was a significant interaction between patient verbal behavior and patient race on physicians' decisions to prescribe opioids. Among black patients, physicians were significantly more likely to state that they would switch to a higher dose or stronger opioid for patients exhibiting "challenging" behaviors (e.g., demanding a specific narcotic, exhibiting anger) compared to those exhibiting "non-challenging" behaviors (55.1%). For white patients there was an opposite pattern of results in which physicians were slightly more likely to escalate treatment for patients exhibiting "non-challenging" (64.3%) vs. "challenging" (54.5%) verbal behaviors. Results point to the need for better understanding of the way a complex interplay of non-clinical characteristics affects physician behavior in order to improve quality of pain management and other clinical decision-making. Published by Elsevier Ltd.
C1 [Burgess, Diana Jill] VA Med Ctr, Ctr Chron Dis Outcomes Res, Minneapolis, MN 55419 USA.
[Burgess, Diana Jill; Roth, Craig] Univ Minnesota, Dept Med, Minneapolis, MN 55455 USA.
[Crowley-Matoka, Megan] Univ Pittsburgh, Dept Med, Pittsburgh, PA 15260 USA.
[Crowley-Matoka, Megan] Pittsburgh Vet Affairs Med Ctr, Ctr Hlth Equity Res & Promot, Pittsburgh, PA USA.
[Crowley-Matoka, Megan] Univ Pittsburgh, Dept Anthropol, Pittsburgh, PA 15260 USA.
[Phelan, Sean] Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA.
[Dovidio, John F.] Yale Univ, Dept Psychol, New Haven, CT 06520 USA.
[Kerns, Robert; Saha, Somnath] Yale Univ, Dept Psychiat, VA Connecticut Healthcare Syst, New Haven, CT 06520 USA.
[Kerns, Robert; Saha, Somnath] Yale Univ, Dept Neurol, VA Connecticut Healthcare Syst, New Haven, CT 06520 USA.
[Kerns, Robert; Saha, Somnath] Yale Univ, Dept Psychol, VA Connecticut Healthcare Syst, New Haven, CT 06520 USA.
[Roth, Craig] Univ Minnesota, Minneapolis Vet Affairs Med Ctr, Minneapolis, MN 55455 USA.
[van Ryn, Michelle] Univ Minnesota, Div Epidemiol, Minneapolis, MN 55455 USA.
[van Ryn, Michelle] Univ Minnesota, Dept Family Med & Community Hlth, Minneapolis, MN 55455 USA.
[Saha, Somnath] Oregon Hlth & Sci Univ, Portland Vet Affairs Med Ctr, Portland, OR 97201 USA.
[Saha, Somnath] Oregon Hlth & Sci Univ, Dept Med, Portland, OR 97201 USA.
RP Burgess, DJ (reprint author), VA Med Ctr, Ctr Chron Dis Outcomes Res, 1 Vet Dr, Minneapolis, MN 55419 USA.
EM diana.burgess@med.va.gov; mcm29@imap.pitt.edu; phel0085@umn.edu;
john.dovidio@yale.edu; robert.kerns@va.gov; craig.roth@va.gov;
sahas@ohsu.edu; vanry001@umn.edu
RI VAN RYN, MICHELLE/B-1664-2010; Burgess, Diana/A-1946-2016
NR 62
TC 40
Z9 40
U1 3
U2 18
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0277-9536
J9 SOC SCI MED
JI Soc. Sci. Med.
PD DEC
PY 2008
VL 67
IS 11
BP 1852
EP 1860
DI 10.1016/j.socscimed.2008.09.009
PG 9
WC Public, Environmental & Occupational Health; Social Sciences, Biomedical
SC Public, Environmental & Occupational Health; Biomedical Social Sciences
GA 383EZ
UT WOS:000261658200025
PM 18926612
ER
PT J
AU Krieger, N
Chen, JT
Waterman, PD
Hartman, C
Stoddard, AM
Quinn, MM
Sorensen, G
Barbeau, EM
AF Krieger, Nancy
Chen, Jarvis T.
Waterman, Pamela D.
Hartman, Cathy
Stoddard, Anne M.
Quinn, Margaret M.
Sorensen, Glorian
Barbeau, Elizabeth M.
TI The inverse hazard law: Blood pressure, sexual harassment, racial
discrimination, workplace abuse and occupational exposures in US
low-income black, white and Latino workers
SO SOCIAL SCIENCE & MEDICINE
LA English
DT Article
DE Blood pressure; Health inequities; Occupational health; Racial
discrimination; Sexual harassment; Workplace abuse; USA
ID UNITED-STATES; AFRICAN-AMERICANS; SOCIAL HAZARDS; PUBLIC-HEALTH;
RISK-FACTORS; SELF-REPORT; HYPERTENSION; POPULATION; PREVALENCE; ADULTS
AB Research on societal determinants of health suggests the existence of an "inverse hazard law." which we define as: "The accumulation of health hazards tends to vary inversely with the power and resources of the populations affected." Yet, little empirical research has systematically investigated this topic, including in relation to workplace exposures. We accordingly designed the United for Health study (Greater Boston Area, Massachusetts, 2003-2004) to investigate the joint distribution and health implications of workplace occupational hazards (dust, fumes, chemical, noise, ergonomic strain) and social hazards (racial discrimination, sexual harassment, workplace abuse). Focusing on blood pressure as our health outcome, we found that among the 1202 low-income multi-racial/ethnic working class participants in our cohort - of whom 40% lived below the US poverty line 79% reported exposure to at least one social hazard and 82% to at least one high-exposure occupational hazard. Only sexual harassment, the least common social hazard, was associated with elevated systolic blood pressure (SBP) among the women workers. By contrast, no statistically significant associations were detectable between the other additional highly prevalent social and occupational hazards and SBP: we did, however, find suggestive evidence of an association between SBP and response to unfair treatment, implying that in a context of high exposure, differential susceptibility to the exposure matters. These results interestingly contrast to our prior findings for this same cohort, in which we found associations between self-reported experiences of racial discrimination and two other health outcomes: psychological distress and cigarette smoking. Likely explanations for these contrasting findings include: (a) the differential etiologic periods and pathways involving somatic health, mental health, and health behaviors, and (b) the high prevalence of adverse exposures, limiting the ability to detect significant associations. As clarified by the "inverse hazard law," to understand health inequities, research is needed that contrasts exposures and health status population-wide, not just among those most inequitably exposed. (c) 2008 Elsevier Ltd. All rights reserved.
C1 [Krieger, Nancy; Chen, Jarvis T.; Waterman, Pamela D.] Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Boston, MA 02115 USA.
[Hartman, Cathy; Barbeau, Elizabeth M.] Hlth Dialog, Boston, MA 02109 USA.
[Stoddard, Anne M.] New England Res Inst, Watertown, MA 02472 USA.
[Quinn, Margaret M.] Univ Massachusetts, Dept Work Environm, Lowell, MA USA.
[Sorensen, Glorian] Dana Farber Canc Inst, Ctr Community Based Res, Boston, MA 02115 USA.
RP Krieger, N (reprint author), Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Kresge 717,677 Huntington Ave, Boston, MA 02115 USA.
EM nkrieger@hsph.harvard.edu
FU PHS HHS [R01 OHO7366-01, R01 OHO7366-01S]
NR 50
TC 48
Z9 48
U1 3
U2 10
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0277-9536
J9 SOC SCI MED
JI Soc. Sci. Med.
PD DEC
PY 2008
VL 67
IS 12
BP 1970
EP 1981
DI 10.1016/j.socscimed.2008.09.039
PG 12
WC Public, Environmental & Occupational Health; Social Sciences, Biomedical
SC Public, Environmental & Occupational Health; Biomedical Social Sciences
GA 388AY
UT WOS:000261993900005
PM 18950922
ER
PT J
AU Singh, S
Khosla, S
Gupta, V
AF Singh, Sarabjeet
Khosla, Sandeep
Gupta, Vishal
TI The Role of Drug-Eluting Stents in Treating Cardiac Transplant
Vasculopathy
SO SOUTHERN MEDICAL JOURNAL
LA English
DT Editorial Material
ID CORONARY-ARTERY-DISEASE; ALLOGRAFT VASCULOPATHY; RECIPIENTS;
MULTICENTER; ANGIOPLASTY; PREVENTION; REJECTION; OUTCOMES
C1 Chicago Med Sch & Affiliated Hosp, Dept Med, Cardiol Sect, Chicago, IL USA.
Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Intervent Cardiol, Boston, MA USA.
RP Singh, S (reprint author), Mt Sinai Hosp, Dept Cardiol, Chicago, IL 60608 USA.
EM sarabjeetsingh_2000@yahoo.com
NR 11
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0038-4348
J9 SOUTH MED J
JI South.Med.J.
PD DEC
PY 2008
VL 101
IS 12
BP 1198
EP 1199
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 384XR
UT WOS:000261778000005
PM 19005449
ER
PT J
AU Hansson, T
Hansson, E
Malchau, H
AF Hansson, Tommy
Hansson, Elisabeth
Malchau, Henrik
TI Utility of Spine Surgery A Comparison of Common Elective Orthopaedic
Surgical Procedures
SO SPINE
LA English
DT Article
DE quality of life; utility; spine surgery; elective surgery; spinal
stenosis
ID LOW-BACK-PAIN; TRIAL; FUSION; EUROQOL; EQ-5D; STATE; DISC
AB Study Design. A 1-year prospective observational cohort study.
Objective. To compare the utility before and 1 year after elective spine surgery with some other common orthopaedic surgical procedures.
Summary of Background Data. By using global measures like EQ-5D and SF-36 for the determination of the utility, the changes in quality of life, quality of life (QoL) after an intervention different diagnoses, and treatments can be compared. Total hip replacement (THR) has become almost golden standard in this respect.
Methods. Seven hundred seventy-seven subjects with different common orthopaedic diagnoses scheduled for elective surgery were just before surgery and 1 year after surgery answering both EQ-5D and SF-36. Four groups with different spine diagnoses and procedures were formed and compared with 8 other diagnoses and treatment groups. Results. Before surgery, subjects with spine diagnoses reported the lowest QoL of all diagnoses compared. Surgery for spinal stenosis, spondylolisthesis, and instability meant the largest improvement of all surgical interventions. Surgery for NHP gave a moderately good improvement, whereas surgery for CLBP only marginally improved those operated. Particularly THR but also TKR more or less completely normalized QoL but made it from a relatively high preoperative level. The greatest improvements after spine surgery, other surgical procedures, and different diagnoses were in the pain/discomfort domain.
Conclusion. Spinal surgery in spinal stenosis, spondylolisthesis, and instability had in comparison to other types of elective orthopaedic surgery an outstanding better ability to improve the operated subject's health-related quality of life than other types of elective orthopaedic surgery. The utility of HNP surgery was somewhat lower and was rather marginal for those operated for nonspecific CLBP.
C1 [Hansson, Tommy] SU Sahlgrenska Acad, Dept Orthopaed, S-41345 Gothenburg, Sweden.
[Malchau, Henrik] Massachusetts Gen Hosp, Dept Orthopaed, Boston, MA 02114 USA.
RP Hansson, T (reprint author), SU Sahlgrenska Acad, Dept Orthopaed, Bruna Straket 11, S-41345 Gothenburg, Sweden.
EM tommy.hansson@orthop.gu.se
FU FAS, Goteborg University; AFA
FX Supported in part by the grants from FAS, Goteborg University, and AFA.
NR 26
TC 28
Z9 28
U1 3
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0362-2436
J9 SPINE
JI SPINE
PD DEC 1
PY 2008
VL 33
IS 25
BP 2819
EP 2830
DI 10.1097/BRS.0b013e31818e2914
PG 12
WC Clinical Neurology; Orthopedics
SC Neurosciences & Neurology; Orthopedics
GA 378SY
UT WOS:000261345400017
PM 19050588
ER
PT J
AU Eckman, MH
Wong, LKS
Soo, YOY
Lam, W
Yang, SR
Greenberg, SM
Rosand, J
AF Eckman, Mark H.
Wong, Lawrence K. S.
Soo, Yannie O. Y.
Lam, Wynnie
Yang, Song Ran
Greenberg, Steven M.
Rosand, Jonathan
TI Patient-Specific Decision-Making for Warfarin Therapy in Nonvalvular
Atrial Fibrillation How Will Screening With Genetics and Imaging Help?
SO STROKE
LA English
DT Article
DE atrial fibrillation; cerebral hemorrhage; decision support techniques;
genetics; magnetic resonance imaging
ID CEREBRAL AMYLOID ANGIOPATHY; SPONTANEOUS INTRACEREBRAL HEMORRHAGE;
MATTER HYPERINTENSITY VOLUME; RANDOMIZED CONTROLLED-TRIALS;
APOLIPOPROTEIN-E EPSILON-4; GRADIENT-ECHO MRI; QUALITY-OF-LIFE;
RISK-FACTORS; INTRACRANIAL HEMORRHAGE; ANTITHROMBOTIC THERAPY
AB Background and Purpose-Intracerebral hemorrhage (ICH) accounts for a majority of long-term morbidity and mortality associated with bleeding while on warfarin. Both ICH and warfarin-related ICH appear to have a genetic component. Furthermore, advanced neuroimaging using MRI can now identify individuals at increased risk of ICH. We explore whether screening strategies that include genetic profiling and neuroimaging might improve the safety of chronic anticoagulation for atrial fibrillation by identifying individuals from whom warfarin should be withheld.
Methods-We used a Markov state transition decision model. Effectiveness was measured in quality-adjusted life-years. Data sources included the English language literature using MEDLINE searches and bibliographies from selected articles along with empirical data from our institutions. The base case was a 69-year-old man with newly diagnosed nonvalvular atrial fibrillation.
Results-For patients at average risk for thromboembolic events and known to possess a hypothetical genetic profile increasing risk for warfarin ICH, anticoagulation remains the preferred strategy until the relative hazard of ICH exceeds 23.8. Genetic profiling would be favored for patients at low risk of thromboembolism (1.5% per year) if the hypothetical gene variant(s) conferred a relative risk of ICH > 4.1. Screening strategies in which patients underwent genotyping and MRI before anticoagulation did not improve aggregate patient outcomes unless the predictive power of MRI exceeded current best guess estimates and patients were at low to moderate risk of thromboembolism.
Conclusion-Currently identified genetic markers of bleeding risk do not confer a risk of ICH sufficiently high to warrant routine genetic testing for patients at average risk of thromboembolism. Even if patients undergo screening with MRI as well as genotyping, currently available data on the role of MRI on risk of ICH and warfarin ICH do not support use of these tests for withholding anticoagulation in patients with atrial fibrillation. (Stroke. 2008; 39: 3308-3315.)
C1 [Eckman, Mark H.] Univ Cincinnati, Med Ctr, Div Gen Internal Med, Cincinnati, OH 45267 USA.
[Eckman, Mark H.] Univ Cincinnati, Med Ctr, Ctr Clin Effectiveness, Cincinnati, OH 45267 USA.
[Wong, Lawrence K. S.; Soo, Yannie O. Y.; Lam, Wynnie] Chinese Univ Hong Kong, Dept Neurol, Hong Kong, Hong Kong, Peoples R China.
Prince Wales Hosp, Acute Stroke Unit, Hong Kong, Hong Kong, Peoples R China.
[Yang, Song Ran] Sun Yat Sen Univ, Dept Neurol, Guangzhou 510275, Guangdong, Peoples R China.
[Greenberg, Steven M.; Rosand, Jonathan] Massachusetts Gen Hosp, Dept Neurol, Hemorrhag Stroke Res Grp, Boston, MA 02114 USA.
[Rosand, Jonathan] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
RP Eckman, MH (reprint author), Univ Cincinnati, Med Ctr, Div Gen Internal Med, POB 670535, Cincinnati, OH 45267 USA.
EM mark.eckman@uc.edu
RI Wong, Ka Sing Lawrence/N-3434-2015
OI Wong, Ka Sing Lawrence/0000-0002-2031-9866
FU National Institute of Diabetes and Digestive and Kidney Diseases [K23
DK075599]; National Heart, Lung, and Blood Institute [K30 HL078581-01];
Foundation for Informed Medical Decision Making; National Institutes of
Neurological Disorders and Stroke [K23 NS42695-01, R01 NS04217]; Deane
Institute for Integrative Study of Atrial Fibrillation and Stroke
FX This work was supported by the National Institute of Diabetes and
Digestive and Kidney Diseases (K23 DK075599, to M. H. E.), National
Heart, Lung, and Blood Institute (K30 HL078581-01, to M. H. E.), and
Foundation for Informed Medical Decision Making (to M. H. E.); by the
National Institutes of Neurological Disorders and Stroke (K23
NS42695-01, to J. R., and R01 NS04217, to J. R. and S. M. G.), and the
Deane Institute for Integrative Study of Atrial Fibrillation and Stroke
(to J. R.).
NR 68
TC 26
Z9 26
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD DEC
PY 2008
VL 39
IS 12
BP 3308
EP 3315
DI 10.1161/STROKEAHA.108.523159
PG 8
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 377AT
UT WOS:000261224800027
PM 18845797
ER
PT J
AU Murata, Y
Rosell, A
Scannevin, RH
Rhodes, KJ
Wang, XY
Lo, EH
AF Murata, Yoshihiro
Rosell, Anna
Scannevin, Robert H.
Rhodes, Kenneth J.
Wang, Xiaoying
Lo, Eng H.
TI Extension of the Thrombolytic Time Window With Minocycline in
Experimental Stroke
SO STROKE
LA English
DT Article
DE cerebral ischemia; hemorrhagic transformation; edema; tPA;
neuroprotection
ID TISSUE-PLASMINOGEN-ACTIVATOR; FOCAL CEREBRAL-ISCHEMIA;
SPINAL-CORD-INJURY; AMYOTROPHIC-LATERAL-SCLEROSIS; TRAUMATIC
BRAIN-INJURY; CYTOCHROME-C RELEASE; HEMORRHAGIC TRANSFORMATION;
MATRIX-METALLOPROTEINASE; INTRACEREBRAL HEMORRHAGE; NEUTROPHIL
INFILTRATION
AB Background and Purpose-Thrombolysis with tPA is the only FDA-approved therapy for acute ischemic stroke. But its widespread application remains limited by narrow treatment time windows and the related risks of cerebral hemorrhage. In this study, we ask whether minocycline can prevent tPA-associated cerebral hemorrhage and extend the reperfusion window in an experimental stroke model in rats.
Methods-Spontaneously hypertensive rats were subjected to embolic focal ischemia using homologous clots and treated with: saline at 1 hour; early tPA at 1 hour, delayed tPA at 6 hours; minocycline at 4 hours; combined minocycline at 4 hours plus tPA at 6 hours. Infarct volumes and hemorrhagic transformation were quantified at 24 hours. Gelatin zymography was used to measure blood levels of circulating matrix metalloproteinase-9 (MMP-9).
Results-Early 1-hour thrombolysis restored perfusion and reduced infarction. Late 6-hour tPA did not decrease infarction but instead worsened hemorrhagic conversion. Combining minocycline with delayed 6-hour tPA decreased plasma MMP-9 levels, reduced infarction, and ameliorated brain hemorrhage. Blood levels of MMP-9 were also significantly correlated with volumes of infarction and hemorrhage.
Conclusion-Combination therapy with minocycline may extend tPA treatment time windows in ischemic stroke. (Stroke. 2008; 39: 3372-3377.)
C1 [Murata, Yoshihiro; Rosell, Anna; Wang, Xiaoying; Lo, Eng H.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Neuroprotect Res Lab,Dept Neurol, Charlestown, MA USA.
Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Radiol, Charlestown, MA USA.
[Scannevin, Robert H.; Rhodes, Kenneth J.] Biogen IDEC, Cambridge, MA USA.
RP Lo, EH (reprint author), Neuroprotect Res Lab, MGH E 149-2401, Charlestown, MA 02129 USA.
EM Lo@helilx.mgh.harvard.edu
FU NIH [R01-NS37074, R01-NS48422, R01-NS56548, P50-NS10828]; American Heart
Association; Ministerio de Educacion y Ciencia [EXT2006/766]
FX This work was supported in part by NIH grants R01-NS37074, R01-NS48422,
R01-NS56548, P50-NS10828, and a Bugher award from the American Heart
Association. Anna Rosell is the recipient of a postdoctoral grant from
Ministerio de Educacion y Ciencia (EXT2006/766).
NR 39
TC 98
Z9 102
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD DEC
PY 2008
VL 39
IS 12
BP 3372
EP 3377
DI 10.1161/STROKEAHA.108.514026
PG 6
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 377AT
UT WOS:000261224800036
PM 18927459
ER
PT J
AU Foerch, C
Arai, K
Jin, G
Park, KP
Pallast, S
van Leyen, K
Lo, EH
AF Foerch, Christian
Arai, Ken
Jin, Guang
Park, Kyung-Pil
Pallast, Stefanie
van Leyen, Klaus
Lo, Eng H.
TI Experimental Model of Warfarin-Associated Intracerebral Hemorrhage
SO STROKE
LA English
DT Article
DE cerebral hemorrhage; warfarin; mice
ID ORAL ANTICOAGULANT-THERAPY; ATRIAL-FIBRILLATION; HEMATOMA; STROKE; MICE;
MANAGEMENT
AB Background and Purpose-Future demographic changes predict an increase in the number of patients with atrial fibrillation. As long-term anticoagulation for the prevention of ischemic strokes becomes more prevalent, the burden of warfarin-associated intracerebral hemorrhage (W-ICH) is likely to grow. However, little is known about the clinical aspects and pathophysiologic mechanisms of W-ICH. This study describes the development of a mouse model of W-ICH in which hematoma growth and outcomes can be correlated with anticoagulation parameters.
Methods-CD-1 mice were treated with warfarin (2 mg/kg per 24 hours) added to drinking water. ICH was induced by stereotactic injection of collagenase type VII (0.075 U) into the right striatum. Hemorrhagic blood volume was quantified by means of a photometric hemoglobin assay 2 and 24 hours after hemorrhage induction. Neurologic outcomes were assessed on a 5-point scale.
Results-The international normalized ratio in nonanticoagulated mice was 0.8 +/- 0.1. After 24 (W-24) and 30 (W-30) hours of warfarin pretreatment, international normalized ratio values increased to 3.5 +/- 0.9 and 7.2 +/- 3.4, respectively. Compared with nonanticoagulated mice, mean hemorrhagic blood volume determined 24 hours after hemorrhage induction was found to be 2.5-fold larger in W-24 mice (P=0.019) and 3.1-fold larger in W-30 mice (P < 0.001, n=10 per group). Mortality at 24 hours after hemorrhage induction was 0% in nonanticoagulated mice, 10% in W-24 mice, and 30% in W-30 mice. Hematoma enlargement between 2 and 24 hours after hemorrhage induction was -1.4% for nonanticoagulated mice, 22.9% for W-24 mice, and 62.2% for W-30 mice.
Conclusions-This study characterizes the first experimental model of W-ICH. It may be helpful in gaining further insights into the pathophysiology of W-ICH and may be used for testing the efficacy of treatment strategies, such as hemostatic therapy, in this severe subtype of stroke. (Stroke. 2008; 39: 3397-3404.)
C1 [Foerch, Christian; Arai, Ken; Jin, Guang; Park, Kyung-Pil; Pallast, Stefanie; van Leyen, Klaus; Lo, Eng H.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Neuroprotect Res Lab, Charlestown, MA 02129 USA.
RP Foerch, C (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Neuroprotect Res Lab, Room 2414,149 13th St, Charlestown, MA 02129 USA.
EM foerch@em.uni-frankfurt.de
RI van Leyen, Klaus/C-9126-2013;
OI Park, Kyung-Pil/0000-0003-4952-3796
FU Deutsche Forschungsgemeinschaft; National Institutes of Health
[R01-NS37074, R01-NS48422, R01-NS53560, R01-NS56458]
FX This study was supported in part by a grant from the Deutsche
Forschungsgemeinschaft and by National Institutes of Health grants
R01-NS37074, R01-NS48422, R01-NS53560, and R01-NS56458.
NR 25
TC 57
Z9 57
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD DEC
PY 2008
VL 39
IS 12
BP 3397
EP 3404
DI 10.1161/STROKEAHA.108.517482
PG 8
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 377AT
UT WOS:000261224800039
PM 18772448
ER
PT J
AU Veillette, G
Fernandez-del Castillo, C
AF Veillette, Gregory
Fernandez-del Castillo, Carlos
TI Distal Biliary Malignancy
SO SURGICAL CLINICS OF NORTH AMERICA
LA English
DT Article
ID PRIMARY SCLEROSING CHOLANGITIS; EXTRAHEPATIC BILE-DUCTS;
PROGNOSTIC-FACTORS; PANCREATIC FISTULAS; CHOLANGIOCARCINOMA;
PANCREATICODUODENECTOMY; MANAGEMENT; CANCER; EXPERIENCE; CARCINOMA
AB Distal cholangiocarcinoma (malignancy in the common bile duct from the cystic duct to the ampulla) remains a rare diagnosis. Most of these lesions are adenocarcinomas, and typically present with painless jaundice. If suspected, a high-quality CT scan and endoscopic retrograde cholangiopancreatography are required for diagnosis and staging. In addition, identification of risk factors, use of tumor markers, and advanced molecular testing may enhance diagnostic and prognostic capabilities. The treatment of choice for resectable disease is pancreaticoduodenectomy and the overall 5-year survival for resected distal cholangiocarcinoma remains 20% to 30%.
C1 [Veillette, Gregory; Fernandez-del Castillo, Carlos] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
RP Veillette, G (reprint author), Massachusetts Gen Hosp, Dept Surg, 15 Parkman St,Wang Ambulatory Care Ctr Suite 460, Boston, MA 02114 USA.
EM gveillette@partners.org
NR 68
TC 14
Z9 14
U1 1
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0039-6109
J9 SURG CLIN N AM
JI Surg. Clin.-North Am.
PD DEC
PY 2008
VL 88
IS 6
BP 1429
EP +
DI 10.1016/j.suc.2008.07.003
PG 20
WC Surgery
SC Surgery
GA 383SP
UT WOS:000261694000017
PM 18992603
ER
PT J
AU Lancaster, RT
Hutter, MM
AF Lancaster, Robert T.
Hutter, Matthew M.
TI Bands and bypasses: 30-day morbidity and mortality of bariatric surgical
procedures as assessed by prospective, multi-center, risk-adjusted
ACS-NSQIP data
SO SURGICAL ENDOSCOPY AND OTHER INTERVENTIONAL TECHNIQUES
LA English
DT Article; Proceedings Paper
CT Annual Meeting of the
Society-of-American-Gastrointestinal-and-Endoscopic-Surgeons
CY APR 09-12, 2008
CL Philadelphia, PA
SP Soc Amer Gastrointestinal & Endoscop Surg
DE Bariatric surgery; Adjustable gastric band; Gastric bypass; NSQIP;
Laparoscopic; Open
ID ROUX-EN-Y; LAPAROSCOPIC GASTRIC BYPASS; POSTOPERATIVE MORTALITY;
RANDOMIZED-TRIAL; NATIONAL TRENDS; SEVERE OBESITY; UNITED-STATES; US
ADULTS; FOLLOW-UP; SURGERY
AB Background Previous multi-institution comparisons of open and laparoscopic Roux-en-Y gastric bypass (ORYGB and LRYGB), and laparoscopic adjustable gastric banding (LAGB) have been limited by the lack of unique current procedural terminology (CPT) codes. Specific codes have been available for LRYGB and LAGB since 2005 and 2006, respectively. We compare the short-term safety of these procedures, using risk-adjusted clinical data from a multi-institutional quality improvement program.
Methods The America College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) Participant Use File (PUF) was used to compare patients undergoing LRYGB with those undergoing ORYGB or LAGB.
Results ORYGB versus LRYGB: The 2-year study period (2005-2006) included 5,777 patients (ORYGB = 1,146, LRYGB = 4,631). Patients undergoing ORYGB experienced a higher 30-day incidence of mortality (0.79% vs. 0.17%; p = 0.002), major complications rate (7.42% vs. 3.37%; p < 0.0001), any complication rate (13.18% vs. 6.69%; p < 0.0001), return visits to the OR (4.97% vs. 3.56%; p = 0.032), and longer postoperative length of stay (LOS) (median 3 vs. 2 days; p < 0.0001). After risk adjustment, ORYGB continued to demonstrate higher odds of major complication (OR = 2.04; [1.54, 2.69]). LAGB versus LRYGB: Analysis of 1 year of data from 2006 included 4,756 patients (LRYGB = 3,580, LAGB = 1,176). Those treated with LAGB experienced an equivalent 30-day mortality (0.09% vs. 0.14%; p = 1.0), and a lower rate of major complications (1.0% vs. 3.3%; p < 0.0001), any complication (2.6% vs. 6.7%; p < 0.0001), return visits to the OR (0.94% vs. 3.6%; p < 0.0001), and shorter postoperative LOS (median 1 vs. 2 days; p < 0.0001). Risk adjustment showed that LAGB was associated with a lower major complication odds (OR = 0.29; [0.16, 0.53]).
Conclusions Compared with LRYGB, ORYGB is associated with higher 30-day mortality and higher risk-adjusted major complication rate. While ORYGB may sometimes be indicated, a laparoscopic approach may be safer for RYGB when feasible. LAGB, compared with LRYGB, has a similarly low mortality rate and a small but statistically significant decrease in risk-adjusted 30-day complications. Clinical efficacy and long-term outcomes will need to be evaluated to determine superiority between these procedures.
C1 [Lancaster, Robert T.; Hutter, Matthew M.] Massachusetts Gen Hosp, Dept Surg, Codman Ctr Clin Effectiveness Surg, Boston, MA 02114 USA.
RP Hutter, MM (reprint author), Massachusetts Gen Hosp, Dept Surg, Codman Ctr Clin Effectiveness Surg, 15 Parkman St Wang ACC 335, Boston, MA 02114 USA.
EM rtlancaster@partners.org; mhutter@partners.org
NR 42
TC 69
Z9 69
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0930-2794
J9 SURG ENDOSC
JI Surg. Endosc.
PD DEC
PY 2008
VL 22
IS 12
BP 2554
EP 2563
DI 10.1007/s00464-008-0074-y
PG 10
WC Surgery
SC Surgery
GA 389JR
UT WOS:000262089200003
PM 18806945
ER
PT J
AU Rusby, JE
Smith, BL
AF Rusby, Jennifer E.
Smith, Barbara L.
TI Unanswered questions in nipple-sparing mastectomy
SO SURGICAL ONCOLOGY-OXFORD
LA English
DT Editorial Material
ID TRANSPLANTED NIPPLE; BREAST-CANCER; CARCINOMA
C1 [Rusby, Jennifer E.; Smith, Barbara L.] Massachusetts Gen Hosp, Div Surg Oncol, Boston, MA 02114 USA.
RP Smith, BL (reprint author), Massachusetts Gen Hosp, Div Surg Oncol, Yawkey 9A,55 Fruit St, Boston, MA 02114 USA.
EM blsmith1@partners.org
NR 10
TC 2
Z9 2
U1 0
U2 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0960-7404
J9 SURG ONCOL
JI Surg. Oncol.-Oxf.
PD DEC
PY 2008
VL 17
IS 4
BP 259
EP 260
DI 10.1016/j.suronc.2008.05.006
PG 2
WC Oncology; Surgery
SC Oncology; Surgery
GA 370IF
UT WOS:000260755200001
PM 18602258
ER
PT J
AU Riboldi, M
Chen, GTY
Baroni, G
Paganetti, H
Seco, J
AF Riboldi, M.
Chen, G. T. Y.
Baroni, G.
Paganetti, H.
Seco, J.
TI Design and Testing of a Simulation Framework for Dosimetric Motion
Studies Integrating an Anthropomorphic Computational Phantom into
Four-dimensional Monte Carlo
SO TECHNOLOGY IN CANCER RESEARCH & TREATMENT
LA English
DT Article
DE Monte Carlo; 4D dosimetry; Computational phantom; Organ motion
ID ORGAN MOTION; COMPUTED-TOMOGRAPHY; ELECTRON-TRANSPORT; TISSUE
PARAMETERS; DOSE CALCULATIONS; IMRT TREATMENTS; HUMAN ANATOMY;
LUNG-CANCER; CT NUMBERS; RADIOTHERAPY
AB We have designed a simulation framework for motion studies in radiation therapy by integrating the anthropomorphic NCAT phantom into a 4D Monte Carlo dose calculation engine based on DPM. Representing an artifact-free environment, the system can be used to identify class solutions as a function of geometric and dosimetric parameters. A pilot dynamic conformal study for three lesions (similar to 2.0 cm) in the right lung was performed (70 Gy prescription dose). Tumor motion changed as a function of tumor location, according to the anthropomorphic deformable motion model. Conformal plans were simulated with 0 to 2 cm margin for the aperture, with additional 0.5 cm for beam penumbra. The dosimetric effects of intensity modulated radiotherapy (IMRT) vs. conformal treatments were compared in a static case. Results show that the Monte Carlo simulation framework can model tumor tracking in deformable anatomy with high accuracy, providing absolute doses for IMRT and conformal radiation therapy. A target underdosage of up to 3.67 Gy (lower lung) was highlighted in the composite dose distribution mapped at exhale. Such effects depend on tumor location and treatment margin and are affected by lung deformation and ribcage motion. In summary, the complexity in the irradiation of moving targets has been reduced to a controlled simulation environment, where several treatment options can be accurately modeled and quantified The implemented tools will be utilized for extensive motion study in lung/liver irradiation.
C1 [Riboldi, M.; Baroni, G.] Univ Milan, Dept Bioengn Politecn, TBMLab, I-20133 Milan, Italy.
[Chen, G. T. Y.; Paganetti, H.; Seco, J.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Chen, G. T. Y.; Paganetti, H.; Seco, J.] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
RP Riboldi, M (reprint author), Univ Milan, Dept Bioengn Politecn, TBMLab, P Za Leonardo Da Vinci 32, I-20133 Milan, Italy.
EM marco.riboldi@polimi.it
RI Baroni, Guido/D-3012-2011; Riboldi, Marco/I-2980-2014
OI Riboldi, Marco/0000-0002-2431-4966
FU NCI/NIH [R01-CA 111590]; Progetto Rocca foundation
FX The work is partly supported by NCI/NIH R01-CA 111590. We also
acknowledge the Progetto Rocca foundation for the support.
NR 35
TC 1
Z9 1
U1 0
U2 4
PU ADENINE PRESS
PI SCHENECTADY
PA 2066 CENTRAL AVE, SCHENECTADY, NY 12304 USA
SN 1533-0346
J9 TECHNOL CANCER RES T
JI Technol. Cancer Res. Treat.
PD DEC
PY 2008
VL 7
IS 6
BP 449
EP 456
PG 8
WC Oncology
SC Oncology
GA 388PR
UT WOS:000262032200006
PM 19044324
ER
PT J
AU Allen, AM
Wolfsberger, L
Tishler, RB
Court, LE
AF Allen, Aaron M.
Wolfsberger, Luciant
Tishler, Roy B.
Court, Laurence E.
TI Options for Combining Altered Fractionation with IMRT
SO TECHNOLOGY IN CANCER RESEARCH & TREATMENT
LA English
DT Article
DE Altered fractionation; IMRT; Head and Neck
ID INTENSITY-MODULATED RADIOTHERAPY; QUALITY-OF-LIFE; NECK-CANCER;
RADIATION-THERAPY; ACCELERATED FRACTIONATION; CONVENTIONAL
FRACTIONATION; OROPHARYNGEAL CARCINOMA; RANDOMIZED TRIAL; ADVANCED HEAD;
2ND CANCERS
AB We set out to investigate IMRT-based concomitant boost. Eight patients with stage III/IV squamous cell carcinoma of the head and neck treated with once daily with chemoradiotherapy at the Dana-Farber/Brigham and Women's Hospital had their treatment plans reviewed with IRB approval. Each case was replanned for treatment with a a concomitant boost regimen. Plans delivered 1.9 Gy in 30 fractions to 57 Gy with a boost of 1.5 Gy in 10 fractions for a total dose of 72 Gy. The boost was planned with both IMRT and 3-D conformal, to compare the two techniques. For each patient, both plans (IMRT-IMRT and IMRT-3DCRT) were evaluated for target and avoidance coverage, monitor units and integral dose. Finally, we evaluated the plans for time to completion. The IMRT-IMRT and IMRT-3-DCRT techniques were equivalent for target coverage. 100% coverage of the GTV and PTV was achieved with 97% of the prescription dose. Hot spots were seen 104% to 108% with IMRT-IMRT plan and from 102-111% with the IMRT-3DCRT plans. The IMRT-IMRT boost had double the monitor units as the 3-DCRT boosts. When the total monitor units from both the initial and boost portions of the plans were e combined there was not a significant differnce. There was a slight increase in integral dose with the IMRT-IMRT plans of mean 3.8%. Planning time was increased for the 3-DCRT boost as opposed to the IMRT boost (mean 3.5 hours vs. 1.5 hours). More time was needed for quality assurance of the IMRT-IMRT plans (3.0 hours vs. 1.5 hours for IMRT-3-DCRT). We found that both IMRT-based concomitant-boost strategies are achievable and produce good dosimetric results.
C1 [Allen, Aaron M.; Wolfsberger, Luciant; Tishler, Roy B.; Court, Laurence E.] Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02215 USA.
RP Allen, AM (reprint author), Dana Farber Canc Inst, Dept Radiat Oncol, 44 Binney St, Boston, MA 02215 USA.
EM aallen@lroc.harvard.edu
NR 19
TC 1
Z9 1
U1 0
U2 0
PU ADENINE PRESS
PI SCHENECTADY
PA 2066 CENTRAL AVE, SCHENECTADY, NY 12304 USA
SN 1533-0346
J9 TECHNOL CANCER RES T
JI Technol. Cancer Res. Treat.
PD DEC
PY 2008
VL 7
IS 6
BP 457
EP 461
PG 5
WC Oncology
SC Oncology
GA 388PR
UT WOS:000262032200007
PM 19044325
ER
PT J
AU Bryce, CL
Zickmund, S
Hess, R
McTigue, KM
Olshansky, E
Fitzgerald, K
Fischer, G
AF Bryce, Cindy L.
Zickmund, Susan
Hess, Rachel
McTigue, Kathleen M.
Olshansky, Ellen
Fitzgerald, Katharine
Fischer, Gary
TI Value Versus User Fees: Perspectives of Patients Before and After Using
a Web-Based Portal for Management of Diabetes
SO TELEMEDICINE JOURNAL AND E-HEALTH
LA English
DT Article
DE diabetes; user fee; access fee; patient portal; quantitative and
qualitative methods
ID SELF-MANAGEMENT; HEALTH RECORDS; COMMUNICATION; IMPLEMENTATION;
INFORMATION
AB The objective of this work was to rate the potential or actual usefulness of 15 features of a Web-based portal for diabetes management and assess whether patients would be willing to pay user fees for portal access. We used a combination of qualitative methods (focus group discussions) and quantitative methods (survey responses) to examine patients' perspectives. We enrolled 21 patients before the diabetes-specific portal was released ("preportal" group) and 18 patients after it was released ("portal-users" group). The two groups were similar except that 67% of preportal patients and 100% of portal users were Internet users. Overall, portal features that were rated most favorably were the online calculator to estimate blood glucose control (characterized as "very useful" by 74% of patients), appointment reminder systems (74%), e-mail access to health team (74%), personal tracking logs (69%), and online scheduling (69%). More patients from the preportal group than the portal-users group favored personal logs (86% versus 50%; p = 0.015) and opportunities to form interest groups (62% versus 28%; p = 0.034). Of the 30 patients who assigned a dollar amount for 1 month of portal access, 20 assigned zero dollars. Discussions about payment focused on equity and access. Because fees are expected to discourage portal usage, many patients believed that the potential benefits associated with self-management would not be realized. Others felt that the health system would benefit financially from a portal and should therefore absorb the costs. Even if portals are valued, patients may be resistant to paying for them. This opposition stems from concerns about fairness and from the recognition that health systems may experience cost savings if patients manage their diabetes successfully.
C1 [Bryce, Cindy L.; Zickmund, Susan; Hess, Rachel; McTigue, Kathleen M.; Fitzgerald, Katharine; Fischer, Gary] Univ Pittsburgh, Ctr Res Hlth Care, Pittsburgh, PA 15213 USA.
[Bryce, Cindy L.; Zickmund, Susan; Hess, Rachel; McTigue, Kathleen M.; Olshansky, Ellen; Fitzgerald, Katharine; Fischer, Gary] Univ Pittsburgh, Sch Med, Dept Med, Pittsburgh, PA 15213 USA.
[Bryce, Cindy L.] Univ Pittsburgh, Sect Decis Sci & Clin Syst Modeling, Pittsburgh, PA 15213 USA.
[Bryce, Cindy L.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Hlth Policy & Management, Pittsburgh, PA 15213 USA.
[Zickmund, Susan] VA Pittsburgh Healthcare Syst, Ctr Hlth Equity Res & Promot, Pittsburgh, PA USA.
[Olshansky, Ellen] Univ Calif Irvine, Coll Hlth Sci, Program Nursing Sci, Irvine, CA USA.
RP Bryce, CL (reprint author), Univ Pittsburgh, Ctr Res Hlth Care, 200 Meyran Ave,Suite 200, Pittsburgh, PA 15213 USA.
EM brycecl@upmc.edu
OI Bryce, Cindy/0000-0001-6356-6675
FU United States Air Force [W81XWH-04-2-003]; VA Health Services Research
and Development Merit Review
FX Portions of this research were sponsored by funding from the United
States Air Force, administered by the U. S. Army Medical Research
Acquisition Activity, Fort Detrick, Maryland, Award Number
W81XWH-04-2-003. Review of material does not imply Department of the Air
Force endorsement of factual accuracy or opinion. Dr. Zickmund is
supported by a VA Health Services Research and Development Merit Review
Grant.
NR 17
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U1 0
U2 4
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1530-5627
J9 TELEMED J E-HEALTH
JI Telemed. J. e-Health
PD DEC
PY 2008
VL 14
IS 10
BP 1035
EP 1043
DI 10.1089/tmj.2008.0005
PG 9
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA 394UD
UT WOS:000262473600004
PM 19119825
ER
PT J
AU Calfee, CS
Ware, LB
Eisner, MD
Parsons, PE
Thompson, BT
Wickersham, N
Matthay, MA
AF Calfee, C. S.
Ware, L. B.
Eisner, M. D.
Parsons, P. E.
Thompson, B. T.
Wickersham, N.
Matthay, M. A.
CA NHLBI Ards Network
TI Plasma receptor for advanced glycation end products and clinical
outcomes in acute lung injury
SO THORAX
LA English
DT Article
ID RESPIRATORY-DISTRESS-SYNDROME; RANDOMIZED CONTROLLED-TRIAL; TIDAL VOLUME
VENTILATION; SOLUBLE RECEPTOR; I CELLS; MECHANICAL VENTILATION;
TRANSPORT PROTEINS; FLUID TRANSPORT; ALVEOLAR; RAGE
AB Objectives: To determine whether baseline plasma levels of the receptor for advanced glycation end products (RAGE), a novel marker of alveolar type I cell injury, are associated with the severity and outcomes of acute lung injury, and whether plasma RAGE levels are affected by lower tidal volume ventilation.
Design, setting and participants: Measurement of plasma RAGE levels from 676 subjects enrolled in a large randomised controlled trial of lower tidal volume ventilation in acute lung injury.
Measurements and main results: Higher baseline plasma RAGE was associated with increased severity of lung injury. In addition, higher baseline RAGE was associated with increased mortality (OR for death 1.38 (95% CI 1.13 to 1.68) per 1 log increment in RAGE; p = 0.002) and fewer ventilator free and organ failure free days in patients randomised to higher tidal volumes. These associations persisted in multivariable models that adjusted for age, gender, severity of illness and the presence of sepsis or trauma. Plasma RAGE was not associated with outcomes in the lower tidal volume group (p = 0.09 for interaction in unadjusted analysis). In both tidal volume groups, plasma RAGE levels declined over the first 3 days; however, the decline was 15% greater in the lower tidal volume group (p = 0.02; 95% CI 2.4% to 25.0%).
Conclusions: Baseline plasma RAGE levels are strongly associated with clinical outcomes in patients with acute lung injury ventilated with higher tidal volumes. Lower tidal volume ventilation may be beneficial in part by decreasing injury to the alveolar epithelium.
C1 [Calfee, C. S.; Eisner, M. D.; Matthay, M. A.] Univ Calif San Francisco, Div Pulm & Crit Care Med, Dept Med, San Francisco, CA 94143 USA.
[Calfee, C. S.; Matthay, M. A.] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA.
[Ware, L. B.; Wickersham, N.] Vanderbilt Univ, Dept Med, Div Allergy Pulm & Crit Care, Nashville, TN USA.
[Eisner, M. D.; Matthay, M. A.] Univ Calif San Francisco, Dept Anesthesia, San Francisco, CA 94143 USA.
[Parsons, P. E.] Univ Vermont, Dept Med, Div Pulm & Crit Care Med, Burlington, VT USA.
[Thompson, B. T.] Massachusetts Gen Hosp, Dept Med, Pulm & Crit Care Med Unit, Boston, MA 02114 USA.
[Thompson, B. T.] Massachusetts Gen Hosp, Biostat Unit, Boston, MA 02114 USA.
RP Calfee, CS (reprint author), Univ Calif San Francisco, Div Pulm & Crit Care, 505 Parnassus Ave, San Francisco, CA 94143 USA.
EM carolyn.calfee@ucsf.edu
FU National Heart, Lung, and Blood Institute (NHLBI) [N01-HR 46054, 46055,
46056, 46057, 46058, 46059, 46060, 46061, 46062, 46063, 46064, HL 51856,
HL081332]; National Center for Research Resources [KL2RR024130]; Flight
Attendant Medical Research Institute
FX This work was supported by contracts (N01-HR 46054, 46055, 46056, 46057,
46058, 46059, 46060, 46061, 46062, 46063, and 46064) from the National
Heart, Lung, and Blood Institute (NHLBI). MAM was supported by NHLBI
Grant HL 51856. CSC was supported by KL2RR024130 from the National
Center for Research Resources, a component of the NIH, and by the Flight
Attendant Medical Research Institute. LBW was supported by NHLBI Grant
HL081332.
NR 40
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U1 0
U2 1
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0040-6376
J9 THORAX
JI Thorax
PD DEC
PY 2008
VL 63
IS 12
BP 1083
EP 1089
DI 10.1136/thx.2008.095588
PG 7
WC Respiratory System
SC Respiratory System
GA 374HG
UT WOS:000261033800013
PM 18566109
ER
PT J
AU Yeiung, A
Kam, R
AF Yeiung, Albert
Kam, Raymond
TI Ethical and Cultural Considerations in Delivering Psychiatric Diagnosis:
Reconciling the Gap Using MDD Diagnosis Delivery in Less-Acculturated
Chinese Patients
SO TRANSCULTURAL PSYCHIATRY
LA English
DT Article
DE discussing psychiatric diagnoses; depression; illness beliefs; cultural
sensitivity; Chinese
ID NEURASTHENIA; DEPRESSION; TRANSFORMATION; PSYCHOTHERAPY; PERSPECTIVE;
COMPETENCE; AMERICANS; ATTITUDES; AUTONOMY; CONTEXT
AB Talking to patients from diverse cultural backgrounds about their psychiatric disorders requires knowledge of one's own culture, the patients' cultures, and the ways in which they might interact, both in positive and unexpectedly negative ways. In this paper, we discuss the issues raised by discussing psychiatric diagnoses with Chinese-Americans who hold traditional illness beliefs and are not familiar with Western conceptions of psychiatric disorders. We explore how cultural values influence this aspect of medical practice, and suggest practical approaches to communicating the diagnosis of major depressive disorder in a culturally sensitive manner. Our clinical approach is to develop co-constructed illness narratives with patients, and to aid this process by refraining different elements of the clinical process into more culturally resonant forms. The following steps are suggested: 1) elicit patient's illness beliefs; 2) understand and acknowledge multiple explanatory models; 3) contextualize depressive symptoms into patient's physical health and social system; 4) introduce Western psychiatric theories in ways that reflect assumptions shared by Traditional Chinese Medicine (TCM); 5) involve patients' families whenever possible; and 6) use terminology that avoids unintended stigma.
C1 [Yeiung, Albert] Massachusetts Gen Hosp, Depress Clin & Res Program, Boston, MA 02114 USA.
[Yeiung, Albert; Kam, Raymond] S Cove Community Hlth Ctr, Boston, MA USA.
[Kam, Raymond] Childrens Hosp, Boston, MA 02115 USA.
[Yeiung, Albert; Kam, Raymond] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
RP Yeiung, A (reprint author), Massachusetts Gen Hosp, Depress Clin & Res Program, 50 Staniford St,Suite 401, Boston, MA 02114 USA.
NR 49
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Z9 0
U1 2
U2 6
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1363-4615
EI 1461-7471
J9 TRANSCULT PSYCHIATRY
JI Transcult. Psychiatry
PD DEC
PY 2008
VL 45
IS 4
BP 531
EP 552
DI 10.1177/1363461508100781
PG 22
WC Anthropology; Psychiatry
SC Anthropology; Psychiatry
GA 393BR
UT WOS:000262346400001
ER
PT J
AU Powers, A
Stowell, CP
Dzik, WH
Saidman, SL
Lee, H
Makar, RS
AF Powers, Amy
Stowell, Christopher P.
Dzik, Walter H.
Saidman, Susan L.
Lee, Hang
Makar, Robert S.
TI Testing only donors with a prior history of pregnancy or transfusion is
a logical and cost-effective transfusion-related acute lung injury
prevention strategy
SO TRANSFUSION
LA English
DT Article
ID BLOOD-DONORS; TRALI; ANTIBODIES; PLASMA; IMPACT; SENSITIZATION; ANTIGEN
AB Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related fatality reported to the Food and Drug Administration. Donor screening may reduce TRALI risk. This study sought to compare the efficacy and safety of different TRALI risk-reduction strategies at a hospital-based donor center.
Samples from 1053 donors who answered questions regarding pregnancy and transfusion history were tested for HLA Class I and II antibodies using a flow cytometry-based screening assay. Donor history was compared with the presence of HLA alloantibodies. These data were used to model several TRALI risk-reduction strategies. The medical records of patients transfused fresh-frozen plasma (FFP) from highly alloimmunized donors were retrospectively reviewed for TRALI.
HLA alloimmunization was observed among 25.4 percent (256/1009) of all female donors and among 12.0 percent (3/25) of those male donors who gave a history of prior transfusion. Prior pregnancy, reported by 52.6 percent (531/1009) of females, correlated significantly with HLA alloimmunization (p < 0.0001). The rate of HLA alloimmunization increased with parity. A positive pregnancy history was a sensitive (87.9%) screen for HLA alloimmunization with a negative predictive value of 93.5 percent (95% confidence interval, 91.3%-95.7%). Although 5.9 percent (27/459) of nulliparous, untransfused females demonstrated a positive screening test, only 1 percent (7/459) had a confirmed HLA alloantibody. Transfusion of FFP from donors found retrospectively to be highly alloimmunized led to reactions suggestive of TRALI in 2 of 26 recipients.
Donor history is a reliable predictor of HLA alloimmunization. Testing only donors with a prior history of pregnancy or transfusion is a logical and cost-effective TRALI prevention strategy.
C1 [Makar, Robert S.] Massachusetts Gen Hosp, Blood Transfus Serv, Dept Pathol, Boston, MA 02114 USA.
Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
Massachusetts Gen Hosp, Histocompatibil Lab, Dept Pathol, Boston, MA 02114 USA.
Beth Israel Deaconess Med Ctr, Div Lab & Transfus Med, Boston, MA 02215 USA.
RP Makar, RS (reprint author), Massachusetts Gen Hosp, Blood Transfus Serv, Dept Pathol, 55 Fruit St,GRJ 206C, Boston, MA 02114 USA.
EM rmakar@partners.org
FU Evelyn and Robert Luick Memorial Fund
FX This work was supported by the Evelyn and Robert Luick Memorial Fund.
The authors have no conflicts of interest to disclose.
NR 34
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U1 1
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0041-1132
J9 TRANSFUSION
JI Transfusion
PD DEC
PY 2008
VL 48
IS 12
BP 2549
EP 2558
DI 10.1111/j.1537-2995.2008.01902.x
PG 10
WC Hematology
SC Hematology
GA 380BG
UT WOS:000261439900012
PM 18717778
ER
PT J
AU Fehr, T
Sykes, M
AF Fehr, Thomas
Sykes, Megan
TI Clinical experience with mixed chimerism to induce transplantation
tolerance
SO TRANSPLANT INTERNATIONAL
LA English
DT Review
DE bone marrow transplantation; clinical trial; mixed chimerism; myeloma;
tolerance
ID BONE-MARROW-TRANSPLANTATION; TOTAL LYMPHOID IRRADIATION; STEM-CELL
TRANSPLANTATION; RENAL-ALLOGRAFT RECIPIENTS; ANTIGEN-SPECIFIC
HYPOREACTIVITY; DONOR LIVER-TRANSPLANTATION; IDENTICAL LITTERMATE DOGS;
HUMANIZED ANTI-CD2 MAB; VERSUS-HOST-DISEASE; HEMATOPOIETIC CHIMERISM
AB Lymphohematopoietic chimerism was first shown to be associated with donor-specific allograft tolerance more than 60 years ago. However, early clinical experience with bone marrow transplantation soon revealed that conventional, myeloablative approaches were far too toxic and the risk of graft-versus-host disease too great to justify using this technology for the purpose of organ allograft tolerance induction in the absence of malignant disease. In this review, we discuss a step-wise approach that has been applied by several centers to establish less toxic approaches to using hematopoietic cell transplantation (HCT) for tolerance induction. These steps include (i) feasibility and efficacy data for tolerance induction in large animal models; (ii) safety data in clinical trials for patients with hematologic malignancies; and (iii) pilot trials of combined HCT and kidney transplantation for tolerance induction. Thus far, only one published trial conducted at the Massachusetts General Hospital in Boston has achieved long-term acceptance of human leukocyte antigen-mismatched kidney allografts without chronic immunosuppressive therapy. Alternative protocols have been successful in large animals, but long-term organ allograft tolerance has not been reported in patients. Thus, proof-of-principle that nonmyeloablative induction of mixed chimerism can be used intentionally to induce organ allograft tolerance has now been achieved. Directions for further research to make this approach applicable for a broader patient population are discussed.
C1 [Sykes, Megan] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Transplantat Biol Res Ctr,Bone Marrow Transplanta, Boston, MA 02129 USA.
[Fehr, Thomas] Univ Zurich Hosp, Sch Med, Dept Internal Med, Clin Nephrol, CH-8091 Zurich, Switzerland.
RP Sykes, M (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Transplantat Biol Res Ctr,Bone Marrow Transplanta, MGH E CNY 149,13th St, Boston, MA 02129 USA.
EM megan.sykes@tbrc.mgh.harvard.edu
FU NIH; NCI; NHLBI; NIAID; Juvenile Diabetes Research Foundation; Multiple
Myeloma Research Foundation; Swiss Foundation for Medical and
Biological; Novartis Switzerland; Walter and Gertrud Siegenthaler
Foundation; University of Zurich, Switzerland
FX We thank Dr Yong-Guang and Dr Toshiki Saito for critical review of this
manuscript and Ms Kelly Walsh for expert assistance with the manuscript.
Megan Sykes was supported by NIH grants from the NCI, NHLBI and NIAID
and by grants from the Juvenile Diabetes Research Foundation and
Multiple Myeloma Research Foundation. Thomas Fehr was supported by a
research fellowship of the Swiss Foundation for Medical and Biological
Grants (with support from Novartis Switzerland) and a research
fellowship of the Walter and Gertrud Siegenthaler Foundation (Medical
Faculty, University of Zurich, Switzerland).
NR 95
TC 49
Z9 54
U1 1
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0934-0874
J9 TRANSPL INT
JI Transpl. Int.
PD DEC
PY 2008
VL 21
IS 12
BP 1118
EP 1135
DI 10.1111/j.1432-2277.2008.00783.x
PG 18
WC Surgery; Transplantation
SC Surgery; Transplantation
GA 369WF
UT WOS:000260723900002
PM 18954364
ER
PT J
AU Saidi, RF
Kennealey, PT
Elias, N
Kawai, T
Hertl, M
Farrell, M
Goes, N
Hartono, C
Tolkoff-Rubin, N
Cosimi, AB
Ko, DSC
AF Saidi, R. F.
Kennealey, P. T.
Elias, N.
Kawai, T.
Hertl, M.
Farrell, M.
Goes, N.
Hartono, C.
Tolkoff-Rubin, N.
Cosimi, A. B.
Ko, D. S. C.
TI Deceased Donor Kidney Transplantation in Elderly Patients: Is There a
Difference in Outcomes?
SO TRANSPLANTATION PROCEEDINGS
LA English
DT Article
ID CADAVERIC RENAL-TRANSPLANTATION; REPLACEMENT THERAPIES; AGE; OLDER;
RECIPIENTS; EXPERIENCE; DIALYSIS; HEMODIALYSIS; SURVIVAL; REGISTRY
AB Introduction. There is a paucity of data on long-term outcomes of older kidney recipients. Our aim was to compare the early and long-term outcomes of deceased donor kidney transplantation in patients aged >= 60 years with outcomes in younger recipients.
Materials and Methods. From 1998 to 2005, we performed 271 deceased donor kidney transplants. There were 76 recepients (28.1%) >60 years old. Older candidates were carefully selected based on their physiologic, cardiac, and performance status. Demographic data, including clinical characteristics, early complications, mortality, and patient and graft survival rates, were collected and analyzed.
Results. Older patients had comparable perioperative mortality and morbidity, incidence of delayed graft function (DGF), length of stay, and readmissions compared with younger patients. The rates of acute rejection and major infections were also comparable between the 2 study groups. Among older recipients, 25/76 (32.1%) patients received extended criteria donor kidneys compared with only 35/195 (17.9%) of younger patients (P <.001). Nevertheless, equivalent 1-, 3-, and 5-year allograft survival rates were observed in elderly and young patients; 91.5% versus, 92.5%, 78.5% versus 81.9%, and 75.6% versus 78.5%, respectively. Overall patient survival was also comparable in both groups.
Conclusion. Kidney transplantation in appropriately selected elderly recipients provides equivalent outcomes compared with those observed in younger patients. These observations support the notion that older recipients should not lose access to deceased donor kidney transplantation in the effort to achieve a perceived gain in social utility.
C1 [Saidi, R. F.; Kennealey, P. T.; Elias, N.; Kawai, T.; Hertl, M.; Farrell, M.; Cosimi, A. B.; Ko, D. S. C.] Massachusetts Gen Hosp, Dept Surg, Transplantat Unit, Boston, MA 02114 USA.
[Goes, N.; Hartono, C.; Tolkoff-Rubin, N.] Massachusetts Gen Hosp, Renal Unit, Boston, MA 02114 USA.
RP Ko, DSC (reprint author), Massachusetts Gen Hosp, Dept Surg, Transplantat Unit, Blake 655,55 Fruit St, Boston, MA 02114 USA.
EM dko@partners.org
NR 25
TC 3
Z9 4
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0041-1345
J9 TRANSPL P
JI Transplant. Proc.
PD DEC
PY 2008
VL 40
IS 10
BP 3413
EP 3417
DI 10.1016/j.transproceed.2008.08.127
PG 5
WC Immunology; Surgery; Transplantation
SC Immunology; Surgery; Transplantation
GA 389ZE
UT WOS:000262133300029
PM 19100401
ER
PT J
AU Welters, HJ
Kulkarni, RN
AF Welters, Hannah J.
Kulkarni, Rohit N.
TI Wnt signaling: relevance to beta-cell biology and diabetes
SO TRENDS IN ENDOCRINOLOGY AND METABOLISM
LA English
DT Review
ID TRANSCRIPTION-FACTOR-7-LIKE-2 TCF7L2 GENE; INSULIN-SECRETION; PROTEIN
INTERACTIONS; PANCREATIC-ISLETS; CATENIN PATHWAY; GROWTH; PROLIFERATION;
MICE; GLUCOSE; EXPRESSION
AB Interest in the importance of Wnt signaling in diabetes has risen after identification of the transcription factor TCF7L2, a component of this pathway, as a strong risk factor for type 2 diabetes. Here, we review emerging new evidence that Wnt signaling influences endocrine pancreas development and modulates mature beta-cell functions including insulin secretion, survival and proliferation. Alterations in Wnt signaling might also impact other metabolic tissues involved in the pathogenesis of diabetes, with TCF7L2 proposed to modulate adipogenesis and regulate GLP-1 production. Together, these studies point towards a role for Wnt signaling in the pathogenesis of type 2 diabetes, highlighting the importance of further investigation of this pathway to develop new therapies for this disease.
C1 [Welters, Hannah J.] Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02215 USA.
Harvard Univ, Sch Med, Dept Med, Boston, MA 02215 USA.
RP Welters, HJ (reprint author), Harvard Univ, Sch Med, Joslin Diabet Ctr, 1 Joslin Pl, Boston, MA 02215 USA.
EM hannah.welters@joslin.harvard.edu
FU NIH [RO1 DK 67536, RO1 DK 68721]; Astra Zeneca
FX Funding from NIH RO1 DK 67536, NIH RO1 DK 68721 and Astra Zeneca.
NR 72
TC 78
Z9 81
U1 2
U2 11
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 1043-2760
J9 TRENDS ENDOCRIN MET
JI Trends Endocrinol. Metab.
PD DEC
PY 2008
VL 19
IS 10
BP 349
EP 355
DI 10.1016/j.tem.2008.08.004
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 380PM
UT WOS:000261477600001
PM 18926717
ER
PT J
AU El Khoury, J
Luster, AD
AF El Khoury, Joseph
Luster, Andrew D.
TI Mechanisms of microglia accumulation in Alzheimer's disease: therapeutic
implications
SO TRENDS IN PHARMACOLOGICAL SCIENCES
LA English
DT Review
ID CENTRAL-NERVOUS-SYSTEM; BETA-AMYLOID FIBRILS; BONE-MARROW;
HEMATOPOIETIC-CELLS; REACTIVE MICROGLIA; SCAVENGER RECEPTOR; BLOOD
MONOCYTES; MOUSE MODEL; MICE; BRAIN
AB In Alzheimer's disease (AD), and other conditions affecting integrity of the blood-brain barrier, microglia can originate in the bone marrow, migrate into the blood and enter the brain in a chemokine-dependent manner. CCR2, a chemokine receptor that controls mononuclear phagocyte infiltration into the brain in multiple sclerosis, bacterial meningitis and neuropathic pain, also regulates microglia accumulation in mouse models of AD. CCR2 deficiency leads to lower microglia accumulation and higher brain beta-amyloid (A beta) levels, indicating that early microglial accumulation promotes A beta clearance. In support of this protective role, enhancing microglia accumulation delays progression of AD. AD mice that constitutively express interieukin-1 in the brain, or that are deficient in peripheral mononuclear phagocyte transforming growth factor-beta signaling, have increased microglia accumulation around beta-amyloid plaques and reduced AD-like pathology. Regulating microglia recruitment into the brain is a novel therapeutic strategy to delay or stop progression of AD. Here, we review the role of microglia in AD and the mechanisms of their accumulation and discuss implications for AD therapy.
C1 [El Khoury, Joseph; Luster, Andrew D.] Harvard Univ, Sch Med, Ctr Immunol & Inflammatory Dis, Massachusetts Gen Hosp,Div Rheumatol Allergy & Im, Charlestown, MA 02129 USA.
[El Khoury, Joseph] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Infect Dis, Charlestown, MA 02129 USA.
RP El Khoury, J (reprint author), Harvard Univ, Sch Med, Ctr Immunol & Inflammatory Dis, Massachusetts Gen Hosp,Div Rheumatol Allergy & Im, 149 13th St, Charlestown, MA 02129 USA.
EM jelkhoury@partners.org
FU National Institute of Neurological Disorders and Stroke [NS059005,
NS044973]; Dana Foundation
FX This work was supported by grants NS059005 (J.E.K.) and NS044973
(A.D.L.) from the National Institute of Neurological Disorders and
Stroke (www.ninds.nih.gov) and a grant from the Dana Foundation
(www.dana.org) Neuro-Immunology program (J.E.K.).
NR 64
TC 91
Z9 92
U1 2
U2 16
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0165-6147
J9 TRENDS PHARMACOL SCI
JI Trends Pharmacol. Sci.
PD DEC
PY 2008
VL 29
IS 12
BP 626
EP 632
DI 10.1016/j.tips.2008.08.004
PG 7
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 384AD
UT WOS:000261714800005
PM 18835047
ER
PT J
AU Sartor, AO
Hricak, H
Wheeler, TM
Coleman, J
Penson, DF
Carroll, PR
Rubin, MA
Scardino, PT
AF Sartor, A. Oliver
Hricak, Hedvig
Wheeler, Thomas M.
Coleman, Jonathan
Penson, David F.
Carroll, Peter R.
Rubin, Mark A.
Scardino, Peter T.
TI Evaluating Localized Prostate Cancer and Identifying Candidates for
Focal Therapy
SO UROLOGY
LA English
DT Review
ID PREDICT PATHOLOGICAL STAGE; BEAM RADIATION-THERAPY; 3-DIMENSIONAL
CONFORMAL RADIOTHERAPY; TMPRSS2-ERG FUSION TRANSCRIPTS; GUIDED TEMPLATE
BIOPSY; MR-IMAGING FINDINGS; RADICAL PROSTATECTOMY; PREOPERATIVE
NOMOGRAM; NEEDLE-BIOPSY; PRETREATMENT NOMOGRAM
AB Can focal therapy successfully control prostate cancer? Also, if so, which patients should be considered eligible? With limited data available from relatively few patients, these questions are difficult to answer. At this writing, the most likely candidates for focal therapy are patients with low-risk, small-volume tumors, located in 1 region or sector of the prostate, who would benefit from early intervention. The difficulty lies in reliably identifying these men.
The larger number of cores obtained in each needle biopsy session has increased both the detection of prostate cancer and the potential risk of overtreating many patients whose cancers pose very little risk to life or health. Urologists typically perform at least a 12-core template biopsy. Although the debate continues about the optimal template, laterally and peripherally directed biopsies have been shown to improve the diagnostic yield. However, as many as 25% of tumors arise anteriorly and can be missed with peripherally directed techniques.
Prostate cancer tends to be multifocal, even in its earliest stages. However, the secondary cancers are usually smaller and less aggressive than the index cancer. They appear similar to the incidental cancers found in cystoprostatectomy specimens and appear to have little effect on prognosis in surgical series. When a single focus of cancer is found in I core, physicians rightly suspect that more foci of cancer are present in the prostate. Assessing the risk in these patients is challenging when determined by the biopsy data alone.
To predict the presence of a very low-risk or "indolent" cancer, nomograms have been developed to incorporate clinical stage, Gleason grade, prostate-specific antigen levels, and prostate volume, along with the quantitative analysis of the biopsy results. Transperineal "mapping" or "saturation" biopsies have been advocated to detect cancers missed or underestimated by previous transrectal biopsies. This approach could provide the accurate staging, grading, and tumor localization needed for a focal therapy program. Nevertheless, for men with minimal cancer who are amenable to active surveillance or focal therapy, consensus about the most accurate biopsy strategy has not yet been reached.
Imaging, particularly magnetic resonance imaging and magnetic resonance spectroscopic imaging, has been used to assess men with early-stage prostate cancer. Large-volume cancers can be seen reasonably well, but small lesions have been difficult to detect reliably or measure accurately. Factors such as voxel resolution, organ movement, biopsy artifact, and benign changes have limited the consistent estimation of the quantitative tumor volume. Nevertheless, magnetic resonance imaging and magnetic resonance spectroscopic imaging can aid in evaluating patients with prostate cancer being considered for focal therapy by providing additional evidence that the patient does not harbor an otherwise undetected high-risk, aggressive cancer. In some cases, imaging can usefully identify the location of even a limited-sized index cancer. When imaging findings are substantiated by mapping biopsy results, confidence in the accurate characterization of the cancer is enhanced. Correlating the imaging results with tissue changes during and after treatment can be of use in monitoring the ablative effects in the prostate and in assessing for tumor recurrence. More work is necessary before staging studies can uniformly characterize a prostate cancer before therapy, much less reliably identify and locate small-volume cancer within the prostate. However, exploring the role of focal ablation as a therapeutic option for selected men with low-risk, clinically localized, prostate cancer need not await the emergence of perfectly accurate staging studies, any more than the application of radical surgery or radiotherapy have. Modern biopsy strategies, combined with optimal imaging and nomograms to estimate the pathologic stage and risk, taken together, provide a sound basis for the selection of appropriate patients for entry into prospective clinical trials of focal therapy. UROLOGY 72 (Suppl 6A): 12-24, 2008. (C) 2008 Published by Elsevier Inc.
C1 [Sartor, A. Oliver] Harvard Univ, Sch Med, Dana Farber Canc Inst, Lank Ctr Genitourinary Oncol,Dept Med, Boston, MA 02115 USA.
[Hricak, Hedvig; Scardino, Peter T.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Wheeler, Thomas M.] Baylor Coll Med, Houston, TX 77030 USA.
[Penson, David F.] Univ So Calif, Kenneth Norris Jr Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
[Carroll, Peter R.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Rubin, Mark A.] Weill Cornell Med Ctr, New York, NY USA.
RP Sartor, AO (reprint author), Tulane Canc Ctr, Dept Med, New Orleans, LA 70115 USA.
EM osartor@tulane.edu
OI Hricak, Hedvig/0000-0003-2240-9694; Rubin, Mark/0000-0002-8321-9950;
Coleman, Jonathan/0000-0002-6428-7835
FU Steba Biotech
FX The members of the International Task Force on Prostate Cancer and the
Focal Lesion Paradigm are particularly indebted to the following people
for their guidance and support: Pierre Dussault, Aurelie Hubert,
Stephanie Adam, and Karyn Wagner from the task force scientific support
team in Montreal, Canada. We are grateful to the following people for
their scientific contributions: Fernando J. Bianco, MD, of The George
Washington University Cancer Institute, Washington, DC, USA; Mark
Einberton, MD, of University College London, London, United Kingdom;
Avigdor Scherz, PhD, of the Weizmann Institute of Science, Rehovot,
Israel; and John Trachtenberg, MD, of Princess Margaret Hospital,
University Health Network, Toronto, Canada. We would also like to thank
the medical editors from Memorial Sloan-Kettering Cancer Center, New
York, NY, USA, for bibliographic, editorial, and writing assistance:
Susan Aiello, DVM, ELS; Melissa Bogen, ELS; Barbara Kristaponis; Hope J.
Lafferty, ELS; Michael McGregor, MA; Peggy McPartland; and Jennifer
Swartz-Turfle. The task force was made possible in part with financial
support from Steba Biotech.
NR 109
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U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0090-4295
J9 UROLOGY
JI Urology
PD DEC
PY 2008
VL 72
IS 6A
BP 12
EP 24
DI 10.1016/j.urology.2008.10.004
PG 13
WC Urology & Nephrology
SC Urology & Nephrology
GA 389VE
UT WOS:000262121800003
PM 19095124
ER
PT J
AU Hu, JC
Kwan, L
Krupski, TL
Anger, JT
Maliski, SL
Connor, S
Litwin, MS
AF Hu, Jim C.
Kwan, Lorna
Krupski, Tracey L.
Anger, Jennifer T.
Maliski, Sally L.
Connor, Sarah
Litwin, Mark S.
TI Determinants of Treatment Regret in Low-Income, Uninsured Men With
Prostate Cancer
SO UROLOGY
LA English
DT Article
ID QUALITY-OF-LIFE; MEMORIAL ANXIETY SCALE; RADICAL PROSTATECTOMY;
TREATMENT DECISIONS; MAX-PC; VALIDITY; RELIABILITY; UNCERTAINTY;
RECURRENCE; CAPSURE
AB OBJECTIVES The regret of a prostate cancer treatment choice, a significant dimension of health-related quality of life, has not been well-characterized. Little is known about its association with the fear of cancer recurrence or spirituality.
METHODS We drew subjects from a men's health study composed of a clinically heterogeneous sample of subjects enrolled from a statewide, publicly funded assistance program that provided free prostate cancer treatment for uninsured, low-income men in California. We included men who completed a telephone interviews and self-administered questionnaires at Study enrollment and at 6 months of follow-up. Using validated instruments, we measured regret, health-related quality of life, fear of cancer recurrence, and spirituality through telephone interviews and self-administered questionnaires.
RESULTS Of the 195 men, 90 underwent radical prostatectomy (46%), 50 underwent external beam radiotherapy (28%), and 51 underwent hormonal therapy (26%). Of these 195 men, 36 (18%) regretted their treatment choice. Multivariate analyses revealed that nonwhite men were more likely than white men to experience decisional regret (odds ratio [OR] range 7.27 to 12.26). Conversely, men confident of cancer cure (OR 0.19, 95% confident interval 0.04 to 0.86), rnen with greater spirituality (OR 0.91, 95% confidence interval 0.87 to 0.96), and men with acute treatment effects (OR 0.34, 95% confidence interval 0.12 to 0.93) were less likely to regret their treatment decisions.
CONCLUSIONS In Our study, a fear of cancer recurrence, less spirituality, a longer interval since treatment, and nonwhite race were associated with treatment regret in low-income, underserved men with prostate cancer. Attempts to decrease anxiety and enhance spirituality in men treated for prostate cancer might diminish treatment regret. Additional Studies in racially diverse cohorts are needed to examine the association of regret with race. UROLOGY 72: 1274-1279, 2008. (C) 2008 Elsevier Inc.
C1 [Hu, Jim C.] Harvard Univ, Brigham & Womens Hosp, Sch Med,Div Urol, Dana Farber Canc Inst,Lank Ctr Genitourinary Onco, Boston, MA 02115 USA.
Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90024 USA.
Duke Univ, Sch Med, Div Urol, Durham, NC USA.
Univ Calif Los Angeles, David Geffen Sch Med, Dept Urol, Los Angeles, CA 90095 USA.
Univ Calif Los Angeles, Sch Publ Hlth, Dept Hlth Serv, Los Angeles, CA 90024 USA.
RP Hu, JC (reprint author), Harvard Univ, Brigham & Womens Hosp, Sch Med,Div Urol, Dana Farber Canc Inst,Lank Ctr Genitourinary Onco, 45 Francis St,ASBII-3, Boston, MA 02115 USA.
EM jhu2@partners.org
FU California Department of Health Services Cancer Detection Section
FX This study was supported by an award from the California Department of
Health Services Cancer Detection Section.
NR 25
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Z9 21
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0090-4295
J9 UROLOGY
JI Urology
PD DEC
PY 2008
VL 72
IS 6
BP 1274
EP 1279
DI 10.1016/j.urology.2007.11.066
PG 6
WC Urology & Nephrology
SC Urology & Nephrology
GA 389VB
UT WOS:000262121500020
PM 18313115
ER
PT J
AU Armstrong, D
Lipsky, B
Boulton, A
AF Armstrong, David
Lipsky, Benjamin
Boulton, Andrew
TI A Closer Look At The Prevalence Of MRSA And Its Impact On Empiric
Therapy
SO WOUNDS-A COMPENDIUM OF CLINICAL RESEARCH AND PRACTICE
LA English
DT Article
C1 [Armstrong, David] Univ Arizona, Coll Med, SALSA, Tucson, AZ 85721 USA.
[Boulton, Andrew] Univ Manchester, Manchester M13 9PL, Lancs, England.
Coatesville Vet Affairs Med Ctr, Coatesville, PA USA.
Roxborough Mem Hosp, Philadelphia, PA USA.
[Lipsky, Benjamin] Univ Washington, Sch Med, Seattle, WA 98195 USA.
[Lipsky, Benjamin] Gen Internal Med Clin, Seattle, WA USA.
[Lipsky, Benjamin] Vet Affairs Puget Sound Hlth Care Syst, Antibiot Res Clin, Seattle, WA USA.
RP Armstrong, D (reprint author), Univ Arizona, Coll Med, SALSA, Tucson, AZ 85721 USA.
RI Lipsky, Benjamin/B-4645-2013
NR 0
TC 0
Z9 0
U1 0
U2 1
PU H M P COMMUNICATIONS
PI MALVERN
PA 83 GENERAL WARREN BLVD, STE 100, MALVERN, PA 19355 USA
SN 1044-7946
J9 WOUNDS
JI Wounds-Compend. Clin. Res. Pract.
PD DEC
PY 2008
BP 5
EP 10
PG 6
WC Dermatology; Surgery
SC Dermatology; Surgery
GA 393EI
UT WOS:000262353300001
ER
PT J
AU Armstrong
Boulton
Rogers
Lipsky
AF Dr Armstrong
Dr Boulton
Dr Rogers
Dr Lipsky
TI A Guide To Current MRSA Treatment Options
SO WOUNDS-A COMPENDIUM OF CLINICAL RESEARCH AND PRACTICE
LA English
DT Article
C1 [Dr Armstrong] Univ Arizona, Coll Med, SALSA, Tucson, AZ 85721 USA.
[Dr Boulton] Univ Manchester, Manchester M13 9PL, Lancs, England.
Roxborough Mem Hosp, Philadelphia, PA USA.
Coatesville Vet Affairs Med Ctr, Coatesville, PA USA.
[Dr Lipsky] Univ Washington, Sch Med, Seattle, WA 98195 USA.
[Dr Lipsky] Gen Internal Med Clin, Seattle, WA USA.
[Dr Lipsky] Vet Affairs Puget Sound Hlth Care Syst, Antibiot Res Clin, Seattle, WA USA.
[Dr Rogers] Broadlawns Med Ctr, Amputat Prevent Ctr, Des Moines, IA USA.
RP Armstrong (reprint author), Univ Arizona, Coll Med, SALSA, Tucson, AZ 85721 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU H M P COMMUNICATIONS
PI MALVERN
PA 83 GENERAL WARREN BLVD, STE 100, MALVERN, PA 19355 USA
SN 1044-7946
J9 WOUNDS
JI Wounds-Compend. Clin. Res. Pract.
PD DEC
PY 2008
BP 11
EP 17
PG 7
WC Dermatology; Surgery
SC Dermatology; Surgery
GA 393EI
UT WOS:000262353300002
ER
PT J
AU Ceol, CJ
Houvras, Y
White, RM
Zon, LI
AF Ceol, Craig J.
Houvras, Yariv
White, Richard M.
Zon, Leonard I.
TI Melanoma Biology and the Promise of Zebrafish
SO ZEBRAFISH
LA English
DT Review
ID ENDOTHELIN-B RECEPTOR; C-KIT PROTOONCOGENE; NEURAL-CREST; TRANSCRIPTION
FACTOR; MALIGNANT-MELANOMA; WAARDENBURG-SYNDROME; CUTANEOUS MELANOMA;
IN-VIVO; METASTATIC MELANOMA; GENE-EXPRESSION
AB Advantageous organismal and technical attributes of the zebrafish are being increasingly applied to study cancer biology. Along with other tumor models, zebrafish that develop melanomas have been generated. In both genetics and phenotype, zebrafish melanomas are strikingly similar to their human counterparts. For this reason, studies in the zebrafish are poised to make significant contributions to melanoma biology. In this review, we summarize important features of human melanoma and discuss how the zebrafish can be used to address many questions that remain unanswered about this devastating disease.
C1 [Zon, Leonard I.] Childrens Hosp, Karp Res Labs, Stem Cell Program, Boston, MA 02115 USA.
[Ceol, Craig J.; Houvras, Yariv; White, Richard M.; Zon, Leonard I.] Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA.
[Ceol, Craig J.; Houvras, Yariv; White, Richard M.; Zon, Leonard I.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Harvard Stem Cell Inst,Howard Hughes Med Inst, Boston, MA 02115 USA.
[Houvras, Yariv] Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
RP Zon, LI (reprint author), Childrens Hosp, Karp Res Labs, Stem Cell Program, 300 Longwood Ave,7th Floor, Boston, MA 02115 USA.
EM zon@enders.tch.harvard.edu
FU Charles A. King Trust Postdoctoral Fellowship; Bank of America; National
Institutes of Health [K08-DK075432, R01-DK53298-08]; American Society
for Clinical Oncology Young Investigator Award; Aid for Cancer Research
Fellowship
FX We are grateful to members of the Zon laboratory, especially Michael
Dovey, for helpful discussions. C.J.C. is supported by a Charles A. King
Trust Postdoctoral Fellowship, Bank of America, Co-Trustee; Y.H. by a
National Institutes of Health K08 award (K08-DK075432); and R.M.W. by an
American Society for Clinical Oncology Young Investigator Award and an
Aid for Cancer Research Fellowship. Melanoma research by L.I.Z. is
funded by NIH Grant R01-DK53298-08.
NR 101
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Z9 20
U1 0
U2 8
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1545-8547
EI 1557-8542
J9 ZEBRAFISH
JI Zebrafish
PD DEC
PY 2008
VL 5
IS 4
BP 247
EP 255
DI 10.1089/zeb.2008.0544
PG 9
WC Developmental Biology; Zoology
SC Developmental Biology; Zoology
GA 396QE
UT WOS:000262605400004
PM 19133823
ER
PT J
AU Sessa, AK
White, R
Houvras, Y
Burke, C
Pugach, E
Baker, B
Gilbert, R
Look, AT
Zon, LI
AF Sessa, Anna K.
White, Richard
Houvras, Yariv
Burke, Christopher
Pugach, Emily
Baker, Barry
Gilbert, Rharaka
Look, A. Thomas
Zon, Leonard I.
TI The Effect of a Depth Gradient on the Mating Behavior, Oviposition Site
Preference, and Embryo Production in the Zebrafish, Danio rerio
SO Zebrafish
LA English
DT Article
ID REPRODUCTION
AB Captive zebrafish (Danio rerio) exhibit a limited repertoire of mating behaviors, likely due to the somewhat unnatural environment of aquaria. Observations in their natural habitat led us to believe that a depth gradient within the mating setup would positively affect fish mating. By tilting the tank to produce a depth gradient, we observed novel behaviors along with a preference for oviposition in the shallow area. Although we did not see an increase in the likelihood of a pair of fish to mate, we did see an increase in the embryo output in both adults and juveniles. In the adults, tilting led to a significant increase in embryo production (436 +/- 35 tilted vs. 362 +/- 34 untilted; p < 0.05). A similar effect was seen in juvenile fish as they progressed through sexual maturity. These results suggest that tilting of mating cages in the laboratory setting will lead to demonstrable improvements in embryo production for zebrafish researchers, and highlights the possibility of other manipulations to increase fecundity.
C1 [Sessa, Anna K.; White, Richard; Houvras, Yariv; Burke, Christopher; Pugach, Emily; Zon, Leonard I.] Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA.
[White, Richard; Baker, Barry; Gilbert, Rharaka; Look, A. Thomas; Zon, Leonard I.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[White, Richard; Zon, Leonard I.] Harvard Univ, Sch Med, Boston, MA USA.
[Houvras, Yariv] Brigham & Womens Hosp, Boston, MA 02115 USA.
RP Zon, LI (reprint author), Karp Family Res Labs, 300 Longwood Ave,Room 7211, Boston, MA 02115 USA.
EM zon@enders.tch.harvard.edu
FU NIDDK NIH HHS [P30 DK049216-139002, P30 DK049216]
NR 17
TC 12
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U1 1
U2 8
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1545-8547
J9 ZEBRAFISH
JI Zebrafish
PD DEC
PY 2008
VL 5
IS 4
BP 335
EP 339
DI 10.1089/zeb.2008.0535
PG 5
WC Developmental Biology; Zoology
SC Developmental Biology; Zoology
GA 396QE
UT WOS:000262605400013
PM 19133832
ER
PT J
AU Weiner, DK
Perera, S
Rudy, TE
Glick, RM
Shenoy, S
Delitto, A
AF Weiner, Debra K.
Perera, Subashan
Rudy, Thomas E.
Glick, Ronald M.
Shenoy, Sonali
Delitto, Anthony
TI Efficacy of percutaneous electrical nerve stimulation and therapeutic
exercise for older adults with chronic low back pain: A randomized
controlled trial
SO PAIN
LA English
DT Article
DE Chronic low back pain; Older adults; Percutaneous electrical nerve
stimulation; Exercise
ID SELF-RATED HEALTH; LOWER-EXTREMITY FUNCTION; PHYSICAL PERFORMANCE
BATTERY; FOLLOW-UP; NEUROPSYCHOLOGICAL PERFORMANCE; SUBSEQUENT
DISABILITY; BODY-COMPOSITION; FITNESS PROGRAM; ACUPUNCTURE; SCALE
AB Chronic low back pain (CLBP) in older adults may be disabling and therapeutically challenging, largely because of the inefficacy and/or morbidity associated with traditional pain treatment. We conducted a randomized controlled trial in 200 men and women >= age 65 with CLBP to evaluate the efficacy of percutaneous electrical nerve stimulation (PENS) with and without general conditioning and aerobic exercise (GCAE), for reducing pain and improving physical function. Participants were randomized to receive (1) PENS, (2) control-PENS (brief electrical stimulation to control for treatment expectancy), (3) PENS + GCAE, or (4) control-PENS + GCAE, twice a week for 6 weeks. All (Our groups experienced significantly reduced pain (range -2.3 to -4.1 on the McGill Pain Questionnaire short form), improved self-reported disability (range -2.1 to -3.0 on Roland scale) and improved gait velocity (0.04-0.07 m/s), Sustained at 6 months. The GCAE groups experienced significantly fewer fear avoidance beliefs immediately post-intervention and at 6 months than non-GCAE groups. There were no significant side effects. Since brief electrical stimulation (i.e., control-PENS) facilitated comparably reduced pain and improved function at 6 months as compared with PENS, the exact dose of electrical stimulation required for analgesia cannot be determined. GCAE was more effective than PENS alone in reducing fear avoidance beliefs, but not in reducing pain or in improving physical function. Published by Elsevier B.V. on behalf of International Association For the Study of Pain.
C1 [Weiner, Debra K.] VA Pittsburgh Healthcare Syst, Ctr Geriatr Res Educ & Clin, Pittsburgh, PA 15213 USA.
[Weiner, Debra K.; Perera, Subashan] Univ Pittsburgh, Dept Med, Pittsburgh, PA 15260 USA.
[Weiner, Debra K.; Rudy, Thomas E.] Univ Pittsburgh, Dept Anesthesiol, Pittsburgh, PA 15260 USA.
[Weiner, Debra K.; Rudy, Thomas E.; Glick, Ronald M.] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15260 USA.
[Perera, Subashan; Rudy, Thomas E.] Univ Pittsburgh, Dept Biostat, Pittsburgh, PA 15260 USA.
[Glick, Ronald M.] Univ Pittsburgh, Ctr Integrat Med, Pittsburgh, PA 15260 USA.
[Shenoy, Sonali; Delitto, Anthony] Univ Pittsburgh, Dept Phys Therapy, Pittsburgh, PA 15260 USA.
RP Weiner, DK (reprint author), VA Pittsburgh Healthcare Syst, Ctr Geriatr Res Educ & Clin, 3471 5th Ave,Suite 500, Pittsburgh, PA 15213 USA.
EM dweiner@pitt.edu
RI Perera, Subashan/D-7603-2014
FU National Center [R01 AT000985]; National Institute on Aging; National
Institutes of Health; Older Americans Independence Center [NIA P30
AG-024827]
FX This work was supported in by Grant R01 AT000985 from the National
Center for Complementary and Alternative Medicine and the National
Institute on Aging, National Institutes of Health. Dr. Percra was also
supported by the Pittsburgh Claude D. Pepper Older Americans
Independence Center (NIA P30 AG-024827).
NR 71
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U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-3959
EI 1872-6623
J9 PAIN
JI Pain
PD NOV 30
PY 2008
VL 140
IS 2
BP 344
EP 357
DI 10.1016/j.pain.2008.09.005
PG 14
WC Anesthesiology; Clinical Neurology; Neurosciences
SC Anesthesiology; Neurosciences & Neurology
GA 381QT
UT WOS:000261551700011
PM 18930352
ER
PT J
AU Wynn, JK
Green, MF
Engel, S
Korb, A
Lee, J
Glahn, D
Nuechterlein, KH
Cohen, MS
AF Wynn, Jonathan K.
Green, Michael F.
Engel, Stephen
Korb, Alex
Lee, Junghee
Glahn, David
Nuechterlein, Keith H.
Cohen, Mark S.
TI Increased extent of object-selective cortex in schizophrenia
SO PSYCHIATRY RESEARCH-NEUROIMAGING
LA English
DT Article
DE Schizophrenia; visual processing; functional MRI; object processing
ID HUMAN VISUAL-CORTEX; BRAIN; RECOGNITION; AREAS; FMRI; REGISTRATION;
DYSFUNCTION; ACTIVATION; RELATIVES; ACCURATE
AB Schizophrenia patients exhibit deficits in various stages of visual information processing. Despite recent informative efforts to examine visual processing in schizophrenia with functional magnetic resonance imaging (fMRI), much remains unknown about the basic function, structure, and organization of key early visual processing areas in schizophrenia. This study examined magnitude and topography of regional brain activity in three early visual processing areas: early retinotopically organized areas (V1-V4), motion-sensitive areas (human area MT, hMT+), and object-recognition areas (lateral occipital complex, LO). Using visual stimuli that are known to preferentially activate each respective region, we compared responses in these areas in 22 schizophrenia patients and 19 normal controls. Activity in all three regions was of similar amplitude in schizophrenia patients and normal controls. Activity in retinotopically organized areas and hMT+ showed good spatial overlap between groups. However, activation of LO was more widely distributed in patients compared with normal controls. The findings of abnormal spatial organization of LO in schizophrenia patients may converge with behavioral evidence of deficits in schizophrenia patients for object-recognition tasks that are believed to be mediated by LO activity. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
C1 [Wynn, Jonathan K.; Green, Michael F.; Lee, Junghee] VA Greater Los Angeles Healthcare Syst, MIRECC, Los Angeles, CA 90073 USA.
[Wynn, Jonathan K.; Green, Michael F.; Korb, Alex; Lee, Junghee; Nuechterlein, Keith H.; Cohen, Mark S.] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA.
[Engel, Stephen; Nuechterlein, Keith H.; Cohen, Mark S.] Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90024 USA.
[Glahn, David] Univ Texas Hlth Sci Ctr San Antonio, Dept Psychiat, San Antonio, TX 78229 USA.
RP Wynn, JK (reprint author), VA Greater Los Angeles Healthcare Syst, MIRECC, Bldg 210,11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM jkwynn@ucla.edu
RI Wynn, Jonathan/H-3749-2014; Cohen, Mark/C-6610-2011; Lee,
Junghee/C-5226-2014
OI Wynn, Jonathan/0000-0002-1763-8540; Cohen, Mark/0000-0001-6731-4053;
Lee, Junghee/0000-0001-9567-8700
FU NIMH [MH43292, MH065707]; Brain Mapping Medical Research Organization;
Brain Mapping Support Foundation; Pierson-Lovelace Foundation; Ahmanson
Foundation; William M. and Linda R. Dietel Philanthropic Fund at the
Northern Piedmont Community Foundation; Tamkin Foundation; Jennifer
Jones-Simon Foundation; Capital Group Companies Charitable Foundation;
Robson Family; Northstar Fund
FX Support for this study came from NIMH Grant MH43292 (PI: Michael F.
Green, Ph.D) and NIMH Grant MH065707 (PI: Michael F. Green, Ph.D.). For
generous support, we also thank the Brain Mapping Medical Research
Organization, Brain Mapping Support Foundation, Pierson-Lovelace
Foundation, The Ahmanson Foundation, William M. and Linda R. Dietel
Philanthropic Fund at the Northern Piedmont Community Foundation, Tamkin
Foundation, Jennifer Jones-Simon Foundation, Capital Group Companies
Charitable Foundation, Robson Family, and Northstar Fund. The authors
thank Poorang Nori and Alisa Malin for assistance in data collection.
NR 39
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U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0925-4927
J9 PSYCHIAT RES-NEUROIM
JI Psychiatry Res. Neuroimaging
PD NOV 30
PY 2008
VL 164
IS 2
BP 97
EP 105
DI 10.1016/j.pscychresns.2008.01.005
PG 9
WC Clinical Neurology; Neuroimaging; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 381QS
UT WOS:000261551600001
PM 18938066
ER
PT J
AU Ruan, PK
Gray, RJ
AF Ruan, Ping K.
Gray, Robert J.
TI Analyses of cumulative incidence functions via non-parametric multiple
imputation
SO STATISTICS IN MEDICINE
LA English
DT Article
DE censoring complete data; competing risks; missing data; multiple
imputation; partial likelihood estimation; penalized spline
ID PROPORTIONAL HAZARDS MODEL; CENSORED REGRESSION DATA; SURVIVAL ANALYSIS;
COMPETING RISK; AUXILIARY VARIABLES; SUBDISTRIBUTION; SPLINES; TESTS
AB We describe a non-parametric multiple imputation method that recovers the missing potential censoring information from competing risks failure times for the analysis of cumulative incidence functions. The method can be applied in the settings of stratified analyses, time-varying covariates, weighted analysis of case-cohort samples and clustered survival data analysis, where no current available methods can be readily implemented. The method uses a Kaplan-Meier imputation method for the censoring times to form an imputed data set, SO Cumulative incidence can be analyzed using techniques and software developed for ordinary right censored survival data. We discuss the methodology and show from both simulations and real data examples that the method yields valid estimates and performs well. The method can be easily implemented via available software with a minor programming requirement (for the imputation step). It provides a practical, alternative analysis tool for otherwise complicated analyses of cumulative incidence of competing risks data. Copyright (C) 2008 John Wiley & Sons, Ltd.
C1 [Ruan, Ping K.] Harvard Univ, Ctr Biostat AIDS Res, Boston, MA 02115 USA.
[Ruan, Ping K.] Harvard Univ, Dept Biostat, Boston, MA 02115 USA.
[Gray, Robert J.] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
RP Ruan, PK (reprint author), Harvard Univ, Ctr Biostat AIDS Res, 655 Huntington Ave, Boston, MA 02115 USA.
EM pkruan@sdac.harvard.edu
NR 26
TC 29
Z9 29
U1 0
U2 9
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD NOV 29
PY 2008
VL 27
IS 27
BP 5709
EP 5724
DI 10.1002/sim.3402
PG 16
WC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Medicine, Research &
Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Research & Experimental
Medicine; Mathematics
GA 372MP
UT WOS:000260906000010
PM 18712779
ER
PT J
AU Casas, A
Di Venosa, G
Vanzulli, S
Perotti, C
Mamome, L
Rodriguez, L
Simian, M
Juarranz, A
Pontiggia, O
Hasan, T
Batlle, A
AF Casas, Adriana
Di Venosa, Gabriela
Vanzulli, Silvia
Perotti, Christian
Mamome, Leandro
Rodriguez, Lorena
Simian, Marina
Juarranz, Angeles
Pontiggia, Osvaldo
Hasan, Tayyaba
Batlle, Alcira
TI Decreased metastatic phenotype in cells resistant to aminolevulinic
acid-photodynamic therapy
SO CANCER LETTERS
LA English
DT Article
DE Photodynamic therapy; Aminolevulinic acid; Metastasis; Invasion;
Adhesion
ID MAMMARY ADENOCARCINOMA CELLS; 5-AMINOLEVULINIC ACID; PROSTATE-CANCER;
EXTRACELLULAR-MATRIX; GLIOMA-CELLS; IN-VITRO; TUMOR; ADHESION; MODEL;
FLUORESCENCE
AB Photodynamic therapy (PDT) is a novel cancer treatment utilising a photosensitiser, visible light and oxygen. PDT often leaves a significant number of surviving tumour cells. In a previous work, we isolated and studied two PDT resistant clones derived from the mammary adenocarcinoma LM3 line (Int. J. Oncol. 29 (2006) 397-405). The isolated Clon 4 and Clon 8 exhibited a more fibroblastic, dendritic pattern and were larger than the parentals. In the present work we studied the metastatic potential of the two clones in comparison with LM3.
We found that 100% of LM3 invaded Matrigel, whereas only 19 +/- 6% and 24 +/- 7% of Clon 4 and Clon 8 cells invaded. In addition, 100% of LM3 cells migrated towards a chemotactic stimulus whereas 38 +/- 8% and 73 +/- 10% of Clones 4 and 8, respectively, were able to migrate. In vivo, 100% of the LM3 injected mice developed spontaneous lung metastasis, whereas none of the Clon 8 did, and only one of the mice injected with Clon 4 did. No differences were found in the proteolytic enzyme profiles among the cells. Anchorage-dependent adhesion was also impaired in vivo in the resistant clones, evidenced by the lower tumour take, latency time and growth rates, although both clones showed in vitro higher binding to collagen I without overexpression of beta 1 integrin.
This is the first work where the metastatic potential of cells surviving to PDT has been studied. PDT strongly affects the invasive phenotype of these cells, probably related to a higher binding to collagen. These findings may be crucial for the outcome of ALA-PDT of metastatic tumours, although further studies are needed to extrapolate the results to the clinic employing another photosensitisers and cell types. (c) 2008 Elsevier Ireland Ltd. All rights reserved.
C1 [Casas, Adriana; Di Venosa, Gabriela; Perotti, Christian; Mamome, Leandro; Rodriguez, Lorena; Batlle, Alcira] Univ Buenos Aires, CONICET, CIPYP, Buenos Aires, DF, Argentina.
[Casas, Adriana; Di Venosa, Gabriela; Perotti, Christian; Mamome, Leandro; Rodriguez, Lorena; Batlle, Alcira] Univ Buenos Aires, Hosp Clin Jose de San Martin, Buenos Aires, DF, Argentina.
[Vanzulli, Silvia] Acad Nacl Med Buenos Aires, Inst Estudios Oncol, RA-3092 Buenos Aires, DF, Argentina.
[Simian, Marina; Pontiggia, Osvaldo] Inst Angel H Roffo, RA-5481 Buenos Aires, DF, Argentina.
[Juarranz, Angeles] Univ Autonoma Madrid, Fac Ciencias, Dept Biol, E-28049 Madrid, Spain.
[Hasan, Tayyaba] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Dermatol,Wellman Labs Photomed WEL 224, Boston, MA 02114 USA.
RP Casas, A (reprint author), Univ Buenos Aires, CONICET, CIPYP, Viamonte 1881,10 A,1056 Ciudad Buenos Aires,Cordo, Buenos Aires, DF, Argentina.
EM adriana@qb.fcen.uba.ar
RI Juarranz, Angeles/L-2446-2013
OI Juarranz, Angeles/0000-0002-6574-2887
FU National Cancer Center [PO1 CA84203]; National Institutes for Health
[RO1 AR040352, PO1 CA084203]; Department of Defense [FA 9550-04-1-0079];
Argentine National Research Council; CONICET [PIP 4108/96, 5263/05,
105508/99-00]; Bunge y Born Foundation and Jorge Oster Argentina
FX This research was funded by grants from the National Cancer Center PO1
CA84203, the National Institutes for Health RO1 AR040352, the Department
of Defense FA 9550-04-1-0079, and the Argentine National Research
Council (CONICET) (PIP 4108/96, 5263/05 and 105508/99-00). During the
writing of this article, support to the authors was provided by National
Institute of Health Grants PO1 CA084203 and RO1 AR040352. A.C. thanks
Bunge y Born Foundation and Jorge Oster Argentina for financial support.
NR 66
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Z9 19
U1 0
U2 4
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0304-3835
J9 CANCER LETT
JI Cancer Lett.
PD NOV 28
PY 2008
VL 271
IS 2
BP 342
EP 351
DI 10.1016/j.canlet.2008.06.023
PG 10
WC Oncology
SC Oncology
GA 373YV
UT WOS:000261010300017
PM 18662847
ER
PT J
AU Oberdoerffer, P
Michan, S
Mcvay, M
Mostoslavsky, R
Vann, J
Park, SK
Hartlerode, A
Stegmuller, J
Hafner, A
Loerch, P
Wright, SM
Mills, KD
Bonni, A
Yankner, BA
Scully, R
Prolla, TA
Alt, FW
Sinclair, DA
AF Oberdoerffer, Philipp
Michan, Shaday
Mcvay, Michael
Mostoslavsky, Raul
Vann, James
Park, Sang-Kyu
Hartlerode, Andrea
Stegmuller, Judith
Hafner, Angela
Loerch, Patrick
Wright, Sarah M.
Mills, Kevin D.
Bonni, Azad
Yankner, Bruce A.
Scully, Ralph
Prolla, Tomas A.
Alt, Frederick W.
Sinclair, David A.
TI SIRT1 Redistribution on Chromatin Promotes Genomic Stability but Alters
Gene Expression during Aging
SO CELL
LA English
DT Article
ID DOUBLE-STRAND BREAKS; EMBRYONIC STEM-CELLS; SACCHAROMYCES-CEREVISIAE;
LIFE-SPAN; DNA-DAMAGE; HISTONE H2AX; HETEROCHROMATIN FORMATION; CELLULAR
SENESCENCE; GENOTOXIC STRESS; MATING-TYPE
AB Genomic instability and alterations in gene expression are hallmarks of eukaryotic aging. The yeast histone deacetylase Sir2 silences transcription and stabilizes repetitive DNA, but during aging or in response to a DNA break, the Sir complex relocalizes to sites of genomic instability, resulting in the desilencing of genes that cause sterility, a characteristic of yeast aging. Using embryonic stem cells, we show that mammalian Sir2, SIRT1, represses repetitive DNA and a functionally diverse set of genes across the mouse genome. In response to DNA damage, SIRT1 dissociates from these loci and relocalizes to DNA breaks to promote repair, resulting in transcriptional changes that parallel those in the aging mouse brain. Increased SIRT1 expression promotes survival in a mouse model of genomic instability and suppresses age-dependent transcriptional changes. Thus, DNA damage-induced redistribution of SIRT1 and other chromatin-modifying proteins may be a conserved mechanism of aging in eukaryotes.
C1 [Oberdoerffer, Philipp; Michan, Shaday; Mcvay, Michael; Stegmuller, Judith; Hafner, Angela; Loerch, Patrick; Bonni, Azad; Yankner, Bruce A.; Sinclair, David A.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Oberdoerffer, Philipp; Michan, Shaday; Mcvay, Michael; Stegmuller, Judith; Hafner, Angela; Loerch, Patrick; Bonni, Azad; Yankner, Bruce A.; Sinclair, David A.] Harvard Univ, Sch Med, Glenn Labs Aging Res, Boston, MA 02115 USA.
[Mostoslavsky, Raul] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Vann, James; Park, Sang-Kyu; Prolla, Tomas A.] Univ Wisconsin, Dept Genet & Med Genet, Madison, WI 53706 USA.
[Hartlerode, Andrea; Scully, Ralph] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[Hartlerode, Andrea; Scully, Ralph] Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA.
[Wright, Sarah M.; Mills, Kevin D.] Jackson Lab, Bar Harbor, ME 04609 USA.
[Alt, Frederick W.] Harvard Univ, Sch Med, Howard Hughes Med Inst, Childrens Hosp,Immune Dis Inst, Boston, MA 02115 USA.
[Alt, Frederick W.] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
RP Sinclair, DA (reprint author), Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
EM david_sinclair@hms.harvard.edu
RI Scully, Ralph/F-5008-2013;
OI Sinclair, David/0000-0002-9936-436X
FU National Space Biomedical Research Institute [PF00903]; National
Institutes of Health [NIH] [RO1GM068072, R01AG19719, NS047188, GM
073894, R01AG 020681]; Glenn Foundation for Medical Research
FX D. A. S. wishes to thank B. Stillman and C. Westphal for advice and
scientific discussions. We are also grateful to K. Rajewsky, D.
Reinberg, D. Lamming, L. Guarente, A. Vaquero, and M. Jasin for advice
and reagents. We thank E. Vollmann, J. Campbell, and D. Zimmerman for
technical assistance and R. Bronson for mouse necropsy. We are
especially grateful to P. Glenn, M. Collins, and L. Ellison for their
support of aging research. P. O. was supported by a fellowship from the
National Space Biomedical Research Institute (grant PF00903), the
Sinclair Lab by grants RO1GM068072 and R01AG19719 (National Institutes
of Health [NIH]), and the Glenn Foundation for Medical Research. D. A.
S. and F. W. A. are Ellison Medical Foundation Senior Scholars. R. M. is
a V and Kimmel Foundation Scholar. A. B. supported by NIH grant
NS047188; R. S. by GM 073894; and J. V., S. P., and T. A. P. by R01AG
020681. F. W. A. is an Investigator of the Howard Hughes Medical
Institute. D. A. S. is a consultant to Shaklee, Genocea, and Sirtris (a
GSK company developing sirtuin-based drugs) and an inventor on Harvard
patents licensed to GSK.
NR 70
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Z9 403
U1 2
U2 25
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD NOV 28
PY 2008
VL 135
IS 5
BP 907
EP 918
DI 10.1016/j.cell.2008.10.025
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 376LA
UT WOS:000261183900021
PM 19041753
ER
PT J
AU Araujo, P
Nguyen, TT
Froyland, L
Wang, JD
Kang, JX
AF Araujo, Pedro
Nguyen, Thu-Thao
Froyland, Livar
Wang, Jingdong
Kang, Jing X.
TI Evaluation of a rapid method for the quantitative analysis of fatty
acids in various matrices
SO JOURNAL OF CHROMATOGRAPHY A
LA English
DT Article
DE Methylation; Methylation models; Gas chromatography; High performance
thin layer chromatography
ID METHYLATION; CHOLESTEROL; LIVER
AB A simplified method for quantitative analysis of fatty acids in various matrices by gas chromatography is proposed as an alternative to the conventional method and the variables of the protocol examined to optimize the processing conditions. The modified method involves direct methylation of fatty acids in homogenized samples with boron trihalide (BF(3) or BCl(3) in methanol) followed by extraction with hexane. The addition of hexane to the reaction mixture after the methylation process can enhance the efficiency of fatty acid methylation and is critical for those samples that contain high levels of triglycerides. A mechanism underlying this effect is proposed. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Araujo, Pedro; Nguyen, Thu-Thao; Froyland, Livar] Natl Inst Nutr & Seafood Res NIFES, N-5817 Bergen, Norway.
[Wang, Jingdong; Kang, Jing X.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Wang, Jingdong; Kang, Jing X.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Araujo, P (reprint author), Natl Inst Nutr & Seafood Res NIFES, POB 2029 Nordnes, N-5817 Bergen, Norway.
EM pedro.araujo@nifes.no
FU NIH [R01CA113605]
FX This study was partially Supported by the NIH grant (R01CA113605)
(J.X.K.).
NR 17
TC 40
Z9 42
U1 1
U2 21
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0021-9673
J9 J CHROMATOGR A
JI J. Chromatogr. A
PD NOV 28
PY 2008
VL 1212
IS 1-2
BP 106
EP 113
DI 10.1016/j.chroma.2008.10.006
PG 8
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 377TF
UT WOS:000261272800015
PM 18937951
ER
PT J
AU Smith, ER
Loeffler, J
Misra, M
Pomerantz, SR
Stemmer-Rachamimov, A
Post, MD
Harris, NL
McKenna, M
AF Smith, Edward R.
Loeffler, Jay
Misra, Madhusmita
Pomerantz, Stuart R.
Stemmer-Rachamimov, Anat
Post, Miriam D.
Harris, Nancy Lee
McKenna, Michael
TI A Boy with a Pituitary Tumor and Skull Abnormalities Pituitary adenoma,
prolactin secreting, with atypical features and a high proliferation
fraction. Osteoblastoma of the skull
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID VALVULAR HEART-DISEASE; TRICUSPID REGURGITATION; MEDICAL THERAPY;
CABERGOLINE; ADOLESCENTS; CHILDREN; HEADACHE; LESIONS; BROMOCRIPTINE;
AMENORRHEA
C1 [Smith, Edward R.] Childrens Hosp, Dept Neurosurg, Boston, MA 02115 USA.
[Loeffler, Jay] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
[Misra, Madhusmita] Massachusetts Gen Hosp, Dept Pediat, Boston, MA 02114 USA.
[Pomerantz, Stuart R.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Stemmer-Rachamimov, Anat; Post, Miriam D.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Smith, Edward R.] Harvard Univ, Sch Med, Dept Surg, Cambridge, MA 02138 USA.
[Loeffler, Jay] Harvard Univ, Sch Med, Dept Radiat Oncol, Cambridge, MA 02138 USA.
[Misra, Madhusmita] Harvard Univ, Sch Med, Dept Pediat, Cambridge, MA 02138 USA.
[Pomerantz, Stuart R.] Harvard Univ, Sch Med, Dept Radiol, Cambridge, MA 02138 USA.
[Stemmer-Rachamimov, Anat; Post, Miriam D.] Harvard Univ, Sch Med, Dept Pathol, Cambridge, MA 02138 USA.
RP Smith, ER (reprint author), Childrens Hosp, Dept Neurosurg, 300 Longwood Ave, Boston, MA 02115 USA.
FU Tercica; Ortho-McNeil Pharmaceutical; GE HealthCare
FX Dr. Loeffler reports receiving consulting fees or being on the paid
advisory boards of TransMolecular and Procore and having equity
ownership in Procore; Dr. Misra, receiving grant support from Tercica
and Ortho-McNeil Pharmaceutical, and Dr. Pomerantz, receiving lecture
fees and grant support from GE HealthCare. No other potential conflict
of interest relevant to this article was reported.
NR 30
TC 1
Z9 1
U1 0
U2 1
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 27
PY 2008
VL 359
IS 22
BP 2367
EP 2377
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 377SG
UT WOS:000261270300010
PM 19038883
ER
PT J
AU Blumenthal, D
Morone, J
AF Blumenthal, David
Morone, James
TI The Lessons of Success - Revisiting the Medicare Story
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
C1 [Blumenthal, David] Massachusetts Gen Hosp, Inst Hlth Policy, Boston, MA 02114 USA.
[Morone, James] Brown Univ, Dept Polit Sci, Providence, RI 02912 USA.
RP Blumenthal, D (reprint author), Massachusetts Gen Hosp, Inst Hlth Policy, Boston, MA 02114 USA.
NR 24
TC 3
Z9 3
U1 0
U2 0
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 27
PY 2008
VL 359
IS 22
BP 2384
EP 2389
DI 10.1056/NEJMhpr0806879
PG 6
WC Medicine, General & Internal
SC General & Internal Medicine
GA 377SG
UT WOS:000261270300013
PM 19038885
ER
PT J
AU Doria, A
Wojcik, J
Xu, R
Gervino, EV
Hauser, TH
Johnstone, MT
Nolan, D
Hu, FB
Warram, JH
AF Doria, Alessandro
Wojcik, Joanna
Xu, Rui
Gervino, Ernest V.
Hauser, Thomas H.
Johnstone, Michael T.
Nolan, David
Hu, Frank B.
Warram, James H.
TI Interaction Between Poor Glycemic Control and 9p21 Locus on Risk of
Coronary Artery Disease in Type 2 Diabetes
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; CARDIOVASCULAR-DISEASE; MYOCARDIAL-INFARCTION;
ADIPONECTIN GENE; META-ANALYSIS; INSULIN; EPIDEMIOLOGY; POLYMORPHISM;
MELLITUS; SUSCEPTIBILITY
AB Context A common allele on chromosome 9p21 has been repeatedly associated with increased risk of coronary artery disease ( CAD) in the general population. However, the magnitude of this effect in the population with diabetes has not been well characterized.
Objective To examine the association of the 9p21 variant with CAD in individuals with type 2 diabetes and evaluate its interaction with poor glycemic control.
Design, Setting, and Participants ( 1) Case- control study of 734 type 2 diabetes patients ( 322 with angiographically diagnosed CAD and 412 with no evidence of CAD) who were recruited between 2001 and 2006 at the Joslin Clinic, Beth Israel Deaconess Medical Center; and ( 2) independent cohort study of 475 type 2 diabetes patients from the Joslin Clinic whose survival status was monitored from their recruitment between 1993 and 1996 until December 31, 2004. Participants for both studies were genotyped for a representative single- nucleotide polymorphism at 9p21 ( rs2383206) and characterized for their long- term glycemic control by averaging multiple hemoglobin A(1c) ( HbA(1c)) measurements taken in the years before study entry.
Main Outcome Measures For the case- control study, association between single-nucleotide polymorphism rs2383206 and CAD defined as angiographically documented stenosis greater than 50% in a major coronary artery or a main branch thereof was assessed and for the cohort study, cumulative 10- year mortality was documented.
Results Individuals who were homozygous for the risk allele were significantly more frequent among case than control participants ( 42.3% vs 28.9P=. 0002). This association was unaffected by adjustment for cardiovascular risk factors, but the effect of the risk genotype was significantly magnified ( adjusted P for interaction=. 048) in the presence of poor glycemic control ( worst tertile of the distribution of HbA(1c) at examination). Relative to the CAD risk for patients with neither a 9p21 risk allele nor poor glycemic control, the CAD odds for participants having 2 risk alleles but not poor glycemic control were increased 2- fold ( odds ratio [ OR], 1.99; 95% confidence interval [ CI], 1.17- 3.41), whereas the odds for study participants with the same genotype and with poor glycemic control were increased 4- fold ( OR, 4.27; 95% CI, 2.26- 8.01). The interaction was stronger ( adjusted P=. 005) when a measure of long- term glycemic control ( 7- year average rather than most recent HbA(1c)) was used with ORs of 7.83 ( 95% CI, 3.49- 17.6) for participants having 2 risk alleles and a history of poor glycemia and 1.54 ( 95% CI, 0.72- 3.30) for participants with the same genotype but without this exposure. A similar interaction between 9p21 variant and poor glycemic control was observed with respect to cumulative 10- year mortality in the cohort study ( 43.6% in patients with 2 risk alleles and poor glycemic control, 23.1% in individuals with only the 2 risk alleles, 30.0% in individuals with only poor glycemic control, and 31.6% in individuals with neither factor, P for interaction, =. 036).
Conclusion In this study population, the CAD risk associated with the 9p21 variant was increased in the presence of poor glycemic control in type 2 diabetes.
C1 [Doria, Alessandro; Wojcik, Joanna; Xu, Rui; Nolan, David; Warram, James H.] Joslin Diabet Ctr, Div Res, Sect Genet & Epidemiol, Boston, MA 02215 USA.
[Doria, Alessandro; Wojcik, Joanna; Xu, Rui; Gervino, Ernest V.; Hauser, Thomas H.; Hu, Frank B.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Gervino, Ernest V.; Hauser, Thomas H.] Beth Israel Deaconess Med Ctr, Div Cardiovasc, Boston, MA 02215 USA.
[Johnstone, Michael T.] Caritas St Elizabeth Med Ctr, Boston, MA USA.
[Hu, Frank B.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Doria, Alessandro; Hu, Frank B.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
RP Doria, A (reprint author), Joslin Diabet Ctr, Div Res, Sect Genet & Epidemiol, 1 Joslin Pl, Boston, MA 02215 USA.
EM alessandro.doria@joslin.harvard.edu
FU National Institutes of Health [HL73168, HL71981]; Genetics Core of the
Diabetes and Endocrinology Research Center at the Joslin Diabetes Center
[DK36836]; Donald W. Reynolds Foundation
FX This study was supported by National Institutes of Health grants
HL73168, HL71981, and DK36836 (Genetics Core of the Diabetes and
Endocrinology Research Center at the Joslin Diabetes Center), and a
grant from the Donald W. Reynolds Foundation. Role of the Sponsors: None
of the funding agencies had any role in the design and conduct of the
study, in the collection, management, analysis, and interpretation of
the data, or in the preparation, review, or approval of the manuscript.
NR 40
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U1 0
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 26
PY 2008
VL 300
IS 20
BP 2389
EP 2397
DI 10.1001/jama.2008.649
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 375YX
UT WOS:000261150800021
PM 19033589
ER
PT J
AU Lyamin, OI
Kosenko, PO
Lapierre, JL
Mukhametov, LM
Siegel, JM
AF Lyamin, Oleg I.
Kosenko, Peter O.
Lapierre, Jennifer L.
Mukhametov, Lev M.
Siegel, Jerome M.
TI Fur Seals Display a Strong Drive for Bilateral Slow-Wave Sleep While on
Land
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE EEG asymmetry; bilateral slow-wave sleep; slow-wave activity; sleep
deprivation; sleep-wake cycle; Callorhinus ursinus
ID UNIHEMISPHERIC SLEEP; SPECTRAL POWER; DEPRIVATION; EEG; ASYMMETRY;
STIMULATION; DOLPHINS; RAT
AB Fur seals (pinnipeds of the family Otariidae) display two fundamentally different patterns of sleep: bilaterally symmetrical slow-wave sleep (BSWS) as seen in terrestrial mammals and slow-wave sleep (SWS) with a striking interhemispheric EEG asymmetry (asymmetrical SWS or ASWS) as observed in cetaceans. We examined the effect of preventing fur seals from sleeping in BSWS on their pattern of sleep. Four northern fur seals (Callorhinus ursinus) kept on land were sleep deprived (SD) of BSWS for 3 consecutive days, followed by 1 recovery day. EEG asymmetry was evaluated both visually and by EEG spectral analysis. SD significantly reduced the percentage of high-voltage BSWS (on average to 14% of baseline) and REM sleep (to 60% of baseline) whereas the percentage of low-voltage BSWS was not affected. During the SD period, all seals repeatedly tried to enter BSWS (109-411 attempts per day). SD significantly increased the amount of ASWS in each seal when scored visually (to 116-235% of baseline) and the difference in the EEG slow-wave activity (spectral power in the range of 1.2-4.0 Hz) between the two hemispheres (117-197%) as measured by the asymmetry index. High-voltage BSWS and the amount of SWS in each hemisphere were significantly elevated during the first 4 h of recovery. These data indicate that fur seals display a homeostatic response to the loss of SWS and that alternating SWS in the two hemispheres does not adequately compensate for the absence of BSWS.
C1 [Lyamin, Oleg I.; Lapierre, Jennifer L.; Siegel, Jerome M.] Vet Affairs Greater Los Angeles Healthcare Syst, Neurobiol Res 151A3, North Hills, CA 91343 USA.
[Lyamin, Oleg I.; Lapierre, Jennifer L.; Siegel, Jerome M.] Univ Calif Los Angeles, Dept Psychiat, Sch Med, North Hills, CA 91343 USA.
[Lyamin, Oleg I.; Kosenko, Peter O.; Mukhametov, Lev M.] Utrish Dolphinarium Ltd, Moscow 119071, Russia.
RP Lyamin, OI (reprint author), Vet Affairs Greater Los Angeles Healthcare Syst, Neurobiol Res 151A3, 16111 Plummer St, North Hills, CA 91343 USA.
EM olyamin@ucla.edu
FU National Science Foundation [0234687]; Defense Advanced Research
Projects Agency [BAA0412F8034]; Department of Veterans Affairs; Utrish
Dolphinarium, Ltd
FX This work was supported by the National Science Foundation (Grant
0234687), the Defense Advanced Research Projects Agency (Grant
BAA0412F8034), the Medical Research Service of the Department of
Veterans Affairs, and the Utrish Dolphinarium, Ltd. We thank E. Belyaev,
A. Kibalnikov, E. Nazarenko, J. Pryaslova, and O. Shpak for their
assistance during the experiments.
NR 28
TC 11
Z9 11
U1 2
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 NOV 26
PY 2008
VL 28
IS 48
BP 12614
EP 12621
DI 10.1523/JNEUROSCI.2306-08.2008
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 376OA
UT WOS:000261191700003
PM 19036955
ER
PT J
AU Weissman, JR
Kelley, RI
Bauman, ML
Cohen, BH
Murray, KF
Mitchell, RL
Kern, RL
Natowicz, MR
AF Weissman, Jacqueline R.
Kelley, Richard I.
Bauman, Margaret L.
Cohen, Bruce H.
Murray, Katherine F.
Mitchell, Rebecca L.
Kern, Rebecca L.
Natowicz, Marvin R.
TI Mitochondrial Disease in Autism Spectrum Disorder Patients: A Cohort
Analysis
SO PLOS ONE
LA English
DT Article
ID RESPIRATORY-CHAIN DISORDERS; MTDNA MUTATIONS; GASTROINTESTINAL SYMPTOMS;
DEVELOPMENTAL REGRESSION; DIAGNOSTIC-CRITERIA; LACTIC-ACIDOSIS; DNA
MUTATIONS; COMPLEX-I; CHILDREN; DYSFUNCTION
AB Background: Previous reports indicate an association between autism spectrum disorders (ASD) and disorders of mitochondrial oxidative phosphorylation. One study suggested that children with both diagnoses are clinically indistinguishable from children with idiopathic autism. There are, however, no detailed analyses of the clinical and laboratory findings in a large cohort of these children. Therefore, we undertook a comprehensive review of patients with ASD and a mitochondrial disorder.
Methodology/Principal Findings: We reviewed medical records of 25 patients with a primary diagnosis of ASD by DSM-IV-TR criteria, later determined to have enzyme- or mutation-defined mitochondrial electron transport chain (ETC) dysfunction. Twenty-four of 25 patients had one or more major clinical abnormalities uncommon in idiopathic autism. Twenty-one patients had histories of significant non-neurological medical problems. Nineteen patients exhibited constitutional symptoms, especially excessive fatigability. Fifteen patients had abnormal neurological findings. Unusual developmental phenotypes included marked delay in early gross motor milestones (32%) and unusual patterns of regression (40%). Levels of blood lactate, plasma alanine, and serum ALT and/or AST were increased at least once in 76%, 36%, and 52% of patients, respectively. The most common ETC disorders were deficiencies of complex I (64%) and complex III (20%). Two patients had rare mtDNA mutations of likely pathogenicity.
Conclusions/Significance: Although all patients' initial diagnosis was idiopathic autism, careful clinical and biochemical assessment identified clinical findings that differentiated them from children with idiopathic autism. These and prior data suggest a disturbance of mitochondrial energy production as an underlying pathophysiological mechanism in a subset of individuals with autism.
C1 [Weissman, Jacqueline R.; Natowicz, Marvin R.] Cleveland Clin, Lerner Coll Med, Cleveland, OH 44106 USA.
[Kelley, Richard I.; Kern, Rebecca L.] Kennedy Krieger Inst, Division of Metabolism, Baltimore, MD USA.
[Kelley, Richard I.; Kern, Rebecca L.] Johns Hopkins Univ, Med Ctr, Dept Pediat, Baltimore, MD 21218 USA.
[Bauman, Margaret L.; Murray, Katherine F.] Massachusetts Gen Hosp, LADDERS, Dept Pediat, Boston, MA 02114 USA.
[Cohen, Bruce H.; Natowicz, Marvin R.] Cleveland Clin, Pediatrics Inst, Neurol Inst, Cleveland, OH USA.
[Mitchell, Rebecca L.; Natowicz, Marvin R.] Cleveland Clin, Genom Med Inst, Cleveland, OH USA.
[Natowicz, Marvin R.] Cleveland Clin, Lab Med Inst, Cleveland, OH USA.
RP Weissman, JR (reprint author), Cleveland Clin, Lerner Coll Med, Cleveland, OH 44106 USA.
EM natowim@ccf.org
FU Solving the Mystery of Autism Foundation, Inc; Green Foundation
FX This work was supported in part by a grant from the Solving the Mystery
of Autism Foundation, Inc. and from the Green Foundation. The funders
had no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 63
TC 93
Z9 97
U1 0
U2 10
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 26
PY 2008
VL 3
IS 11
AR e3815
DI 10.1371/journal.pone.0003815
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 436YG
UT WOS:000265451400007
PM 19043581
ER
PT J
AU Van den Stock, J
Grezes, J
de Gelder, B
AF Van den Stock, Jan
Grezes, Julie
de Gelder, Beatrice
TI Human and animal sounds influence recognition of body language
SO BRAIN RESEARCH
LA English
DT Article; Proceedings Paper
CT 8th International Multisensory Research Forum
CY JUL, 2007
CL Univ Sydney, Sydney, AUSTRALIA
HO Univ Sydney
DE Multisensory; Body perception; Emotion
ID COMBINED PERCEPTION; VOICE; FACE; EXPRESSIONS; EMOTION; INTEGRATION;
RESPONSES; AMYGDALA; BINDING; FEAR
AB In naturalistic settings emotional events have multiple correlates and are simultaneously perceived by several sensory systems. Recent studies have shown that recognition of facial expressions is biased towards the emotion expressed by a simultaneously presented emotional expression in the voice even if attention is directed to the face only. So far, no study examined whether this phenomenon also applies to whole body expressions, although there is no obvious reason why this crossmodal influence would be specific for faces. Here we investigated whether perception of emotions expressed in whole body movements is influenced by affective information provided by human and by animal vocalizations. Participants were instructed to attend to the action displayed by the body and to categorize the expressed emotion. The results indicate that recognition of body language is biased towards the emotion expressed by the simultaneously presented auditory information, whether it consist of human or of animal sounds. Our results show that a crossmodal influence from auditory to visual emotional information obtains for whole body video images with the facial expression blanked and includes human as well as animal sounds. (c) 2008 Elsevier B.V. All rights reserved.
C1 [de Gelder, Beatrice] Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[de Gelder, Beatrice] Harvard Univ, Sch Med, Charlestown, MA USA.
[Van den Stock, Jan; de Gelder, Beatrice] Tilburg Univ, Cognit & Affect Neurosci Lab, Tilburg, Netherlands.
[Van den Stock, Jan] Univ Hosp Leuven, Dept Old Age Psychiat, Louvain, Belgium.
[Grezes, Julie] Ecole Normale Super, Cognit Neurosci Lab, INSERM, U742 & DEC, Paris, France.
RP de Gelder, B (reprint author), Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, Room 417,Bldg 36,1st St, Charlestown, MA 02129 USA.
EM degelder@nmr.mgh.harvard.edu
RI Van den Stock, Jan/F-1906-2014; Grezes, Julie/E-5060-2016
OI Van den Stock, Jan/0000-0001-5756-3195;
NR 26
TC 33
Z9 33
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD NOV 25
PY 2008
VL 1242
BP 185
EP 190
DI 10.1016/j.brainres.2008.05.040
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA 386EQ
UT WOS:000261865500019
PM 18617158
ER
PT J
AU Ridker, PM
Paynter, NP
Rifai, N
Gaziano, JM
Cook, NR
AF Ridker, Paul M.
Paynter, Nina P.
Rifai, Nader
Gaziano, J. Michael
Cook, Nancy R.
TI C-Reactive Protein and Parental History Improve Global Cardiovascular
Risk Prediction The Reynolds Risk Score for Men
SO CIRCULATION
LA English
DT Article
DE epidemiology; prevention; inflammation; genetics; risk factors
ID TREATMENT PANEL-III; ROC CURVE; DISEASE; MODELS; PREVENTION;
CHOLESTEROL; RECLASSIFICATION; RECOMMENDATIONS; VALIDATION; ABILITY
AB Background-High-sensitivity C-reactive protein and family history are independently associated with future cardiovascular events and have been incorporated into risk prediction models for women (the Reynolds Risk Score for women); however, no cardiovascular risk prediction algorithm incorporating these variables currently exists for men.
Methods and Results-Among 10 724 initially healthy American nondiabetic men who were followed up prospectively over a median period of 10.8 years, we compared the test characteristics of global model fit, discrimination, calibration, and reclassification in 2 prediction models for incident cardiovascular events, one based on age, blood pressure, smoking status, total cholesterol, and high-density lipoprotein cholesterol (traditional model) and the other based on these risk factors plus high-sensitivity C-reactive protein and parental history of myocardial infarction before age 60 years (Reynolds Risk Score for men). A total of 1294 cardiovascular events accrued during study follow-up. Compared with the traditional model, the Reynolds Risk Score had better global fit (likelihood ratio test P<0.001), a superior (lower) Bayes information criterion, and a larger C-index (P<0.001). For the end point of all cardiovascular events, the Reynolds Risk Score for men reclassified 17.8% (1904/10 724) of the study population (and 20.2% [1392/6884] of those at 5% to 20% 10-year risk) into higher-or lower-risk categories, with markedly improved accuracy among those reclassified. For this model comparison, the net reclassification index was 5.3%, and the clinical net reclassification index was 14.2% (both P<0.001). In models based on the Adult Treatment Panel III preferred end point of coronary heart disease and limited to men not taking lipid-lowering therapy, 16.7% of the study population (and 20.1% of those at 5% to 20% 10-year risk) were reclassified to higher- or lower-risk groups, again with significantly improved global fit, larger C-index (P<0.001), and markedly improved accuracy among those reclassified. For this model, the net reclassification index was 8.4% and the clinical net reclassification index was 15.8% (both P<0.001).
Conclusions-As previously shown in women, a prediction model in men that incorporates high-sensitivity C-reactive protein and parental history significantly improves global cardiovascular risk prediction. (Circulation. 2008; 118: 2243-2251.)
C1 [Ridker, Paul M.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Ctr Cardiovasc Dis Prevent,Div Prevent Med, Boston, MA 02215 USA.
Harvard Univ, Sch Med, Brigham & Womens Hosp, Ctr Cardiovasc Dis Prevent,Div Cardiovasc Med, Boston, MA 02215 USA.
Harvard Univ, Sch Med, Brigham & Womens Hosp, Donald W Reynolds Ctr Cardiovasc Res, Boston, MA 02215 USA.
VA Boston Hlth Care Syst, MAVERIC, Boston, MA USA.
RP Ridker, PM (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Ctr Cardiovasc Dis Prevent,Div Prevent Med, 900 Commonwealth Ave E, Boston, MA 02215 USA.
EM pridker@partners.org
FU National Heart, Lung, and Blood Institute (Bethesda, Md); Donald W.
Reynolds Foundation (Las Vegas, Nev); National Heart, Lung, and Blood
Institute
FX These analyses were funded by grants from the National Heart, Lung, and
Blood Institute (Bethesda, Md) and the Donald W. Reynolds Foundation
(Las Vegas, Nev). The Physicians Health Study is supported by grants
from the National Heart, Lung, and Blood Institute. The funding agencies
had no involvement in the design and conduct of the study; the
collection, management, analysis, and interpretation of the data; or the
drafting of the manuscript.
NR 23
TC 402
Z9 423
U1 2
U2 19
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 25
PY 2008
VL 118
IS 22
BP 2243
EP 4
DI 10.1161/CIRCULATIONAHA.108.814251
PG 13
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 377AO
UT WOS:000261224300005
PM 18997194
ER
PT J
AU Velagaleti, RS
Gona, P
Levy, D
Aragam, J
Larson, MG
Tofler, GH
Lieb, W
Wang, TJ
Benjamin, EJ
Vasan, RS
AF Velagaleti, Raghava S.
Gona, Philimon
Levy, Daniel
Aragam, Jayashri
Larson, Martin G.
Tofler, Geoffrey H.
Lieb, Wolfgang
Wang, Thomas J.
Benjamin, Emelia J.
Vasan, Ramachandran S.
TI Relations of Biomarkers Representing Distinct Biological Pathways to
Left Ventricular Geometry
SO CIRCULATION
LA English
DT Article
DE aldosterone; biological markers; echocardiography; hypertrophy;
remodeling; renin
ID C-REACTIVE PROTEIN; ANGIOTENSIN-ALDOSTERONE SYSTEM; CONVERTING
ENZYME-INHIBITOR; CORONARY HEART-DISEASE; TARGET ORGAN DAMAGE;
ESSENTIAL-HYPERTENSION; BLOOD-PRESSURE; METABOLIC SYNDROME; SERUM
ALDOSTERONE; RISK-FACTORS
AB Background-Several biological pathways are activated concomitantly during left ventricular (LV) remodeling. However, the relative contribution of circulating biomarkers representing these distinct pathways to LV geometry is unclear.
Methods and Results-We evaluated 2119 Framingham Offspring Study participants (mean age, 57 years; 57% women) who underwent measurements of biomarkers of inflammation (C-reactive protein), hemostasis (fibrinogen and plasminogen activator inhibitor-1), neurohormonal activation (B-type natriuretic peptide), and renin-angiotensin-aldosterone system (aldosterone and renin modeled as a ratio [ARR]) and echocardiography at a routine examination. LV geometry was defined on the basis of sex-specific distributions of LV mass (LVM) and relative wall thickness (RWT): normal (LVM and RWT <80th percentile), concentric remodeling (LVM <80th percentile but RWT >= 80th percentile), eccentric hypertrophy (LVM >= 80th percentile but RWT <80th percentile), and concentric hypertrophy (LVM and RWT >80th percentile). We related the biomarker panel to LV geometry using polytomous logistic regression adjusting for clinical covariates and used backwards elimination to identify a parsimonious set of biomarkers associated with LV geometry. Modeled individually, C-reactive protein, fibrinogen, plasminogen activator inhibitor-1, and ARR were related to LV geometry (P<0.01). In multivariable analyses, the biomarker panel was significantly related to altered LV geometry (P<0.0001). On backwards elimination, logARR alone was significantly and positively associated with eccentric (odds ratio per SD increment, 1.20; 95% confidence interval, 1.05 to 1.37) and concentric LV hypertrophy (odds ratio per SD increment, 1.29; 95% confidence interval, 1.06 to 1.58).
Conclusions-Our cross-sectional observations on a large community-based sample identified ARR as a key correlate of concentric and eccentric LV hypertrophy, consistent with a major role for the renin-angiotensin-aldosterone system in LV remodeling. (Circulation. 2008; 118: 2252-2258.)
C1 [Velagaleti, Raghava S.; Gona, Philimon; Levy, Daniel; Larson, Martin G.; Lieb, Wolfgang; Wang, Thomas J.; Benjamin, Emelia J.; Vasan, Ramachandran S.] Framingham Heart Dis Epidemiol Study, Newark, NJ 07102 USA.
[Aragam, Jayashri] Vet Adm Hosp, W Roxbury, MA USA.
[Levy, Daniel] NHLBI, Ctr Populat Studies, W Roxbury, MA USA.
[Gona, Philimon; Larson, Martin G.] Dept Math & Stat, W Roxbury, MA USA.
[Wang, Thomas J.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Tofler, Geoffrey H.] Royal N Shore Hosp, Dept Cardiol, Sydney, NSW, Australia.
[Benjamin, Emelia J.; Vasan, Ramachandran S.] Boston Univ, Dept Sch Publ Hlth, Sch Med & Epidemiol, Prevent Med Sect, Boston, MA 02215 USA.
[Benjamin, Emelia J.; Vasan, Ramachandran S.] Boston Univ, Dept Sch Publ Hlth, Sch Med & Epidemiol, Cardiol Sect, Boston, MA 02215 USA.
RP Vasan, RS (reprint author), Framingham Heart Dis Epidemiol Study, 73 Mt Wayte Ave, Newark, NJ 07102 USA.
EM vasan@bu.edu
RI Lieb, Wolfgang/C-1990-2012;
OI Larson, Martin/0000-0002-9631-1254; Ramachandran,
Vasan/0000-0001-7357-5970; Benjamin, Emelia/0000-0003-4076-2336
FU National Heart, Lung, and Blood Institute [N01-HC-25195]; National
Institutes of Health [RO1-HL086875, RO1 HL67288, IIL080124, K24-HL04334]
FX This work was supported by the National Heart, Lung, and Blood Institute
(contract N01-HC-25195) and National Institutes of Health grants
RO1-HL086875 (Dr Wang), RO1 HL67288, IIL080124, and K24-HL04334 (Dr
Vasan).
NR 48
TC 14
Z9 14
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 25
PY 2008
VL 118
IS 22
BP 2252
EP U161
DI 10.1161/CIRCULATIONAHA.108.817411
PG 12
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 377AO
UT WOS:000261224300006
ER
PT J
AU Davis, BR
Kostis, JB
Simpson, LM
Black, HR
Cushman, WC
Einhorn, PT
Farber, MA
Ford, CE
Levy, D
Massie, BM
Nawaz, S
AF Davis, Barry R.
Kostis, John B.
Simpson, Lara M.
Black, Henry R.
Cushman, William C.
Einhorn, Paula T.
Farber, Michael A.
Ford, Charles E.
Levy, Daniel
Massie, Barry M.
Nawaz, Shah
CA ALLHAT Collaborative Res Grp
TI Heart Failure With Preserved and Reduced Left Ventricular Ejection
Fraction in the Antihypertensive and Lipid-Lowering Treatment to Prevent
Heart Attack Trial
SO CIRCULATION
LA English
DT Article
DE angiotensin-converting enzyme inhibitors; antihypertensive agents;
calcium channel blockers; diuretics; heart failure; hypertension;
ventricular ejection fraction
ID SYSTOLIC FUNCTION; DIASTOLIC DYSFUNCTION; CARDIOVASCULAR HEALTH; OLMSTED
COUNTY; PREVALENCE; COMMUNITY; POPULATION; PROGNOSIS; ALLHAT; MECHANISMS
AB Background-Heart failure (HF) developing in hypertensive patients may occur with preserved or reduced left ventricular ejection fraction (PEF [>= 50%] or REF [<50%]). In the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), 42 418 high-risk hypertensive patients were randomized to chlorthalidone, amlodipine, lisinopril, or doxazosin, providing an opportunity to compare these treatments with regard to occurrence of hospitalized HFPEF or HFREF.
Methods and Results-HF diagnostic criteria were prespecified in the ALLHAT protocol. EF estimated by contrast ventriculography, echocardiography, or radionuclide study was available in 910 of 1367 patients (66.6%) with hospitalized events meeting ALLHAT criteria. Cox regression models adjusted for baseline characteristics were used to examine treatment differences for HF (overall and by PEF and REF). HF case fatality rates were examined. Of those with EF data, 44.4% had HFPEF and 55.6% had HFREF. Chlorthalidone reduced the risk of HFPEF compared with amlodipine, lisinopril, or doxazosin; the hazard ratios were 0.69 (95% confidence interval [CI], 0.53 to 0.91; P=0.009), 0.74 (95% CI, 0.56 to 0.97; P=0.032), and 0.53 (95% CI, 0.38 to 0.73; P<0.001), respectively. Chlorthalidone reduced the risk of HFREF compared with amlodipine or doxazosin; the hazard ratios were 0.74 (95% CI, 0.59 to 0.94; P=0.013) and 0.61 (95% CI, 0.47 to 0.79; P<0.001), respectively. Chlorthalidone was similar to lisinopril with regard to incidence of HFREF (hazard ratio, 1.07; 95% CI, 0.82 to 1.40; P=0.596). After HF onset, death occurred in 29.2% of participants (chlorthalidone/amlodipine/lisinopril) with new-onset HFPEF versus 41.9% in those with HFREF (P<0.001; median follow-up, 1.74 years); and in the chlorthalidone/doxazosin comparison that was terminated early, 20.0% of HFPEF and 26.0% of HFREF patients died (P=0.185; median follow-up, 1.55 years).
Conclusions-In ALLHAT, with adjudicated outcomes, chlorthalidone significantly reduced the occurrence of new-onset hospitalized HFPEF and HFREF compared with amlodipine and doxazosin. Chlorthalidone also reduced the incidence of new-onset HFPEF compared with lisinopril. Among high-risk hypertensive men and women, HFPEF has a better prognosis than HFREF. (Circulation. 2008; 118: 2259-2267.)
C1 [Davis, Barry R.; Simpson, Lara M.; Ford, Charles E.] Univ Texas Houston, Hlth Sci Ctr, Sch Publ Hlth, Houston, TX 77030 USA.
[Kostis, John B.] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, New Brunswick, NJ USA.
[Black, Henry R.] NYU, Sch Med, New York, NY USA.
[Cushman, William C.] Memphis Vet Affairs Med Ctr, Memphis, TN USA.
[Einhorn, Paula T.] NHLBI, Div Prevent & Populat Sci, Bethesda, MD 20892 USA.
[Farber, Michael A.] Crozer Keystone Hlth Network, Upland, PA USA.
[Levy, Daniel] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Massie, Barry M.] San Francisco VA Med Ctr, San Francisco, CA USA.
RP Davis, BR (reprint author), Univ Texas Houston, Hlth Sci Ctr, Sch Publ Hlth, 1200 Herman Pressler,Suite E801, Houston, TX 77030 USA.
EM barry.r.davis@uth.tmc.edu
FU National Heart, Lung, and Blood Institute, National Institutes of
Health, US Department of Health and Human Services Bethesda, Md
[N01-HC-35130]
FX This research was supported by Health and Human Services contract
N01-HC-35130 from the National Heart, Lung, and Blood Institute,
National Institutes of Health, US Department of Health and Human
Services, Bethesda, Md. The ALLHAT investigators acknowledge
contributions of study medications supplied by Pfizer Inc (amlodipine
and doxazosin), AstraZeneca (atenolol and lisinopril), and Bristol-Myers
Squibb (pravastatin) and financial support provided by Pfizer Inc.
NR 45
TC 73
Z9 77
U1 2
U2 31
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 25
PY 2008
VL 118
IS 22
BP 2259
EP 2267
DI 10.1161/CIRCULATIONAHA.107.762229
PG 9
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 377AO
UT WOS:000261224300007
PM 19001024
ER
PT J
AU Gupta, V
Truong, QA
Okada, DR
Kiernan, TJ
Yan, BP
Cubeddu, RJ
Roberts, DJ
Abbara, S
MacGillivray, TE
Palacios, IF
AF Gupta, Vishal
Truong, Quynh A.
Okada, David R.
Kiernan, Thomas J.
Yan, Bryan P.
Cubeddu, Roberto J.
Roberts, David J.
Abbara, Suhny
MacGillivray, Thomas E.
Palacios, Igor F.
TI Giant Left Circumflex Coronary Artery Aneurysm With Arteriovenous
Fistula to the Coronary Sinus
SO CIRCULATION
LA English
DT Editorial Material
C1 [Gupta, Vishal; Kiernan, Thomas J.; Yan, Bryan P.; Cubeddu, Roberto J.; Palacios, Igor F.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Truong, Quynh A.; Okada, David R.; Abbara, Suhny] Massachusetts Gen Hosp, Cardiac MR PET CT Program, Boston, MA 02114 USA.
[MacGillivray, Thomas E.] Massachusetts Gen Hosp, Dept Cardiac Surg, Boston, MA 02114 USA.
[Roberts, David J.] N Shore Med Ctr, Div Cardiol, Salem, MA USA.
RP Gupta, V (reprint author), Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
EM vishalgupta@yahoo.com
RI Yan, Bryan/C-3390-2008; Yan, Bryan/P-5928-2015
FU NHLBI NIH HHS [T32HL076136]
NR 4
TC 8
Z9 8
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 25
PY 2008
VL 118
IS 22
BP 2304
EP 2307
DI 10.1161/CIRCULATIONAHA.108.781617
PG 4
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 377AO
UT WOS:000261224300012
PM 19029479
ER
PT J
AU Gutierrez, GM
Kong, E
Sabbagh, Y
Brown, NE
Lee, JS
Demay, MB
Thomas, DM
Hind, PW
AF Gutierrez, Gabriel M.
Kong, Elizabeth
Sabbagh, Yves
Brown, Nelson E.
Lee, Jong-Seo
Demay, Marie B.
Thomas, David M.
Hind, Philip W.
TI Impaired bone development and increased mesenchymal progenitor cells in
calvaria of RB1(-/-) mice
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE differentiation; retinoblastoma protein; osteoprogenitors
ID RETINOBLASTOMA PROTEIN; TARGETED DISRUPTION; ADIPOCYTE DIFFERENTIATION;
OSTEOBLAST LINEAGE; MAMMARY-GLAND; MUSCLE-CELLS; IN-VITRO; RB; GENE;
INACTIVATION
AB We have previously shown that the retinoblastoma protein (pRb) can activate expression of Runx2-dependent, bone-specific genes in cultured cells. We now show that pRb also plays a role early in osteogenesis, and that in primary RB1(-/-) calvarial cells there is an increased osteoprogenitor pool. To understand pRb's function in vivo, we generated a conditional RB1-KO mouse in which pRb expression is efficiently extinguished in osteoblasts. These animals display an apparent developmental defect in bones, most strikingly in the calvaria. Cultured RB1(-/-) calvarial osteoblasts fail to cease proliferation upon reaching confluence or following differentiation. Re-plating assays of primary RB1(-/-) calvarial cells after differentiation showed a clear adipogenic ability with increased multipotency. RB1(-/-) osteoblasts display a severe reduction in levels of mRNAs expressed late in differentiation. In this study, we present strong evidence that pRb has multiple regulatory roles in osteogenesis. Furthermore, in the absence of RB1(-/-) there is a larger pool of multipotent cells compared with the WT counterpart. This increased pool of osteoprogenitor cells may be susceptible to additional transforming events leading to osteosarcoma, and is therefore key to understanding RB1 as a target in malignancy.
C1 [Gutierrez, Gabriel M.; Kong, Elizabeth; Brown, Nelson E.; Hind, Philip W.] Tufts Med Ctr, Mol Oncol Res Inst, Boston, MA 02111 USA.
[Sabbagh, Yves; Demay, Marie B.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Endocrine Unit, Boston, MA 02114 USA.
[Lee, Jong-Seo] Ewha Womans Univ, Div Mol Life Sci, Seoul 120750, South Korea.
[Thomas, David M.] Peter MacCallum Canc Ctr, Sir Donald & Lady Trescowthick Labs, Melbourne, Vic 3002, Australia.
[Thomas, David M.] Peter MacCallum Canc Ctr, Sir Donald & Lady Trescowthick Labs, Melbourne, Vic 3002, Australia.
[Thomas, David M.] Ian Potter Fdn, Ctr Canc Genom & Predict Med, Melbourne, Vic 3002, Australia.
RP Hind, PW (reprint author), Tufts Med Ctr, Mol Oncol Res Inst, Boston, MA 02111 USA.
EM phinds@tuftsmedicalcenter.org
OI Sabbagh, Yves/0000-0001-5339-6705; Gutierrez,
Gabriel/0000-0001-8487-0414
FU National Institutes of Health [AG020208]
FX The authors thank C. Kuperwasser and P. Yelick for helpful comments.
This work was supported by National Institutes of Health Grant AG020208
(to P.W.H.).
NR 43
TC 38
Z9 39
U1 0
U2 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 25
PY 2008
VL 105
IS 47
BP 18402
EP 18407
DI 10.1073/pnas.0805925105
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 380TY
UT WOS:000261489300066
PM 19020086
ER
PT J
AU Breckwoldt, MO
Chen, JW
Stangenberg, L
Aikawa, E
Rodriguez, E
Qiu, SM
Moskowitz, MA
Weissleder, R
AF Breckwoldt, Michael O.
Chen, John W.
Stangenberg, Lars
Aikawa, Elena
Rodriguez, Elisenda
Qiu, Shumei
Moskowitz, Michael A.
Weissleder, Ralph
TI Tracking the inflammatory response in stroke in vivo by sensing the
enzyme myeloperoxidase
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE inflammation; ischemia; molecular imaging; MRI; brain
ID ISCHEMIC-STROKE; ENHANCED MRI; CEREBRAL-ISCHEMIA; FOCAL ISCHEMIA; BRAIN
ISCHEMIA; INJURY; NEUTROPHILS; INFARCTION; TRANSIENT; DISEASE
AB Inflammation can extend ischemic brain injury and adversely affect outcome in experimental animal models. A key difficulty in translating animal studies to humans is the lack of a definitive method to confirm and track inflammation in the brain in vivo. Myeloper-oxidase (MPO), a key inflammatory enzyme secreted by activated neutrophils and macrophages/microglia, can generate highly reactive oxygen species to cause additional damage in cerebral ischemia. We report here that a functional, enzyme-activatable MRI agent can accurately track the oxidative activity of MPO noninvasively in stroke in living animals. We found that MPO is widely distributed in ischemic tissues, correlates positively with infarct size, and is detected even 3 weeks postinfarction. The peak level of MPO activity, determined by activation of the MPO-sensing agent in vivo and confirmed by MPO activity and quantitative RT-PCR assays, occurred on day 3 after ischemia. Both neutrophils and macrophages/microglia contribute to secrete MPO in the ischemic brain, although neutrophils peak earlier (days 1-3) whereas macrophages/microglia are most abundant later (days 3-7). In contrast to the conventional MRI agent diethylenetriamine-pentatacetate gadolinium, which reports blood-brain barrier disruption, MPO imaging is able to additionally track MPO activity and confirm inflammation on the molecular level in vivo, information that was previously only possible to obtain on ex vivo brain sections and impossible to assess in living human patients. Our findings could allow efficient noninvasive serial screening of therapies targeting inflammation and the use of MPO imaging as an imaging biomarker to risk-stratify patients.
C1 [Breckwoldt, Michael O.; Chen, John W.; Weissleder, Ralph] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Syst Biol, Charlestown, MA 02129 USA.
[Breckwoldt, Michael O.; Chen, John W.; Stangenberg, Lars; Aikawa, Elena; Rodriguez, Elisenda; Weissleder, Ralph] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Mol Imaging Res, Charlestown, MA 02129 USA.
[Qiu, Shumei; Moskowitz, Michael A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Stroke & Neurovasc Regulat Lab, Charlestown, MA 02129 USA.
[Chen, John W.; Moskowitz, Michael A.; Weissleder, Ralph] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Charlestown, MA 02129 USA.
RP Chen, JW (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Syst Biol, CNY 149,13th St, Charlestown, MA 02129 USA.
EM chenjo@helix.mgh.harvard.edu
FU German National Academic Foundation; Boehringer Ingelheim Fonds; German
Research Foundation; Marie Curie Fellowship; National Institutes of
Health [5K08HL081170, P50-NS10828-32, R24-CA92782, R01-HL078641]
FX We thank Carlos Rangel, Claire Kaufman, Anne Yu, Jenny Chan, Vincent
Lok, Todd Sponholtz, Yoshiko Iwamoto, and Ying Wei for experimental
assistance and Peter Panizzi for helpful discussions. We acknowledge
early contributions by Alexei Bogdanov and Manel Querol in developing
MPO-Gd. M.O..B. was supported by the German National Academic Foundation
and Boehringer Ingelheim Fonds. L.S. received support from the German
Research Foundation. E.R. was supported by the Marie Curie Fellowship.
This work was supported in part by National Institutes of Health Grants
5K08HL081170 (to J.W.C.), P50-NS10828-32 (to M.M.), and R24-CA92782 and
R01-HL078641 (to R.W.).
NR 35
TC 133
Z9 137
U1 2
U2 15
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 25
PY 2008
VL 105
IS 47
BP 18584
EP 18589
DI 10.1073/pnas.0803945105
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 380TY
UT WOS:000261489300097
PM 19011099
ER
PT J
AU Ongusaha, PP
Qi, HH
Raj, L
Kim, YB
Aaronson, SA
Davis, RJ
Shi, Y
Liao, JK
Lee, SW
AF Ongusaha, Pat P.
Qi, Hank H.
Raj, Lakshmi
Kim, Young-Bum
Aaronson, Stuart A.
Davis, Roger J.
Shi, Yang
Liao, James K.
Lee, Sam W.
TI Identification of ROCK1 as an Upstream Activator of the JIP-3 to JNK
Signaling Axis in Response to UVB Damage
SO SCIENCE SIGNALING
LA English
DT Article
AB Although apoptosis triggered by ultraviolet B (UVB)-mediated activation of the c-Jun N-terminal kinase (JNK) pathway is mediated by both intrinsic and extrinsic pathways, the mechanism of initiation of JNK activation remains obscure. Here, we report the characterization of the JNK-interacting protein 3 (JIP-3) scaffolding protein as an interacting partner of Rho-associated kinase 1 (ROCK1), as determined by tandem affinity protein purification. Upon UVB-induced stress in keratinocytes, ROCK1 was activated, bound to JIP-3, and activated the JNK pathway. Moreover, phosphorylation of JIP-3 by ROCK1 was crucial for the recruitment of JNK. Inhibition of the activity of ROCK1 in keratinocytes resulted in decreased activation of the JNK pathway and thus a reduction in apoptosis. ROCK1(+/-) mice exhibited decreased UVB-mediated activation of JNK and apoptosis relative to wild-type mice. Our findings present a new molecular mechanism by which ROCK1 functions as a UVB sensor that regulates apoptosis, an important event in the prevention of skin cancer.
C1 [Ongusaha, Pat P.; Raj, Lakshmi; Lee, Sam W.] Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA 02129 USA.
[Ongusaha, Pat P.; Raj, Lakshmi; Lee, Sam W.] Harvard Univ, Sch Med, Charlestown, MA 02129 USA.
[Qi, Hank H.; Shi, Yang] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Kim, Young-Bum] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA.
[Kim, Young-Bum] Harvard Univ, Sch Med, Boston, MA 02215 USA.
[Aaronson, Stuart A.] Mt Sinai Sch Med, Dept Oncol Sci, New York, NY 10029 USA.
[Davis, Roger J.] Univ Massachusetts, Sch Med, Howard Hughes Med Inst, Worcester, MA 01605 USA.
[Davis, Roger J.] Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA 01605 USA.
[Liao, James K.] Brigham & Womens Hosp, Vasc Med Res Unit, Cambridge, MA 02139 USA.
[Liao, James K.] Harvard Univ, Sch Med, Cambridge, MA 02139 USA.
RP Lee, SW (reprint author), Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, 13th St,Bldg 149, Charlestown, MA 02129 USA.
EM swlee@partners.org
FU NCI NIH HHS [R01 CA127247, R01 CA085214, P01 CA080058, R01 CA085681];
NHLBI NIH HHS [R01 HL070274, R01 HL052233-12, R01 HL052233, R01
HL080187-03, R01 HL070274-05, R01 HL080187]; NIDDK NIH HHS [R01
DK062729-05, R01 DK062729]; NINDS NIH HHS [P01 NS010828-330036, P01
NS010828]
NR 52
TC 24
Z9 28
U1 2
U2 6
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1937-9145
J9 SCI SIGNAL
JI Sci. Signal.
PD NOV 25
PY 2008
VL 1
IS 47
AR ra14
DI 10.1126/scisignal.1161938
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA V10XU
UT WOS:000207497500004
PM 19036714
ER
PT J
AU Li, XY
Gounari, F
Protopopov, A
Khazaie, K
von Boehmer, H
AF Li, Xiaoyu
Gounari, Fotini
Protopopov, Alexei
Khazaie, Khashayarsha
von Boehmer, Harald
TI Oncogenesis of T-ALL and nonmalignant consequences of overexpressing
intracellular NOTCH1
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; C-MYC; CELL-RECEPTOR; GENE-EXPRESSION;
LYMPHOCYTE DEVELOPMENT; TUMOR-SUPPRESSOR; TRANSGENIC MICE;
DOWN-REGULATION; ALPHA-BETA; PT-ALPHA
AB Mutations resulting in overexpression of intracellular Notch1 (ICN1) are frequently observed in human T cell acute lymphoblastic leukemia (T-ALL). We have determined the consequences of ICN1 overexpression from retroviral vectors introduced into bone marrow cells. Early consequences are the generation of polyclonal nontumorigenic CD4(+)8(+) T cell receptor (TCR)-alpha beta(+) cells that do not qualify as tumor precursors despite the observation that they overexpress Notch 1 and c-Myc and degrade the tumor suppressor E2A by post-translational modification. The first tumorigenic cells are detected among more immature CD4(-)8(+)TCR-alpha beta(-) cells that give rise to monoclonal tumors with a single, unique TCR-beta chain and diverse TCR-alpha chains, pinpointing malignant transformation to a stage after pre-TCR signaling and before completion of TCR-alpha rearrangement. In T-ALL, E2A deficiency is accompanied by further transcriptional up-regulation of c-Myc and concomitant dysregulation of the c-Myc-p53 axis at the transcriptional level. Even though the tumors consist of phenotypically heterogeneous cells, no evidence for tumor stem cells was found. As judged by array-based comparative genomic hybridization (array CGH) and spectral karyotype (SKY) analysis, none of the tumors arise because of genomic instability.
C1 [Li, Xiaoyu; Gounari, Fotini; Protopopov, Alexei; Khazaie, Khashayarsha; von Boehmer, Harald] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Gounari, Fotini] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
[Khazaie, Khashayarsha] Northwestern Univ, Dept Microbiol Immunol, Chicago, IL 60611 USA.
RP von Boehmer, H (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
EM harald_von_boehmer@dfci.harvard.edu
FU National Institutes of Health (NIH) [P01 CA109901, R01 AI45846,
T32-CA70083]; Lymphoma Research Foundation
FX This work was supported by National Institutes of Health (NIH) grants
P01 CA109901 and R01 AI45846. X. Li is supported by the Lymphoma
Research Foundation, Lee Fellowship, and NIH training grant T32-CA70083.
NR 40
TC 57
Z9 58
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
J9 J EXP MED
JI J. Exp. Med.
PD NOV 24
PY 2008
VL 205
IS 12
BP 2851
EP U72
DI 10.1084/jem.20081561
PG 13
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 378BE
UT WOS:000261295300018
PM 18981238
ER
PT J
AU Hezel, AF
Bardeesy, N
AF Hezel, A. F.
Bardeesy, N.
TI LKB1; linking cell structure and tumor suppression
SO ONCOGENE
LA English
DT Review
DE polarity; mouse models; Peutz-Jeghers; cancer; hamartoma; STK11
ID PEUTZ-JEGHERS-SYNDROME; ACTIVATED PROTEIN-KINASE; LUNG-CANCER CELLS;
SOMATIC MUTATIONS; METABOLIC CHECKPOINT; GLUCOSE-HOMEOSTASIS;
ENDOTHELIAL-CELLS; LKB1-AMPK PATHWAY; CYCLE PROGRESSION; ENERGETIC
STRESS
AB Germ line mutations in the LKB1 tumor suppressor gene are associated with the Peutz-Jeghers polyposis and cancer syndrome. Somatic mutations in Lkb1 are observed in sporadic pulmonary, pancreatic and biliary cancers and melanomas. The LKB1 serine-threonine kinase functionally and biochemically links control of cellular structure and energy utilization through activation of the AMPK family of kinases. Lkb1 regulates cell polarity through downstream kinases including AMPKs, MARKs and BRSKs, and nutrient utilization and cellular metabolism through the AMPK-mTOR pathway. LKB1 has been shown to affect normal chromosomal segregation, TGF-beta signaling in the mesenchyme and WNT and p53 activity. Although each of the LKB1-dependent processes and downstream pathways have been individually delineated through work across a range of experimental systems, how they relate to Lkb1's role as a tumor suppressor remains to be fully explored and elucidated. The recent development of mouse cancer models harboring engineered mutations in Lkb1 have offered insights into how LKB1 may be functioning to restrain tumorigenesis and how its role as a master regulator of polarity and metabolism could contribute to its tumor suppressor function.
C1 [Hezel, A. F.; Bardeesy, N.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Canc,Dept Med, Boston, MA 02114 USA.
RP Bardeesy, N (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Canc,Dept Med, Boston, MA 02114 USA.
EM Bardeesy.Nabeel@MGH.Harvard.edu
NR 127
TC 112
Z9 118
U1 2
U2 20
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD NOV 24
PY 2008
VL 27
IS 55
BP 6908
EP 6919
DI 10.1038/onc.2008.342
PG 12
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA 375IU
UT WOS:000261108200004
PM 19029933
ER
PT J
AU Sharma, U
Chang, EW
Yun, SH
AF Sharma, Utkarsh
Chang, Ernest W.
Yun, Seok H.
TI Long-wavelength optical coherence tomography at 1.7 mu m for enhanced
imaging depth
SO OPTICS EXPRESS
LA English
DT Article
ID MULTIPLE-SCATTERING; IN-VIVO; SPECTRAL RANGE; DENSE TISSUE; MONTE-CARLO;
NM; ATTENUATION; MICROSCOPY; CONTRAST; SIGNAL
AB Multiple scattering in a sample presents a significant limitation to achieve meaningful structural information at deeper penetration depths in optical coherence tomography (OCT). Previous studies suggest that the spectral region around 1.7 mu m may exhibit reduced scattering coefficients in biological tissues compared to the widely used wavelengths around 1.3 mu m. To investigate this long-wavelength region, we developed a wavelength-swept laser at 1.7 mu m wavelength and conducted OCT or optical frequency domain imaging (OFDI) for the first time in this spectral range. The constructed laser is capable of providing a wide tuning range from 1.59 to 1.75 mu m over 160 nm. When the laser was operated with a reduced tuning range over 95 nm at a repetition rate of 10.9 kHz and an average output power of 12.3 mW, the OFDI imaging system exhibited a sensitivity of about 100 dB and axial and lateral resolution of 24 mu m and 14 mu m, respectively. We imaged several phantom and biological samples using 1.3 mu m and 1.7 mu m OFDI systems and found that the depth-dependent signal decay rate is substantially lower at 1.7 mu m wavelength in most, if not all samples. Our results suggest that this imaging window may offer an advantage over shorter wavelengths by increasing the penetration depths as well as enhancing image contrast at deeper penetration depths where otherwise multiple scattered photons dominate over ballistic photons. (c) 2008 Optical Society of America
C1 [Yun, Seok H.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
RP Yun, SH (reprint author), Harvard Univ, Sch Med, 40 Blossom St, Boston, MA 02114 USA.
EM syun@hms.harvard.edu
FU National Institute Health [R33CA110130]; National Science Foundation
[ECCS-0801412]
FX This work was supported in part by National Institute Health (Grant
R33CA110130) and National Science Foundation (Grant ECCS-0801412).
Authors are grateful to M. Suter, B. Vakoc, G. Tearney, and B. Bouma for
access to the 1.3-mu m system and P. Heim for helpful discussion.
NR 27
TC 62
Z9 63
U1 0
U2 4
PU OPTICAL SOC AMER
PI WASHINGTON
PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA
SN 1094-4087
J9 OPT EXPRESS
JI Opt. Express
PD NOV 24
PY 2008
VL 16
IS 24
BP 19712
EP 19723
DI 10.1364/OE.16.019712
PG 12
WC Optics
SC Optics
GA 381UR
UT WOS:000261561900031
PM 19030057
ER
PT J
AU Lietha, D
Eck, MJ
AF Lietha, Daniel
Eck, Michael J.
TI Crystal Structures of the FAK Kinase in Complex with TAE226 and Related
Bis-Anilino Pyrimidine Inhibitors Reveal a Helical DFG Conformation
SO PLOS ONE
LA English
DT Article
AB Focal Adhesion Kinase (FAK) is a non-receptor tyrosine kinase required for cell migration, proliferation and survival. FAK overexpression has been documented in diverse human cancers and is associated with a poor clinical outcome. Recently, a novel bis-anilino pyrimidine inhibitor, TAE226, was reported to efficiently inhibit FAK signaling, arrest tumor growth and invasion and prolong the life of mice with glioma or ovarian tumor implants. Here we describe the crystal structures of the FAK kinase bound to TAE226 and three related bis-anilino pyrimidine compounds. TAE226 induces a conformation of the N-terminal portion of the kinase activation loop that is only observed in FAK, but is distinct from the conformation in both the active and inactive states of the kinase. This conformation appears to require a glycine immediately N-terminal to the "DFG motif", which adopts a helical conformation stabilized by interactions with TAE226. The presence of a glycine residue in this position contributes to the specificity of TAE226 and related compounds for FAK. Our work highlights the fact that kinases can access conformational space that is not necessarily utilized for their native catalytic regulation, and that such conformations can explain and be exploited for inhibitor specificity.
C1 [Lietha, Daniel; Eck, Michael J.] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Lietha, Daniel; Eck, Michael J.] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA USA.
RP Lietha, D (reprint author), Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
EM eck@red.dfci.harvard.edu
RI Lietha, Daniel/L-8041-2014
OI Lietha, Daniel/0000-0002-6133-6486
FU NIH [HL048675, CA080942]; Leukemia and Lymphoma Society; NCI
[5T32CA09361]
FX The research was supported in part by NIH grants HL048675 and CA080942
(MJE). MJE is the recipient of a Scholar Award from the Leukemia and
Lymphoma Society. DL was supported by an institutional training grant
from the NCI (5T32CA09361). The funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.
NR 38
TC 27
Z9 28
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 24
PY 2008
VL 3
IS 11
AR e3800
DI 10.1371/journal.pone.0003800
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 436YA
UT WOS:000265450800010
PM 19030106
ER
PT J
AU Moulton, EA
Burstein, R
Tully, S
Hargreaves, R
Becerra, L
Borsook, D
AF Moulton, Eric A.
Burstein, Rami
Tully, Shannon
Hargreaves, Richard
Becerra, Lino
Borsook, David
TI Interictal Dysfunction of a Brainstem Descending Modulatory Center in
Migraine Patients
SO PLOS ONE
LA English
DT Article
AB Background: The brainstem contains descending circuitry that can modulate nociceptive processing (neural signals associated with pain) in the dorsal horn of the spinal cord and the medullary dorsal horn. In migraineurs, abnormal brainstem function during attacks suggest that dysfunction of descending modulation may facilitate migraine attacks, either by reducing descending inhibition or increasing facilitation. To determine whether a brainstem dysfunction could play a role in facilitating migraine attacks, we measured brainstem function in migraineurs when they were not having an attack (i.e. the interictal phase).
Methods and Findings: Using fMRI (functional magnetic resonance imaging), we mapped brainstem activity to heat stimuli in 12 episodic migraine patients during the interictal phase. Separate scans were collected to measure responses to 41 degrees C and noxious heat (pain threshold+1 degrees C). Stimuli were either applied to the forehead on the affected side (as reported during an attack) or the dorsum of the hand. This was repeated in 12 age-gender-matched control subjects, and the side tested corresponded to that in the matched migraine patients. Nucleus cuneiformis (NCF), a component of brainstem pain modulatory circuits, appears to be hypofunctional in migraineurs. 3 out of the 4 thermal stimulus conditions showed significantly greater NCF activation in control subjects than the migraine patients.
Conclusions: Altered descending modulation has been postulated to contribute to migraine, leading to loss of inhibition or enhanced facilitation resulting in hyperexcitability of trigeminovascular neurons. NCF function could potentially serve as a diagnostic measure in migraine patients, even when not experiencing an attack. This has important implications for the evaluation of therapies for migraine.
C1 [Moulton, Eric A.; Tully, Shannon; Becerra, Lino; Borsook, David] Harvard Univ, McLean Hosp, Sch Med, PAIN Grp,Brain Imaging Ctr, Belmont, MA 02178 USA.
[Moulton, Eric A.; Becerra, Lino; Borsook, David] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Psychiat, Boston, MA USA.
[Burstein, Rami] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Boston, MA USA.
[Hargreaves, Richard] Merck & Co Inc, West Point, PA USA.
[Becerra, Lino; Borsook, David] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Athinoula Martinos Ctr Bioengn, Dept Radiol, Charlestown, MA USA.
RP Moulton, EA (reprint author), Harvard Univ, McLean Hosp, Sch Med, PAIN Grp,Brain Imaging Ctr, Belmont, MA 02178 USA.
EM dborsook@partners.org
FU NIH/NINDS [R01NS056195-02, R01NS051484-04]; Merck and Co
FX This study was financially supported by NIH/NINDS grants to David
Borsook (R01NS056195-02) and Rami Burstein (R01NS051484-04), and by an
unrestricted grant from Merck and Co. These financial sponsors did not
have a direct role in this study, and did not participate in the
preparation of this manuscript.
NR 46
TC 94
Z9 94
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 NOV 24
PY 2008
VL 3
IS 11
AR e3799
DI 10.1371/journal.pone.0003799
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 436YA
UT WOS:000265450800009
PM 19030105
ER
PT J
AU Ono, K
Condron, MM
Ho, L
Wang, J
Zhao, W
Pasinetti, GM
Teplow, DB
AF Ono, Kenjiro
Condron, Margaret M.
Ho, Lap
Wang, Jun
Zhao, Wei
Pasinetti, Giulio M.
Teplow, David B.
TI Effects of Grape Seed-derived Polyphenols on Amyloid beta-Protein
Self-assembly and Cytotoxicity
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID FIBRILS IN-VITRO; ALZHEIMERS-DISEASE; CROSS-LINKING; SYNAPTIC
PLASTICITY; WINE CONSUMPTION; APOLIPOPROTEIN-E; TRANSGENIC MICE;
ALPHA-SYNUCLEIN; FRENCH PARADOX; MOUSE MODEL
AB Epidemiological evidence suggests that moderate consumption of red wine reduces the incidence of Alzheimer disease (AD). To study the protective effects of red wine, experiments recently were executed in the Tg2576 mouse model of AD. These studies showed that a commercially available grape seed polyphenolic extract, MegaNatural-AZ (MN), significantly attenuated AD-type cognitive deterioration and reduced cerebral amyloid deposition (Wang, J., Ho, L., Zhao, W., Ono, K., Rosensweig, C., Chen, L., Humala, N., Teplow, D. B., and Pasinetti, G. M. (2008) J. Neurosci. 28, 6388-6392). To elucidate the mechanistic bases for these observations, here we used CD spectroscopy, photo-induced cross-linking of unmodified proteins, thioflavin T fluorescence, size exclusion chromatography, and electron microscopy to examine the effects of MN on the assembly of the two predominant disease-related amyloid beta-protein alloforms, A beta 40 and A beta 42. We also examined the effects of MN on A beta-induced cytotoxicity by assaying 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide metabolism and lactate dehydrogenase activity in A beta-treated, differentiated pheochromocytoma (PC12) cells. Initial studies revealed that MN blocked A beta fibril formation. Subsequent evaluation of the assembly stage specificity of the effect showed thatMNwas able to inhibit protofibril formation, pre-protofibrillar oligomerization, and initial coil -> alpha-helix/beta-sheet secondary structure transitions. Importantly, MN had protective effects in assays of cytotoxicity in which MN was mixed with A beta prior to peptide assembly or following assembly and just prior to peptide addition to cells. These data suggest that MN is worthy of consideration as a therapeutic agent for AD.
C1 [Ho, Lap; Wang, Jun; Zhao, Wei; Pasinetti, Giulio M.] Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA.
[Ono, Kenjiro; Condron, Margaret M.; Teplow, David B.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA.
[Ono, Kenjiro; Condron, Margaret M.; Teplow, David B.] Univ Calif Los Angeles, Inst Mol Biol, Los Angeles, CA 90095 USA.
[Ono, Kenjiro; Condron, Margaret M.; Teplow, David B.] Univ Calif Los Angeles, Brain Res Inst, Los Angeles, CA 90095 USA.
[Ono, Kenjiro] Kanazawa Univ, Grad Sch Med Sci, Dept Neurol & Neurobiol, Kanazawa, Ishikawa 9208640, Japan.
[Ho, Lap; Wang, Jun; Zhao, Wei; Pasinetti, Giulio M.] Mt Sinai Sch Med, Dept Neurosci, New York, NY 10029 USA.
[Ho, Lap; Pasinetti, Giulio M.] Bronx Vet Adm Med Ctr, Bronx, NY 10468 USA.
RP Pasinetti, GM (reprint author), Mt Sinai Sch Med, Dept Psychiat, 1468 Madison Ave,Rm 14-94C, New York, NY 10029 USA.
EM giulio.pasinetti@mssm.edu; dteplow@ucla.edu
RI Zhao, Wei/B-3220-2010; Zhao, Wei/A-2206-2010
FU National Institutes of Health [PO1 AT004511]; NCCAM; Department of
Veterans Affairs Merit Review; James J. Peters Veterans Affairs Medical
Center Geriatric Research Education Clinical Center Program, and
Polyphenolics; Japan Human Science Foundation and the Mochida Memorial
Foundation for Medical and Pharmaceutical Research; Alzheimer's
Association; Jim Easton Consortium for Alzheimer's Drug Discovery and
Biomarkers at UCLA; [AG027818]
FX This work was supported, in whole or in part, by National Institutes of
Health Grant PO1 AT004511 through the NCCAM (to L. H., G. M. P., and D.
B. T.) and Grant AG027818(to (D. B. T.). This work also was supported by
the Department of Veterans Affairs Merit Review grant and a grant from
the James J. Peters Veterans Affairs Medical Center Geriatric Research
Education Clinical Center Program, and Polyphenolics (to G. M. P.);
grants from the Japan Human Science Foundation and the Mochida Memorial
Foundation for Medical and Pharmaceutical Research (to K. O.); and
grants from the Alzheimer's Association, and the Jim Easton Consortium
for Alzheimer's Drug Discovery and Biomarkers at UCLA (to D. B. T.). The
costs of publication of this article were defrayed in part by the
payment of page charges. This article must therefore be hereby marked
"advertisement" in accordance with 18 U. S. C. Section 1734 solely to
indicate this fact.
NR 53
TC 103
Z9 109
U1 2
U2 27
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 21
PY 2008
VL 283
IS 47
BP 32176
EP 32187
DI 10.1074/jbc.M806154200
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 372HW
UT WOS:000260893700004
PM 18815129
ER
PT J
AU Stamler, R
Keutmann, HT
Sidis, Y
Kattamuri, C
Schneyer, A
Thompson, TB
AF Stamler, Robin
Keutmann, Henry T.
Sidis, Yisrael
Kattamuri, Chandramohan
Schneyer, Alan
Thompson, Thomas B.
TI The Structure of FSTL3.Activin A Complex DIFFERENTIAL BINDING OF
N-TERMINAL DOMAINS INFLUENCES FOLLISTATIN-TYPE ANTAGONIST SPECIFICITY
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID BONE-MORPHOGENETIC PROTEIN; TGF-BETA SUPERFAMILY; ACTIVIN-BINDING;
RECEPTOR-BINDING; FAMILY; GENE; CELL; MECHANISMS; MYOSTATIN; RECOGNITION
AB Transforming growth factor beta family ligands are neutralized by a number of structurally divergent antagonists. Follistatin-type antagonists, which include splice variants of follistatin (FS288 and FS315) and follistatin-like 3 (FSTL3), have high affinity for activin A but differ in their affinity for other ligands, particularly bone morphogenetic proteins. To understand the structural basis for ligand specificity within FS-type antagonists, we determined the x-ray structure of activin A in complex with FSTL3 to a resolution of 2.5 angstrom. Similar to the previously resolved FS.activin A structures, the ligand is encircled by two antagonist molecules blocking all ligand receptor-binding sites. Recently, the significance of the FS N-terminal domain interaction at the ligand type I receptor site has been questioned; however, our data show that for FSTL3, the N-terminal domain forms a more intimate contact with activin A, implying that this interaction is stronger than that for FS. Furthermore, binding studies revealed that replacing the FSTL3 N-terminal domain with the corresponding FS domain considerably lowers activin A affinity. Therefore, both structural and biochemical evidence support a significant interaction of the N-terminal domain of FSTL3 with activin A. In addition, structural comparisons with bone morphogenetic proteins suggest that the interface where the N-terminal domain binds may be the key site for determining FS-type antagonist specificity.
C1 [Stamler, Robin; Kattamuri, Chandramohan; Thompson, Thomas B.] Univ Cincinnati, Dept Mol Genet Biochem & Microbiol, Cincinnati, OH 45267 USA.
[Keutmann, Henry T.] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
[Sidis, Yisrael] Massachusetts Gen Hosp, Reprod Endocrine Unit, Boston, MA 02114 USA.
[Schneyer, Alan] Baystate Med Ctr, Pioneer Valley Life Sci Inst, Springfield, MA 01107 USA.
RP Thompson, TB (reprint author), Univ Cincinnati, Dept Mol Genet Biochem & Microbiol, Med Sci Bldg,231 Albert Sabin Way, Cincinnati, OH 45267 USA.
EM tom.thompson@ucmail.uc.edu
FU National Institutes of Health [GM084186, DK053828]
FX This work was supported, in whole or in part, by National Institutes of
Health Grants GM084186 ( to T. B. T.) and DK053828 ( to H. T. K.).
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PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 21
PY 2008
VL 283
IS 47
BP 32831
EP 32838
DI 10.1074/jbc.M801266200
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 372HW
UT WOS:000260893700072
PM 18768470
ER
PT J
AU Shen, XH
Liu, YC
Hsu, YJ
Fujiwara, Y
Kim, J
Mao, XH
Yuan, GC
Orkin, SH
AF Shen, Xiaohua
Liu, Yingchun
Hsu, Yu-Jung
Fujiwara, Yuko
Kim, Jonghwan
Mao, Xiaohong
Yuan, Guo-Cheng
Orkin, Stuart H.
TI EZH1 Mediates Methylation on Histone H3 Lysine 27 and Complements EZH2
in Maintaining Stem Cell Identity and Executing Pluripotency
SO MOLECULAR CELL
LA English
DT Article
ID POLYCOMB GROUP PROTEINS; METHYLTRANSFERASE ACTIVITY; MOUSE DEVELOPMENT;
DEVELOPMENTAL REGULATORS; DROSOPHILA ESC; DIFFERENTIATION; ENHANCER;
EED; COMPLEXES; MESODERM
AB Trimethylation on H3K27 (H3K27me3) mediated by Polycomb repressive complex 2 (PRC2) has been linked to embryonic stem cell (ESC) identity and pluripotency. EZH2, the catalytic subunit of PRC2, has been reported as the sole histone methyltransferase that methylates H3K27 and mediates transcriptional silencing. Analysis of Ezh2(-/-) ESCs suggests existence of an additional enzyme(s) catalyzing H3K27 methylation. We have identified EZH1, a homolog of EZH2 that is physically present in a noncanonical PRC2 complex, as an H3K27 methyltransferase in vivo and in vitro. EZH1 colocalizes with the H3K27me3 mark on chromatin and preferentially preserves this mark on development-related genes in Ezh2(-/-) ESCs. Depletion of Ezh1 in cells lacking Ezh2 abolishes residual methylation on H3K27 and derepresses H3K27me3 target genes, demonstrating a role of EZH1 in safeguarding ESC identity. Ezh1 partially complements Ezh2 in executing pluripotency during ESC differentiation, suggesting that cell-fate transitions require epigenetic specificity.
C1 [Shen, Xiaohua; Hsu, Yu-Jung; Fujiwara, Yuko; Kim, Jonghwan; Orkin, Stuart H.] Childrens Hosp, Dept Pediat Oncol, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Shen, Xiaohua; Hsu, Yu-Jung; Fujiwara, Yuko; Kim, Jonghwan; Orkin, Stuart H.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Liu, Yingchun; Yuan, Guo-Cheng] Harvard Univ, Sch Publ Hlth, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Kim, Jonghwan; Orkin, Stuart H.] Howard Hughes Med Inst, Boston, MA 02115 USA.
[Mao, Xiaohong] Novartis Inst Biomed Res Inc, Cambridge, MA 02139 USA.
[Orkin, Stuart H.] Harvard Stem Cell Inst, Boston, MA 02115 USA.
RP Orkin, SH (reprint author), Childrens Hosp, Dept Pediat Oncol, Dana Farber Canc Inst, Boston, MA 02115 USA.
EM stuart_orkin@dfci.harvard.edu
FU Claudia Adams Barr Program in Cancer Research
FX We are grateful to T. Magnuson for Eed-/- ESCs, G. Keller for
T-GFP ESCs, A. Glaser, S., Schaft, J., Lubitz, S., Vintersten, K., van
der Hoeven, F., Tufteland, Smith for 46C cells, and K. Helin for EED
antibody. We thank R. Tomaino for K.R., Aasland, R., Anastassiadis, K.,
Ang, S.L., and Stewart, A.F. (2006). performing LC-MS/MS, DFCI
Microarray Core for processing microarray sam- Multiple epigenetic
maintenance factors implicated by the loss of M112 in ples, and W. Li,
T. Liu, and X.S. Liu for assistance with MAT. We thank B. Wil- mouse
development. Development 133, 1423-1432. son, C. Roberts, D. Levasseur,
and X. Xia for criticism, and members of the Johnson, W.E., Li, W.,
Meyer, C.A., Gottardo, R., Carroll, J.S., Brown, M., and Orkin lab for
their assistance. G.-C.Y. is supported by the Claudia Adams Barr Program
in Cancer Research. S.H.O. is an Investigator of the HHMI.
NR 47
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PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1097-2765
J9 MOL CELL
JI Mol. Cell
PD NOV 21
PY 2008
VL 32
IS 4
BP 491
EP 502
DI 10.1016/j.molcel.2008.10.016
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 377ZD
UT WOS:000261290000007
PM 19026780
ER
PT J
AU Yang, G
Li, YT
Nishimura, EK
Xin, H
Zhou, AY
Guo, YS
Dong, L
Denning, MF
Nickoloff, BJ
Cui, RT
AF Yang, Guang
Li, Yitang
Nishimura, Emi K.
Xin, Hong
Zhou, Anyu
Guo, Yinshi
Dong, Liang
Denning, Mitchell F.
Nickoloff, Brian J.
Cui, Rutao
TI Inhibition of PAX3 by TGF-beta Modulates Melanocyte Viability
SO MOLECULAR CELL
LA English
DT Article
ID GROWTH-FACTOR-BETA; MICROPHTHALMIA GENE-PRODUCT; WAARDENBURG-SYNDROME;
TRANSCRIPTION FACTOR; HUMAN SKIN; HUMAN MELANOMAS; CELL SURVIVAL;
ULTRAVIOLET-B; IN-VIVO; EXPRESSION
AB The protein encoded by paired-box homeotic gene 3 (PAX3) is a key regulator of the microphthalmia-associated transcription factor (Mito in the melanocyte lineage. Here, we show that PAX3 expression in skin is directly inhibited by TGF-beta/Smads. UV irradiation represses TGF-beta in keratinocytes, and the repression of TGF-beta/Smads upregulates PAX3 in melanocytes, which is associated with a UV-induced melanogenic response and consequent pigmentation. Furthermore, the TGF-beta-PAX3 signaling pathway interacts with the p53-POMC/MSH-MC1R signaling pathway, and both are crucial in melanogenesis. The activation of p53-POMC/MSH-MC1R signaling is required for the UV-induced melanogenic response because PAX3 functions in synergy with SOX10 in a cAMP-response element (CRE)-dependent manner to regulate the transcription of Mitf. This study will provide a rich foundation for further research on skin cancer prevention by enabling us to identify targeted small molecules in the signaling pathways of the UV-induced melanogenic response that are highly likely to induce naturally protective pigmentation.
C1 [Xin, Hong; Guo, Yinshi; Dong, Liang; Denning, Mitchell F.; Nickoloff, Brian J.; Cui, Rutao] Loyola Univ Chicago, Dept Pathol, Inst Oncol, Cardinal Bernardin Canc Ctr,Stritch Sch Med, Maywood, IL 60153 USA.
[Yang, Guang; Li, Yitang; Zhou, Anyu] Harvard Univ, Sch Med, Dept Med Oncol, Dana Farber Canc Inst,Childrens Hosp Boston, Boston, MA 02115 USA.
[Nishimura, Emi K.] Kanazawa Univ, Dept Stem Cell Med, Canc Res Inst, Kanazawa, Ishikawa 9200934, Japan.
RP Cui, RT (reprint author), Loyola Univ Chicago, Dept Pathol, Inst Oncol, Cardinal Bernardin Canc Ctr,Stritch Sch Med, 2160 S 1st Ave, Maywood, IL 60153 USA.
EM rcui@lumc.edu
FU American Cancer Society [RSG-09022-01-CNE]; American Cancer
Society-Illinois Division [08-026]; Elsa U. Pardee Foundation
FX We thank Dr. Michel Goossens for the PAX3 construct. We also thank Dr.
David E. Fisher, Dr. Scott R. Granter, Dr. Hans R Widlund, Dr. Jinyan
Du, Dr. Xiansi Zhao, Dr. Jiwang Zhang, Dr. Guo Wei, Dr. Wei Li, and Dr.
Hai Li for helpful comments. This work was supported by American Cancer
Society (RSG-09022-01-CNE), American Cancer Society-Illinois Division
(08-026), and Elsa U. Pardee Foundation (R.C.). No potential conflicts
of interest were disclosed.
NR 61
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PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1097-2765
J9 MOL CELL
JI Mol. Cell
PD NOV 21
PY 2008
VL 32
IS 4
BP 554
EP 563
DI 10.1016/j.molcel.2008.11.002
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 377ZD
UT WOS:000261290000012
PM 19026785
ER
PT J
AU Swanson, KD
Tang, Y
Ceccarelli, DF
Poy, F
Sliwa, JP
Neel, BG
Eck, MJ
AF Swanson, Kenneth D.
Tang, Yong
Ceccarelli, Derek F.
Poy, Florence
Sliwa, Jan P.
Neel, Benjamin G.
Eck, Michael J.
TI The Skap-hom Dimerization and PH Domains Comprise a 3
'-Phosphoinositide-Gated Molecular Switch
SO MOLECULAR CELL
LA English
DT Article
ID PLECKSTRIN HOMOLOGY DOMAINS; MEDIATED INTEGRIN ACTIVATION; T-CELL;
CRYSTAL-STRUCTURE; ACTIN CYTOSKELETON; SIGNALING MODULE; STRUCTURAL
BASIS; TYROSINE KINASE; PROTEIN; ADAPTER
AB PH domains, by binding to phosphoinositides, often serve as membrane-targeting modules. Using crystallographic, biochemical, and cell biological approaches, we have uncovered a mechanism that the integrin-signaling adaptor Skap-hom uses to mediate cytoskeletal interactions. Skap-hom is a homodimer containing an N-terminal four-helix bundle dimerization domain, against which its two PH domains pack in a conformation incompatible with phosphoinositide binding. The isolated PH domains bind PI[3,4,5]P(3), and mutations targeting the dimerization domain or the PH domain's PI[3,4,5]P(3)-binding pocket prevent Skap-hom localization to ruffles. Targeting is retained when the PH domain is deleted or by combined mutation of the PI[3,4,5]P(3)-binding pocket and the PH/dimerization domain interface. Thus, the dimerization and PH domain form a PI[3,4,5]P(3)-responsive molecular switch that controls Skap-hom function.
C1 [Swanson, Kenneth D.; Neel, Benjamin G.] Beth Israel Deaconess Med Ctr, Canc Biol Program, Div Hematol Oncol, Dept Med, Boston, MA 02115 USA.
[Tang, Yong; Ceccarelli, Derek F.; Poy, Florence; Sliwa, Jan P.; Eck, Michael J.] Harvard Univ, Sch Med, Dept Canc Biol, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Tang, Yong; Ceccarelli, Derek F.; Poy, Florence; Eck, Michael J.] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
RP Neel, BG (reprint author), Univ Toronto, Ontario Canc Inst, Dept Med Biophys, Toronto, ON M5G 1L7, Canada.
EM bneel@uhnresearch.ca; eck@red.dfci.harvard.edu
FU National Institutes of Health (NIH) [R01CA080942, P01HL048675, R37CA
41952, R01CA114945, 2T32 HL07623-23]; Canadian Institute of Health
Research; Canadian-Strategic Training in Health Research fellowship
FX We thank Q. Hao at MacCHESS beamline Al, T. Boggon and Y. Xu for
assistance with data collection, R. Marmorstein for critical reading of
the manuscript, F. Sicheri for help with FP, and L.C. Cantley for his
support. This work was supported by National Institutes of Health (NIH)
grants R01CA080942 and P01HL048675 to M.J.E., R37CA 41952 and
R01CA114945 to B.G.N., and 2T32 HL07623-23 to K.D.S. and by the Canadian
Institute of Health Research, the Canadian-Strategic Training in Health
Research fellowship, to D.F.C. pEBHA-Fyb and mCherry-tagged actin were
gifts from Chris Rudd (University of Cambridge) and Max Krummel
(University of California, San Francisco), respectively. The authors
declare that they have no competing financial interests.
NR 48
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U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1097-2765
J9 MOL CELL
JI Mol. Cell
PD NOV 21
PY 2008
VL 32
IS 4
BP 564
EP 575
DI 10.1016/j.molcel.2008.09.022
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 377ZD
UT WOS:000261290000013
PM 19026786
ER
PT J
AU Roberts, DA
Hansen, VN
Niven, AC
Thompson, MG
Seco, J
Evans, PM
AF Roberts, D. A.
Hansen, V. N.
Niven, A. C.
Thompson, M. G.
Seco, J.
Evans, P. M.
TI A low Z linac and flat panel imager: comparison with the conventional
imaging approach
SO PHYSICS IN MEDICINE AND BIOLOGY
LA English
DT Article
ID BEAM COMPUTED-TOMOGRAPHY; MONTE-CARLO-SIMULATION; BREMSSTRAHLUNG BEAMS;
RADIATION-THERAPY; VERIFICATION; FEASIBILITY; ACCELERATOR; IRRADIATION;
PROSTATE; POSITION
AB Experimental and Monte Carlo simulations were conducted for an Elekta Ltd Precise Treatment System linac fitted with a low Z insert of sufficient thickness to remove all primary electrons. A variety of amorphous silicon based panels employing different scintillators were modelled to determine their response to a variety of x-ray spectra and produce an optimized portal imaging system. This study has shown that in a low Z configuration the vast majority of x-rays are produced in the nickel electron window, and with a combination of a carbon insert and caesium iodide based XVI-panel, significant improvement in the object contrast was achieved. For thin, head and neck-type geometries, contrast is 4.62 times greater for 1.6 cm bone in 5.8 cm water than the standard 6MV/iViewGT system. For thicker, pelvis-type geometries contrast increases by a factor of 1.3 for 1.6 cm of bone in 25.8 cm water. To obtain images with the same signal-to-noise ratio as the 6 MV/iViewGT system, dose reductions of a factor of 15 and 4.2 are possible for 5.8 cm and 25.8 cm phantoms respectively. This design has the advantage of being easily implemented on a standard linac and provides a portal image directly from the therapy beam aperture.
C1 [Roberts, D. A.; Hansen, V. N.; Evans, P. M.] Inst Canc Res, Joint Dept Phys, Sutton, Surrey, England.
[Roberts, D. A.; Hansen, V. N.; Evans, P. M.] Royal Marsden NHS Fdn Trust, Sutton, Surrey, England.
[Niven, A. C.; Thompson, M. G.] Elekta Ltd, Crawley, W Sussex, England.
[Seco, J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Roberts, DA (reprint author), Inst Canc Res, Joint Dept Phys, Downs Rd, Sutton, Surrey, England.
RI Evans, Philip/A-6257-2009; Seco, Joao/J-4451-2012
FU Elekta Ltd; The Institute of Cancer Research; Cancer Research UK
[C46/A3970]
FX This work is supported by Elekta Ltd and The Institute of Cancer
Research. Work of the radiotherapy physics group is partially supported
by Cancer Research UK under programme grant C46/A3970. We are grateful
for information provided by Elekta Ltd and Perkin Elmer for the purposes
of modelling the linac and detectors. We are extremely grateful to
Andrew Lake for helping with the experiments and to Alan Hitchings for
advice on the target holder design. Also to Nick Smith, Clive Long and
Craig Cummings for manufacturing and modifying the target insert and to
Mike Partridge for useful discussions relating to detectors. We would
also like to thank all the ICR/RMH physics staff who have contributed
with comments or help with this work.
NR 22
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U1 0
U2 3
PU IOP PUBLISHING LTD
PI BRISTOL
PA TEMPLE CIRCUS, TEMPLE WAY, BRISTOL BS1 6BE, ENGLAND
SN 0031-9155
J9 PHYS MED BIOL
JI Phys. Med. Biol.
PD NOV 21
PY 2008
VL 53
IS 22
BP 6305
EP 6319
DI 10.1088/0031-9155/53/22/003
PG 15
WC Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging
SC Engineering; Radiology, Nuclear Medicine & Medical Imaging
GA 370JL
UT WOS:000260758400003
PM 18936518
ER
PT J
AU Stenman, JM
Rajagopal, J
Carroll, TJ
Ishibashi, M
McMahon, J
McMahon, AP
AF Stenman, Jan M.
Rajagopal, Jay
Carroll, Thomas J.
Ishibashi, Makoto
McMahon, Jill
McMahon, Andrew P.
TI Canonical Wnt Signaling Regulates Organ-Specific Assembly and
Differentiation of CNS Vasculature
SO SCIENCE
LA English
DT Article
ID BETA-CATENIN GENE; ENDOTHELIAL-CELLS; MOUSE DEVELOPMENT; RECEPTOR GENE;
EXPRESSION; PROLIFERATION; ANGIOGENESIS; INACTIVATION; DISRUPTION;
PATHWAY
AB Every organ depends on blood vessels for oxygen and nutrients, but the vasculature associated with individual organs can be structurally and molecularly diverse. The central nervous system (CNS) vasculature consists of a tightly sealed endothelium that forms the blood- brain barrier, whereas blood vessels of other organs are more porous. Wnt7a and Wnt7b encode two Wnt ligands produced by the neuroepithelium of the developing CNS coincident with vascular invasion. Using genetic mouse models, we found that these ligands directly target the vascular endothelium and that the CNS uses the canonical Wnt signaling pathway to promote formation and CNS- specific differentiation of the organ's vasculature.
C1 [Stenman, Jan M.; Rajagopal, Jay; Carroll, Thomas J.; Ishibashi, Makoto; McMahon, Jill; McMahon, Andrew P.] Harvard Univ, Dept Mol & Cellular Biol, Cambridge, MA 02138 USA.
[Rajagopal, Jay] Massachusetts Gen Hosp, Dept Internal Med, Boston, MA 02114 USA.
[McMahon, Andrew P.] Harvard Univ, Harvard Stem Cell Inst, Cambridge, MA 02138 USA.
RP McMahon, AP (reprint author), Harvard Univ, Dept Mol & Cellular Biol, Cambridge, MA 02138 USA.
EM mcmahon@mcb.harvard.edu
FU Wenner-Gren Foundations (Sweden); National Heart, Lung, and Blood
Institute [HL076393]; NIH [DK054364]
FX We thank P. D'Amore for helpful discussions. Supported by a Wenner-Gren
Foundations (Sweden) postdoctoral fellowship (J.M.S.), National Heart,
Lung, and Blood Institute grant HL076393 (J.R.), and NIH grant DK054364
(A.P.M.). The authors have a patent pending on the basis of the results
reported in this paper. A.P.M. has been a paid consultant for Merck,
Genentech, and Wythe in the past 3 years.
NR 27
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U2 15
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD NOV 21
PY 2008
VL 322
IS 5905
BP 1247
EP 1250
DI 10.1126/science.1164594
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 374HC
UT WOS:000261033400042
PM 19023080
ER
PT J
AU Heinrich, MC
Maki, RG
Corless, CL
Antonescu, CR
Harlow, A
Griffith, D
Town, A
McKinley, A
Ou, WB
Fletcher, JA
Fletcher, CDM
Huang, X
Cohen, DP
Baum, CM
Demetri, GD
AF Heinrich, Michael C.
Maki, Robert G.
Corless, Christopher L.
Antonescu, Cristina R.
Harlow, Amy
Griffith, Diana
Town, Ajia
McKinley, Arin
Ou, Wen-Bin
Fletcher, Jonathan A.
Fletcher, Christopher D. M.
Huang, Xin
Cohen, Darrel P.
Baum, Charles M.
Demetri, George D.
TI Primary and Secondary Kinase Genotypes Correlate With the Biological and
Clinical Activity of Sunitinib in Imatinib-Resistant Gastrointestinal
Stromal Tumor
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article; Proceedings Paper
CT AACR International Conference on Molecular Diagnostics in Cancer
Therapeutic Development
CY SEP 12-15, 2006
CL Chicago, IL
SP Amer Assoc Canc Res
ID ACQUIRED-RESISTANCE; KIT MUTATIONS; INHIBITOR SU11248; MISSENSE
MUTATION; SARCOMA-GROUP; GROWTH-FACTOR; IN-VITRO; MESYLATE; CANCER;
EFFICACY
AB Purpose
Most gastrointestinal stromal tumors (GISTs) harbor mutant KIT or platelet-derived growth factor receptor alpha (PDGFRA) kinases, which are imatinib targets. Sunitinib, which targets KIT, PDGFRs, and several other kinases, has demonstrated efficacy in patients with GIST after they experience imatinib failure. We evaluated the impact of primary and secondary kinase genotype on sunitinib activity.
Patients and Methods
Tumor responses were assessed radiologically in a phase I/II trial of sunitinib in 97 patients with metastatic, imatinib-resistant/intolerant GIST. KIT/PDGFRA mutational status was determined for 78 patients by using tumor specimens obtained before and after prior imatinib therapy. Kinase mutants were biochemically profiled for sunitinib and imatinib sensitivity.
Results
Clinical benefit (partial response or stable disease for >= 6 months) with sunitinib was observed for the three most common primary GIST genotypes: KIT exon 9 (58%), KIT exon 11 (34%), and wild-type KIT/PDGFRA (56%). Progression-free survival (PFS) was significantly longer for patients with primary KIT exon 9 mutations (P = .0005) or with a wild-type genotype (P = .0356) than for those with KIT exon 11 mutations. The same pattern was observed for overall survival (OS). PFS and OS were longer for patients with secondary KIT exon 13 or 14 mutations (which involve the KIT-adenosine triphosphate binding pocket) than for those with exon 17 or 18 mutations (which involve the KIT activation loop). Biochemical profiling studies confirmed the clinical results.
Conclusion
The clinical activity of sunitinib after imatinib failure is significantly influenced by both primary and secondary mutations in the predominant pathogenic kinases, which has implications for optimization of the treatment of patients with GIST.
C1 [Heinrich, Michael C.] Portland VA Med Ctr, Dept Med, Div Hematol Oncol, Portland, OR 97239 USA.
Portland VA Med Ctr, Dept Cell & Dev Biol, Div Hematol Oncol, Portland, OR 97239 USA.
Oregon Hlth & Sci Univ, Inst Canc, Portland, OR 97239 USA.
Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Brigham & Womens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Boston, MA USA.
Pfizer Global Res & Dev, La Jolla, CA USA.
RP Heinrich, MC (reprint author), Portland VA Med Ctr, Dept Med, Div Hematol Oncol, R&D 19,3710 SW US Vet Hosp Rd, Portland, OR 97239 USA.
EM Heinrich@ohsu.edu
FU NCI NIH HHS [1P50 CA127003-01, CA 47179]
NR 39
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U1 3
U2 9
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 20
PY 2008
VL 26
IS 33
BP 5352
EP 5359
DI 10.1200/JCO.2007.15.7461
PG 8
WC Oncology
SC Oncology
GA 376RA
UT WOS:000261199500009
PM 18955458
ER
PT J
AU Heinrich, MC
Owzar, K
Corless, CL
Hollis, D
Borden, EC
Fletcher, CDM
Ryan, CW
von Mehren, M
Blanke, CD
Rankin, C
Benjamin, RS
Bramwell, VH
Demetri, GD
Bertagnolli, MM
Fletcher, JA
AF Heinrich, Michael C.
Owzar, Kouros
Corless, Christopher L.
Hollis, Donna
Borden, Ernest C.
Fletcher, Christopher D. M.
Ryan, Christopher W.
von Mehren, Margaret
Blanke, Charles D.
Rankin, Cathryn
Benjamin, Robert S.
Bramwell, Vivien H.
Demetri, George D.
Bertagnolli, Monica M.
Fletcher, Jonathan A.
TI Correlation of Kinase Genotype and Clinical Outcome in the North
American Intergroup Phase III Trial of Imatinib Mesylate for Treatment
of Advanced Gastrointestinal Stromal Tumor: CALGB 150105 Study by Cancer
and Leukemia Group B and Southwest Oncology Group
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID RECEPTOR TYROSINE KINASE; OF-FUNCTION MUTATIONS; TERM-FOLLOW-UP; C-KIT;
DOSE IMATINIB; SARCOMA-GROUP; GENE; INHIBITOR; EFFICACY; SAFETY
AB Purpose
Imatinib mesylate is standard treatment for patients who have advanced gastrointestinal stromal tumor (GIST), but not all patients benefit equally. In previous studies, GIST genotype correlated with treatment outcome and optimal imatinib dosing.
Patients and Methods
We examined the relationship between kinase genotype and treatment outcome for 428 patients enrolled on the North American phase III study SWOG S0033/CALGB 150105 and treated with either 400 mg or 800 mg daily doses of imatinib.
Results
The presence of KIT exon 11-mutant genotype (n = 283) correlated with improved treatment outcome when compared with KIT exon 9-mutant (n = 32) and wild-type (WT; n = 67) genotypes for objective response (complete response [CR]/ partial response [PR], 71.7% v 44.4% [P = .007]; and 44.6% [P = .0002], respectively); time to tumor progression (TTP; median 24.7 months v 16.7 and 12.8 months, respectively); and overall survival (OS; median 60.0 months v 38.4 and 49.0 months, respectively). The survival outcomes for patients with exon 9-mutant, exon 11-mutant or WT GIST were not affected by imatinib dose. However, there was evidence of improved response rates for patients with exon 9-mutant tumors treated with imatinib 800 mg versus 400 mg (CR/PR, 67% v 17%; P = .02). Patients who had CD117-negative GIST had similar TTP but inferior OS compared with patients who had CD117-positive disease, which suggests that patients who have CD117-negative GIST may benefit from imatinib treatment. In addition, we identified novel but rare mutations of the KIT extracellular domain (exons 8 and 9).
Conclusion
We confirmed the favorable impact of KIT exon 11 genotype when compared with KIT exon 9 and wild-type genotype for patients with advanced GIST who are treated with imatinib.
C1 [Heinrich, Michael C.] Portland VA Med Ctr, Portland, OR 97239 USA.
Oregon Hlth & Sci Univ, Div Hematol Oncol, Portland, OR 97239 USA.
Duke Univ, Med Ctr, Dept Biostat & Bioinformat, Durham, NC USA.
Cleveland Clin Fdn, Cleveland, OH 44195 USA.
Brigham & Womens Hosp, Dept Surg, Boston, MA 02115 USA.
Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
SW Oncol Grp, Ctr Stat, Seattle, WA USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Tom Baker Canc Clin, Calgary, AB, Canada.
RP Heinrich, MC (reprint author), Portland VA Med Ctr, 3710 SW US Vet Hosp Rd,R&D 19, Portland, OR 97239 USA.
EM heinrich@ohsu.edu
FU National Cancer Institute (NCI) [CA33601, CA04919, CA32291, CA27525,
CA31946, CA32102, CA77202, U01-CA70172-01, N01-CM-17003]; Veterans
Affairs Merit Review; Novartis Pharmaceuticals
FX Supported in part by Grants No. CA33601, CA04919, CA32291, CA27525,
CA31946, CA32102, and CA77202 from the National Cancer Institute (NCI);
by Grants No. U01-CA70172-01 and N01-CM-17003 from the NCI; by a
Veterans Affairs Merit Review Grant (M. H.); and by research funding
from Novartis Pharmaceuticals.
NR 28
TC 274
Z9 297
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 20
PY 2008
VL 26
IS 33
BP 5360
EP 5367
DI 10.1200/JCO.2008.17.4284
PG 8
WC Oncology
SC Oncology
GA 376RA
UT WOS:000261199500010
PM 18955451
ER
PT J
AU Heymach, JV
Paz-Ares, L
De Braud, F
Sebastian, M
Stewart, DJ
Eberhardt, WEE
Ranade, AA
Cohen, G
Trigo, JM
Sandler, AB
Bonomi, PD
Herbst, RS
Krebs, AD
Vasselli, J
Johnson, BE
AF Heymach, John V.
Paz-Ares, Luis
De Braud, Filippo
Sebastian, Martin
Stewart, David J.
Eberhardt, Wilfried E. E.
Ranade, Anantbhushan A.
Cohen, Graham
Trigo, Jose Manuel
Sandler, Alan B.
Bonomi, Philip D.
Herbst, Roy S.
Krebs, Annetta D.
Vasselli, James
Johnson, Bruce E.
TI Randomized Phase II Study of Vandetanib Alone or With Paclitaxel and
Carboplatin as First-Line Treatment for Advanced Non-Small-Cell Lung
Cancer
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article; Proceedings Paper
CT 12th World Conference on Lung Cancer
CY SEP 02-06, 2007
CL Seoul, SOUTH KOREA
ID RECEPTOR TYROSINE KINASE; PREVIOUSLY TREATED PATIENTS; ENDOTHELIAL
GROWTH-FACTOR; CLINICAL-EVALUATION; MALIGNANT-TUMORS; TRIAL; ZD6474;
GEFITINIB; COMBINATION; INHIBITOR
AB Purpose
Vandetanib is a once-daily, oral inhibitor of vascular endothelial growth factor receptor and epidermal growth factor receptor signaling. The antitumor activity of vandetanib monotherapy or vandetanib with paclitaxel and carboplatin (VPC) was compared with paclitaxel and carboplatin (PC) in previously untreated patients with non-small-cell lung cancer (NSCLC).
Patients and Methods
All NSCLC histologies and previously treated CNS metastases were permitted in this partially blinded, placebo-controlled, randomized phase II study. Patients were randomly assigned 2:1:1 to receive vandetanib, VPC, or PC. Progression-free survival (PFS) was the primary end point, and the study was powered to detect a reduced risk of progression with VPC versus PC (hazard ratio = 0.70; one-sided P < .2) and to demonstrate noninferiority for vandetanib versus PC. Overall survival was a secondary assessment.
Results
The risk of progression was reduced for patients receiving VPC (n = 56) versus PC (n = 52; hazard ratio = 0.76, one-sided P = .098); median PFS was 24 weeks (VPC) and 23 weeks (PC). The vandetanib monotherapy arm (n = 73) was discontinued after a planned interim PFS analysis met the criterion for discontinuation (hazard ratio > 1.33 v PC). Overall survival was not significantly different between patients receiving VPC or PC. Rash, diarrhea, and hypertension were common adverse events; no pulmonary or CNS hemorrhage events required intervention.
Conclusion
VPC could be safely administered to patients with NSCLC, including those with squamous cell histology and treated brain metastases. Compared with the PC control arm, patients receiving VPC had longer PFS, meeting the prespecified study end point, whereas those receiving vandetanib monotherapy had
C1 [Johnson, Bruce E.] Dana Farber Canc Inst, Boston, MA 02115 USA.
Doce Octubre Univ Hosp, Madrid, Spain.
Hosp Clin Virgen Victoria, Malaga, Spain.
European Inst Oncol, Milan, Italy.
Johannes Gutenberg Univ Mainz, Med Klin 3, Mainz, Germany.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Univ Duisburg Essen, Univ Klinikum Essen, Essen, Germany.
Deenanath Mangeshkar Hosp & Res Ctr, Pune, Maharashtra, India.
Mary Potter Oncol Ctr, Pretoria, South Africa.
Vanderbilt Univ, Med Ctr, Nashville, TN USA.
Rush Univ, Med Ctr, Chicago, IL 60612 USA.
Astra Zeneca, Wilmington, DE USA.
RP Johnson, BE (reprint author), Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA.
EM bruce_johnson@dfci.harvard.edu
RI IBIS, NUEVAS TERAPIA/P-3415-2015; de Braud, Filippo/B-9997-2017
OI de Braud, Filippo/0000-0003-0103-730X
NR 32
TC 150
Z9 153
U1 1
U2 14
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 20
PY 2008
VL 26
IS 33
BP 5407
EP 5415
DI 10.1200/JCO.2008.17.3138
PG 9
WC Oncology
SC Oncology
GA 376RA
UT WOS:000261199500017
PM 18936474
ER
PT J
AU Meigs, JB
Shrader, P
Sullivan, LM
McAteer, JB
Fox, CS
Dupuis, J
Manning, AK
Florez, JC
Wilson, PWF
D'Agostino, RB
Cupples, LA
AF Meigs, James B.
Shrader, Peter
Sullivan, Lisa M.
McAteer, Jarred B.
Fox, Caroline S.
Dupuis, Josee
Manning, Alisa K.
Florez, Jose C.
Wilson, Peter W. F.
D'Agostino, Ralph B., Sr.
Cupples, L. Adrienne
TI Genotype Score in Addition to Common Risk Factors for Prediction of Type
2 Diabetes
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; GLUCOSE-TOLERANCE; LIFE-STYLE; LOCI;
POLYMORPHISMS; MELLITUS; DISEASE; METAANALYSIS; REPLICATION; POPULATION
AB Background: Multiple genetic loci have been convincingly associated with the risk of type 2 diabetes mellitus. We tested the hypothesis that knowledge of these loci allows better prediction of risk than knowledge of common phenotypic risk factors alone.
Methods: We genotyped single-nucleotide polymorphisms (SNPs) at 18 loci associated with diabetes in 2377 participants of the Framingham Offspring Study. We created a genotype score from the number of risk alleles and used logistic regression to generate C statistics indicating the extent to which the genotype score can discriminate the risk of diabetes when used alone and in addition to clinical risk factors.
Results: There were 255 new cases of diabetes during 28 years of follow-up. The mean (+/-SD) genotype score was 17.7+/-2.7 among subjects in whom diabetes developed and 17.1+/-2.6 among those in whom diabetes did not develop (P<0.001). The sex-adjusted odds ratio for diabetes was 1.12 per risk allele (95% confidence interval, 1.07 to 1.17). The C statistic was 0.534 without the genotype score and 0.581 with the score (P=>0.01). In a model adjusted for sex and self-reported family history of diabetes, the C statistic was 0.595 without the genotype score and 0.615 with the score (P=0.11). In a model adjusted for age, sex, family history, body-mass index, fasting glucose level, systolic blood pressure, high-density lipoprotein cholesterol level, and triglyceride level, the C statistic was 0.900 without the genotype score and 0.901 with the score (P=0.49). The genotype score resulted in the appropriate risk reclassification of, at most, 4% of the subjects.
Conclusions: A genotype score based on 18 risk alleles predicted new cases of diabetes in the community but provided only a slightly better prediction of risk than knowledge of common risk factors alone.
C1 [Meigs, James B.; Shrader, Peter] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[Meigs, James B.; Shrader, Peter; Florez, Jose C.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[McAteer, Jarred B.; Florez, Jose C.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[McAteer, Jarred B.; Florez, Jose C.] Massachusetts Gen Hosp, Diabet Unit, Dept Med, Boston, MA 02114 USA.
[Sullivan, Lisa M.; Dupuis, Josee; Manning, Alisa K.; Cupples, L. Adrienne] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[McAteer, Jarred B.; Florez, Jose C.] Broad Inst Harvard & MIT, Program Med & Populat Genet, Cambridge, MA USA.
[Fox, Caroline S.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Endocrinol Diabet & Hypertens, Boston, MA USA.
[Fox, Caroline S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Wilson, Peter W. F.] Emory Univ, Sch Med, Emory Program Cardiovasc Outcomes Res & Epidemiol, Atlanta, GA USA.
[D'Agostino, Ralph B., Sr.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
RP Meigs, JB (reprint author), Massachusetts Gen Hosp, Div Gen Med, 50 Staniford St,9th Fl, Boston, MA 02114 USA.
EM jmeigs@partners.org
OI Cupples, L. Adrienne/0000-0003-0273-7965; Dupuis,
Josee/0000-0003-2871-3603; Sullivan, Lisa/0000-0003-0726-7149
FU National Heart, Lung, and Blood Institute's Framingham Heart Study
[N01-HC-25195]; National Institute for Diabetes and Digestive and Kidney
Diseases [R01 DK078616, K24 DK080140, K23 DK65978]; Boston University
Linux Cluster for Genetic Analysis; National Institutes of Health
National Center for Research Resources Shared Instrumentation
[1S10RR163736-01A1]; Sanofi-Aventis; GlaxoSmithKline; Merck; Publicis
Healthcare Communications Group
FX Supported by a contract from the National Heart, Lung, and Blood
Institute's Framingham Heart Study (N01-HC-25195), grants from the
National Institute for Diabetes and Digestive and Kidney Diseases
(NIDDK) (R01 DK078616 and K24 DK080140, to Dr. Meigs), an NIDDK Research
Career Award (K23 DK65978, to Dr. Florez), and the Boston University
Linux Cluster for Genetic Analysis, funded by a grant from the National
Institutes of Health National Center for Research Resources Shared
Instrumentation (1S10RR163736-01A1). Dr. Meigs reports serving on a
consultancy board for Interleukin Genetics and receiving grants from
Sanofi-Aventis and GlaxoSmithKline; and Dr. Florez, receiving consulting
fees from Merck and Publicis Healthcare Communications Group, a global
advertising agency engaged by Amylin Pharmaceuticals. No other potential
conflict of interest relevant to this article was reported.
NR 40
TC 392
Z9 405
U1 1
U2 14
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 20
PY 2008
VL 359
IS 21
BP 2208
EP 2219
DI 10.1056/NEJMoa0804742
PG 12
WC Medicine, General & Internal
SC General & Internal Medicine
GA 373SW
UT WOS:000260994000004
PM 19020323
ER
PT J
AU Lyssenko, V
Jonsson, A
Almgren, P
Pulizzi, N
Isomaa, B
Tuomi, T
Berglund, G
Altshuler, D
Nilsson, P
Groop, L
AF Lyssenko, Valeriya
Jonsson, Anna
Almgren, Peter
Pulizzi, Nicolo
Isomaa, Bo
Tuomi, Tiinamaija
Berglund, Goran
Altshuler, David
Nilsson, Peter
Groop, Leif
TI Clinical Risk Factors, DNA Variants, and the Development of Type 2
Diabetes.
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; INSULIN SENSITIVITY; LOCI; PREDICTION;
MELLITUS; REPLICATION; SECRETION; INDEXES; GENE
AB Background: Type 2 diabetes mellitus is thought to develop from an interaction between environmental and genetic factors. We examined whether clinical or genetic factors or both could predict progression to diabetes in two prospective cohorts.
Methods: We genotyped 16 single-nucleotide polymorphisms (SNPs) and examined clinical factors in 16,061 Swedish and 2770 Finnish subjects. Type 2 diabetes developed in 2201 (11.7%) of these subjects during a median follow-up period of 23.5 years. We also studied the effect of genetic variants on changes in insulin secretion and action over time.
Results: Strong predictors of diabetes were a family history of the disease, an increased body-mass index, elevated liver-enzyme levels, current smoking status, and reduced measures of insulin secretion and action. Variants in 11 genes (TCF7L2, PPARG, FTO, KCNJ11, NOTCH2, WFS1, CDKAL1, IGF2BP2, SLC30A8, JAZF1, and HHEX) were significantly associated with the risk of type 2 diabetes independently of clinical risk factors; variants in 8 of these genes were associated with impaired beta-cell function. The addition of specific genetic information to clinical factors slightly improved the prediction of future diabetes, with a slight increase in the area under the receiver-operating-characteristic curve from 0.74 to 0.75; however, the magnitude of the increase was significant (P=1.0 x 10(-4)). The discriminative power of genetic risk factors improved with an increasing duration of follow-up, whereas that of clinical risk factors decreased.
Conclusions: As compared with clinical risk factors alone, common genetic variants associated with the risk of diabetes had a small effect on the ability to predict the future development of type 2 diabetes. The value of genetic factors increased with an increasing duration of follow-up.
C1 [Lyssenko, Valeriya; Jonsson, Anna; Almgren, Peter; Berglund, Goran; Nilsson, Peter; Groop, Leif] Lund Univ, Dept Clin Sci, Malmo, Sweden.
[Pulizzi, Nicolo] Univ Pisa, Pisa, Italy.
[Isomaa, Bo; Tuomi, Tiinamaija] Folkhalsan Res Ctr, Helsinki, Finland.
[Tuomi, Tiinamaija; Groop, Leif] Univ Helsinki, Cent Hosp, Helsinki, Finland.
[Altshuler, David] Broad Inst Harvard & MIT, Program Med & Populat Genet, Cambridge, MA USA.
[Altshuler, David] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Lyssenko, V (reprint author), Lund Univ, Malmo Univ Hosp, Dept Clin Sci Diabet & Endocrinol, CRC, S-20502 Malmo, Sweden.
EM valeri.lyssenko@med.lu.se
RI Altshuler, David/A-4476-2009
OI Altshuler, David/0000-0002-7250-4107
FU Swedish Research Council; Linne [31475113580]; Heart and Lung
Foundation; Swedish Diabetes Research Society; Nordic Center of
Excellence Grant in Disease Genetics; Diabetes Program at the Lund
University; Finnish Diabetes Research Society; Sigrid Juselius
Foundation; Pahlsson Foundation; Crafoord Foundation; Folkhalsan
Research Foundation; Novo Nordisk Foundation; European Network of
Genomic and Genetic Epidemiology; Wallenberg Foundation; European
Foundation for the Study of Diabetes; Tethys; Merck; Eisai; MPM Capital;
Novartis; Bristol-Myers Squibb Foundation; Eli Lilly; GlaxoSmithKline;
Aventis; Sanofi
FX Supported by grants from the Swedish Research Council (including Linne
grant 31475113580), the Heart and Lung Foundation, the Swedish Diabetes
Research Society, a Nordic Center of Excellence Grant in Disease
Genetics, the Diabetes Program at the Lund University, the Finnish
Diabetes Research Society, the Sigrid Juselius Foundation, the Pahlsson
Foundation, the Crafoord Foundation, the Folkhalsan Research Foundation,
the Novo Nordisk Foundation, the European Network of Genomic and Genetic
Epidemiology, the Wallenberg Foundation, and the European Foundation for
the Study of Diabetes. Dr. Lyssenko reports receiving consulting fees
from Tethys; Dr. Altshuler, receiving consulting fees from Merck, Eisai,
and MPM Capital and grant support from Novartis, receiving an
unrestricted grant from the Bristol-Myers Squibb Foundation, and having
an equity interest in MPM Capital; and Dr. Groop, receiving consulting
fees from Tethys, Eli Lilly, GlaxoSmithKline, Aventis, and Sanofi,
lecture fees from Aventis and Sanofi, and grant support from Novartis.
No other potential conflict of interest relevant to this article was
reported. We thank the patients for their participation and Anna
Berglund, Margareta Svensson, and Malin Neptin for their excellent
technical assistance.
NR 30
TC 461
Z9 482
U1 4
U2 41
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 20
PY 2008
VL 359
IS 21
BP 2220
EP 2232
DI 10.1056/NEJMoa0801869
PG 13
WC Medicine, General & Internal
SC General & Internal Medicine
GA 373SW
UT WOS:000260994000005
PM 19020324
ER
PT J
AU Brass, SD
Durand, ML
Stone, JH
Chen, JW
Stone, JR
Cohen, AB
Harris, NL
Friday, RP
Utz, AL
AF Brass, Steven D.
Durand, Marlene L.
Stone, John H.
Chen, John W.
Stone, James R.
Cohen, Adam B.
Harris, Nancy Lee
Friday, Robert P.
Utz, Andrea L.
TI A Man with Chronic Daily Headache Giant-cell arteritis, involving the
superficial temporal artery and small dural arteries
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID SLEEP-APNEA SYNDROME; HYPERTROPHIC CRANIAL PACHYMENINGITIS; QUALITY
STANDARDS SUBCOMMITTEE; NERVOUS-SYSTEM HISTOPLASMOSIS;
CEREBROSPINAL-FLUID LEAKS; WEGENERS-GRANULOMATOSIS; INTRACRANIAL
HYPOTENSION; PRACTICE PARAMETER; AMERICAN-ACADEMY; SARCOIDOSIS
C1 [Brass, Steven D.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Durand, Marlene L.; Stone, John H.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Chen, John W.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Stone, James R.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Brass, Steven D.] Harvard Univ, Sch Med, Dept Neurol, Cambridge, MA 02138 USA.
[Stone, John H.] Harvard Univ, Sch Med, Dept Med, Cambridge, MA 02138 USA.
[Chen, John W.] Harvard Univ, Sch Med, Dept Radiol, Cambridge, MA 02138 USA.
[Stone, James R.] Harvard Univ, Sch Med, Dept Pathol, Cambridge, MA 02138 USA.
RP Brass, SD (reprint author), Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
FU Teva Neuroscience; EMD Serono; Biogen; Bayer; Merck; Zymogenetics;
Muscle Tech; GlaxoSmithKline; Proteon Therapeutics
FX Dr. Brass reports receiving consulting fees from Teva Neuroscience, EMD
Serono, Biogen, and Bayer; Dr. John Stone, consulting fees from Merck
and Zymogenetics; and Dr. James Stone, consulting fees from Merck,
Muscle Tech, GlaxoSmithKline, and Proteon Therapeutics. No other
potential conflict of interest relevant to this article was reported.
NR 59
TC 8
Z9 9
U1 0
U2 3
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 20
PY 2008
VL 359
IS 21
BP 2267
EP 2278
PG 12
WC Medicine, General & Internal
SC General & Internal Medicine
GA 373SW
UT WOS:000260994000012
PM 19020329
ER
PT J
AU Maggard, MA
Yermilov, I
Li, Z
Maglione, M
Newberry, S
Suttorp, M
Hilton, L
Santry, HP
Morton, JM
Livingston, EH
Shekelle, PG
AF Maggard, Melinda A.
Yermilov, Irina
Li, Zhaoping
Maglione, Margaret
Newberry, Sydne
Suttorp, Marika
Hilton, Lara
Santry, Heena P.
Morton, John M.
Livingston, Edward H.
Shekelle, Paul G.
TI Pregnancy and Fertility Following Bariatric Surgery A Systematic Review
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Review
ID GASTRIC-BYPASS-SURGERY; VERTICAL-BANDED GASTROPLASTY;
VITAMIN-A-DEFICIENCY; NEURAL-TUBE DEFECTS; MORBID-OBESITY;
BILIOPANCREATIC DIVERSION; WEIGHT-LOSS; CARDIOVASCULAR-DISEASE;
METABOLIC SYNDROME; PHYSICAL-ACTIVITY
AB Context Use of bariatric surgery has increased dramatically during the past 10 years, particularly among women of reproductive age.
Objectives To estimate bariatric surgery rates among women aged 18 to 45 years and to assess the published literature on pregnancy outcomes and fertility after surgery.
Evidence Acquisition Search of the Nationwide Inpatient Sample ( 1998- 2005) and multiple electronic databases ( Medline, EMBASE, Controlled Clinical Trials Register Database, and the Cochrane Database of Reviews of Effectiveness) to identify articles published between 1985 and February 2008 on bariatric surgery among women of reproductive age. Search terms included bariatric procedures, fertility, contraception, pregnancy, and nutritional deficiencies. Information was abstracted about study design, fertility, and nutritional, neonatal, and pregnancy outcomes after surgery.
Evidence Synthesis Of 260 screened articles, 75 were included. Women aged 18 to 45 years accounted for 49% of all patients undergoing bariatric surgery ( > 50 000 cases annually for the 3 most recent years). Three matched cohort studies showed lower maternal complication rates after bariatric surgery than in obese women without bariatric surgery, or rates approaching those of nonobese controls. In 1 matched cohort study that compared maternal complication rates in women after laparoscopic adjustable gastric band surgery with obese women without surgery, rates of gestational diabetes ( 0% vs 22.1%, P <. 05) and preeclampsia ( 0% vs 3.1%, P <. 05) were lower in the bariatric surgery group. Findings were supported by 13 other bariatric cohort studies. Neonatal outcomes were similar or better after surgery compared with obese women without laparoscopic adjustable gastric band surgery ( 7.7% vs 7.1% for premature delivery; 7.7% vs 10.6% for low birth weight, P <. 05; 7.7% vs 14.6% for macrosomia, P <. 05). No differences in neonatal outcomes were found after gastric bypass compared with nonobese controls ( 26.3%- 26.9% vs 22.4%- 20.2% for premature delivery, P= not reported [ 1 study] and P=. 43 [ 1 study]; 7.7% vs 9.0% for low birth weight, P= not reported [ 1 study]; and 0% vs 2.6%- 4.3% for macrosomia, P= not reported [ 1 study and P=. 28 [ 1 study]). Findings were supported by 10 other studies. Studies regarding nutrition, fertility, cesarean delivery, and contraception were limited.
Conclusion Rates of many adverse maternal and neonatal outcomes may be lower in women who become pregnant after having had bariatric surgery compared with rates in pregnant women who are obese; however, further data are needed from rigorously designed studies.
C1 [Maggard, Melinda A.; Yermilov, Irina; Li, Zhaoping; Maglione, Margaret; Shekelle, Paul G.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Surg, Los Angeles, CA 90095 USA.
[Maggard, Melinda A.; Maglione, Margaret; Newberry, Sydne; Suttorp, Marika; Hilton, Lara; Shekelle, Paul G.] RAND Corp, Santa Monica, CA USA.
[Yermilov, Irina; Li, Zhaoping; Shekelle, Paul G.] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Santry, Heena P.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Morton, John M.] Stanford Univ, Sch Med, Dept Surg, Palo Alto, CA 94304 USA.
[Livingston, Edward H.] Univ Texas Southwestern Sch Med, Dept Surg, Dallas, TX USA.
RP Maggard, MA (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Surg, CHS 72-215,10833 Le Conte Ave, Los Angeles, CA 90095 USA.
EM mmaggard@mednet.ucla.edu
FU Agency for Healthcare Research and Quality [290-02-0003]; US Department
of Health and Human Services to the Southern California Evidence Based
Practice Center; Robert Wood Johnson Physician Faculty Scholars program
FX This project was funded under contract 290-02-0003 from the Agency for
Healthcare Research and Quality, US Department of Health and Human
Services to the Southern California Evidence Based Practice Center. Dr
Maggard's time was supported in part by a grant from the Robert Wood
Johnson Physician Faculty Scholars program. This work was requested by
the American College of Obstetricians and Gynecologists.
NR 84
TC 199
Z9 204
U1 2
U2 15
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 19
PY 2008
VL 300
IS 19
BP 2286
EP 2296
DI 10.1001/jama.2008.641
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 373IO
UT WOS:000260965500029
PM 19017915
ER
PT J
AU Stewart, AJ
O'Farrell, DA
Cormack, RA
Hansen, JL
Khan, AJ
Mutyala, S
Devlin, PM
AF Stewart, Alexandra J.
O'Farrell, Desmond A.
Cormack, Robert A.
Hansen, Jorgen L.
Khan, Atif J.
Mutyala, Subhakar
Devlin, Philip M.
TI Dose volume histogram analysis of normal structures associated with
accelerated partial breast irradiation delivered by high dose rate
brachytherapy and comparison with whole breast external beam
radiotherapy fields
SO RADIATION ONCOLOGY
LA English
DT Article
ID INITIAL CLINICAL-EXPERIENCE; RADIATION-THERAPY; MAMMOSITE BRACHYTHERAPY;
INTERSTITIAL BRACHYTHERAPY; BALLOON BRACHYTHERAPY; CONSERVING THERAPY;
AMERICAN-SOCIETY; REGISTRY TRIAL; CANCER; TOXICITY
AB Purpose: To assess the radiation dose delivered to the heart and ipsilateral lung during accelerated partial breast brachytherapy using a MammoSite (TM) applicator and compare to those produced by whole breast external beam radiotherapy (WBRT).
Materials and methods: Dosimetric analysis was conducted on patients receiving MammoSite breast brachytherapy following conservative surgery for invasive ductal carcinoma. Cardiac dose was evaluated for patients with left breast tumors with a CT scan encompassing the entire heart. Lung dose was evaluated for patients in whom the entire lung was scanned. The prescription dose of 3400 cGy was 1 cm from the balloon surface. MammoSite dosimetry was compared to simulated WBRT fields with and without radiobiological correction for the effects of dose and fractionation. Dose parameters such as the volume of the structure receiving 10 Gy or more (V10) and the dose received by 20 cc of the structure (D20), were calculated as well as the maximum and mean doses received.
Results: Fifteen patients were studied, five had complete lung data and six had left-sided tumors with complete cardiac data. Ipsilateral lung volumes ranged from 925-1380 cc. Cardiac volumes ranged from 337-551 cc. MammoSite resulted in a significantly lower percentage lung V30 and lung and cardiac V20 than the WBRT fields, with and without radiobiological correction.
Conclusion: This study gives low values for incidental radiation received by the heart and ipsilateral lung using the MammoSite applicator. The volume of heart and lung irradiated to clinically significant levels was significantly lower with the MammoSite applicator than using simulated WBRT fields of the same CT data sets.
Trial registration: Dana Farber Trial Registry number 03-179
C1 [O'Farrell, Desmond A.; Cormack, Robert A.; Hansen, Jorgen L.; Devlin, Philip M.] Harvard Univ, Sch Med, Dana Faber Brigham & Womens Canc Ctr, Dept Radiat Oncol,Div Brachytherapy, Boston, MA 02115 USA.
[Stewart, Alexandra J.] Royal Surrey Cty Hosp, St Lukes Canc Ctr, Surrey, England.
[Mutyala, Subhakar] Montefiore Med Ctr, Dept Radiat Oncol, Bronx, NY 10467 USA.
[Mutyala, Subhakar] Albert Einstein Coll Med, Bronx, NY 10467 USA.
RP Devlin, PM (reprint author), Harvard Univ, Sch Med, Dana Faber Brigham & Womens Canc Ctr, Dept Radiat Oncol,Div Brachytherapy, Boston, MA 02115 USA.
EM ajsintheus@yahoo.co.uk; dofarrell@lroc.harvard.edu;
rcormack@lroc.harvard.edu; jhansen@lroc.harvard.edu;
atif.j.khan@gmail.com; smutyala@montefiore.org; pdevlin@lroc.harvard.edu
OI Cormack, Robert/0000-0001-5553-9984; Khan, Atif/0000-0001-8640-8530
NR 39
TC 23
Z9 23
U1 0
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
J9 RADIAT ONCOL
JI Radiat. Oncol.
PD NOV 19
PY 2008
VL 3
AR 39
DI 10.1186/1748-717X-3-39
PG 11
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 394IY
UT WOS:000262441600001
PM 19019216
ER
PT J
AU Wang, TY
Xiao, L
Alexander, KP
Rao, SV
Kosiborod, MN
Rumsfeld, JS
Spertus, JA
Peterson, ED
AF Wang, Tracy Y.
Xiao, Lan
Alexander, Karen P.
Rao, Sunil V.
Kosiborod, Mikhail N.
Rumsfeld, John S.
Spertus, John A.
Peterson, Eric D.
TI Antiplatelet Therapy Use After Discharge Among Acute Myocardial
Infarction Patients With In-Hospital Bleeding
SO CIRCULATION
LA English
DT Article
DE anticoagulants; antiplatelet therapy; bleeding; myocardial infarction
ID ACUTE CORONARY SYNDROMES; ST-SEGMENT ELEVATION; HIGH-RISK PATIENTS;
CLINICAL-OUTCOMES; COLLABORATIVE METAANALYSIS; RANDOMIZED-TRIALS;
BLOOD-TRANSFUSION; IMPACT; PREDICTORS; REGISTRY
AB Background-Bleeding among patients with acute myocardial infarction (AMI) is associated with worse long-term outcomes. Although the mechanism underlying this association is unclear, a potential explanation is that withholding antiplatelet therapies long beyond resolution of the bleeding event may contribute to recurrent events.
Methods and Results-We examined medication use at discharge, 1, 6, and 12 months after AMI among 2498 patients in the Prospective Registry Evaluating Myocardial Infarction: Events and Recovery (PREMIER) registry. Bleeding was defined as non-coronary artery bypass graft-related Thrombolysis of Myocardial Infarction major/minor bleeding or transfusion among patients with baseline hematocrit >= 28%. Logistic regression was used to evaluate the association between bleeding during the index AMI hospitalization and medication use. In-hospital bleeding occurred in 301 patients (12%) with AMI. Patients with in-hospital bleeding were less likely to be discharged on aspirin or thienopyridine (adjusted odds ratio = 0.45; 95% CI, 0.31 to 0.64; and odds ratio = 0.62; 95% CI, 0.42 to 0.91, respectively). At 1 month after discharge, although patients with in-hospital bleeding remained significantly less likely to receive aspirin (odds ratio = 0.68; 95% CI, 0.50 to 0.92), use of thienopyridines in the 2 groups started to become similar. By 1 year, antiplatelet therapy use was similar among patients with and without bleeding. Postdischarge cardiology follow-up was associated with greater antiplatelet therapy use than either primary care or no clinical follow-up.
Conclusions-Patients whose index AMI is complicated by bleeding are less likely to be treated with antiplatelet therapies during the first 6 months after discharge. Early reassessment of antiplatelet eligibility may represent an opportunity to reduce the long-term risk of adverse outcomes associated with bleeding. (Circulation. 2008; 118: 2139-2145.)
C1 [Wang, Tracy Y.; Alexander, Karen P.; Rao, Sunil V.; Peterson, Eric D.] Duke Clin Res Inst, Durham, NC 27705 USA.
[Wang, Tracy Y.; Alexander, Karen P.; Rao, Sunil V.; Peterson, Eric D.] Duke Univ, Med Ctr, Durham, NC 27705 USA.
[Xiao, Lan; Kosiborod, Mikhail N.; Spertus, John A.] Univ Missouri, Kansas City, MO 64110 USA.
[Xiao, Lan; Kosiborod, Mikhail N.; Spertus, John A.] St Lukes Hosp, Mid Amer Heart Inst, Kansas City, MO 64111 USA.
[Rumsfeld, John S.] Denver Vet Affairs Med Ctr, Denver, CO USA.
RP Wang, TY (reprint author), Duke Clin Res Inst, 2400 Pratt St,Room 0311,Terrace Level, Durham, NC 27705 USA.
EM wang0085@mc.duke.edu
FU Cardiovascular Outcomes, Inc; Cardiovascular Therapeutics, Inc, Palo
Alto, Calif; Duke Clinical Research Institute, Durham, NC; CV
Therapeutics, Inc, Palo Alto, Calif
FX The PREMIER Quality Improvement Registry was organized by Cardiovascular
Outcomes, Inc, a nonprofit 501( c)( 3) organization dedicated to the
advancement of outcomes research and improvement of cardiovascular
healthcare quality, and is funded by Cardiovascular Therapeutics, Inc,
Palo Alto, Calif. More information on the PREMIER Quality Improvement
Registry can be found at http://www.cvoutcomes.org. Funding and support
for this publication were provided by the Duke Clinical Research
Institute, Durham, NC. Funding for statistical analysis was provided by
CV Therapeutics, Inc, Palo Alto, Calif.
NR 27
TC 69
Z9 72
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 18
PY 2008
VL 118
IS 21
BP 2139
EP 2145
DI 10.1161/CIRCULATIONAHA.108.787143
PG 7
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 373FB
UT WOS:000260955300005
PM 18981304
ER
PT J
AU Tolle, JJ
Waxman, AB
Van Horn, TL
Pappagianopoulos, PP
Systrom, DM
AF Tolle, James J.
Waxman, Aaron B.
Van Horn, Teresa L.
Pappagianopoulos, Paul P.
Systrom, David M.
TI Exercise-Induced Pulmonary Arterial Hypertension
SO CIRCULATION
LA English
DT Article
DE circulation; exercise; hemodynamics; hypertension, pulmonary; physiology
ID RIGHT ATRIAL PRESSURE; VASCULAR-RESISTANCE; ANAEROBIC THRESHOLD;
DOPPLER-ECHOCARDIOGRAPHY; HEMODYNAMIC-RESPONSE; SYSTEMIC-SCLEROSIS;
DIAGNOSIS; PATHOGENESIS; LIMIT
AB Background-The clinical relevance of exercise-induced pulmonary arterial hypertension (PAH) is uncertain, and its existence has never been well studied by direct measurements of central hemodynamics. Using invasive cardiopulmonary exercise testing, we hypothesized that exercise-induced PAH represents a symptomatic stage of PAH, physiologically intermediate between resting pulmonary arterial hypertension and normal.
Methods and Results-A total of 406 consecutive clinically indicated cardiopulmonary exercise tests with radial and pulmonary arterial catheters and radionuclide ventriculographic scanning were analyzed. The invasive hemodynamic phenotype of exercise-induced PAH (n = 78) was compared with resting PAH (n = 15) and normals (n = 16). Log-log plots of mean pulmonary artery pressure versus oxygen uptake ((V)over dotO(2)) were obtained, and a "join-point" for a least residual sum of squares for 2 straight-line segments (slopes m1, m2) was determined; m2m1 = "takeoff" pattern. At maximum exercise, (V) over dotO(2) (55.8 +/- 20.3% versus 66.5 +/- 16.3% versus 91.7 +/- 13.7% predicted) was lowest in resting PAH, intermediate in exercise-induced PAH, and highest in normals, whereas mean pulmonary artery pressure (48.4 +/- 11.1 versus 36.6 +/- 5.7 versus 27.4 + 3.7 mm Hg) and pulmonary vascular resistance (294 +/- 158 versus 161 +/- 60 versus 62 +/- 20 dyne . s . cm(-5), respectively; P<0.05) followed an opposite pattern. An exercise-induced PAH plateau (n = 32) was associated with lower (V) over dotO(2)max (60.6 +/- 15.1% versus 72.0 +/- 16.1% predicted) and maximum cardiac output (78.2 +/- 17.1% versus 87.8 +/- 18.3% predicted) and a higher resting pulmonary vascular resistance (247 +/- 101 versus 199 +/- 56 dyne . s . cm(-5); P<0.05) than takeoff (n = 40). The plateau pattern was most common in resting PAH, and the takeoff pattern was present in nearly all normals.
Conclusions-Exercise-induced PAH is an early, mild, and clinically relevant phase of the PAH spectrum. (Circulation. 2008; 118: 2183-2189.)
C1 [Tolle, James J.; Waxman, Aaron B.; Van Horn, Teresa L.; Pappagianopoulos, Paul P.; Systrom, David M.] Harvard Univ, Pulm & Crit Care Unit, Sch Med, Massachusetts Gen Hosp,Med Serv, Boston, MA 02114 USA.
RP Tolle, JJ (reprint author), Harvard Univ, Pulm & Crit Care Unit, Sch Med, Massachusetts Gen Hosp,Med Serv, BUL 1-148,55 Fruit St, Boston, MA 02114 USA.
EM jjtolle@yahoo.com
OI Systrom, David/0000-0002-9610-6330
FU National Institutes of Health [K24HL04022-05]
FX This work was supported by grant K24HL04022-05 from the National
Institutes of Health.
NR 46
TC 152
Z9 157
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 18
PY 2008
VL 118
IS 21
BP 2183
EP 2189
DI 10.1161/CIRCULATIONAHA.108.787101
PG 7
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 373FB
UT WOS:000260955300010
PM 18981305
ER
PT J
AU Chiu, IM
Chen, A
Zheng, Y
Kosaras, B
Tsiftsoglou, SA
Vartanian, TK
Brown, RH
Carroll, MC
AF Chiu, Isaac M.
Chen, Adam
Zheng, Yi
Kosaras, Bela
Tsiftsoglou, Stefanos A.
Vartanian, Timothy K.
Brown, Robert H., Jr.
Carroll, Michael C.
TI T lymphocytes potentiate endogenous neuroprotective inflammation in a
mouse model of ALS
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE amyotrophic lateral sclerosis; microglia; neuroimmunology;
neuroinflammation; T cells
ID AMYOTROPHIC-LATERAL-SCLEROSIS; MOTOR-NEURON DEGENERATION; WILD-TYPE
MICROGLIA; SPINAL-CORD; EXTEND SURVIVAL; NADPH OXIDASE; FAMILIAL ALS;
MICE; CELLS; DISEASE
AB Amyotrophic Lateral Sclerosis (ALS) is an adult-onset, progressive, motor neuron degenerative disease, in which the role of inflammation is not well established. Innate and adaptive immunity were investigated in the CNS of the Superoxide Dismutase 1 (SOD1)(G93A) transgenic mouse model of ALS. CD4(+) and CD8+ T cells infiltrated SOD1(G93A) spinal cords during disease progression. Cell-specific flow cytometry and gene expression profiling showed significant phenotypic changes in microglia, including dendritic cell receptor acquisition, and expression of genes linked to neuroprotection, cholesterol metabolism and tissue remodeling. Microglia dramatically up-regulated IGF-1 and down-regulated IL-6 expression. When mutant SOD1 mice were bred onto a TCR beta deficient background, disease progression was significantly accelerated at the symptomatic stage. In addition, microglia reactivity and IGF-1 levels were reduced in spinal cords of SOD1(G93A) (TCR beta(-/-)) mice. These results indicate that T cells play an endogenous neuroprotective role in ALS by modulating a beneficial inflammatory response to neuronal injury.
C1 [Chiu, Isaac M.; Zheng, Yi; Tsiftsoglou, Stefanos A.; Carroll, Michael C.] Harvard Univ, Sch Med, Immune Dis Inst, Dept Pathol, Boston, MA 02115 USA.
[Chen, Adam; Brown, Robert H., Jr.] Massachusetts Gen Hosp, Day Neuromuscular Res Lab, Charlestown, MA 02129 USA.
[Kosaras, Bela; Vartanian, Timothy K.] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA.
RP Chiu, IM (reprint author), Harvard Univ, Sch Med, Immune Dis Inst, Dept Pathol, Boston, MA 02115 USA.
EM chiu@fas.haward.edu
FU Amyotrophic Lateral Sclerosis Association; National Institutes of Health
Training [Al 007306-23]; ALS Association; National Institute for
Neurological Disease and Stroke; National Institute for Aging; ALS
Research Foundation; Al-Athel Amyotrophic Lateral Sclerosis Foundation
FX We thank Michael Haas, Vijay Kuchroo, and Tammy Hshieh for helpful,
critical discussions; Eugene Ponomarev for CNS cell isolation and adult
microglia culture advice; Laura Santambrogio, Jeng-Shin Lee, and Viraga
Haridas for technical help; and Monica Carrasco for help with image
analysis. This work was funded by the Amyotrophic Lateral Sclerosis
Association (M.C.C., I.M.C.); National Institutes of Health Training
Grant Al 007306-23 (to I.M.C.); and the ALS Association, National
Institute for Neurological Disease and Stroke, National Institute for
Aging, Angel Fund, Project ALS, Pierre L. de Bourgknect ALS Research
Foundation, and Al-Athel Amyotrophic Lateral Sclerosis Foundation
(R.B.).
NR 36
TC 154
Z9 156
U1 0
U2 7
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 18
PY 2008
VL 105
IS 46
BP 17913
EP 17918
DI 10.1073/pnas.0804610105
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 377BB
UT WOS:000261225600063
PM 18997009
ER
PT J
AU Kahn, JM
Asch, RJ
Iwashyna, TJ
Rubenfeld, GD
Angus, DC
Asch, DA
AF Kahn, Jeremy M.
Asch, Rebecca J.
Iwashyna, Theodore J.
Rubenfeld, Gordon D.
Angus, Derek C.
Asch, David A.
TI Perceived barriers to the regionalization of adult critical care in the
United States: a qualitative preliminary study
SO BMC HEALTH SERVICES RESEARCH
LA English
DT Article
ID HOSPITAL VOLUME; DELIVERY; ILL; ORGANIZATION; MORTALITY; MEDICINE;
SERVICES; OUTCOMES; IMPACT
AB Background: Regionalization of adult critical care services may improve outcomes for critically ill patients. We sought to develop a framework for understanding clinician attitudes toward regionalization and potential barriers to developing a tiered, regionalized system of care in the United States.
Methods: We performed a qualitative study using semi-structured interviews of critical care stakeholders in the United States, including physicians, nurses and hospital administrators. Stakeholders were identified from a stratified-random sample of United States general medical and surgical hospitals. Key barriers and potential solutions were identified by performing content analysis of the interview transcriptions.
Results: We interviewed 30 stakeholders from 24 different hospitals, representing a broad range of hospital locations and sizes. Key barriers to regionalization included personal and economic strain on families, loss of autonomy on the part of referring physicians and hospitals, loss of revenue on the part of referring physicians and hospitals, the potential to worsen outcomes at small hospitals by limiting services, and the potential to overwhelm large hospitals. Improving communication between destination and source hospitals, provider education, instituting voluntary objective criteria to become a designated referral center, and mechanisms to feed back patients and revenue to source hospitals were identified as potential solutions to some of these barriers.
Conclusion: Regionalization efforts will be met with significant conceptual and structural barriers. These data provide a foundation for future research and can be used to inform policy decisions regarding the design and implementation of a regionalized system of critical care.
C1 [Kahn, Jeremy M.; Asch, Rebecca J.] Univ Penn, Div Pulm Allergy & Crit Care, Sch Med, Philadelphia, PA 19104 USA.
[Kahn, Jeremy M.; Asch, David A.] Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA.
[Kahn, Jeremy M.] Univ Penn, Sch Med, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
[Iwashyna, Theodore J.] Univ Michigan, Div Pulm & Crit Care Med, Ann Arbor, MI 48109 USA.
[Rubenfeld, Gordon D.] Univ Toronto, Sunnybrook Hlth Sci Ctr, Program Trauma Emergency & Crit Care, Toronto, ON M4N 3M5, Canada.
[Angus, Derek C.] Univ Pittsburgh, Sch Med, Dept Crit Care Med, CRISMA Lab, Pittsburgh, PA USA.
[Asch, David A.] Philadelphia Vet Affairs Med Ctr, Ctr Hlth Equ Res & Promot, Philadelphia, PA 19104 USA.
RP Kahn, JM (reprint author), Univ Penn, Div Pulm Allergy & Crit Care, Sch Med, 3400 Spruce St, Philadelphia, PA 19104 USA.
EM jmkahn@mail.med.upenn.edu; aschrj@mail.med.upenn.edu;
tiwashyn@umich.edu; gordon.rubenfeld@sunnybrook.ca;
angusdc@ccm.upmc.edu; asch@wharton.upenn.edu
RI Angus, Derek/E-9671-2012;
OI Asch, David/0000-0002-7970-286X; Iwashyna, Theodore/0000-0002-4226-9310
FU United States National Institutes of Health [K23 HL082650]
FX This work was supported by the University of Pennsylvania Leschly Fund.
Dr. Kahn is supported by a career development award from the United
States National Institutes of Health (K23 HL082650). The funding source
had no role in the design, implementation, analysis or decision to
publish this research.
NR 28
TC 11
Z9 11
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1472-6963
J9 BMC HEALTH SERV RES
JI BMC Health Serv. Res.
PD NOV 17
PY 2008
VL 8
AR 239
DI 10.1186/1472-6963-8-239
PG 7
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA 391LA
UT WOS:000262233600002
PM 19014704
ER
PT J
AU Friedberg, JW
Sharman, J
Schaefer-Cutillo, J
Johnston, PB
De Vos, S
LaCasce, A
Leonard, JP
Cripe, LD
Sinha, R
Gregory, SA
Sweetenham, J
Vose, JM
Lowe, AM
Levy, R
Shipp, MA
AF Friedberg, Jonatan W.
Sharman, Jeff
Schaefer-Cutillo, Julia
Johnston, Patrick B.
De Vos, Sven
LaCasce, Ann
Leonard, John P.
Cripe, Larry D.
Sinha, Rajni
Gregory, Stephanie A.
Sweetenham, John
Vose, Julie M.
Lowe, Ann M.
Levy, R.
Shipp, Margaret A.
TI Fostamatinib Disodium (FosD), An Oral Inhibitor of Syk, Is
Well-Tolerated and Has Significant Clinical Activity in Diffuse Large B
Cell Lymphoma (DLBCL) and Chronic Lymphocytic Leukemia (SLL/CLL)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Friedberg, Jonatan W.; Schaefer-Cutillo, Julia] Univ Rochester, James P Wilmot Canc Ctr, Rochester, NY USA.
[Sharman, Jeff] Stanford Univ, Stanford, CA 94305 USA.
[Johnston, Patrick B.] Mayo Clin, Grad Sch Med, Rochester, MN USA.
[De Vos, Sven] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[LaCasce, Ann; Shipp, Margaret A.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Leonard, John P.] Weill Cornell Med Coll, Div Hem Onc, New York, NY USA.
[Cripe, Larry D.] Indiana Univ, Simon Canc Ctr, Indianapolis, IN 46204 USA.
[Sinha, Rajni] Emory Univ, Atlanta, GA 30322 USA.
[Gregory, Stephanie A.] Rush Univ, Med Ctr, Sect Hematol & Stem Cell Transplantat, Chicago, IL 60612 USA.
[Sweetenham, John] Taussig Canc Inst, Cleveland Clin, Cleveland, OH USA.
[Vose, Julie M.] Univ NE Med Ctr, Omaha, NE USA.
[Lowe, Ann M.] Rigel Pharmaceut, San Francisco, CA USA.
[Levy, R.] Stanford Univ, Stanford, CA 94305 USA.
NR 0
TC 20
Z9 20
U1 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 3
EP 4
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700004
ER
PT J
AU Kikushige, Y
Miyamoto, T
Lino, T
Ishikawa, F
Akashi, K
AF Kikushige, Yoshikane
Miyamoto, Toshihiro
Lino, Tadafumi
Ishikawa, Fumihiko
Akashi, Koichi
TI Hematopoictic Stem tells Are Primarily Involved in Pathogenesis of
Chronic Lymphocytic Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Kikushige, Yoshikane; Miyamoto, Toshihiro] Kyushu Univ Hosp, Ctr Cellular & Mol Med, Fukuoka 812, Japan.
[Lino, Tadafumi; Akashi, Koichi] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Ishikawa, Fumihiko] RIKEN Rsrch Ctr Allergy & Immunol, Rsrch Unit Human Dis Models, Yokohama, Kanagawa, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 17
EP 17
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700030
ER
PT J
AU Ramsay, AG
Gorgun, G
Holderried, TAW
Zahrieh, D
Liu, FL
Quackenbush, J
Croce, CM
Gribben, JG
AF Ramsay, Alan G.
Gorgun, Gullu
Holderried, Tobias A. W.
Zahrieh, David
Liu, Fenglong
Quackenbush, John
Croce, Carlo M.
Gribben, John G.
TI A Mouse Model for Immunotherapeutic Reversal of Leukemia-induced T Cell
Dysfunction
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ramsay, Alan G.; Gribben, John G.] Barts & London Queen Marys Sch Med & Dent, Inst Canc, Ctr Med Oncol, London, England.
[Gorgun, Gullu; Holderried, Tobias A. W.; Zahrieh, David; Liu, Fenglong; Quackenbush, John] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Croce, Carlo M.] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 17
EP 17
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700031
ER
PT J
AU Rowe, JM
Sun, ZX
Cassileth, PA
Appelbaum, FR
Wiernik, PH
Lazarus, HM
Blume, KG
Fernandez, HF
Litzow, MR
Tallman, MS
AF Rowe, Jacob M.
Sun, Zhuoxin
Cassileth, Peter A.
Appelbaum, Frederick R.
Wiernik, Peter H.
Lazarus, Hillard M.
Blume, Karl G.
Fernandez, Hugo F.
Litzow, Mark R.
Tallman, Martin S.
TI Treatment-Related Mortality and Relapse Rate from Time of Initiation of
Post-Remission Therapy for Patients Receiving Allogeneic
Transplantation, Autologous Transplantation or Intensive Chemotherapy: A
Report from the Eastern Cooperative Oncology Group (ECOG)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Rowe, Jacob M.] Technion Israel Inst Technol, Haifa, Israel.
[Sun, Zhuoxin] Dana Farber Canc Inst, Boston, MA USA.
[Cassileth, Peter A.] Univ Miami, Sylvester Canc Ctr, Miami, FL USA.
[Appelbaum, Frederick R.] Univ Washington, Fred Hutchinson Canc Res Ctr, Sch Med, Seattle, WA 98195 USA.
[Wiernik, Peter H.] New York Med Coll, Our Lady Mercy Canc Ctr, Bronx, NY USA.
[Lazarus, Hillard M.] Univ Hosp Cleveland, Ireland Canc Ctr, Cleveland, OH 44106 USA.
[Blume, Karl G.] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
[Fernandez, Hugo F.] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
[Litzow, Mark R.] Mayo Clin, Rochester, MN USA.
[Tallman, Martin S.] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 25
EP 25
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700050
ER
PT J
AU Navarro, WH
Agovi, MA
Logan, B
Bacigalupo, A
Ballen, KK
Bolwell, BJ
Frangoul, H
Gupta, V
Hahn, T
Juckett, M
Lazarus, HM
Litzow, MR
Liesveld, J
Moreb, J
Marks, D
McCarthy, PL
Rizzo, JD
AF Navarro, Willis H.
Agovi, Manza-A
Logan, Brent
Bacigalupo, Andrea
Ballen, Karen K.
Bolwell, Brian J.
Frangoul, Haydar
Gupta, Vikas
Hahn, Theresa
Juckett, Mark
Lazarus, Hillard M.
Litzow, Mark R.
Liesveld, Jane
Moreb, Jan
Marks, David
McCarthy, Philip L.
Rizzo, J. Douglas
TI Obesity Does Not Preclude Safe and Effective Myeloablative Hematopoietic
Cell Transplantation (HCT) for Acute Myeloid Leukemia (AML) in Adults
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Navarro, Willis H.] Natl Marrow Donor Program, Minneapolis, MN USA.
[Agovi, Manza-A; Logan, Brent; Rizzo, J. Douglas] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
[Bacigalupo, Andrea] San Martino Hosp, Genoa, Italy.
[Ballen, Karen K.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Bolwell, Brian J.] Cleveland Clin, Cleveland, OH 44106 USA.
[Frangoul, Haydar] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
[Gupta, Vikas] Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
[Hahn, Theresa; Liesveld, Jane; McCarthy, Philip L.] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[Juckett, Mark] Univ WI Hosp & Clin, Madison, WI USA.
[Lazarus, Hillard M.] Univ Hosp Case Med Ctr, Cleveland, OH USA.
[Litzow, Mark R.] Mayo Clin, Rochester, MN USA.
[Moreb, Jan] Univ Florida, Shands Hosp, Gainesville, FL USA.
[Marks, David] United Bristol Healthcare Trust, Bristol, Avon, England.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 26
EP 26
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700052
ER
PT J
AU Alousi, A
Weisdorf, DJ
Logan, BR
Bolanos-Meade, J
Goldstein, SC
Ho, VT
Hayes-Lattin, B
Wingard, JR
Horowitz, MM
Levine, JE
AF Alousi, Amin
Weisdorf, Daniel J.
Logan, Brent R.
Bolanos-Meade, Javier
Goldstein, Steven C.
Ho, Vincent T.
Hayes-Lattin, Brandon
Wingard, John R.
Horowitz, Mary M.
Levine, John E.
TI BMT CTN 0302: A Phase II Randomized Trial Evaluating Etanercept,
Mycophenolate Mofetil (MMF), Denileukin Diftitox, and Pentostatin in
Combination with Corticosteroids in 180 Patients (pts) with Newly
Diagnosed Acute Graft Vs. Host Disease (aGVHD)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Alousi, Amin] Univ Texas MD Anderson Canc Ctr, Stem Cell Transplantat & Cellular Therapy, Houston, TX 77030 USA.
[Weisdorf, Daniel J.] Univ Minnesota, Minneapolis, MN USA.
[Logan, Brent R.] Med Coll Wisconsin, Div Biostat, Milwaukee, WI 53226 USA.
[Bolanos-Meade, Javier] Johns Hopkins Univ, Baltimore, MD USA.
[Goldstein, Steven C.] Univ Penn, Philadelphia, PA 19104 USA.
[Ho, Vincent T.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Hayes-Lattin, Brandon] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Wingard, John R.] Univ Florida, Shands Canc Ctr, Gainesville, FL USA.
[Horowitz, Mary M.] Ctr Int Blood & Marrow Transplant Res, Ctr Clin Canc, Froedtert & Med Coll Wisconsin, Milwaukee, WI USA.
[Levine, John E.] Univ Michigan, Blood & Marrow Transplantat Program, Ann Arbor, MI 48109 USA.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 27
EP 28
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700056
ER
PT J
AU Kumar, S
Flinn, IW
Noga, SJ
Hari, P
Rifkin, RM
Callander, NS
Bhandari, M
Wolf, JL
Gasparetto, C
Krishnan, A
Grosman, DD
Glass, J
Sahovic, EA
Shi, H
Webb, IJ
Richardson, P
Rajkumar, SV
AF Kumar, Shaji
Flinn, Ian W.
Noga, Stephen J.
Hari, Parameswaran
Rifkin, Robert M.
Callander, Natalie Scott
Bhandari, Manish
Wolf, Jeffrey Lee
Gasparetto, Cristina
Krishnan, Amrita
Grosman, Daren D.
Glass, Jonathan
Sahovic, Entezam Asim
Shi, Hongliang
Webb, Iain J.
Richardson, Paul
Rajkumar, S. Vincent
TI Safety and Efficacy of Novel Combination Therapy with Bortezomib,
Dexamethasone, Cyclophosphamide, and Lenalidomide in Newly Diagnosed
Multiple Myeloma: Initial Results from the Phase I/II MultiCenter
EVOLUTION Study
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Rajkumar, S. Vincent] Mayo Clin, Coll Med, Rochester, MN USA.
[Flinn, Ian W.] Sarah Cannon Res Inst, Nashville, TN USA.
[Noga, Stephen J.] Alvin & Lois Lapidus Canc Inst, Baltimore, MD USA.
[Hari, Parameswaran] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
[Rifkin, Robert M.] Rocky Mt Canc Ctr, Denver, CO USA.
[Callander, Natalie Scott] Univ Washington, Madison, WI USA.
[Bhandari, Manish] Christ Hosp, Cincinnati, OH 45219 USA.
[Wolf, Jeffrey Lee] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Gasparetto, Cristina] Duke Univ, Med Ctr, Durham, NC USA.
[Krishnan, Amrita] City Hope Natl Med Ctr, Duarte, CA 91010 USA.
[Grosman, Daren D.] Mem Healthcare Canc Ctr, Hollywood, FL USA.
[Glass, Jonathan] LSUHSC Shreveport, Feist Weiller Canc Ctr, Dept Med, Shreveport, LA USA.
[Sahovic, Entezam Asim] Western Penn Hosp, Pittsburgh, PA 15224 USA.
[Shi, Hongliang] Millennium Pharmaceut Takeda Oncol Co, Clin Biostat, Cambridge, MA USA.
[Richardson, Paul] Dana Farber Canc Inst, Boston, MA 02115 USA.
RI Kumar, Shaji/A-9853-2008
OI Kumar, Shaji/0000-0001-5392-9284
NR 0
TC 4
Z9 5
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 41
EP 42
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700094
ER
PT J
AU Richardson, P
Lonial, S
Jakubowiak, A
Jagannath, S
Raje, NS
Avigan, D
Ghobrial, IM
Schlossman, RL
Mazumder, A
Munshi, NC
Vesole, DH
Joyce, R
Doss, D
Warren, DL
Hayes, SW
Kaster, S
Delaney, C
Lauria, M
Mitsiades, C
Hideshima, T
Knight, RD
Esseltine, DL
Anderson, KC
AF Richardson, Paul
Lonial, Sagar
Jakubowiak, Andrzej
Jagannath, Sundar
Raje, Noopur S.
Avigan, David
Ghobrial, Irene M.
Schlossman, Robert L.
Mazumder, Amitabha
Munshi, Nikhil C.
Vesole, David H.
Joyce, Robin
Doss, Deborah
Warren, Diane L.
Hayes, Stephen W.
Kaster, Sarah
Delaney, Carol
Lauria, Marisa
Mitsiades, Constantine
Hideshima, Teru
Knight, Robert D.
Esseltine, Dixie-Lee
Anderson, Kenneth C.
TI Lenalidomide, Bortezomib, and Dexamethasone in Patients with Newly
Diagnosed Multiple Myeloma: Encouraging Efficacy in High Risk Groups
with Updated Results of a Phase I/II Study
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Richardson, Paul; Ghobrial, Irene M.; Schlossman, Robert L.; Munshi, Nikhil C.; Doss, Deborah; Warren, Diane L.; Hayes, Stephen W.; Mitsiades, Constantine; Hideshima, Teru; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Lonial, Sagar] Emory Univ, Atlanta, GA 30322 USA.
[Jakubowiak, Andrzej] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Jagannath, Sundar; Mazumder, Amitabha; Vesole, David H.] St Vincents Comprehens Canc Ctr, New York, NY USA.
[Raje, Noopur S.; Kaster, Sarah] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Avigan, David; Joyce, Robin; Delaney, Carol; Lauria, Marisa] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Knight, Robert D.] Celgene Corp, Summit, NJ 07901 USA.
[Esseltine, Dixie-Lee] Millennium Pharmaceut Takeda Oncol Co, Cambridge, MA USA.
NR 0
TC 7
Z9 8
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 41
EP 41
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700093
ER
PT J
AU Adamia, S
AvetLoiseau, H
Amin, SB
Tai, YT
Treon, SP
Moreau, P
Minvielle, S
Li, C
Anderson, KC
Munshi, NC
AF Adamia, Sophia
AvetLoiseau, Herve
Amin, Samirkumar B.
Tai, Yu-Tzu
Treon, Steven P.
Moreau, Philippe
Minvielle, Stephane
Li, Cheng
Anderson, Kenneth C.
Munshi, Nikhil C.
TI Microrna Expression Profile Identifies Distinct Clinically Relevant
Sub-Groups in Multiple Myeloma: Novel Prognostic Markers and Potential
Targets for Therapy
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Amin, Samirkumar B.; Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Dis Ctr, Boston, MA 02115 USA.
[AvetLoiseau, Herve; Moreau, Philippe; Minvielle, Stephane] Hop Nantes, Dept Hematol, F-44093 Nantes, France.
[Munshi, Nikhil C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston VA Canc Healthcare Syst, Boston, MA 02115 USA.
RI Minvielle, Stephane/K-8251-2015; richard, chrystelle/K-8595-2015
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 43
EP 43
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700097
ER
PT J
AU Pardanani, AD
Gotlib, J
Jamieson, C
Cortes, J
Talpaz, M
Stone, RM
Silverman, MH
Shorr, J
Gilliland, DG
Tefferi, A
AF Pardanani, Animesh D.
Gotlib, Jason
Jamieson, Catriona
Cortes, Jorge
Talpaz, Moshe
Stone, Richard M.
Silverman, Michael H.
Shorr, Jolene
Gilliland, D. Gary
Tefferi, Ayalew
TI A Phase I Study of TG101348, An Orally Bioavailable JAK2-Selective
Inhibitor, in Patients with Myelofibrosis
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Pardanani, Animesh D.] Mayo Clin, Rochester, MN USA.
[Gotlib, Jason] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
[Jamieson, Catriona] Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA.
[Jamieson, Catriona] Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA.
[Cortes, Jorge] Univ Texas Houston, MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Talpaz, Moshe] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Stone, Richard M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Silverman, Michael H.] Biosirateg Consulting Ltd, Marblehead, MA USA.
[Gilliland, D. Gary] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Shorr, Jolene] TargeGen Inc, San Diego, CA USA.
[Tefferi, Ayalew] Mayo Clin Grad Sch Med, Div Hematol, Rochester, MN USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 43
EP 44
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700098
ER
PT J
AU Shah, NP
Olszynski, P
Sokol, L
Verstovsek, S
Hoffman, R
List, AF
Cortes, J
Kantadian, HM
Gilliland, DG
Clary, DO
Bui, LA
Wadleigh, M
AF Shah, Neil P.
Olszynski, Patrycja
Sokol, Lubomir
Verstovsek, Srdan
Hoffman, Ronald
List, Alan F.
Cortes, Jorge
Kantadian, Hagop M.
Gilliland, D. Gary
Clary, Douglas O.
Bui, Lynne A.
Wadleigh, Martha
TI A Phase I Study of XL019, a Selective JAK2 Inhibitor, in Patients with
Primary Myelofibrosis, Post-Polycythemia Vera, or Post-Essential
Thrombocythemia Myelofibrosis
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Shah, Neil P.; Olszynski, Patrycja] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Sokol, Lubomir; List, Alan F.] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Verstovsek, Srdan; Cortes, Jorge] Univ Texas Houston, MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Hoffman, Ronald] Mt Sinai Sch Med, New York, NY USA.
[List, Alan F.] Res Inst, Tampa, FL USA.
[Kantadian, Hagop M.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Gilliland, D. Gary] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Clary, Douglas O.; Bui, Lynne A.] Exelixis Inc, San Francisco, CA USA.
[Wadleigh, Martha] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 4
Z9 4
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 44
EP 44
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700099
ER
PT J
AU Gyurkocza, B
Storb, RF
Storer, B
Chauncey, T
Niederwieser, D
Shizuru, J
Langston, A
Pulsipher, M
Bredeson, C
Maziarz, RT
Bruno, B
Petersen, F
Maris, M
Agura, E
Yeager, AM
Bethge, WA
Sahebi, F
Vindelov, L
McSweeney, PA
Appelbaum, FR
Maloney, DG
Sandmaier, BM
AF Gyurkocza, Boglarka
Storb, Rainer F.
Storer, Barry
Chauncey, Thomas
Niederwieser, Dietger
Shizuru, Judith
Langston, Amelia
Pulsipher, Michael
Bredeson, Christopher
Maziarz, Richard T.
Bruno, Benedetto
Petersen, Finn
Maris, Michael
Agura, Edward
Yeager, Andrew M.
Bethge, Wolfgang A.
Sahebi, Firoozeh
Vindelov, Lars
McSweeney, Peter A.
Appelbaum, Frederick R.
Maloney, David G.
Sandmaier, Brenda M.
TI Nonmyeloablative Allogeneic Hematopoietic Cell Transplantation in
Patients with De Novo and Secondary Acute Myeloid Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Chauncey, Thomas] Univ Washington, Fred Hutchinson Canc Res Ctr, VA Puget Sound Hlth Care Syst, Seattle, WA 98195 USA.
[Niederwieser, Dietger] Univ Leipzig, Leipzig, Germany.
[Shizuru, Judith] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
[Langston, Amelia] Emory Univ, Atlanta, GA 30322 USA.
[Pulsipher, Michael] Univ Utah, Med Ctr, Salt Lake City, UT USA.
[Bredeson, Christopher] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Maziarz, Richard T.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Bruno, Benedetto] Univ Turin, Turin, Italy.
[Petersen, Finn] LDS Hosp, Salt Lake City, UT USA.
[Maris, Michael; McSweeney, Peter A.] Rocky Mt Canc Ctr, Denver, CO USA.
[Agura, Edward] Baylor Univ, Med Ctr, Dallas, TX USA.
[Yeager, Andrew M.] Univ Arizona, Tucson, AZ USA.
[Bethge, Wolfgang A.] Univ Tubingen, Med Ctr, Tubingen, Germany.
[Sahebi, Firoozeh] City Hope Natl Med Ctr, Duarte, CA USA.
[Vindelov, Lars] Univ Copenhagen, Rigshosp, DK-2100 Copenhagen, Denmark.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 61
EP 61
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700150
ER
PT J
AU Roti, G
Ross, KN
Mecucci, C
Ferrando, AA
Aster, JC
Stegmaier, K
AF Roti, Giovanni
Ross, Kenneth N.
Mecucci, Cristina
Ferrando, Adolfo A.
Aster, Jon C.
Stegmaier, Kimberly
TI Chemical Genomic Screen Identifies Ionophores as Modulators of Notch1 in
T-ALL
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Roti, Giovanni; Stegmaier, Kimberly] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Ross, Kenneth N.] Harvard Univ, Broad Inst, Canc Program, Cambridge, MA 02138 USA.
[Ross, Kenneth N.] MIT, Cambridge, MA 02139 USA.
[Ferrando, Adolfo A.] Columbia Univ, Inst Canc Genet, New York, NY USA.
[Aster, Jon C.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Stegmaier, Kimberly] Harvard Univ, Broad Inst, Boston, MA 02115 USA.
[Stegmaier, Kimberly] MIT, Boston, MA USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 81
EP 81
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700201
ER
PT J
AU Davies, J
Yuk, D
Nadler, L
Guinan, E
AF Davies, Jeff
Yuk, Dongin
Nadler, Lee
Guinan, Eva
TI Alloanergization of HILA-Mismatched Human Donor T Cells Results in the
Generation of Allosuppressive CD4(+) T Regulatory Cells Both in Vitro
and in Vivo
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology/ASH/ASCO Joint
Symposium
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol, Sanofi Aventis U.S.
C1 [Davies, Jeff; Yuk, Dongin; Nadler, Lee; Guinan, Eva] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 83
EP 84
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700208
ER
PT J
AU Ooi, MG
McMillin, DW
Negri, JM
Delmore, J
Klippel, S
Mitsiades, N
Richardson, PG
Anderson, KC
Mitsiades, CS
AF Ooi, Melissa G.
McMillin, Douglas W.
Negri, Joseph M.
Delmore, Jake
Klippel, Steffen
Mitsiades, Nicholas
Richardson, Paul G.
Anderson, Kenneth C.
Mitsiades, Constantine S.
TI Compartment-Specific Bioluminescence Imaging (CS-BLI) High-Throughput
Assays Provide Comparative Insights into the Impact of Osteoclasts Vs.
Stromal Cells on Activity of Anti-Myeloma Therapeutics
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ooi, Melissa G.; McMillin, Douglas W.; Negri, Joseph M.; Delmore, Jake; Klippel, Steffen; Mitsiades, Nicholas; Richardson, Paul G.; Anderson, Kenneth C.; Mitsiades, Constantine S.] Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 88
EP 88
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700220
ER
PT J
AU Freedman, AS
Neelapu, S
Nichols, CR
Robertson, M
Djulbegovic, B
Winter, JN
Gold, D
Bender, J
Stewart, M
Ghalie, RG
Hamlin, PA
AF Freedman, Arnold S.
Neelapu, Sattva
Nichols, Craig R.
Robertson, Michael
Djulbegovic, Benjamin
Winter, Jane N.
Gold, Daniel
Bender, John
Stewart, Morgan
Ghalie, Richard G.
Hamlin, Paul A., Jr.
TI A Placebo-Controlled Phase III Trial of Patient-Specific Immunotherapy
with Mitumprotimut-T (ID-KLR) and GM-CSF Following Rituximab in Patients
with CD20+Follicular Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Freedman, Arnold S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Neelapu, Sattva] Univ Texas MD Anderson Canc Ctr, Dept Lymphoma & Myeloma, Houston, TX 77030 USA.
[Nichols, Craig R.] Providence Canc Ctr, Portland, OR USA.
[Robertson, Michael] Indiana Univ, Med Ctr, Indianapolis, IN USA.
[Djulbegovic, Benjamin] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Winter, Jane N.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Gold, Daniel; Bender, John; Stewart, Morgan; Ghalie, Richard G.] Favrille Inc, San Diego, CA USA.
[Hamlin, Paul A., Jr.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
RI Djulbegovic, Benjamin/I-3661-2012
OI Djulbegovic, Benjamin/0000-0003-0671-1447
NR 0
TC 1
Z9 1
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 94
EP 94
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700237
ER
PT J
AU Bianchi, G
Oliva, L
Cascio, P
Pengo, N
Orsi, A
Fontana, F
Pasqualetto, E
Mezghrani, A
Cerruti, F
Calbi, V
Palladini, G
Giuliani, N
Chauhan, D
Anderson, KC
Sitia, R
Cenci, S
AF Bianchi, Giada
Oliva, Laura
Cascio, Paolo
Pengo, Niccolo
Orsi, Andrea
Fontana, Francesca
Pasqualetto, Elena
Mezghrani, Alexandre
Cerruti, Fulvia
Calbi, Valeria
Palladini, Giovanni
Giuliani, Nicola
Chauhan, Dharminder
Anderson, Kenneth C.
Sitia, Roberto
Cenci, Simone
TI Proteasome Stress Causes Apoptotic Sensitivity of Multiple Myeloma Cells
to Proteasome Inhibition
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Bianchi, Giada; Chauhan, Dharminder; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Oliva, Laura; Pengo, Niccolo; Orsi, Andrea; Fontana, Francesca; Pasqualetto, Elena; Sitia, Roberto; Cenci, Simone] Ist Sci San Raffaele, DiBiT, Dept Biol & Technol, I-20132 Milan, Italy.
[Cascio, Paolo; Cerruti, Fulvia] Univ Turin, Dept Vet Morphophysiol, Turin, Italy.
[Mezghrani, Alexandre] CNRS, Inst Genet Humaine, Montpellier, France.
[Calbi, Valeria] Ist Sci San Raffaele, Hematol & BMT Unit, I-20132 Milan, Italy.
[Palladini, Giovanni] Univ Pavia, Dept Biochem, I-27100 Pavia, Italy.
[Palladini, Giovanni] Univ Pavia, Ctr Amyloidosis, Fdn IRCCS Policlin San Matteo, I-27100 Pavia, Italy.
[Giuliani, Nicola] Univ Parma, Hematol Unit, I-43100 Parma, Italy.
[Giuliani, Nicola] Univ Parma, BMT, I-43100 Parma, Italy.
RI Palladini, Giovanni/G-1763-2010
OI Palladini, Giovanni/0000-0001-5994-5138
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 98
EP 98
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700248
ER
PT J
AU Santo, L
Vallet, S
Hideshima, T
Cirstea, D
Pozzi, S
Vaghela, N
Ikeda, H
Okawa, Y
Gorgun, G
Perrone, G
Calabrese, E
Squires, MS
Ladetto, M
Munshi, NC
Boccadoro, M
Anderson, KC
Raje, N
AF Santo, Loredana
Vallet, Sonia
Hideshima, Teru
Cirstea, Diana
Pozzi, Samantha
Vaghela, Nileshwari
Ikeda, Hiroshi
Okawa, Yutaka
Gorgun, Gullu
Perrone, Giulia
Calabrese, Elisabetta
Squires, Matthew S.
Ladetto, Marco
Munshi, Nikhil C.
Boccadoro, Mario
Anderson, Kenneth C.
Raje, Noopur
TI AT7519, a Novel Small Molecule Multi-Cyclin Dependent Kinase Inhibitor,
Induces Apoptosis in Multiple Myeloma VIA GSK3 beta
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Santo, Loredana; Hideshima, Teru; Cirstea, Diana; Pozzi, Samantha; Ikeda, Hiroshi; Okawa, Yutaka; Gorgun, Gullu; Perrone, Giulia; Calabrese, Elisabetta; Munshi, Nikhil C.; Anderson, Kenneth C.; Raje, Noopur] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Vallet, Sonia; Vaghela, Nileshwari] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Squires, Matthew S.] Astex Therapeut Ltd, Cambridge, England.
[Ladetto, Marco; Boccadoro, Mario] Univ Turin, Div Hematol, Turin, Italy.
RI Pozzi, Samantha/A-7617-2012
OI Pozzi, Samantha/0000-0001-7917-1774
NR 0
TC 2
Z9 2
U1 1
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 NOV 16
PY 2008
VL 112
IS 11
BP 99
EP 100
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700252
ER
PT J
AU Rickles, RJ
Pierce, L
Giordano, T
Avery, W
Farwell, M
Crowe, D
Tam, WF
Chen, M
Kansra, V
McMillin, DW
Anderson, KC
Mitsiades, C
Lee, MS
AF Rickles, Richard J.
Pierce, Laura
Giordano, Thomas
Avery, William
Farwell, Melissa
Crowe, David
Tam, Winnie F.
Chen, Mei
Kansra, Vikram
McMillin, Douglas W.
Anderson, Kenneth C.
Mitsiades, Constantine
Lee, Margaret S.
TI Preclinical Evaluation of CRx-501, a Potent Selective A2A Agonist as a
Novel Drug Candidate for the Treatment of Multiple Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Rickles, Richard J.; Pierce, Laura; Giordano, Thomas; Avery, William; Farwell, Melissa; Crowe, David; Tam, Winnie F.; Chen, Mei; Kansra, Vikram; Lee, Margaret S.] CombinatoRx Inc, Cambridge, MA USA.
[McMillin, Douglas W.; Anderson, Kenneth C.; Mitsiades, Constantine] Harvard Univ, Sch Med, Dana Farber Canc Inst,Dept Med, Jerome Lipper Multiple Myeloma Ctr,Dept Med Oncol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 100
EP 100
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700253
ER
PT J
AU Zhao, BQ
Chauhan, AK
Patten, IS
Dockal, M
Scheiflinger, F
Wagner, DD
AF Zhao, Bing-Qiao
Chauhan, Anil Kumar
Patten, Ian S.
Dockal, Michael
Scheiflinger, Friedrich
Wagner, Denisa D.
TI VWF-Cleaving Protease ADAMTS13 Reduces Brain Injury Following Ischemic
Stroke in Mice: Essential Role for VWF in Stroke
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Zhao, Bing-Qiao; Chauhan, Anil Kumar; Patten, Ian S.; Wagner, Denisa D.] Harvard Univ, Sch Med, Dept Pathol, Immune Dis Inst, Boston, MA 02115 USA.
[Dockal, Michael] Baxter Biosci, Prot Engn, Orth, Austria.
[Scheiflinger, Friedrich] Baxter Innovat GmbH, Discovery Res, Vienna, Austria.
NR 0
TC 0
Z9 0
U1 3
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 NOV 16
PY 2008
VL 112
IS 11
BP 102
EP 102
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700260
ER
PT J
AU O'Connor, OA
Pro, B
Pinter-Brown, L
Popplewell, L
Barlett, N
Shustov, A
Lechowicz, MJ
Savage, KJ
Coiffier, B
Jacobsen, E
Zinzani, PL
Goy, A
Zain, J
Wilroy, S
Patterson, M
Boyd, A
Saunders, ME
Cagnoni, P
Horwitz, SM
AF O'Connor, Owen A.
Pro, Barbara
Pinter-Brown, Lauren
Popplewell, Leslie
Barlett, Nancy
Shustov, Andrei
Lechowicz, Mary Jo
Savage, Kerry J.
Coiffier, Bertrand
Jacobsen, Eric
Zinzani, Pier Luigi
Goy, Andre
Zain, Jasmine
Wilroy, Shannon
Patterson, Molly
Boyd, Adam
Saunders, Michael E.
Cagnoni, Pablo
Horwitz, Steven M.
TI PROPEL: A Multi-Center Phase 2 Open-Label Study of Pralatrexate (PDX)
with Vitamin B-12 and Folic Acid Supplementation in Patients with
Replapsed or Refractory Peripheral T-Cell Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology/ASH/ASCO Joint
Symposium
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol, Sanofi Aventis U.S.
C1 [O'Connor, Owen A.; Zain, Jasmine; Patterson, Molly] CUMC, New York, NY USA.
[Pro, Barbara] Univ Texas MD Anderson Canc Ctr, Dept Lymphoma Myeloma, Houston, TX 77030 USA.
[Pinter-Brown, Lauren] Univ Calif Los Angeles, Dept Internal Med, Div Oncol, Los Angeles, CA USA.
[Popplewell, Leslie] City Hope Natl Med Ctr, Duarte, CA USA.
[Barlett, Nancy] Washington Univ Med, Dept Internal Med, Div Oncol, St Louis, MO USA.
[Shustov, Andrei] Univ Washington, Seattle, WA USA.
[Lechowicz, Mary Jo] Emory Univ, Atlanta, GA 30322 USA.
[Savage, Kerry J.] British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada.
[Coiffier, Bertrand] Ctr Hosp Lyon Sud, F-69310 Pierre Benite, France.
[Jacobsen, Eric] Dana Farber, Boston, MA USA.
[Zinzani, Pier Luigi] Univ Bologna, Dept Hematol Oncol, Bologna, Italy.
[Goy, Andre] HUMC, Ctr Canc, Hackensack, NJ USA.
[Wilroy, Shannon; Boyd, Adam; Saunders, Michael E.; Cagnoni, Pablo] Allos Therapeut Inc, Westminster, CO USA.
[Horwitz, Steven M.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
RI Zinzani, Pier Luigi/J-9182-2016
OI Zinzani, Pier Luigi/0000-0002-2112-2651
NR 0
TC 2
Z9 2
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 103
EP 103
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700262
ER
PT J
AU Leonard, JP
LaCasce, A
Smith, MR
Noy, A
Yap, JT
Van den Abbeele, AD
Yu, JQ
Chen-Kiang, S
Ely, SA
Vallabhajosula, S
Chirieac, LR
Larson, SM
Shapiro, GI
Schoder, H
AF Leonard, John P.
LaCasce, Ann
Smith, Mitchell R.
Noy, Ariela
Yap, Jeffrey T.
Van den Abbeele, Annick D.
Yu, Jian Q.
Chen-Kiang, Selina
Ely, Scott A.
Vallabhajosula, Shankar
Chirieac, Lucian R.
Larson, Steven M.
Shapiro, Geoffrey I.
Schoder, Heiko
TI Cdk4/6 Inhibitor PD 0332991 Demonstrates Cell Cycle Inhibition Via
FLT-PET Imaging and Tissue Analysis in Patients with Recurrent Mantle
Cell Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Leonard, John P.; Chen-Kiang, Selina; Ely, Scott A.] Weill Cornell Med Coll, Div Hem Onc, New York, NY USA.
[LaCasce, Ann; Yap, Jeffrey T.; Van den Abbeele, Annick D.; Chirieac, Lucian R.; Shapiro, Geoffrey I.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Smith, Mitchell R.; Yu, Jian Q.] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[Noy, Ariela; Larson, Steven M.; Schoder, Heiko] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Vallabhajosula, Shankar] Weill Cornell Med Ctr, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 104
EP 104
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700265
ER
PT J
AU Rhodes, KE
Gekas, C
Gereige, L
Helgadottir, H
Ferrari, R
Kurdistani, S
Montecino-Rodriguez, E
Basel-Duby, R
Olson, E
Orkin, SH
Pellegrini, M
Mikkola, H
AF Rhodes, Katrin E.
Gekas, Christos
Gereige, Laurraine
Helgadottir, Hildur
Ferrari, Roberto
Kurdistani, Siavash
Montecino-Rodriguez, Encarnacion
Basel-Duby, Rhonda
Olson, Eric
Orkin, Stuart H.
Pellegrini, Matteo
Mikkola, Hanna
TI Mef2C Is a Lineage-Restricted Target Gene of Scl/Tal1 and Regulates
Megakaryopoiesis and B-Cell Homeostasis
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Mikkola, Hanna] Univ Calif Los Angeles, ICSBM, MCDB, Los Angeles, CA USA.
[Helgadottir, Hildur; Orkin, Stuart H.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Basel-Duby, Rhonda; Olson, Eric] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 109
EP 109
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700279
ER
PT J
AU Gavathiotis, E
Suzuki, M
Davis, ML
Pitter, K
Bird, GH
Katz, SG
Tu, HC
Kim, H
Cheng, E
Tjandra, N
Walensky, LD
AF Gavathiotis, Evripidis
Suzuki, Motoshi
Davis, Marguerite L.
Pitter, Kenneth
Bird, Gregory H.
Katz, Samuel G.
Tu, Ho-Chou
Kim, Hyungjin
Cheng, Emily
Tjandra, Nico
Walensky, Loren D.
TI Structural Analysis of a BAX-BIM SAHB Complex Reveals a Novel BH3
Interaction Site on BAX for Therapeutic Activation of Apoptosis
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Gavathiotis, Evripidis; Davis, Marguerite L.; Pitter, Kenneth; Bird, Gregory H.; Katz, Samuel G.; Walensky, Loren D.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Childrens Hosp Boston, Boston, MA 02115 USA.
[Suzuki, Motoshi; Tjandra, Nico] NHLBI, Lab Mol Biophys, Bethesda, MD 20892 USA.
[Tu, Ho-Chou; Kim, Hyungjin; Cheng, Emily] Washington Univ, St Louis Sch Med, Div Mol Oncol, St Louis, MO USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 117
EP 117
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700301
ER
PT J
AU Bolli, N
Payne, E
Grabher, C
Johnston, A
Kanki, J
Look, AT
AF Bolli, Niccolo
Payne, Elspeth
Grabher, Clemens
Johnston, Adam
Kanki, John
Look, A. Thomas
TI Human Nucleophosmin (NPM1) Perturbs Myeloid Development in Zebrafish in
Vivo
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Bolli, Niccolo; Payne, Elspeth; Grabher, Clemens; Johnston, Adam; Kanki, John; Look, A. Thomas] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 120
EP 120
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700309
ER
PT J
AU Kuter, DJ
Bussel, JB
Newland, A
de Wolf, JTM
Guthrie, T
Wasser, J
Gehl, L
Nie, K
Berger, D
AF Kuter, Davrt J.
Bussel, James B.
Newland, Adrian
de Wolf, Joost T. M.
Guthrie, Troy
Wasser, Jeffrey
Gehl, Lara
Nie, Kun
Berger, Dietmar
TI Long-Term Treatment with Romiplostim in Patients with Chronic Immune
Thrombocytopenic Purpura (ITP): 3-Year Update from An Open-Label
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology/ASH/ASCO Joint
Symposium
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol (ASH), Sanofi Aventis U.S.
C1 [Kuter, Davrt J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Bussel, James B.] New York Presbyterian Hosp, Dept Pediat & med, Div Hematol, New York, NY USA.
[Newland, Adrian] Royal London Hosp, Dept Haematol, London E1 1BB, England.
[de Wolf, Joost T. M.] Univ Groningen, Univ Med Ctr Groningen, NL-9713 AV Groningen, Netherlands.
[Guthrie, Troy] Univ Florida, Baptist Canc Inst, Jacksonville, FL USA.
[Wasser, Jeffrey] DeQuttro Community Canc Ctr, Manchester, CT USA.
[Gehl, Lara; Nie, Kun; Berger, Dietmar] Amgen Inc, Thousand Oaks, CA 91320 USA.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 154
EP 154
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700403
ER
PT J
AU Parmar, K
Kim, JM
Shimamura, A
Stuckert, A
DeLoach, MK
Zhu, K
Mauch, PM
Kutok, J
Aster, J
Akashi, K
Gilliland, G
D'Andrea, AD
AF Parmar, Kalindi
Kim, Jung Min
Shimamura, Akiko
Stuckert, Anna
DeLoach, Mary K.
Zhu, Kaya
Mauch, Peter M.
Kutok, Jeffery
Aster, Jon
Akashi, Koichi
Gilliland, Gary
D'Andrea, Alan D.
TI Hematopoietic Stem Cell Defects in Novel Fanconi Anemia Mouse Models
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Parmar, Kalindi; Kim, Jung Min; Stuckert, Anna; DeLoach, Mary K.; Zhu, Kaya; Mauch, Peter M.; Akashi, Koichi; D'Andrea, Alan D.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Shimamura, Akiko] Univ Washington, Seattle, WA 98195 USA.
[Kutok, Jeffery; Aster, Jon] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Gilliland, Gary] Harvard Univ, Sch Med, Howard Hughes Med Inst, Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 168
EP 168
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700441
ER
PT J
AU Baccarani, M
Rosti, G
Saglio, G
Cortes, J
Stone, R
Niederwieser, DW
Bleickardt, E
Sinha, R
Simonsson, B
AF Baccarani, Michele
Rosti, Gianantonio
Saglio, Giuseppe
Cortes, Jorge
Stone, Richard
Niederwieser, Dietger W.
Bleickardt, Eric
Sinha, Ritwik
Simonsson, Bengt
TI Dasatinib Time to and Durability of Major and Complete Cytogenetic
Response (MCyR and CCyR) in Patients with Chronic Myeloid Leukemia in
Chronic Phase (CML-CP)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Baccarani, Michele; Rosti, Gianantonio] Ist Ematol, Bologna, Italy.
[Saglio, Giuseppe] Univ Turin, Dept Clin & Biol Sci, Turin, Italy.
[Cortes, Jorge] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Stone, Richard] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Niederwieser, Dietger W.] Univ Leipzig, Hamatol Onkol Abt, Leipzig, Germany.
[Bleickardt, Eric; Sinha, Ritwik] Bristol Myers Squibb Co, Wallingford, CT 06492 USA.
[Simonsson, Bengt] Univ Hosp, Dept Hematol, Uppsala, Sweden.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 172
EP 172
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700451
ER
PT J
AU Ofran, Y
Brusic, V
Kim, HT
Soiffer, RJ
Antin, JH
Ritz, J
AF Ofran, Yishay
Brusic, Vladimir
Kim, H. T.
Soiffer, Robert J.
Antin, J. H.
Ritz, Jerome
TI Diverse Patterns of T Cell Reactivity Directed against Multiple Y
Chromosome-Derived, HLA a*0201 Restricted, Peptides in Patients with
chronic Gvhd
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Brusic, Vladimir] Dana Farber Canc Inst, Canc Vaccine Ctr, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 177
EP 177
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700465
ER
PT J
AU Neuwirth, AK
Campagna, DR
Fleming, MD
Bottomley, SS
Neufeld, EJ
AF Neuwirth, Anke K.
Campagna, Dean R.
Fleming, Mark D.
Bottomley, Sylvia S.
Neufeld, Ellis J.
TI Systematic Analysis of Known Candidate Genes in 58 Probands with
Previously Uncharacterized Congenital Sideroblastic Anemia: Evidence for
Genetic Heterogeneity and Identification of Novel Mutations in ALAS2 and
PUS1
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Fleming, Mark D.; Neufeld, Ellis J.] Harvard Univ, Childrens Hosp, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Bottomley, Sylvia S.] Univ Oklahoma, Hlth Sci Ctr, Hematol Oncol Sect, Oklahoma City, OK USA.
RI Neufeld, Ellis/F-9331-2011
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 184
EP 184
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700485
ER
PT J
AU Sankaran, VG
Menne, TF
Akie, TE
Lettre, G
Hirschhorn, JN
Cantor, AB
Orkin, SH
AF Sankaran, Vijay G.
Menne, Tobias F.
Akie, Thomas E.
Lettre, Guillaume
Hirschhorn, Joel N.
Cantor, Alan B.
Orkin, Stuart H.
TI Human Fetal Hemoglobin Expression Is Regulated by the Developmental
Stage-Specific Repressor BCL11A
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Sankaran, Vijay G.; Menne, Tobias F.; Akie, Thomas E.; Lettre, Guillaume; Hirschhorn, Joel N.; Cantor, Alan B.] Childrens Hosp, Boston, MA 02115 USA.
[Orkin, Stuart H.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 185
EP 186
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700488
ER
PT J
AU Chapman, MA
Brunet, JP
Baker, A
Keats, J
Ahmann, G
Schinzel, AC
Moore, A
Shanmugam, V
Perkins, LM
Auclair, D
Hahn, WC
Bergsagel, PL
Fonseca, R
Carpten, J
Trent, J
Golub, TR
AF Chapman, Michael A.
Brunet, Jean-Philippe
Baker, Angela
Keats, Jonathan
Ahmann, Gregory
Schinzel, Anna C.
Moore, Anna
Shanmugam, Vijayalakshmi
Perkins, Louise M.
Auclair, Daniel
Hahn, William C.
Bergsagel, P. Leif
Fonseca, Rafael
Carpten, John
Trent, Jeffrey
Golub, Todd R.
TI Interim Analyses of the MMRC Reference Collection Identifies Recurrent
Genomic-Level Events in Multiple Myeloma and Demonstrates That
CDKN2C/p18 Deletion Is the Pre-Eminent Copy Number Alteration in Poor
Prognosis Disease
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Chapman, Michael A.; Brunet, Jean-Philippe] Broad Inst, Cambridge, MA USA.
[Baker, Angela; Moore, Anna; Shanmugam, Vijayalakshmi; Carpten, John] Translat Genom Res Inst, Integrated Canc Genom Div, Phoenix, AZ USA.
[Keats, Jonathan; Ahmann, Gregory; Bergsagel, P. Leif; Fonseca, Rafael] Mayo Clin Arizona, Scottsdale, AZ USA.
[Schinzel, Anna C.; Hahn, William C.; Golub, Todd R.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Perkins, Louise M.; Auclair, Daniel] Multiple Myeloma Res Fdn, Norwalk, CT USA.
[Trent, Jeffrey] Translat Genom Res Inst, Genet Basis Human Dis Div, Phoenix, AZ USA.
RI Keats, Jonathan/B-2047-2009
NR 0
TC 0
Z9 0
U1 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 188
EP 189
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700498
ER
PT J
AU Munshi, NC
Li, C
Minvielle, S
Amin, SB
Moreau, P
Magrangeas, F
Anderson, KC
Avet-Loiseau, H
AF Munshi, Nikhil C.
Li, Cheng
Minvielle, Stephane
Amin, Samir B.
Moreau, Philippe
Magrangeas, Florence
Anderson, Kenneth C.
Avet-Loiseau, Herve
TI Alternate Splicing Is a Frequent Event and Impacts Clinical Outcome in
Myeloma: A High-Density Exon Array Analysis of Uniformly Treated
Newly-Diagnosed Myeloma Patients
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Munshi, Nikhil C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston VA Canc Healthcare Syst, Boston, MA 02115 USA.
[Li, Cheng] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Li, Cheng] Harvard Univ, Sch Publ Hlth, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Minvielle, Stephane; Moreau, Philippe; Magrangeas, Florence; Avet-Loiseau, Herve] Hop Nantes, Dept Hematol, Nantes, France.
[Amin, Samir B.; Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Dis Ctr, Boston, MA 02115 USA.
RI Magrangeas, Florence/L-3080-2015; Minvielle, Stephane/K-8251-2015;
richard, chrystelle/K-8595-2015
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 189
EP 189
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700499
ER
PT J
AU Payne, E
Bolli, N
Grabher, C
Rhodes, J
Kanki, J
Galinsky, I
Stone, R
Cotter, FE
Look, AT
AF Payne, Elspeth
Bolli, Niccolo
Grabher, Clemens
Rhodes, Jennifer
Kanki, John
Galinsky, Ilene
Stone, Richard
Cotter, Finbar E.
Look, A. Thomas
TI The Role of RNA Helicase Dead Box 18 in Zebrafish Hematopoiesis and
Human MDS
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Payne, Elspeth] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Cotter, Finbar E.] Barts & London Queen Marys Sch Med & Dent, Ctr Haematol, London, England.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 189
EP 190
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700501
ER
PT J
AU Mercher, T
Raffel, GD
Moore, SA
Cornejo, MG
Baudry-Bluteau, D
Cagnard, N
Jesneck, J
Pikman, Y
Cullen, DE
Williams, I
Akashi, K
Shigematsu, H
Bourquin, JP
Giovannini, M
Vainchenker, W
Levine, RL
Lee, BH
Bernard, O
Gilliland, DG
AF Mercher, Thomas
Raffel, Glen D.
Moore, Sandra A.
Cornejo, Melanie G.
Baudry-Bluteau, Dominique
Cagnard, Nicolas
Jesneck, Jonathan
Pikman, Yana
Cullen, Dana E.
Williams, Ifor
Akashi, Koichi
Shigematsu, Hirokazu
Bourquin, Jean-Pierre
Giovannini, Marco
Vainchenker, William
Levine, Ross L.
Lee, Benjamin H.
Bernard, Olivier
Gilliland, D. Gary
TI OTT-MAL Activates the Notch Signaling Transcription Factor RBPJ and
Cooperates with Mutant MPL to Induce Acute Megakaryoblastic Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Cullen, Dana E.] Brigham & Womens Hosp, Dept Med, Div Hematol, Boston, MA 02115 USA.
[Mercher, Thomas; Cagnard, Nicolas] Univ Paris 05, INSERM, EMI0210, Paris, France.
[Raffel, Glen D.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Cornejo, Melanie G.; Cullen, Dana E.] Harvard Univ, Sch Med, Boston, MA USA.
[Baudry-Bluteau, Dominique; Vainchenker, William] INSERM, U790, Villejuif, France.
[Jesneck, Jonathan; Cullen, Dana E.; Akashi, Koichi; Shigematsu, Hirokazu] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Williams, Ifor] Emory Univ, Atlanta, GA 30322 USA.
[Bourquin, Jean-Pierre] Univ Zurich, Zurich, Switzerland.
[Giovannini, Marco] INSERM, U434, Paris, France.
[Levine, Ross L.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Bernard, Olivier] Hop Necker Enfants Malad, Hematol Lab, Paris, France.
RI Mercher, Thomas/J-2446-2014
OI Mercher, Thomas/0000-0003-1552-087X
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 192
EP 192
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700509
ER
PT J
AU Tian, M
Campagna, DR
Langer, N
Choe, SK
Paw, BH
Justice, MJ
Fleming, MD
AF Tian, Meng
Campagna, Dean R.
Langer, Nathaniel
Choe, Seong-Kyu
Paw, Barry H.
Justice, Monica J.
Fleming, Mark D.
TI Rsp1 Is Indispensable for mRNA Stability during Erythroid Terminal
Differentiation
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Campagna, Dean R.] Harvard Univ, Childrens Hosp, Sch Med, Boston, MA 02115 USA.
[Langer, Nathaniel; Choe, Seong-Kyu; Paw, Barry H.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Hematol, Boston, MA 02115 USA.
[Justice, Monica J.] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
[Fleming, Mark D.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Childrens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 200
EP 200
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700533
ER
PT J
AU Arica, M
Schrappe, M
Hunger, S
Carroll, WL
Conter, V
Di Lorenzo, P
Manabe, A
Saba, V
Baruchel, A
Vettenranta, K
Tsuchida, M
Benoit, Y
Pieters, R
Escherich, G
Silverman, LB
Pui, CH
Valsecchi, MG
AF Arica, Maurizio
Schrappe, Martin
Hunger, Stephen
Carroll, William L.
Conter, Valentino
Di Lorenzo, Paola
Manabe, Atsushi
Saba, Vaskar
Baruchel, Andre
Vettenranta, Kim
Tsuchida, Masahiro
Benoit, Yves
Pieters, Rob
Escherich, Gabriele
Silverman, Lewis B.
Pui, Ching-Hon
Valsecchi, Maria Grazia
TI Clinical Outcome of 640 Children with Newly Diagnosed Philadelphia
Chromosome-Positive Acute Lymphoblastic Leukemia Treated Between 1995
and 2005
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology/ASH/ASCO Joint
Symposium
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol, SanofiAventis U.S.
C1 [Arica, Maurizio] Azienda Osped Univ Meyer, Florence, Italy.
[Schrappe, Martin] Univ Med Ctr, Kiel, Germany.
[Hunger, Stephen] Univ Colorado, Coll Med, Pediat Heme Onc BMT, Aurora, CO USA.
[Carroll, William L.] NYU, Sch Med, New York, NY USA.
[Conter, Valentino] Univ Milano Bicocca, Osped S Gerardo, Dept Pediat, Monza, Italy.
[Di Lorenzo, Paola] Univ Milano Bicocca, Dept Clin & Prevent Med, Monza, Italy.
[Manabe, Atsushi] Tokyo Childrens Canc Study Grp, Tokyo, Japan.
[Baruchel, Andre] Hop St Louis, Dept Pediat Hematol, Paris, France.
[Vettenranta, Kim] Univ Helsinki, Childrens Hosp, Helsinki, Finland.
[Tsuchida, Masahiro] Ibaraki Childrens Hosp, Dept Pediat, Mito, Ibaraki, Japan.
[Pieters, Rob] Erasmus MC, Dept Pediat Hem Onc, Rotterdam, Netherlands.
[Escherich, Gabriele] Univ Klinikum Hamburg Eppendorf, Hamburg, Germany.
[Pui, Ching-Hon] St Jude Childrens Rsch Hosp, Dept Onc, Memphis, TN USA.
[Silverman, Lewis B.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Valsecchi, Maria Grazia] Univ Milano Bicocca, Dept Clin & Prevent Med, Int Childhood Acute Lymphoblast Leukemia Study Gr, Monza, Italy.
RI Schrappe, Martin/A-8109-2010
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 213
EP 214
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700569
ER
PT J
AU Meems, H
Meijer, AB
Cullinan, D
Mertens, K
Gilbert, GE
AF Meems, Henriet
Meijer, Alexander B.
Cullinan, Dave
Mertens, Koen
Gilbert, Gary E.
TI Factor VIII C1 Domain Residues 2092-2093 Participate in Membrane Binding
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Meems, Henriet; Meijer, Alexander B.; Mertens, Koen] Sanquin Blood Supply Fdn, Dept Plasma Proteins, Amsterdam, Netherlands.
[Cullinan, Dave; Gilbert, Gary E.] Harvard Univ, Sch Med, VA Boston Healthcare Syst, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 220
EP 220
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700588
ER
PT J
AU Xu, HM
Geiger, H
Szezur, K
Deira, D
Zheng, Y
Settleman, J
Srour, E
Williams, DA
Flippi, MD
AF Xu, Haiming
Geiger, Hartmut
Szezur, Kathleen
Deira, Deidra
Zheng, Yi
Settleman, Jeffrey
Srour, Edward
Williams, David A.
Flippi, Marie-Dominique
TI Absence of the Rho GTPase Activating Protein p190-B Enhances Long Term
Hematopoietic Stem Cell Engraftment
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Xu, Haiming; Geiger, Hartmut; Szezur, Kathleen; Deira, Deidra; Flippi, Marie-Dominique] Cincinnati Childrens Res Fdn, Cincinnati, OH USA.
[Settleman, Jeffrey] Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
[Settleman, Jeffrey; Williams, David A.] Harvard Univ, Sch Med, Boston, MA USA.
[Srour, Edward] Indiana Univ, Sch Med, Indianapolis, IN USA.
[Williams, David A.] Childrens Hosp, Dept Pediat, Div Hematol Oncol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 229
EP 229
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700615
ER
PT J
AU Braggio, E
Keats, JJ
Lelcu, X
Remstein, E
Van Wier, S
Jimenez-Zepeda, VH
Valdez, R
Schop, R
Price-Troska, T
Sacco, A
Azab, F
Greipp, PR
Gertz, M
Rajkumar, SV
Chesi, M
Stewart, K
Dogan, A
Bergsagel, PL
Ghobrial, I
Fonseca, R
AF Braggio, Esteban
Keats, J. Jonathan
Lelcu, Xavier
Remstein, Ellen
Van Wier, Scott
Jimenez-Zepeda, Victor H.
Valdez, Riccardo
Schop, Roelandt
Price-Troska, Tammy
Sacco, Antonio
Azab, Feda
Greipp, Philip R.
Gertz, Moric
Rajkumar, S. Vincent
Chesi, Marta
Stewart, Keith
Dogan, Ahmet
Bergsagel, Peter Leif
Ghobrial, Irene
Fonseca, Rafael
TI TRAF3 and TNFAIP3, Two Negative Regulators of NF-Kb Signaling Pathways,
Are Mutated in Waldenstrom's Macroglobulinemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Braggio, Esteban; Keats, J. Jonathan; Jimenez-Zepeda, Victor H.; Price-Troska, Tammy; Chesi, Marta; Stewart, Keith; Bergsagel, Peter Leif] Mayo Clin, Scottsdale, AZ USA.
[Lelcu, Xavier; Sacco, Antonio; Azab, Feda; Ghobrial, Irene] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Remstein, Ellen] Mayo Clin, Lab Med & Pathol, Rochester, MN USA.
[Van Wier, Scott; Valdez, Riccardo; Schop, Roelandt] Mayo Clin Arizona, Scottsdale, AZ USA.
[Rajkumar, S. Vincent] Mayo Clin, Coll Med, Rochester, MN USA.
[Fonseca, Rafael] Mayo Clin Scottsdale, Scottsdale, AZ USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 231
EP 231
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700620
ER
PT J
AU Braunstein, MJ
Campagne, F
Mukherjee, P
Carrasco, DR
Sukhdeo, K
Protopopov, A
Anderson, KC
Batuman, O
AF Braunstein, Marc J.
Campagne, Fabien
Mukherjee, Piali
Carrasco, Daniel Ruben
Sukhdeo, Kumar
Protopopov, Alexei
Anderson, Kenneth C.
Batuman, Olcay
TI Genome-Wide Profiling of Endothelial Progenitor Cells in Multiple
Mycloma: Disease-Relevant Pathways and Overlaps with Common Cancer
Biomarkers
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Braunstein, Marc J.; Batuman, Olcay] Suny Downstate Med Ctr, Brooklyn, NY 11203 USA.
[Campagne, Fabien; Mukherjee, Piali] Cornell Univ, Inst Computat Biomed, Weill Med Coll, New York, NY 10021 USA.
[Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
RI Campagne, Fabien/F-5158-2010
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 233
EP 234
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700627
ER
PT J
AU Leleu, X
Hong, FX
Roccaro, AM
Jia, X
Sacco, A
Moreau, AS
Ngo, H
Azab, AK
Azab, F
Melhem, M
Anderson, KC
Ghobrial, IM
AF Leleu, Xaiaer
Hong, Fangxin
Roccaro, Aldo M.
Jia, Xiaoying
Sacco, Antonio
Moreau, Anne-Sophie
Ngo, Hai
Azab, Abdel Kareem
Azab, Feda
Melhem, Molly
Anderson, Kenneth C.
Ghobrial, Irene M.
TI Gene Transcriptional Activity Analysis in the 6q Region in Waldenstrom
Macroglobulinemia (WM) Using ChIP-on-Chip Technology
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Leleu, Xaiaer; Moreau, Anne-Sophie] CHRU Lille, Hop Huriez, Serv Malad Sang, Lille, France.
[Hong, Fangxin; Roccaro, Aldo M.; Jia, Xiaoying; Sacco, Antonio; Ngo, Hai; Azab, Abdel Kareem; Azab, Feda; Melhem, Molly; Anderson, Kenneth C.; Ghobrial, Irene M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 234
EP 234
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700629
ER
PT J
AU Loiseau, HA
Li, C
Magrangeas, F
Guerin, C
Gouraud, W
Harousseau, JL
Attal, M
Marit, G
Mathiot, C
Facon, T
Moreau, P
Anderson, KC
Campion, L
Munshi, NC
Minvielle, S
AF Loiseau, Herve Avet
Li, Cheng
Magrangeas, Florence
Guerin, Catherine
Gouraud, Wilfried
Harousseau, Jean-Luc
Attal, Michel
Marit, Gerald
Mathiot, Claire
Facon, Thierry
Moreau, Philippe
Anderson, Kenneth C.
Campion, Loic
Munshi, Nikhil C.
Minvielle, Stephane
TI In Myeloma, the Prognostic Impact of Hyperdiploidy Is Mainly Related to
the Gain of Chromosome 5
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Loiseau, Herve Avet; Magrangeas, Florence; Guerin, Catherine; Gouraud, Wilfried; Harousseau, Jean-Luc; Moreau, Philippe; Minvielle, Stephane] Hop Nantes, Dept Hematol, Nantes, France.
[Li, Cheng] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Li, Cheng] Harvard Univ, Sch Publ Hlth, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Attal, Michel] Hop Purpan, Toulouse, France.
[Marit, Gerald] CHU Bordeaux, Bordeaux, France.
[Mathiot, Claire] Inst Curie, Dept Hematol, F-75231 Paris, France.
[Facon, Thierry] CHRU Lille, Serv HA Matol, Lille, France.
[Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Dis Ctr, Boston, MA 02115 USA.
[Campion, Loic] Ctr Rene Gauducheau, St Herblain, France.
[Munshi, Nikhil C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston VA Canc Healthcare Syst, Boston, MA 02115 USA.
RI FACON, THIERRY/M-9736-2014; Magrangeas, Florence/L-3080-2015; Minvielle,
Stephane/K-8251-2015; richard, chrystelle/K-8595-2015
OI FACON, THIERRY/0000-0001-7705-8460;
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 235
EP 235
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700633
ER
PT J
AU Roccaro, AM
Sacco, A
Chen, CZ
Leleu, X
Runnels, J
Azab, F
Azab, AK
Jia, XY
Ngo, HT
Melhem, MR
Burwick, N
Quang, P
Varticovski, L
Novina, CD
Rollins, BJ
Anderson, KC
Ghobrial, IM
AF Roccaro, Aldo M.
Sacco, Antonio
Chen, Changzhong
Leleu, Xavier
Runnels, Judith
Azab, Feda
Azab, Abdel Kareem
Jia, Xiaoying
Ngo, Hai T.
Melhem, Molly R.
Burwick, Nicholas
Quang, Phong
Varticovski, Lyuba
Novina, Carl D.
Rollins, Barrett J.
Anderson, Kenneth C.
Ghobrial, Irene M.
TI MicroRNA Signature in Waldenstrom Macroglobulinemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Roccaro, Aldo M.; Sacco, Antonio; Chen, Changzhong; Leleu, Xavier; Runnels, Judith; Azab, Feda; Azab, Abdel Kareem; Jia, Xiaoying; Ngo, Hai T.; Melhem, Molly R.; Burwick, Nicholas; Quang, Phong; Novina, Carl D.; Rollins, Barrett J.; Anderson, Kenneth C.; Ghobrial, Irene M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Varticovski, Lyuba] Natl Canc Ctr, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 235
EP 235
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700631
ER
PT J
AU Ngo, HT
Hatjiharissi, E
Leontovich, AA
Chug, W
Farag, M
Leleu, X
Jia, XY
Runnels, J
Roccaro, A
Azab, AK
Azab, F
Sacco, A
Burwick, N
Melhem, MR
Anderson, KC
Fonseca, R
Witzig, TE
Ghobrial, IM
AF Ngo, Hai T.
Hatjiharissi, Evdoxia
Leontovich, Alexey A.
Chug, Wee
Farag, Mena
Leleu, Xavier
Jia, Xiaoying
Runnels, Judith
Roccaro, Aldo
Azab, Abdel Kareem
Azab, Feda
Sacco, Antonio
Burwick, Nicholas
Melhem, Molly R.
Anderson, Kenneth C.
Fonseca, Rafael
Witzig, Thomas E.
Ghobrial, Irene M.
TI Proteomic Analysis of Multiple Myeloma Identifies Upregulation of CRIK
Protein, a Novel Protein Regulating Migration and Adhesion
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ngo, Hai T.; Hatjiharissi, Evdoxia; Farag, Mena; Leleu, Xavier; Jia, Xiaoying; Runnels, Judith; Roccaro, Aldo; Azab, Abdel Kareem; Azab, Feda; Sacco, Antonio; Burwick, Nicholas; Melhem, Molly R.; Anderson, Kenneth C.; Ghobrial, Irene M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Hatjiharissi, Evdoxia] Mayo Clin, Coll Med, Rochester, MN USA.
[Fonseca, Rafael] Mayo Clin, Coll Med, Scottsdale, AZ USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 239
EP 240
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700644
ER
PT J
AU Vallet, S
Mukherjee, S
Vaghela, N
Pozzi, S
Santo, L
Cirstea, D
Fulciniti, M
Rahemtullah, A
Attar, E
Guimaraes, AR
Xie, WL
Patel, C
Schoonmaker, J
Weller, E
Hideshima, T
Munshi, NC
Seehra, J
Scadden, DT
Anderson, KC
Raje, N
AF Vallet, Sonia
Mukherjee, Siddhartha
Vaghela, Nileshwari
Pozzi, Samantha
Santo, Loredana
Cirstea, Diana
Fulciniti, Mariateresa
Rahemtullah, Aliyah
Attar, Eyal
Guimaraes, Alexander R.
Xie, Wanling
Patel, Chirayu
Schoonmaker, Jesse
Weller, Edie
Hideshima, Teru
Munshi, Nilchil C.
Seehra, Jas
Scadden, David T.
Anderson, Kenneth C.
Raje, Noopur
TI Restoration of Bone Balance Via Activin a Inhibition Results in
Anti-Myeloma Activity
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Vallet, Sonia; Vaghela, Nileshwari] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Hematol & Oncol, Boston, MA USA.
[Mukherjee, Siddhartha; Patel, Chirayu; Hideshima, Teru; Munshi, Nilchil C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Regenerat Med, Boston, MA USA.
[Pozzi, Samantha; Santo, Loredana; Attar, Eyal; Guimaraes, Alexander R.; Scadden, David T.; Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Mveloma Dis Ctr, Boston, MA 02115 USA.
[Xie, Wanling] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol, Boston, MA USA.
[Schoonmaker, Jesse] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Mol Imaging Res, Boston, MA USA.
[Schoonmaker, Jesse] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Syst Biol, Boston, MA USA.
[Weller, Edie; Seehra, Jas] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Raje, Noopur] Acceleron Pharma Inc, Cambridge, MA USA.
RI Pozzi, Samantha/A-7617-2012
OI Pozzi, Samantha/0000-0001-7917-1774
NR 0
TC 2
Z9 2
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 240
EP 240
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700646
ER
PT J
AU Mani, M
Dutta, J
Zhang, Y
Carrasco, DE
Zhou, YM
Gatt, M
Baerlogie, B
Shaughnessy, JD
Anderson, KC
Carrasco, DR
AF Mani, Mala
Dutta, Jui
Zhang, Yunyu
Carrasco, Daniel E.
Zhou, Yiming
Gatt, Moshe
Baerlogie, Bart
Shaughnessy, John D., Jr.
Anderson, Kenneth C.
Carrasco, Daniel Ruben
TI The BCL9 Oncogene Promotes Tumor Progression by Conferring Enhanced
Proliferative, Metastatic and Angiogenic Properties to Myeloma Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Dis Ctr, Boston, MA 02115 USA.
[Zhou, Yiming; Baerlogie, Bart; Shaughnessy, John D., Jr.] Univ Arkansas Med Sci, Myeloma Inst Res & Therapy, Little Rock, AR 72205 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 241
EP 241
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700649
ER
PT J
AU Runnels, J
Carlson, A
Pitsillides, C
Spencer, J
Wu, J
Azab, AK
Roccaro, AM
Moreau, AS
Leleu, X
Kung, A
Rodig, SJ
Anderson, KC
Lin, CP
Ghobrial, IM
AF Runnels, Judith
Carlson, Alicia
Pitsillides, Costas
Spencer, Joel
Wu, Juwell
Azab, Abdel Kareem
Roccaro, Aldo M.
Moreau, Anne-Sophie
Leleu, Xavier
Kung, Andrew
Rodig, Scott J.
Anderson, Kenneth C.
Lin, Charles P.
Ghobrial, Irene M.
TI In Vivo Imaging Model of Multiple Myeloma and Its Cellular Interaction
with the Bone Marrow Microenvironment
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Runnels, Judith; Azab, Abdel Kareem; Roccaro, Aldo M.; Moreau, Anne-Sophie; Leleu, Xavier; Kung, Andrew; Anderson, Kenneth C.; Ghobrial, Irene M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Carlson, Alicia; Pitsillides, Costas; Spencer, Joel; Wu, Juwell; Lin, Charles P.] Massachusetts Gen Hosp, Adv Microscopy Program, Ctr Syst Biol, Boston, MA 02114 USA.
[Carlson, Alicia; Pitsillides, Costas; Spencer, Joel; Wu, Juwell; Lin, Charles P.] Massachusetts Gen Hosp, Adv Microscopy Program, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Rodig, Scott J.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
RI Spencer, Joel/A-4590-2013
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 241
EP 241
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700648
ER
PT J
AU Miguel, JFS
Schlag, R
Khuageva, NK
Dimopoulos, MA
Shpilberg, O
Kropff, MH
Spicka, I
Petrucci, MT
Palumbo, A
Samoilova, OS
Dmoszynska, A
Abdulkadyrov, KM
Schots, R
Jiang, B
Mateos, MV
Anderson, KC
Esseltine, DL
Liu, KV
Cakana, A
van de Velde, H
Richardson, P
AF Miguel, Jesus F. San
Schlag, Rudolf
Khuageva, Nuriet K.
Dimopoulos, Meletios A.
Shpilberg, Ofer
Kropff, Martin H.
Spicka, Ivan
Petrucci, Maria Teresa
Palumbo, Antonio
Samoilova, Olga S.
Dmoszynska, Anna
Abdulkadyrov, Kudrat M.
Schots, Rik
Jiang, Bin
Mateos, Maria-Victoria
Anderson, Kenneth C.
Esseltine, Dixie-Lee
Liu, Kevin
Cakana, Andrew
van de Velde, Helgi
Richardson, Paul
TI Updated Follow-up and Results of Subsequent Therapy in the Phase III
VISTA Trial: Bortezomib Plus Melphalan-Prednisone Versus
Melphalan-Prednisone in Newly Diagnosed Multiple Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Miguel, Jesus F. San] USAL, CSIC, IBMCC, CIC,Hosp Univ Salamanca, Salamanca, Spain.
[Schlag, Rudolf] Praxis Hematol & Oncol, Wurzburg, Germany.
[Khuageva, Nuriet K.] SP Botkin Moscow City Clin Hosp, Dept Hematol, Moscow, Russia.
[Dimopoulos, Meletios A.] Univ Athens, Sch Med, Dept Clin Therapeut, GR-11527 Athens, Greece.
[Shpilberg, Ofer] Rabin Med Ctr, Petah Tiqwa, Israel.
[Kropff, Martin H.] Univ Munster, Munster, Germany.
[Spicka, Ivan] Charles Univ Praha, Dept Int Med 1, Prague, Czech Republic.
[Petrucci, Maria Teresa] Univ Roma La Sapienza, Rome, Italy.
[Palumbo, Antonio] Univ Turin, Div Ematol, AOU San Giovanni Battista, Turin, Italy.
[Samoilova, Olga S.] Nizhnii Novgorod Reg Clin Hosp, Nizhnii Novgorod, Russia.
[Dmoszynska, Anna] Med Univ Lublin, Lublin, Poland.
[Abdulkadyrov, Kudrat M.] St Petersburg Clin Res Inst Hematol & Transfusiol, St Petersburg, Russia.
[Schots, Rik] Belgian Hematol Soc, Myeloma Study Grp, Brussels, Belgium.
[Jiang, Bin] Peking Univ, Peoples Hosp, Beijing, Peoples R China.
[Mateos, Maria-Victoria] Hosp Univ Salamanca, Salamanca, Spain.
[Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Dis Ctr, Boston, MA 02115 USA.
[Esseltine, Dixie-Lee] Takeda Oncol Co, Millennium Pharmaceut, Cambridge, MA USA.
[Liu, Kevin] Johnson & Johnson Pharmaceut Res & Dev, Raritan, NJ USA.
[Cakana, Andrew; van de Velde, Helgi] Johnson & Johnson Pharmaceut Res & Dev, Dept Clin R&D Oncol, Beerse, Belgium.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 242
EP 242
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700651
ER
PT J
AU Patsoukis, N
Lafuente, EM
Meraner, P
Li, LQ
Dombkowski, D
Rao, A
Boussiotis, V
AF Patsoukis, Nikolaos
Lafuente, Esther M.
Meraner, Paul
Li, Lequn
Dombkowski, David
Rao, Anjana
Boussiotis, Vassiliki
TI RIAM Regulate Spatio-Temporal Distribution of PLC-gamma 1 and Calcium
Mobilization during T Cell Activation
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Patsoukis, Nikolaos; Lafuente, Esther M.; Li, Lequn; Boussiotis, Vassiliki] Beth Israel Deaconess Med Ctr, Harvard Inst Med, Boston, MA 02215 USA.
[Meraner, Paul] Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA.
[Dombkowski, David] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Rao, Anjana] Brigham & Womens Hosp, Cambridge, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 251
EP 252
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700674
ER
PT J
AU Matsuoka, K
Cutler, C
Koreth, J
Antin, JH
Soiffer, RJ
Ritz, J
AF Matsuoka, Ken-ichi
Cutler, Corey
Koreth, John
Antin, Joseph H.
Soiffer, Robert J.
Ritz, Jerome
TI Increased Proliferation of FoxP3 Regulatory T Cells after Allogeneic
Hematopoietic Stem Cell Transplantation Is Counterbalanced by Increased
Susceptibility to Apoptosis
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Matsuoka, Ken-ichi; Cutler, Corey; Koreth, John; Antin, Joseph H.; Soiffer, Robert J.; Ritz, Jerome] Dana Farber Canc Inst, Div Hematol Malignancies, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 267
EP 268
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700721
ER
PT J
AU Lin, MI
Zon, LI
AF Lin, Michelle I.
Zon, Leonard I.
TI Genetic Analyses in Zebrafish Reveal That Angiopoietin-Like Proteins 1
and 2 Are Required for HSC Development during Embryogenesis
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Lin, Michelle I.] Harvard Univ, Childrens Hosp, Howard Hughes Med Inst, Sch Med, Boston, MA 02115 USA.
[Zon, Leonard I.] Childrens Hosp, Stem Cell Program, Boston, MA 02115 USA.
[Zon, Leonard I.] Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA.
[Zon, Leonard I.] Harvard Stem Cell Inst, Howard Hughes Med Inst, Dana Farber Canc Inst, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 271
EP 271
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700730
ER
PT J
AU Toro, JJ
Haile, DJ
Chao, JH
Jewell, PS
Lee, S
Freytes, CO
AF Toro, Juan J.
Haile, David J.
Chao, Ju-Hsien
Jewell, Pamela S.
Lee, Shuko
Freytes, Cesar O.
TI The Department of Veterans Affairs Nutritional Status Classification
Scheme Allows for Rapid Assessment of Nutritional Status Before
Autologous Peripheral Blood Stem Cell Transplantation and Identifies
Patients at High-Risk of Transplant-Related Complications
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Toro, Juan J.; Haile, David J.; Chao, Ju-Hsien; Jewell, Pamela S.; Lee, Shuko; Freytes, Cesar O.] Audie L Murphy Mem Vet Adm Med Ctr, San Antonio, TX 78284 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 274
EP 274
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700740
ER
PT J
AU Wang, QF
Dong, JF
Mattison, R
Prabhakar, S
Arimura, FE
Kaberlein, J
Wang, CZ
Wang, QB
Nobrega, M
Thirman, M
AF Wang, Qianfei
Dong, Jingfang
Mattison, Ryan
Prabhakar, Shyam
Arimura, Fabio Eiji
Kaberlein, Joseph
Wang, Chong-zhi
Wang, Qianben
Nobrega, Marcelo
Thirman, Michael
TI Autoregulation of MEIS1 through a Distal Enhancer in Acute Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Wang, Qianfei; Dong, Jingfang; Mattison, Ryan; Arimura, Fabio Eiji; Kaberlein, Joseph; Wang, Chong-zhi; Nobrega, Marcelo; Thirman, Michael] Univ Chicago, Chicago, IL 60637 USA.
[Prabhakar, Shyam] Genome Inst Singapore, Singapore, Singapore.
[Wang, Qianben] Harvard Univ, Sch Med, Boston, MA USA.
[Wang, Qianben] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 276
EP 277
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104700746
ER
PT J
AU Schriber, JR
Agovi, MA
Ballen, KK
Bacigalupo, A
Hale, GA
Gupta, V
Lazarus, HM
Litzow, MR
Marks, DI
Giller, RH
Maziarz, RT
Bornhauser, M
Isola, LM
Bredeson, C
Rizzo, JD
AF Schriber, Jeffrey R.
Agovi, Manza- A.
Ballen, Karen K.
Bacigalupo, Andrea
Hale, Gregory A.
Gupta, Vikas
Lazarus, Hillard M.
Litzow, Mark R.
Marks, David I.
Giller, Roger H.
Maziarz, Richard T.
Bornhauser, Martin
Isola, Luis M.
Bredeson, Christopher
Rizzo, J. Douglas
TI Second Unrelated Donor (URD) Transplant as a Rescue Strategy for 122
Patients with Primary Non Engraftment: Results from the CIBMTR
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Schriber, Jeffrey R.] Banner Good Samaritan Med Ctr, Phoenix, AZ USA.
[Agovi, Manza- A.; Rizzo, J. Douglas] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
[Ballen, Karen K.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Bacigalupo, Andrea] Osped San Martino Genova, Genoa, Italy.
[Hale, Gregory A.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
[Gupta, Vikas] Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
[Lazarus, Hillard M.] Univ Hosp Case Med Ctr, Cleveland, OH USA.
[Litzow, Mark R.] Mayo Clin, Rochester, MN USA.
[Marks, David I.] Bristol Royal Hosp Children, Bristol, Avon, England.
[Giller, Roger H.] Childrens Hosp, Aurora, CO USA.
[Maziarz, Richard T.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Bornhauser, Martin] Univ Hosp Dresden, Dresden, Germany.
[Isola, Luis M.] Mt Sinai Med Ctr, New York, NY 10029 USA.
[Bredeson, Christopher] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 295
EP 295
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701018
ER
PT J
AU Levy, O
Suter, EE
Kalish, LA
Gallington, LC
Teghanemt, A
Viriyakosol, S
Soiffer, RJ
Weiss, J
Scannon, P
Leung, HM
Priebe, G
Russell, J
Walker, P
Wessels, MR
Guinan, E
AF Levy, Ofer
Suter, Eugenie E.
Kalish, Leslie A.
Gallington, Leighanne C.
Teghanemt, Athmane
Viriyakosol, Suganya
Soiffer, Robert J.
Weiss, Jerrold
Scannon, Patrick
Leung, Hoi M.
Priebe, Gregory
Russell, Janice
Walker, Paul
Wessels, Michael R.
Guinan, Eva
TI Myeloablative Hematopoietic Stem Cell Transplantation (HSCT) Is
Accompanied by Endotoxemia, Activation of Endotoxin-Directed Innate
Immunity, and Deficiency of Endogenous Proteins That Limit
Endotoxin-Induced TNF Production
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Levy, Ofer; Suter, Eugenie E.; Gallington, Leighanne C.; Wessels, Michael R.] Childrens Hosp, Div Infect Dis, Boston, MA 02115 USA.
[Kalish, Leslie A.] Childrens Hosp, Clin Res Program, Boston, MA 02115 USA.
[Teghanemt, Athmane; Weiss, Jerrold] Univ Iowa, Dept Med, Iowa City, IA 52242 USA.
[Viriyakosol, Suganya] Univ Calif San Diego, Dept Med, San Diego, CA 92103 USA.
[Soiffer, Robert J.; Russell, Janice] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Scannon, Patrick; Leung, Hoi M.] XOMA US LLC, Berkeley, CA USA.
[Priebe, Gregory] Childrens Hosp, Div Crit Care Med, Boston, MA 02115 USA.
[Walker, Paul] Spectral Diagnost, Toronto, ON, Canada.
RI Gallington, Leighanne/G-9341-2011
OI Gallington, Leighanne/0000-0002-0383-7522
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 297
EP 298
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701024
ER
PT J
AU Juszczynski, P
Chen, L
Polo, JM
Ranuncolo, SM
Dalla-Favera, R
Melnick, A
Shipp, MA
AF Juszczynski, Przemyslaw
Chen, Linfeng
Polo, Jose M.
Ranuncolo, Stella M.
Dalla-Favera, Riccardo
Melnick, Ari
Shipp, Margaret A.
TI BCL6 Regulates Tonic BCR Signaling in Diffuse Large B-Cell Lymphomas by
Repressing the SYK Phosphatase, PTPROt
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Juszczynski, Przemyslaw; Chen, Linfeng; Shipp, Margaret A.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Polo, Jose M.; Ranuncolo, Stella M.; Melnick, Ari] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Dalla-Favera, Riccardo] Columbia Univ, Inst Canc Genet, Dept Pathol & Genet & Dev, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 298
EP 298
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701026
ER
PT J
AU Biernacki, MA
Zhang, G
Zhang, W
Brusic, V
Soiffer, RJ
Neuberg, D
Alyea, EP
Tai, YT
Munshi, NC
Ritz, J
Anderson, KC
Wu, CJ
AF Biernacki, Melinda A.
Zhang, Guanglan
Zhang, Wandi
Brusic, Vladimir
Soiffer, Robert J.
Neuberg, Donna
Alyea, Edwin P.
Tai, Yu-Tzu
Munshi, Nikhil C.
Ritz, Jerome
Anderson, Kenneth C.
Wu, Catherine J.
TI Novel Myeloma-Associated Antigens Revealed in the Context of Successful
Syngeneic Hematopoietic Stem Cell Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Biernacki, Melinda A.] Univ Connecticut, Sch Med, Farmington, CT USA.
[Zhang, Guanglan; Zhang, Wandi; Brusic, Vladimir] Canc Vaccine Ctr, Dana Farber Canc Inst, Boston, MA USA.
[Soiffer, Robert J.; Alyea, Edwin P.; Tai, Yu-Tzu; Munshi, Nikhil C.; Ritz, Jerome; Anderson, Kenneth C.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dana Farber Canc Inst,Dept Med Oncol, Boston, MA USA.
[Neuberg, Donna] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 302
EP 303
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701039
ER
PT J
AU Avigan, D
Rosenblatt, J
Vasir, B
Wu, Z
Bissonnette, A
Somaiya, P
MacNamara, C
Uhl, L
Avivi, I
Katz, T
Zarwan, C
Joyce, R
Levine, JD
Boussiotis, V
Tzachanis, D
Lowe, K
Dombagoda, D
Giallombardo, N
Mortellite, J
Conway, K
Fitzgerald, D
Richardson, P
Anderson, K
Munshi, NC
Tsumer, M
Bisharat, L
Rowe, J
Kufe, D
AF Avigan, David
Rosenblatt, Jacalyn
Vasir, Baldev
Wu, Zekui
Bissonnette, Adam
Somaiya, Poorvi
MacNamara, Claire
Uhl, Lynne
Avivi, Irit
Katz, Tami
Zarwan, Corrine
Joyce, Robin
Levine, James D.
Boussiotis, Vassiliki
Tzachanis, Dimitrios
Lowe, Karen
Dombagoda, Dilani
Giallombardo, Nancy
Mortellite, Jamie
Conway, Katharine
Fitzgerald, Donna
Richardson, Paul
Anderson, Kenneth
Munshi, Nikhil C.
Tsumer, Michal
Bisharat, Lina
Rowe, Jacob
Kufe, Donald
TI Fusion Cell Vaccination in Conjunction with Stem Cell Transplantation Is
Well Tolerated, Induces Anti-Tumor Immunity and Is Associated with
Responses in Patients with Multiple Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Avigan, David; Rosenblatt, Jacalyn; Somaiya, Poorvi; MacNamara, Claire; Uhl, Lynne; Zarwan, Corrine; Joyce, Robin; Levine, James D.; Boussiotis, Vassiliki; Tzachanis, Dimitrios; Lowe, Karen; Dombagoda, Dilani; Giallombardo, Nancy; Mortellite, Jamie; Conway, Katharine; Fitzgerald, Donna] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Vasir, Baldev; Wu, Zekui; Bissonnette, Adam; Richardson, Paul; Anderson, Kenneth; Munshi, Nikhil C.; Kufe, Donald] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Avivi, Irit; Katz, Tami; Tsumer, Michal; Bisharat, Lina; Rowe, Jacob] Rambam Med Ctr, IL-31096 Haifa, Israel.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 306
EP 307
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701050
ER
PT J
AU Ho, V
Dranoff, G
Kim, H
Vanneman, M
Pasek, M
Cutler, C
Koreth, J
Alyea, E
Antin, JH
Jerome, R
Soiffer, RJ
AF Ho, Vincent
Dranoff, Glenn
Kim, Haesook
Vanneman, Matthew
Pasek, Mildred
Cutler, Corey
Koreth, John
Alyea, Edwin
Antin, Joseph H.
Jerome, Ritz
Soiffer, Robert J.
TI GM-CSF Secreting Leukemia Cell Vaccination after Allogeneic Reduced
Intensity Hematopoietic Stem Cell Transplantation for Advanced Myeloid
Malignancies
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ho, Vincent; Dranoff, Glenn; Kim, Haesook; Vanneman, Matthew; Pasek, Mildred; Cutler, Corey; Koreth, John; Alyea, Edwin; Antin, Joseph H.; Jerome, Ritz; Soiffer, Robert J.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 306
EP 306
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701049
ER
PT J
AU Ghobrial, IM
Matous, J
Padmanabhan, S
Badros, A
Schlossman, R
Chuma, S
Leduc, R
Nelson, M
O'Connor, K
Sam, A
Harris, B
Soumerai, J
Warren, D
Birner, A
Munshi, N
Treon, SP
Anderson, KC
Richardson, P
AF Ghobrial, Irene M.
Matous, Jeffrey
Padmanabhan, Swaminathan
Badros, Ashraf
Schlossman, Robert
Chuma, Stacey
Leduc, Renee
Nelson, Marybeth
O'Connor, Kelly
Sam, Amy
Harris, Brianna
Soumerai, Jacob
Warren, Diane
Birner, Ann
Munshi, Nikhil
Treon, Steven P.
Anderson, Kenneth C.
Richardson, Paul
TI Phase II Trial of Combination of Bortezomib and Rituximab in Relapsed
and/or Refractory Waldenstrom Macroglobulinemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ghobrial, Irene M.; Schlossman, Robert; Chuma, Stacey; Leduc, Renee; Nelson, Marybeth; O'Connor, Kelly; Sam, Amy; Harris, Brianna; Soumerai, Jacob; Warren, Diane; Birner, Ann; Munshi, Nikhil; Treon, Steven P.; Anderson, Kenneth C.; Richardson, Paul] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Matous, Jeffrey] Rocky Mt Canc Ctr, Denver, CO USA.
[Padmanabhan, Swaminathan] Roswell Pk Canc Ctr, Buffalo, NY USA.
[Badros, Ashraf] Univ Maryland, Baltimore, MD 21201 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 308
EP 309
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701056
ER
PT J
AU Tai, YT
Soydan, E
Fulciniti, M
Song, WH
Li, XF
Burger, P
Hong, FX
Tonon, G
Kim, K
Rumizen, MJ
Nahar, S
Podar, K
Chauhan, D
Hideshima, T
Carrasco, DR
Munshi, NC
Afar, D
Anderson, KC
AF Tai, Yu-Tzu
Soydan, Ender
Fulciniti, Mariateresa
Song, Weihua
Li, Xian-Feng
Burger, Peter
Hong, Fangxin
Tonon, Giovanni
Kim, Kihyun
Rumizen, Mathew J.
Nahar, Sabikun
Podar, Klaus
Chauhan, Dharminder
Hideshima, Teru
Carrasco, Daniel R.
Munshi, Nikhil C.
Afar, Daniel
Anderson, Kenneth C.
TI CS1 Promotes Multiple Myeloma Cell Adhesion, Clonogenic Growth, and
Tumorigenicity Via C-Maf-Mediated Interactions with Bone Marrow Stromal
Cells (BMSCs)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Tai, Yu-Tzu; Soydan, Ender; Fulciniti, Mariateresa; Song, Weihua; Li, Xian-Feng; Burger, Peter; Hong, Fangxin; Tonon, Giovanni; Kim, Kihyun; Rumizen, Mathew J.; Nahar, Sabikun; Podar, Klaus; Chauhan, Dharminder; Hideshima, Teru; Carrasco, Daniel R.; Munshi, Nikhil C.; Anderson, Kenneth C.] Dana Farber Canc Inst, Med Oncol, Boston, MA 02115 USA.
[Afar, Daniel] PDL BioPharma Inc, Res, Redwood City, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 311
EP 311
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701064
ER
PT J
AU Rickles, RJ
Pierce, L
Giordano, T
Tam, WF
McMillin, DW
Anderson, KC
Mitsiades, C
Lee, MS
AF Rickles, Richard J.
Pierce, Laura
Giordano, Thomas
Tam, Winnie F.
McMillin, Douglas W.
Anderson, Kenneth C.
Mitsiades, Constantine
Lee, Margaret S.
TI Adenosine A2A Receptor Agonism and PDE Inhibition: A Synergistic
Multi-Target Mechanism Discovered through Systematic Combination
Screening in Multiple Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Rickles, Richard J.; Pierce, Laura; Giordano, Thomas; Tam, Winnie F.; Lee, Margaret S.] CombinatoRx Inc, Cambridge, MA USA.
[McMillin, Douglas W.; Anderson, Kenneth C.; Mitsiades, Constantine] Harvard Univ, Sch Med, Dana Farber Canc Inst,Dept Med, Jerome Lipper Multiple Myeloma Ctr,Dept Med Oncol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 313
EP 314
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701071
ER
PT J
AU LaBelle, JL
Lawrence, CE
Bird, GH
Walensky, LD
AF LaBelle, James L.
Lawrence, Chelsea E.
Bird, Gregory H.
Walensky, Loren D.
TI A Stapled BIM BH3 Helix Overcomes the MCL-1-Mediated Apoptotic Blockade
of Refractory Hematologic Cancers
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [LaBelle, James L.; Lawrence, Chelsea E.; Bird, Gregory H.; Walensky, Loren D.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Childrens Hosp Boston,Program Canc Chem Biol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 319
EP 319
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701086
ER
PT J
AU Richardson, P
Wolf, J
Jakubowiak, A
Zonder, J
Lonial, S
Irwin, DH
Densmore, J
Krishnan, A
Raje, N
Bar, MH
Allerton, JP
Schlossman, R
Ghobrial, IM
Munshi, NC
Martin, T
Laubach, J
Colson, K
Dean, S
Tocco, D
Steinfield, E
Kendall, T
O'Riley, K
Hideshima, T
Sportelli, P
Gardner, L
Anderson, KC
AF Richardson, Paul
Wolf, Jeffrey
Jakubowiak, Andrzej
Zonder, Jeffrey
Lonial, Sagar
Irwin, David H.
Densmore, John
Krishnan, Amrita
Raje, Noopur
Bar, Michael H.
Allerton, Jeffrey P.
Schlossman, Robert
Ghobrial, Irene M.
Munshi, Nikhil C.
Martin, Thomas
Laubach, Jacob
Colson, Kathy
Dean, Sarah
Tocco, Deanna
Steinfield, Elizabeth
Kendall, Tara
O'Riley, Kimberly
Hideshima, Teru
Sportelli, Peter
Gardner, Lesa
Anderson, Kenneth C.
TI Phase I/II Results of a Multicenter Trial of Perifosine (KRX-0401) +
Bortezomib in Patients with Relapsed or Relapsed/Refractory Multiple
Myeloma Who Were Previously Relapsed from or Refractory to Bortezomib
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Richardson, Paul; Schlossman, Robert; Ghobrial, Irene M.; Munshi, Nikhil C.; Laubach, Jacob; Colson, Kathy; Dean, Sarah; Tocco, Deanna; Hideshima, Teru; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Wolf, Jeffrey; Martin, Thomas; Steinfield, Elizabeth] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Jakubowiak, Andrzej; Kendall, Tara] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Zonder, Jeffrey; O'Riley, Kimberly] Wayne State Univ, Karmanos Canc Inst, Detroit, MI USA.
[Lonial, Sagar] Emory Univ, Atlanta, GA 30322 USA.
[Irwin, David H.] Alta Bates Comprehens Canc Ctr, Berkeley, CA USA.
[Densmore, John] Univ Virginia, Hlth Sci Ctr, Charlottesville, VA USA.
[Krishnan, Amrita] City Hope Natl Med Ctr, Duarte, CA 91010 USA.
[Raje, Noopur] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Hematol & Oncol, Boston, MA USA.
[Bar, Michael H.] Bennett Canc Ctr, Stamford, CT USA.
[Allerton, Jeffrey P.] Guthrie Clin, Sayre, PA USA.
[Sportelli, Peter; Gardner, Lesa] Keryx Biopharmaceut Inc, New York, NY USA.
NR 0
TC 2
Z9 3
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 321
EP 322
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701094
ER
PT J
AU Weber, D
Badros, AZ
Jagannath, S
Siegel, D
Richon, V
Rizvi, S
Garcia-Vargas, J
Reiser, D
Anderson, KC
AF Weber, Donna
Badros, Ashraf Z.
Jagannath, Sundar
Siegel, David
Richon, Victoria
Rizvi, Syed
Garcia-Vargas, Jose
Reiser, David
Anderson, Kenneth C.
TI Vorinostat Plus Bortezomib for the Treatment of Relapsed/Refractory
Multiple Myeloma: Early Clinical Experience
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Weber, Donna] Univ Texas MD Anderson Canc Ctr, Dept Lymphona & Myeloma, Houston, TX 77030 USA.
[Badros, Ashraf Z.] Univ Maryland, Baltimore, MD 21201 USA.
[Jagannath, Sundar] St Vincents Comp Canc Ctr, New York, NY USA.
[Siegel, David] Hackensack Univ, Med Ctr, Hackensack, NJ USA.
[Richon, Victoria; Rizvi, Syed; Garcia-Vargas, Jose; Reiser, David] Merck & Co Inc, Upper Gwynedd, PA USA.
[Anderson, Kenneth C.] Dana Farber Canc Inst, Brookline, MA USA.
NR 0
TC 6
Z9 6
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 322
EP 322
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701095
ER
PT J
AU Van Bennekom, CM
Abel, G
Anderson, T
Stone, RM
Kaufman, DW
AF Van Bennekom, Carla M.
Abel, Gregory
Anderson, Theresa
Stone, Richard M.
Kaufman, David W.
TI Patterns of Treatment among Patients with Recently-Diagnosed
Myelodysplastic Syndromes in a National Registry, 2006-2008
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Van Bennekom, Carla M.; Anderson, Theresa; Kaufman, David W.] Boston Univ, Slone Epidemiol Ctr, Boston, MA 02215 USA.
[Abel, Gregory; Stone, Richard M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 324
EP 324
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701100
ER
PT J
AU Cortes, J
Seiter, K
Maziarz, RT
Wetzler, M
Craig, M
Matous, J
Luger, S
Dey, B
Schiller, GJ
Pham, D
Abboud, CN
Krishnamurthy, M
Brown, A
Moore, JO
AF Cortes, Jorge
Seiter, Karen
Maziarz, Richard Thomas
Wetzler, Meir
Craig, Michael
Matous, Jeffrey
Luger, Selina
Dey, Bimalangshu
Schiller, Gary J.
Pham, Dat
Abboud, Camille N.
Krishnamurthy, Muthuswamy
Brown, Archie, Jr.
Moore, Joseph O.
TI Superiority of Rasburicase Versus Allopurinol on Serum Uric Acid Control
in Adult Patients with Hematological Malignancies at Risk of Developing
Tumor Lysis Syndrome: Results of a Randomized Comparative Phase III
Study
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Cortes, Jorge] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Seiter, Karen] New York Med Coll, Valhalla, NY 10595 USA.
[Maziarz, Richard Thomas] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Wetzler, Meir] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[Craig, Michael] WVU, Morgantown, WV USA.
[Matous, Jeffrey] Rocky Mt Canc Ctr, Denver, CO USA.
[Luger, Selina] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Dey, Bimalangshu] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Schiller, Gary J.] Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA.
[Pham, Dat] UF Shands Jacksonville, Jacksonville, FL USA.
[Abboud, Camille N.] Washington Univ, St Louis, MO USA.
[Krishnamurthy, Muthuswamy] New York Methodist Hosp, Brooklyn, NY USA.
[Brown, Archie, Jr.] Alton Ochsner Med Fdn & Ochsner Clin, New Orleans, LA 70121 USA.
[Moore, Joseph O.] Duke Med Ctr, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 340
EP 341
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701143
ER
PT J
AU Ottmann, OG
Spencer, A
Prince, HM
Bhalla, KN
Fischer, T
Liu, A
Parker, K
Jalaluddin, M
Laird, G
Woo, M
Scott, JW
DeAngelo, DJ
AF Ottmann, Oliver G.
Spencer, Andrew
Prince, H. Miles
Bhalla, Kapil N.
Fischer, Thomas
Liu, Angela
Parker, Kathryn
Jalaluddin, Muhammad
Laird, Glen
Woo, Margaret
Scott, Jeffrey W.
DeAngelo, Daniel J.
TI Phase IA/II Study of Oral Panobinostat (LBH589), a Novel Pan-Deacetylase
Inhibitor (DACi) Demonstrating Efficacy in Patients with Advanced
Hematologic Malignancies.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ottmann, Oliver G.] Univ Frankfurt, Med Klin 2, Frankfurt, Germany.
[Spencer, Andrew] Alfred Hosp, Clin Haematol & BMT, Melbourne, Vic, Australia.
[Prince, H. Miles] Peter MacCallum Canc Ctr, Dept Haematol, Melbourne, Vic, Australia.
[Bhalla, Kapil N.] Med Coll Georgia, Ctr Canc, Augusta, GA 30912 USA.
[Fischer, Thomas] Univ Magdeburg, Dept Hematol Oncol, D-39106 Magdeburg, Germany.
[Liu, Angela; Parker, Kathryn; Laird, Glen; Woo, Margaret; Scott, Jeffrey W.] Novartis Oncol, Florham Pk, NJ USA.
[Jalaluddin, Muhammad] Novartis Pharmaceut, Florham Pk, NJ USA.
[DeAngelo, Daniel J.] Dana Farber Canc Inst, Boston, MA 02115 USA.
RI Ottmann, Oliver/D-5007-2016
OI Ottmann, Oliver/0000-0001-9559-1330
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 352
EP 353
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701182
ER
PT J
AU Brown, JR
Stevenson, K
Kim, HT
Armand, P
Cutler, C
Fisher, DC
Ho, V
Koreth, J
Ritz, J
Antin, JH
Soiffer, RJ
Gribben, JG
Alyea, E
AF Brown, Jennifer R.
Stevenson, Kristen
Kim, Haesook T.
Armand, Philippe
Cutler, Corey
Fisher, David C.
Ho, Vincent
Koreth, John
Ritz, Jerome
Antin, Joseph H.
Soiffer, Robert J.
Gribben, John G.
Alyea, Edwin
TI Comparative Outcome of Myeloablative and Reduced Intensity Allogeneic
Stem Cell Transplantation for Chronic Lymphocytic Leukemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Brown, Jennifer R.; Stevenson, Kristen; Kim, Haesook T.; Armand, Philippe; Cutler, Corey; Fisher, David C.; Ho, Vincent; Koreth, John; Ritz, Jerome; Antin, Joseph H.; Soiffer, Robert J.; Alyea, Edwin] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Gribben, John G.] Barts & London Queen Marys Sch Med & Dent, Inst Canc, Ctr Med Oncol, London, England.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 357
EP 358
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701196
ER
PT J
AU Canault, M
Duerschmied, D
Brill, A
Patten, IS
Bergmeier, W
Wagner, DD
AF Canault, Matthias
Duerschmied, Daniel
Brill, Alexander
Patten, Ian Sean
Bergmeier, Wolfgang
Wagner, Denisa D.
TI MAPK Inhibition Prevents TACE-Mediated Receptor Shedding and Improves
the Hemostatic Function of Stored Platelets.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Canault, Matthias; Duerschmied, Daniel; Brill, Alexander; Patten, Ian Sean; Wagner, Denisa D.] Harvard Univ, Sch Med, Immune Dis Inst, Boston, MA USA.
[Bergmeier, Wolfgang] Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
RI Canault, Matthias/H-5128-2013
OI Canault, Matthias/0000-0002-7880-5250
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 365
EP 365
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701214
ER
PT J
AU Friedberg, JW
Younes, A
Fisher, DC
Gordon, LI
Moore, JO
Czuczman, MS
Miller, TP
Stiff, PJ
Cheson, BD
Forero-Torres, A
McKinney, B
Leonard, JP
AF Friedberg, Jonathan W.
Younes, Anas
Fisher, David C.
Gordon, Leo I.
Moore, Joseph O.
Czuczman, Myron S.
Miller, Thomas P.
Stiff, Patrick J.
Cheson, Bruce D.
Forero-Torres, Andres
McKinney, Byron
Leonard, John P.
TI Durable Responses in Patients Treated with Galiximab (Anti-CD80) in
Combination with Rituximab for Relapsed or Refractory Follicular
Lymphoma: Long-Term Follow-up of a Phase II Clinical Trial.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Friedberg, Jonathan W.] Univ Rochester, James P Wilmot Canc Ctr, Rochester, NY 77030 USA.
[Younes, Anas] Univ Texas Houston, MD Anderson Canc Ctr, Houston, TX 02115 USA.
[Fisher, David C.] Dana Farber Canc Inst, Boston, MA 60611 USA.
[Gordon, Leo I.] Northwestern Univ, Sch Med, Dept Med, Div Hematol Oncol, Chicago, IL USA.
[Moore, Joseph O.] Duke Med Ctr, Durham, NC 14263 USA.
[Czuczman, Myron S.] Roswell Pk Canc Inst, Buffalo, NY USA.
[Miller, Thomas P.] Univ Arizona, Arizona Canc Ctr, Tucson, AZ 60153 USA.
[Stiff, Patrick J.] Loyola Univ, Med Ctr, Maywood, IL USA.
[Cheson, Bruce D.] Georgetown Univ, Vincent T Lombardi Canc Res Ctr, Washington, DC USA.
[Forero-Torres, Andres] Univ Alabama, Birmingham, AL USA.
[McKinney, Byron] Biogen Idec, San Diego, CA USA.
[Leonard, John P.] Weill Cornell Med Coll, Div Hem Onc, New York, NY USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 369
EP 370
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701228
ER
PT J
AU Ghobrial, IM
Chuma, S
Sam, A
Leduc, R
Nelson, M
O'Connor, K
Harris, B
Soumerai, J
Warren, D
Jacobsen, E
DeAngelo, D
Anderson, KC
Richardson, PG
Witzig, TE
Treon, SP
AF Ghobrial, Irene M.
Chuma, Stacey
Sam, Amy
Leduc, Renee
Nelson, Marybeth
O'Connor, Kelly
Harris, Brianna
Soumerai, Jacob
Warren, Diane
Jacobsen, Eric
DeAngelo, Daniel
Anderson, Kenneth C.
Richardson, Paul G.
Witzig, Thomas E.
Treon, Steven P.
TI Phase II Trial of the mTOR Inhibitor RAD001 in Relapsed and/or
Refractory Waldenstrom Macroglobulinemia: The Dana Farber Cancer
Institute Experience.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ghobrial, Irene M.; Chuma, Stacey; Sam, Amy; Leduc, Renee; Nelson, Marybeth; O'Connor, Kelly; Harris, Brianna; Soumerai, Jacob; Warren, Diane; Jacobsen, Eric; DeAngelo, Daniel; Anderson, Kenneth C.; Richardson, Paul G.; Treon, Steven P.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Witzig, Thomas E.] Mayo Clin, Rochester, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 372
EP 372
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701235
ER
PT J
AU Ghobrial, IM
Leleu, X
Rubin, N
Xie, WL
Hong, FX
Chuma, S
Leduc, R
Nelson, M
O'Connor, K
Sam, A
Harris, B
Warren, D
Sportelli, P
Treon, SP
Weller, E
Anderson, KC
Richardson, PG
AF Ghobrial, Irene M.
Leleu, Xavier
Rubin, Nancy
Xie, Wanling
Hong, Fangxin
Chuma, Stacey
Leduc, Renee
Nelson, Marybeth
O'Connor, Kelly
Sam, Amy
Harris, Brianna
Warren, Diane
Sportelli, Peter
Treon, Steven P.
Weller, Edie
Anderson, Kenneth C.
Richardson, Paul G.
TI Final Results of a Phase II Trial of the Novel Oral Akt Inhibitor
Perifosine in Relapsed and/or Refractory Waldenstrom Macroglobulinemia
(WM).
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ghobrial, Irene M.; Leleu, Xavier; Hong, Fangxin; Chuma, Stacey; Leduc, Renee; Nelson, Marybeth; O'Connor, Kelly; Sam, Amy; Harris, Brianna; Warren, Diane; Treon, Steven P.; Weller, Edie; Anderson, Kenneth C.; Richardson, Paul G.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Rubin, Nancy] Community Hosp Monterey Peninsula, Monterey, CA USA.
[Xie, Wanling] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 372
EP 372
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701234
ER
PT J
AU Kay, NE
Kim, HT
Kempin, S
Secreto, C
Knox, T
Tschumper, R
Jelinek, DF
Smoley, S
Van Dyke, D
Saltzman, J
Rosen, ST
Kahl, B
Tallman, MS
AF Kay, Neil E.
Kim, Haesook T.
Kempin, Sanford
Secreto, Charla
Knox, Traci
Tschumper, Renee
Jelinek, Diane F.
Smoley, Stephanie
Van Dyke, Daniel
Saltzman, Joel
Rosen, Steven T.
Kahl, Brad
Tallman, Martin S.
TI Predictors of Clinical Outcome to Pentostatin, Cyclophosphamide and
Rituximab (PCR) Followed by Campath for Relapsed/Refractory CLL - A
Study of the Eastern Cooperative Oncology Group, E2903.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Kay, Neil E.; Secreto, Charla; Knox, Traci; Tschumper, Renee; Jelinek, Diane F.; Smoley, Stephanie; Van Dyke, Daniel] Mayo Clin, Rochester, MN USA.
[Kim, Haesook T.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Kempin, Sanford] St Vincents Hosp, Ctr Comprehens Canc, New York, NY USA.
[Saltzman, Joel] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Rosen, Steven T.] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
[Kahl, Brad] Univ Wisconsin, Madison, WI USA.
[Tallman, Martin S.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 387
EP 387
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701281
ER
PT J
AU Smoley, SA
Van Dyke, DL
Kay, NE
Heerema, NA
Dell'Aquila, ML
Koduru, P
Dal Cin, P
Rassenti, L
Byrd, JC
Rai, KR
Brown, JR
Greaves, AW
Kipps, TJ
Dewald, GW
AF Smoley, Stephanie A.
Van Dyke, Daniel L.
Kay, Neil E.
Heerema, Nyla A.
dell'Aquila, Marie L.
Koduru, Prasad
Dal Cin, Paola
Rassenti, Laura
Byrd, John C.
Rai, Kanti R.
Brown, Jennifer R.
Greaves, Andrew W.
Kipps, Thomas J.
Dewald, Gordon W.
TI Validation of CLL FISH Panel Scoring by Members of the Chronic
Lymphocytic Leukemia Research Consortium.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Kay, Neil E.] Mayo Clin, Div Hematol Oncol, Rochester, MN USA.
[Heerema, Nyla A.; Byrd, John C.] Ohio State Univ, Columbus, OH 43210 USA.
[dell'Aquila, Marie L.; Greaves, Andrew W.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Koduru, Prasad] Royal N Shore Hosp, Manhasset, NY USA.
[Dal Cin, Paola] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Rassenti, Laura] Moores UCSD Canc Ctr, La Jolla, CA USA.
[Rai, Kanti R.] Long Isl Jewish Med Ctr, New Hyde Pk, NY 11042 USA.
[Brown, Jennifer R.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Kipps, Thomas J.] Univ Calif San Diego, La Jolla, CA 92093 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 390
EP 391
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701291
ER
PT J
AU Davies, J
De Lima, M
Cooper, L
Spitzer, T
Kapoor, N
Brennan, L
Thall, P
McMannis, J
Champlin, R
Nadler, L
Guinan, E
AF Davies, Jeff
De Lima, Marcos
Cooper, Laurence
Spitzer, Thomas
Kapoor, Neena
Brennan, Lisa
Thall, Peter
McMannis, John
Champlin, Richard
Nadler, Lee
Guinan, Eva
TI Phase 1 Clinical Study of Adoptive Immunotherapy with Delayed Infusion
of Alloanergized Donor T Cells to Improve Immune Reconstution after
Haploidentical Stem Cell Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Davies, Jeff; Brennan, Lisa; Nadler, Lee; Guinan, Eva] Dana Farber Canc Inst, Boston, MA 02115 USA.
[De Lima, Marcos; Cooper, Laurence; Thall, Peter; McMannis, John; Champlin, Richard] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Spitzer, Thomas] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Kapoor, Neena] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 422
EP 423
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701378
ER
PT J
AU Koreth, J
Stevenson, K
Kim, HT
Ho, VT
Cutler, CS
Armand, P
Soiffer, RJ
Antin, JH
Alyea, EP
AF Koreth, John
Stevenson, Kristen
Kim, Haesook T.
Ho, Vincent T.
Cutler, Corey S.
Armand, Philippe
Soiffer, Robert J.
Antin, Joseph H.
Alyea, Edwin P., III
TI A Phase I/II Trial of Bortezomib, Tacrolimus and Methotrexate for
Prophylaxis of Acute Graft Versus Host Disease after HLA Mismatched
Reduced Intensity Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Koreth, John; Ho, Vincent T.; Cutler, Corey S.; Armand, Philippe; Soiffer, Robert J.; Antin, Joseph H.; Alyea, Edwin P., III] Dana Farber Canc Inst, Div Hematol Malignancies, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 423
EP 423
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701380
ER
PT J
AU Brown, J
McDonough, S
Stevenson, K
Reynolds, C
Kim, H
Alyea, EP
Antin, JH
Attar, E
Avigan, D
Cutler, CS
Dey, B
Ho, V
Joyce, R
Levine, JD
McAfee, SL
Rosenblatt, J
Soiffer, RJ
Spitzer, T
Tzachanis, D
Ballen, KK
Ritz, J
Boussiotis, V
AF Brown, Julia
McDonough, Sean
Stevenson, Kristin
Reynolds, Carol
Kim, Haesook
Alyea, Edwin P., III
Antin, Joseph H.
Attar, Eyal
Avigan, David
Cutler, Corey S.
Dey, Bimalangshu
Ho, Vincent
Joyce, Robin
Levine, James D.
McAfee, Steven L.
Rosenblatt, Jacalyn
Soiffer, Robert J.
Spitzer, Thomas
Tzachanis, Dimitrios
Ballen, Karen K.
Ritz, Jerome
Boussiotis, Vassiliki
TI Development of CMV-SPECIFIC Immunity after Cord Blood Transplantation in
Adults Depends on Reconstitution of Thymopoiesis and Regeneration of
NAIVE CD8+T Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Brown, Julia; Boussiotis, Vassiliki] Beth Israel Deaconess Med Ctr, Harvard Inst Med, Boston, MA 02215 USA.
[Alyea, Edwin P., III] Dana Farber Canc Inst, Div Hematol Malignancies, Boston, MA 02115 USA.
[Antin, Joseph H.] Brigham & Womens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Attar, Eyal] Harvard Univ, Massachusetts Gen Hosp, Ctr Canc, Sch Med, Boston, MA 02114 USA.
[Dey, Bimalangshu] Mass Gen Hosp, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 426
EP 426
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701389
ER
PT J
AU Skert, C
Prestini, K
Peli, A
Biasi, L
Fili, C
Malagola, M
Bergonzi, C
Mendeni, M
Roccaro, AM
Puoti, M
Russo, D
AF Skert, Cristina
Prestini, Katia
Peli, Annalisa
Biasi, Luciano
Fili, Carla
Malagola, Michele
Bergonzi, Cesare
Mendeni, Monia
Roccaro, Aldo M.
Puoti, Massimo
Russo, Domenico
TI Assessment of Liver Damage with Transient Hepatic Elastography
(FIBROSCAN) in patients with chronic Graft-Versus-Host Disease
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Skert, Cristina; Peli, Annalisa; Fili, Carla] Univ Brescia, Chair Haematol, Stem Cell Transplantat Unit, Brescia, Italy.
[Prestini, Katia; Biasi, Luciano; Mendeni, Monia; Puoti, Massimo] Univ Brescia, Dept Infect & Trop Dis, Brescia, Italy.
[Roccaro, Aldo M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 432
EP 433
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701406
ER
PT J
AU Czibere, A
Singh, R
Bruns, I
Zerbini, LF
Haas, R
AF Czibere, Akos
Singh, Raminder
Bruns, Ingmar
Zerbini, Luiz Fernando
Haas, Rainer
TI Ap-1 Family Members C-Jun, JunB and Fra-2 Mediate Apoptosis and
Differentiation in AML through Activation of GADD45 alpha and ADFP
Following Non-Steroidal Anti-Inflammatory Drug Treatment
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Czibere, Akos; Singh, Raminder; Bruns, Ingmar; Haas, Rainer] Univ Dusseldorf, Dusseldorf, Germany.
[Zerbini, Luiz Fernando] Beth Israel Deaconess Med Ctr, BIDMC Genom Ctr, Boston, MA 02215 USA.
RI Zerbini, Luiz /B-7720-2015
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 436
EP 436
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701418
ER
PT J
AU Rosenblatt, J
Bissonnette, A
Wu, ZK
Vasir, B
Zarwan, C
Keefe, W
Joyce, R
Levine, JD
Glotzbecker, B
Rozenvayn, N
Tzachanis, D
Boussiotis, V
Kufe, D
Avigan, D
AF Rosenblatt, Jacalyn
Bissonnette, Adam
Wu, Zekui
Vasir, Baldev
Zarwan, Corrine
Keefe, Whitney
Joyce, Robin
Levine, James D.
Glotzbecker, Brett
Rozenvayn, Nataliya
Tzachanis, Dimitrios
Boussiotis, Vassiliki
Kufe, Donald
Avigan, David
TI Immunomodulatory Effects of Vitamin D: Implications for the Prevention
and Treatment of Graft Versus Host Disease.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Rosenblatt, Jacalyn; Zarwan, Corrine; Joyce, Robin; Levine, James D.; Glotzbecker, Brett; Rozenvayn, Nataliya; Tzachanis, Dimitrios; Boussiotis, Vassiliki; Avigan, David] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Bissonnette, Adam; Wu, Zekui; Vasir, Baldev; Keefe, Whitney; Kufe, Donald] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 454
EP 454
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701473
ER
PT J
AU Waters, EK
Bernimoulin, M
Foy, M
Steele, BM
Sullivan, M
Falet, H
Hartwig, JH
Maguire, PB
Wagner, DD
AF Waters, Emily K.
Bernimoulin, Michael
Foy, Martina
Steele, Brian M.
Sullivan, Matthew
Falet, Herve
Hartwig, John H.
Maguire, Patricia B.
Wagner, Denisa D.
TI Differential Stimulation of Monocytic Cells Results in Distinct
Populations of Microparticles
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Waters, Emily K.; Bernimoulin, Michael; Wagner, Denisa D.] Harvard Univ, Sch Med, Immune Dis Inst, Boston, MA USA.
[Foy, Martina; Steele, Brian M.; Sullivan, Matthew; Maguire, Patricia B.] UCD Conway Inst, Sch Biomol & Biomed Sci, Dublin 4, Ireland.
[Falet, Herve; Hartwig, John H.] Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 456
EP 456
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701480
ER
PT J
AU Carbo, C
Goerge, T
Hattori, H
Duerschmied, D
Cifuni, SM
Luo, HR
Wagner, DD
AF Carbo, Carla
Goerge, Tobias
Hattori, Hidenori
Duerschmied, Daniel
Cifuni, Stephen M.
Luo, Hongbo R.
Wagner, Denisa D.
TI Integrin-Independent Role of CalDAG-GEFI in Neutrophil Chemotaxis
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Carbo, Carla; Goerge, Tobias; Duerschmied, Daniel; Cifuni, Stephen M.; Wagner, Denisa D.] Harvard Univ, Sch Med, Immune Dis Inst, Boston, MA USA.
[Hattori, Hidenori; Luo, Hongbo R.] Harvard Univ, Childrens Hosp, Sch Med, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 458
EP 459
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701488
ER
PT J
AU Grace, RF
Mednick, RE
Neufeld, EJ
AF Grace, Rachael F.
Mednick, Rachel E.
Neufeld, Ellis J.
TI Compliance with Immunizations in Splenectomized Individuals: A Study of
the Splenectomized Hereditary Spherocytosis Population
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Grace, Rachael F.; Mednick, Rachel E.; Neufeld, Ellis J.] Childrens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
RI Neufeld, Ellis/F-9331-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 476
EP 476
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701538
ER
PT J
AU Corneio, MG
Mercher, T
Growney, JD
Jesneck, J
Maillard, I
Pear, WS
Aster, J
Gilliland, DG
AF Corneio, Melanie G.
Mercher, Thomas
Growney, Joseph D.
Jesneck, Jonathan
Maillard, Ivan
Pear, Warren S.
Aster, Jon
Gilliland, D. Gary
TI Runx1 Is Required for Notch-Induced Specification of Megakaryocyte
Development from Early Hematopoietic Stem and Progenitor Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Corneio, Melanie G.; Growney, Joseph D.; Gilliland, D. Gary] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Div Hematol, Boston, MA 02115 USA.
[Mercher, Thomas] Univ Paris 5 Descartes, INSERM, EM10210, Paris, France.
[Jesneck, Jonathan] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Maillard, Ivan] Ctr Stem Cell Biol, Inst Life Sci, Ann Arbor, MI USA.
[Pear, Warren S.] Univ Penn, Philadelphia, PA 19104 USA.
RI Mercher, Thomas/J-2446-2014
OI Mercher, Thomas/0000-0003-1552-087X
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 492
EP 492
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701592
ER
PT J
AU Wang, JF
Dayyani, F
Brynczka, C
Sweetser, DA
AF Wang, Jianfeng
Dayyani, Farshid
Brynczka, Christopher
Sweetser, David A.
TI Groucho/TLE Corepressors Regulate Myeloid Differentiation and Size of
the Stem Cell/Progenitor Population.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Wang, Jianfeng; Brynczka, Christopher] Massachusetts Gen Hosp, Dept Pediat, Boston, MA 02114 USA.
[Dayyani, Farshid] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 499
EP 499
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701618
ER
PT J
AU Tothova, Z
Sykes, SM
Leeman, DS
Horner, JW
Sharpless, N
DePinho, RA
Gilliland, DG
AF Tothova, Zuzana
Sykes, Stephen M.
Leeman, Dena S.
Horner, James W.
Sharpless, Norman
DePinho, Ronald A.
Gilliland, D. Gary
TI p16(INK4a) Is a Key Downstream Mediator of the Deleterious Effects of
FoxO Deficiency on Maintenance of the Hematopoietic Stem Cell
Compartment.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology/ASH/ASCO Joint
Symposium
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol, Sanofi Aventis U.S.
C1 [Tothova, Zuzana; Sykes, Stephen M.; Leeman, Dena S.; Gilliland, D. Gary] Harvard Univ, Sch Med, Howard Hughes Med Inst, Brigham & Womens Hosp,Div Hematol, Boston, MA 02115 USA.
[Horner, James W.; DePinho, Ronald A.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Sharpless, Norman] Univ N Carolina, Sch Med, Lineberger Canc Res Ctr, Chapel Hill, NC 27599 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 502
EP 502
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701627
ER
PT J
AU Barnes, JA
LaCasce, AS
Toomey, CE
Hochberg, E
Lee, AI
Canellos, GP
Abramson, JS
AF Barnes, Jeffrey A.
LaCasce, Ann S.
Toomey, Christiana E.
Hochberg, Ephraim
Lee, Alfred I.
Canellos, George P.
Abramson, Jeremy S.
TI Early Interim FDG-PET Scan Predicts Outcome in Non-Bulky Limited Stage
Hodgkin Lymphoma, but may Not Guide Use of Consolidative Radiotherapy
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Barnes, Jeffrey A.; Toomey, Christiana E.; Hochberg, Ephraim; Lee, Alfred I.; Abramson, Jeremy S.] Massachusetts Gen Hosp, Ctr Canc, Ctr Lymphoma, Boston, MA USA.
[LaCasce, Ann S.; Canellos, George P.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 3
Z9 3
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 518
EP 518
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701675
ER
PT J
AU Kostakoglu, L
Straus, DJ
Schoder, H
LaCasce, AS
Bartlett, NL
Hall, N
Johnson, JL
Jung, SH
Canellos, GP
Schwartz, LH
Cheson, BD
AF Kostakoglu, Lale
Straus, David J.
Schoeder, Heiko
LaCasce, Ann S.
Bartlett, Nancy L.
Hall, Nathan
Johnson, Jeffrey L.
Jung, Sin-Ho
Canellos, George P.
Schwartz, Lawrence H.
Cheson, Bruce D.
TI Validation of the International Harmonization Project (IHP) Guidelines
in Early Stage Hodgkin Lymphoma (HL) Treated with Adriamycin,
Vinblastine and Gemcitabine (AVG) (CALGB 50203): Early Results
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology/ASH/ASCO Joint
Symposium
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol (ASH), Sanofi Aventis U.S.
C1 [Kostakoglu, Lale] Mt Sinai Med Ctr, New York, NY 10029 USA.
[Straus, David J.] MSKCC, New York, NY USA.
[Schoeder, Heiko; Schwartz, Lawrence H.] Mem Sloan Kettering Canc Ctr, New York, NY USA.
[LaCasce, Ann S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Bartlett, Nancy L.] Washington Univ, Sch Med, St Louis, MO USA.
[Hall, Nathan] Ohio State Univ, Columbus, OH 43210 USA.
[Johnson, Jeffrey L.; Jung, Sin-Ho] Duke Univ, Med Ctr, CALGB Stat Off, Durham, NC USA.
[Canellos, George P.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Cheson, Bruce D.] Georgetown Univ Hosp, Vincent T Lombardi Canc Res Ctr, Washington, DC 20007 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 520
EP 520
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701682
ER
PT J
AU Song, WH
Hideshima, T
Tai, YT
Anderson, KC
Munshi, NC
AF Song, Weihua
Hideshima, Teru
Tai, Yu-Tzu
Anderson, Kenneth C.
Munshi, Nikhil C.
TI Phenotypic and Functional Effects of Novel Akt Inhibitor Perifosine on
Immune System
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Munshi, Nikhil C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston VA Healthcare Syst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 551
EP 552
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701776
ER
PT J
AU Raab, MS
Breitkreutz, I
Rebacz, B
Nguyen, T
Hayden, PJ
Clausen, MH
Larsen, TO
Fruehauf, J
Anderson, KC
Kraemer, A
AF Raab, Marc S.
Breitkreutz, Iris
Rebacz, Blanca
Nguyen, Thu
Hayden, Patrick J.
Clausen, Mads H.
Larsen, Thomas O.
Fruehauf, Johannes
Anderson, Kenneth C.
Kraemer, Alwin
TI GF-15, a Novel Inhibitor of Centrosomal Clustering, Suppresses Tumor
Growth in Vivo
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Raab, Marc S.; Breitkreutz, Iris; Hayden, Patrick J.; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Rebacz, Blanca; Kraemer, Alwin] German Canc Res Ctr, CCU Mol Hematol Oncol, D-6900 Heidelberg, Germany.
[Nguyen, Thu; Fruehauf, Johannes] Beth Israel Deaconess Med Ctr, New York, NY 10003 USA.
[Clausen, Mads H.; Larsen, Thomas O.] Univ Denmark, Bioctr, Lyngby, Denmark.
RI Clausen, Mads/A-9656-2015
OI Clausen, Mads/0000-0001-9649-1729
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 578
EP 579
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701860
ER
PT J
AU Santini, V
Fenaux, P
Mufti, GJ
Hellstrom-Lindberg, E
Silverman, LB
List, A
Gore, SD
Seymour, JF
Backstrom, J
McKenzie, D
Beach, CL
AF Santini, Valeria
Fenaux, Pierre
Mufti, Ghularn J.
Hellstrom-Lindberg, Eva
Silverman, Lewis B.
List, Alan
Gore, Steven D.
Seymour, John F.
Backstrom, Jay
McKenzie, David
Beach, C. L.
TI Management and Supportive Care Measures of Adverse Events (AEs) in
Higher-Risk MDS Patients (Pts) Treated with Azacitidine (AZA)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Santini, Valeria] Azienda Osped Careggi, Florence, Italy.
[Fenaux, Pierre] Univ Paris 13, Hop Avicenne, AP HP, Hematol Clin, Bobigny, France.
[Mufti, Ghularn J.] Kings Coll London, Dept Haematol Med, London, England.
[Hellstrom-Lindberg, Eva] Karolinska Univ Hosp, Stockholm, Sweden.
[Silverman, Lewis B.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[List, Alan] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Gore, Steven D.] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Baltimore, MD USA.
[Seymour, John F.] Peter MacCallum Canc Inst, Dept Haematol, Melbourne, Vic, Australia.
[Backstrom, Jay; McKenzie, David; Beach, C. L.] Celgene, Overland Pk, KS USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 583
EP 584
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701874
ER
PT J
AU Azab, AK
Azab, F
Pitsillides, CM
Ngo, HT
Jia, XY
Melhem, MR
Runnels, J
Roccaro, AM
Sacco, A
Burwick, N
Lin, CP
Anderson, KC
Ghobrial, IM
AF Azab, Abdel Kareem
Azab, Feda
Pitsillides, Costas M.
Ngo, Hai T.
Jia, Xiaoying
Melhem, Molly R.
Runnels, Judith
Roccaro, Aldo M.
Sacco, Antonio
Burwick, Nicholas
Lin, Charles P.
Anderson, Kenneth C.
Ghobrial, Irene M.
TI Rho-a and Rac-1 GTPases Play Major and Differential Roles in SDF1
alpha-Induced Cell Adhesion and Chemotaxis in Multiple Myeloma.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Pitsillides, Costas M.; Lin, Charles P.] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Dis Ctr, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 588
EP 588
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104701887
ER
PT J
AU Burwick, N
Moreau, AS
Jia, XY
Leleu, X
Runnels, J
Ngo, HT
Melhem, MR
Roccaro, AM
Azab, AK
Ghobrial, IM
AF Burwick, Nicholas
Moreau, Anne-Sophie
Jia, Xiaoying
Leleu, Xavier
Runnels, Judith
Ngo, Hai T.
Melhem, Molly R.
Roccaro, Aldo M.
Azab, Abdel Kareem
Ghobrial, Irene M.
TI CXCR7 Regulates SDF-1 Induced Adhesion and Homing in Multiple Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Burwick, Nicholas; Moreau, Anne-Sophie; Jia, Xiaoying; Leleu, Xavier; Runnels, Judith; Ngo, Hai T.; Melhem, Molly R.; Roccaro, Aldo M.; Azab, Abdel Kareem; Ghobrial, Irene M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 591
EP 592
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702008
ER
PT J
AU Kumar, S
Zhang, L
Dispenzieri, A
Van Wier, S
Katzmann, J
Snyder, M
Blood, E
DeGoey, R
Henderson, K
Bradwell, A
Kyle, R
Greipp, P
Rajkumar, SV
Fonseca, R
AF Kumar, Shaji
Zhang, Lijun
Dispenzieri, Angela
Van Wier, Scott
Katzmann, Jerry
Snyder, Melissa
Blood, Emily
DeGoey, Roberta
Henderson, Kim
Bradwell, Arthur
Kyle, Robert
Greipp, Philip
Rajkumar, S. Vincent
Fonseca, Rafael
TI Association of High Levels of Free Light Chain and the Presence of Igh
Translocations in Multiple Myeloma and Prognostic Implications
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Kumar, Shaji; Dispenzieri, Angela; Katzmann, Jerry; Snyder, Melissa; DeGoey, Roberta; Henderson, Kim; Kyle, Robert; Greipp, Philip; Rajkumar, S. Vincent] Mayo Clin, Rochester, MN USA.
[Zhang, Lijun] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Van Wier, Scott; Fonseca, Rafael] Mayo Clin Arizona, Scottsdale, AZ USA.
[Blood, Emily] Dartmouth Coll, Hitchcock Med Ctr, Dartmouth Med Sch, Lebanon, NH 03756 USA.
[Bradwell, Arthur] Univ Birmingham, Sch Med, Dept Immunol, Birmingham, W Midlands, England.
RI Kumar, Shaji/A-9853-2008
OI Kumar, Shaji/0000-0001-5392-9284
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 592
EP 593
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702011
ER
PT J
AU Gorgun, G
Calabrese, E
Hideshima, T
Ikeda, H
Perrone, G
Santo, L
Cirstea, D
Richardson, PG
Anderson, KC
AF Gorgun, Gullu
Calabrese, Elisabetta
Hideshima, Teru
Ikeda, Hiroshi
Perrone, Giulia
Santo, Loredana
Cirstea, Diana
Richardson, Paul G.
Anderson, Kenneth C.
TI Immunomodulatory Effects of Lenalidomide and Bortezomib on Bone Marrow
Stroma Cell and CD4 T Cell Interaction in Multiple Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Gorgun, Gullu; Calabrese, Elisabetta; Hideshima, Teru; Ikeda, Hiroshi; Perrone, Giulia; Santo, Loredana; Cirstea, Diana; Richardson, Paul G.; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 597
EP 597
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702024
ER
PT J
AU Ma, S
Zhan, FH
Ma, CG
Tessel, M
Zhang, L
Rajkumar, SV
Singhal, S
Barlogie, B
Shaughnessy, J
Rosen, ST
Krett, N
AF Ma, Shuo
Zhan, Fenghuang
Ma, Chunguang
Tessel, Michael
Zhang, Lijun
Rajkumar, S. Vincent
Singhal, Seema
Barlogie, Bart
Shaughnessy, John
Rosen, Steven T.
Krett, Nancy
TI Glucocorticoid Receptor Expression Correlates with Clinical Outcome in
Myeloma Patients Treated with Glucocorticoid-Containing Regimens
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ma, Shuo; Ma, Chunguang; Tessel, Michael; Krett, Nancy] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
[Zhan, Fenghuang] Univ Utah, Sch Med, Blood Marrow Transplant & Myeloma Program, Salt Lake City, UT USA.
[Zhang, Lijun] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Rajkumar, S. Vincent] Mayo Clin, Rochester, MN USA.
[Singhal, Seema] Northwestern Univ, Sch Med, Chicago, IL USA.
[Barlogie, Bart] Univ Arkansas Med Sci, Myeloma Inst Res & Therapy, Little Rock, AR 72205 USA.
[Shaughnessy, John] Univ AR Med Sci, Dept Med, Little Rock, AR USA.
[Rosen, Steven T.] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
NR 0
TC 1
Z9 2
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 600
EP 600
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702034
ER
PT J
AU Adamia, S
Amin, SB
Li, C
Patterson, CJ
AvetLoiseau, H
Minvielle, S
Moreau, P
Anderson, KC
Munshi, NC
Treon, S
AF Adamia, Sophia
Amin, Samir B.
Li, Cheng
Patterson, Christopher J.
AvetLoiseau, Herve
Minvielle, Stephane
Moreau, Philippe
Anderson, Kenneth C.
Munshi, Nikhil C.
Treon, Steven
TI High-Throughput Microrna Profiling in Patients with Waldenstrom's
Macroglobulinemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Amin, Samir B.; Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA.
[Li, Cheng] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Li, Cheng] Harvard Univ, Sch Publ Hlth, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Patterson, Christopher J.] Dana Farber Canc Inst, Waldenstroms Macroglubulinemia Ctr, Boston, MA 02115 USA.
[AvetLoiseau, Herve; Minvielle, Stephane; Moreau, Philippe] Hop Nantes, Dept Hematol, Nantes, France.
[Munshi, Nikhil C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston VA Canc Healthcare Syst, Boston, MA 02115 USA.
RI Minvielle, Stephane/K-8251-2015; richard, chrystelle/K-8595-2015
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 601
EP 601
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702038
ER
PT J
AU Ikeda, H
Hideshima, T
Lutz, RJ
Vallet, S
Pozzi, S
Santo, L
Calabrese, E
Daelken, B
Uherek, C
Aigner, S
Osterroth, F
Fultiniti, M
Okawa, Y
Perrone, G
Gorgon, G
Yasui, H
Cristia, D
Raje, N
Munshi, N
Richardson, P
Anderson, KC
AF Ikeda, Hiroshi
Hideshima, Tern
Lutz, Robert J.
Vallet, Sonia
Pozzi, Samantha
Santo, Loredana
Calabrese, Elisabetta
Daelken, Benjamin
Uherek, Christoph
Aigner, Silke
Osterroth, Frank
Fultiniti, Mariateresa
Okawa, Yutaka
Perrone, Giulia
Gorgon, Gullu
Yasui, Hiroshi
Cristia, Diana
Raje, Noopur
Munshi, Nikhil
Richardson, Paul
Anderson, Kenneth C.
TI The Monoclonal Antibody nBT062 Conjugated to Cytotoxic Maytansinoids Has
Potent and Selective Cytotoxicity against CD138 Positive Multiple
Myeloma Cells in Vitro and in Vivo
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Lutz, Robert J.] ImmunoGen Inc, Waltham, MA USA.
[Pozzi, Samantha] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Dis Ctr, Boston, MA USA.
[Daelken, Benjamin; Uherek, Christoph; Aigner, Silke; Osterroth, Frank] Biotest AG, Dreieich, Germany.
[Yasui, Hiroshi] Sapporo Med Univ, Dept Internal Med 1, Sapporo, Hokkaido, Japan.
RI Pozzi, Samantha/A-7617-2012
OI Pozzi, Samantha/0000-0001-7917-1774
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 604
EP 605
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702050
ER
PT J
AU Gorgun, G
Calabrese, E
Mani, M
Hideshima, T
Ikeda, H
Perrone, G
Santo, L
Cirstea, D
Blotta, S
Richardson, PG
Ecsedy, J
Anderson, KC
AF Gorgun, Gullu
Calabrese, Elisabetta
Mani, Mala
Hideshima, Teru
Ikeda, Hiroshi
Perrone, Giulia
Santo, Loredana
Cirstea, Diana
Blotta, Simona
Richardson, Paul G.
Ecsedy, Jefrrey
Anderson, Kenneth C.
TI A Novel Aurora-a Kinase Inhibitor MLN8237 Induces Cytotoxicity and Cell
Cycle Arrest in Experimental Multiple Myeloma Models
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Hideshima, Teru] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Dis Ctr, Boston, MA 02115 USA.
[Ecsedy, Jefrrey] Millennium Pharmaceut Inc, Cambridge, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 605
EP 606
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702053
ER
PT J
AU Dimopoulos, MA
Richardson, P
Schlag, R
Khuageva, NK
Shpilberg, O
Kastritis, E
Kropff, MH
Petrucci, MT
Delforge, M
Alexeeva, JA
Schots, R
Masszi, T
Mateos, MV
Deraedt, W
Liu, K
Cakana, A
van de Velde, H
Miguel, JFS
AF Dimopoulos, Meletios A.
Richardson, Paul
Schlag, Rudolf
Khuageva, Nuriet K.
Shpilberg, Ofer
Kastritis, Efstathios
Kropff, Martin H.
Petrucci, Maria Teresa
Delforge, Michel
Alexeeva, Julia A.
Schots, Rik
Masszi, Tamas
Mateos, Maria-Victoria
Deraedt, William
Liu, Kevin
Cakana, Andrew
van de Velde, Helgi
Miguel, Jesus F. San
TI Bortezomib-Melphalan-Prednisone (VMP) in Newly Diagnosed Multiple
Myeloma Patients with Impaired Renal Function: Cohort Analysis of the
Phase III VISTA Study
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Dimopoulos, Meletios A.; Kastritis, Efstathios] Univ Athens, Sch Med, Dept Clin Therapeut, GR-11527 Athens, Greece.
[Richardson, Paul] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Schlag, Rudolf] Praxis Hematol & Oncol, Wurzburg, Germany.
[Khuageva, Nuriet K.] SP Botkin Moscow City Clin Hosp, Dept Hematol, Moscow, Russia.
[Shpilberg, Ofer] Comprehens Ctr Thalassemia & Hemoglobinopathies, Inst Hematol, Petah Tiqwa, Israel.
[Kropff, Martin H.] Univ Munster, Munster, Germany.
[Petrucci, Maria Teresa] Univ Roma La Sapienza, Rome, Italy.
[Delforge, Michel; Schots, Rik] Belgian Hematol Soc, Myeloma Study Grp, Louvain, Belgium.
[Alexeeva, Julia A.] St Petersburg City Hosp, Dept Haematol, St Petersburg, Russia.
[Masszi, Tamas] St Laszlo Hosp Budapest, Budapest, Hungary.
[Miguel, Jesus F. San] USAL CSIC, IBMCC, CIC, Hosp Univ Salamanca, Salamanca, Spain.
[Deraedt, William; Cakana, Andrew; van de Velde, Helgi] Johnson & Johnson Pharmaceut Res & Dev, Beerse, Belgium.
[Liu, Kevin] Johnson & Johnson Pharmaceut, Res & Dev, Raritan, NJ USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 608
EP 609
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702061
ER
PT J
AU Jacobus, S
Kumar, S
Callander, NS
Abonour, R
Fonseca, R
Siegel, D
Greipp, P
Rajkumar, SV
AF Jacobus, Susanna
Kumar, Shaji
Callander, Natalie Scott
Abonour, Rafat
Fonseca, Rafael
Siegel, David
Greipp, Philip
Rajkumar, S. Vincent
TI Effect of Venous Thrombotic Events on Overall Survival in Multiple
Myeloma: Analysis of Thrombotic Events Occurring in E4A03A Randomized
Trial of Lenalidomide Plus High-Dose Dexamethasone (RD) Versus
Lenalidomide Plus Low-Dose Dexamethasone (Rd) in Newly Diagnosed
Multiple Myeloma, a Trial Coordinated by the Eastern Cooperative
Oncology Group (ECOG).
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Jacobus, Susanna] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Kumar, Shaji; Greipp, Philip; Rajkumar, S. Vincent] Mayo Clin, Rochester, MN USA.
[Callander, Natalie Scott] Univ Wisconsin, Madison, WI USA.
[Abonour, Rafat] Indiana Univ Canc, Indianapolis, IN USA.
[Fonseca, Rafael] Mayo Clin, Scottsdale, AZ USA.
[Siegel, David] Hackensack Univ, Med Ctr, Hackensack, NJ USA.
RI Kumar, Shaji/A-9853-2008
OI Kumar, Shaji/0000-0001-5392-9284
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 613
EP 614
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702074
ER
PT J
AU Richardson, P
Schlag, R
Khuageva, NK
Dimopoulos, MA
Shpilberg, O
Kropff, MH
Delforge, M
Petrucci, MT
Rossiev, VA
Hou, J
Robak, T
Mateos, MV
Anderson, KC
Cakana, A
Liu, K
Deraedt, W
van de Velde, H
Miguel, JFS
AF Richardson, Paul
Schlag, Rudolf
Khuageva, Nuriet K.
Dimopoulos, Meletios A.
Shpilberg, Ofer
Kropff, Martin H.
Delforge, Michel
Petrucci, Maria Teresa
Rossiev, Victor A.
Hou, Jian
Robak, Tadeusz
Mateos, Maria-Victoria
Anderson, Kenneth C.
Cakana, Andrew
Liu, Kevin
Deraedt, William
van de Velde, Heigi
Miguel, Jesus F. San
TI Erythropoiesis-Stimulating Agents Do Not Adversely Affect Long-Term
Outcomes Nor Increase the Risk of Thromboembolic Events in Multiple
Myeloma Patients Treated in the Phase III VISTA Trial
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Richardson, Paul; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Schlag, Rudolf] Praxis Hematol & Oncol, Wurzburg, Germany.
[Khuageva, Nuriet K.] SP Botkin Moscow City Clin Hosp, Dept Hematol, Moscow, Russia.
[Dimopoulos, Meletios A.] Univ Athens, Sch Med, Dept Clin Therapeut, GR-11527 Athens, Greece.
[Shpilberg, Ofer] Rabin Med Ctr, Petah Tiqwa, Israel.
[Kropff, Martin H.] Univ Munster, Munster, Germany.
[Delforge, Michel] Belgian Hematol Soc, Myeloma Study Grp, Brussels, Belgium.
[Petrucci, Maria Teresa] Univ Roma La Sapienza, Rome, Italy.
[Rossiev, Victor A.] Samara Reg Clin Hosp, Dept Haematol, Samara, Russia.
[Hou, Jian] Changzheng Hosp, Shanghai, Peoples R China.
[Robak, Tadeusz] Med Univ Lodz, Dept Hematol, Lodz, Poland.
[Miguel, Jesus F. San] USAL CSIC, IBMCC, CIC, Hosp Univ Salamanca, Salamanca, Spain.
[Cakana, Andrew; Deraedt, William; van de Velde, Heigi] Johnson & Johnson Pharmaceut Res & Dev, Beerse, Belgium.
[Liu, Kevin] Johnson & Johnson Pharmaceut Res & Dev, Raritan, NJ USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 614
EP 614
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702075
ER
PT J
AU Richardson, P
Jagannath, S
Jakubowiak, A
Lonial, S
Raje, N
Alsina, M
Ghobrial, I
Mazumder, A
Munshi, NC
Vesole, DH
Colson, K
McKenney, ML
Lunde, L
Kennedy, S
Kosakowski, K
Mitsiades, C
Hideshima, T
Knight, RD
Esseltine, DL
Anderson, KC
AF Richardson, Paul
Jagannath, Sundar
Jakubowiak, Andrzej
Lonial, Sagar
Raje, Noopur
Alsina, Melissa
Ghobrial, Irene
Mazumder, Amitabha
Munshi, Nikhil C.
Vesole, David H.
Colson, Kathleen
McKenney, Mary L.
Lunde, Laura
Kennedy, Sarah
Kosakowski, Kara
Mitsiades, Constantine
Hideshima, Teru
Knight, Robert D.
Esseltine, Dixie-Lee
Anderson, Kenneth C.
TI Lenalidomide, Bortezomib, and Dexamethasone in Patients with Relapsed or
Relapsed/Refractory Multiple Myeloma (MM): Encouraging Response Rates
and Tolerability with Correlation of Outcome and Adverse Cytogenetics in
a Phase II Study.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Richardson, Paul; Ghobrial, Irene; Munshi, Nikhil C.; Colson, Kathleen; McKenney, Mary L.; Lunde, Laura; Mitsiades, Constantine; Hideshima, Teru; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Jagannath, Sundar; Mazumder, Amitabha; Vesole, David H.; Kennedy, Sarah] St Vincents Comprehens Canc Ctr, New York, NY USA.
[Jakubowiak, Andrzej] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Lonial, Sagar] Emory Univ, Sch Med, Winship Canc Inst, Atlanta, GA USA.
[Raje, Noopur] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Hematol & Oncol, Boston, MA USA.
[Alsina, Melissa; Kosakowski, Kara] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Knight, Robert D.] Celgene Inc, Summit, NJ USA.
Takeda Oncol Co, Millennium Pharmaceut, Cambridge, MA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 614
EP 615
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702076
ER
PT J
AU Yoda, A
Sattler, M
Weinstock, DM
AF Yoda, Alcinori
Sattler, Martin
Weinstock, David M.
TI Functional Oncogene Identification in Patient Leukemia Samples
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Yoda, Alcinori; Sattler, Martin] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Weinstock, David M.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 633
EP 633
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702124
ER
PT J
AU Peyvandi, F
Spreafico, M
Foco, L
Bernardinelli, L
Duga, S
Asselta, R
Ardissino, D
Kathiresan, S
Merlini, P
Mannucci, PM
AF Peyvandi, Flora
Spreafico, Marta
Foco, Luisa
Bernardinelli, Luisa
Duga, Stefano
Asselta, Rosanna
Ardissino, Diego
Kathiresan, Sekar
Merlini, Pierangelica
Mannucci, Pier M.
TI Factor V Leiden Is Associated with Premature Myocardial Infarction
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Peyvandi, Flora; Spreafico, Marta; Mannucci, Pier M.] Univ Milan, Maggiore Hosp, IRCCS, Dept Med & Med Specialties, Milan, Italy.
[Foco, Luisa] Univ Pavia, Diparlimento Sci Sanitarie Applicate & Psicocompo, I-27100 Pavia, Italy.
[Bernardinelli, Luisa] Univ Forvie Site, Inst Publ Hlth, Biostat Unit, MRC, Cambridge, England.
[Duga, Stefano; Asselta, Rosanna] Univ Milan, Dept Biol & Genet Med Sci, Milan, Italy.
[Ardissino, Diego] Univ Parma, Maggiore Hosp, Div Cardiol, I-43100 Parma, Italy.
[Kathiresan, Sekar] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Merlini, Pierangelica] Azienda Osped Niguarda Ca Granda, Div Cardiol, Milan, Italy.
RI Mannucci, Pier/C-3102-2014
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 640
EP 640
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702150
ER
PT J
AU Bergmeier, W
Oh-Hora, M
McCarl, CA
Roden, RC
Bray, PF
Feske, S
AF Bergmeier, Wolfgang
Oh-Hora, Masatsugu
McCarl, Christie-Ann
Roden, R. Claire
Bray, Paul F.
Feske, Stefan
TI R93W Mutation in Orai1 Causes Impaired Calcium Influx in Platelets
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Bergmeier, Wolfgang; Roden, R. Claire; Bray, Paul F.] Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
[Oh-Hora, Masatsugu] Harvard Univ, Sch Med, Immune Dis Inst, Boston, MA USA.
[McCarl, Christie-Ann; Feske, Stefan] NYU, Sch Med, Dept Pathol, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 647
EP 647
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702171
ER
PT J
AU Flaumenhaft, R
Dilks, JR
Rozenvayn, N
Woronowicz, K
AF Flaumenhaft, Robert
Dilks, James R.
Rozenvayn, Nataliya
Woronowicz, Kamil
TI The Platelet Actin Cytoskeleton Associates Directly with Syntaxin-4 and
Participates in alpha-Granule Secretion
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Flaumenhaft, Robert; Dilks, James R.; Rozenvayn, Nataliya; Woronowicz, Kamil] Harvard Univ, Sch Med, Dept Med, BIDMC, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 647
EP 647
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702172
ER
PT J
AU Raffel, GD
Chu, GC
Cullen, DE
Bronson, RT
Bernard, OA
Gilliland, DG
AF Raffel, Glen D.
Chu, Gerry C.
Cullen, Dana E.
Bronson, Roderick T.
Bernard, Olivier A.
Gilliland, D. Gary
TI Vascular Branching Morphogenesis of the Placenta Requires Expression of
Ott1(Rbm15) in the Trophoblast Compartment.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Raffel, Glen D.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Cullen, Dana E.] Brigham & Womens Hosp, Dept Med, Div Hematol, Boston, MA 02115 USA.
[Chu, Gerry C.; Cullen, Dana E.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Bronson, Roderick T.] Harvard Univ, Dept Rodent Pathol, Sch Med, Boston, MA 02115 USA.
[Bernard, Olivier A.] Hop Necker Enfants Malad, Hematol Lab, Paris, France.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 663
EP 663
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702228
ER
PT J
AU Stam, RW
Den Boer, ML
Schneider, P
de Boer, J
Hagelstein, J
Sallan, SE
Brady, HJM
Armstrong, S
Pieters, R
AF Stam, Ronald W.
Den Boer, Monique L.
Schneider, Pauline
de Boer, Jasper
Hagelstein, Jill
Sallan, Stephen E.
Brady, Hugh J. M.
Armstrong, Scott
Pieters, Rob
TI Rearranged Infant Acute Lymphoblastic Leukemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Stam, Ronald W.; Den Boer, Monique L.; Schneider, Pauline; Hagelstein, Jill; Pieters, Rob] Sophia Childrens Univ Hosp, Erasmus MC, Rotterdam, Netherlands.
[de Boer, Jasper; Brady, Hugh J. M.] UCL Inst Child Hlth, Mol Haematol & Canc Biol Unit, London, England.
[de Boer, Jasper; Brady, Hugh J. M.] Great Ormond St Hosp Sick Children, London, England.
[Sallan, Stephen E.; Armstrong, Scott] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 668
EP 668
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702246
ER
PT J
AU Rowe, JM
Yao, XP
Cassileth, PA
Appelbaum, FR
Wiernik, PH
Schiffer, C
Litzow, MR
Luger, S
Bennett, JM
Lazarus, HM
Tallman, MS
AF Rowe, Jacob M.
Yao, Xiaopan
Cassileth, Peter A.
Appelbaum, Frederick R.
Wiernik, Peter H.
Schiffer, Charles
Litzow, Mark R.
Luger, Selina
Bennett, John M.
Lazarus, Hillard M.
Tallman, Martin S.
TI The Pitfalls of Early Publication of Data in Acute Myeloid Leukemia: A
Report from the Eastern Cooperative Oncology Group (ECOG).
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Rowe, Jacob M.] Technion Israel Inst Technol, Haifa, Israel.
[Yao, Xiaopan] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Cassileth, Peter A.] Univ Miami, Sylvester Canc Ctr, Miami, FL USA.
[Appelbaum, Frederick R.] Univ Washington, Fred Hutchinson Canc Res Ctr, Sch Med, Seattle, WA 98195 USA.
[Wiernik, Peter H.] New York Med Coll, Our Lady Mercy Canc Ctr, Bronx, NY USA.
[Schiffer, Charles] Wayne State Univ, Detroit, MI USA.
[Litzow, Mark R.] Mayo Clin, Rochester, MN USA.
[Luger, Selina] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Bennett, John M.] Univ Rochester, Rochester, NY USA.
[Lazarus, Hillard M.] Univ Hosp Cleveland, Ireland Canc Ctr, Cleveland, OH 44106 USA.
[Tallman, Martin S.] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 681
EP 681
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702285
ER
PT J
AU Ballen, KK
Cutler, C
Yeap, BY
McAfee, SL
Dey, BR
Attar, EC
Haspel, RL
Liney, D
Koreth, J
Ho, V
Alyea, EP
Soiffer, RJ
Spitzer, TR
Antin, JH
AF Ballen, Karen K.
Cutler, Corey
Yeap, Beow Y.
McAfee, Steven L.
Dey, Bimalangshu R.
Attar, Eyal C.
Haspel, Richard L.
Liney, Deborah
Koreth, John
Ho, Vincent
Alyea, Edwin P., III
Soiffer, Robert J.
Spitzer, Thomas R.
Antin, Joseph H.
TI High Rate of Second Malignancies after Reduced Intensity Double Cord
Blood Transplants in Adults.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ballen, Karen K.; Yeap, Beow Y.; McAfee, Steven L.; Dey, Bimalangshu R.; Attar, Eyal C.; Spitzer, Thomas R.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Cutler, Corey; Liney, Deborah; Koreth, John; Ho, Vincent; Alyea, Edwin P., III; Soiffer, Robert J.; Antin, Joseph H.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Haspel, Richard L.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 683
EP 683
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702291
ER
PT J
AU Zhou, J
Lu, CF
Yu, HJ
Hou, JX
Liu, SC
Ma, M
Gilbert, G
Shi, JL
AF Zhou, Jin
Lu, Chengfang
Yu, Hongjuan
Hou, Jinxiao
Liu, Shuchuan
Ma, Ming
Gilbert, Gary
Shi, Jialan
TI Elevated Procoagulant Activity Due to Phosphatidylserine Exposure on Red
Blood Cells during Storage
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Zhou, Jin; Lu, Chengfang; Yu, Hongjuan; Hou, Jinxiao; Liu, Shuchuan; Ma, Ming] Harbin Med Coll, Affiliated Hosp 1, Dept Med, Harbin, Peoples R China.
[Gilbert, Gary; Shi, Jialan] Brigham & Womens Hosp, Dept Med, VA Boston Healthcare Syst, Boston, MA 02115 USA.
[Gilbert, Gary; Shi, Jialan] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 696
EP 696
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702329
ER
PT J
AU Ioakimidis, L
Patterson, C
Soumerai, J
Manning, R
Sheehy, P
Treon, S
AF Ioakimidis, Leukothea
Patterson, Christopher
Soumerai, Jacob
Manning, Robert
Sheehy, Patricia
Treon, Steven
TI Comparative Outcomes Following CP-R, CVP-R and CHOP-R in Patients with
Waldenstrom's Macroglobulinemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ioakimidis, Leukothea; Manning, Robert; Sheehy, Patricia] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 702
EP 702
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702344
ER
PT J
AU Wierda, WG
Kipps, TJ
Keating, MJ
Brown, JR
Gribben, JG
Rassenti, LZ
Greaves, AW
Neuberg, D
O'Brien, SM
AF Wierda, William G.
Kipps, Thomas J.
Keating, Michael J.
Brown, Jennifer R.
Gribben, John G.
Rassenti, Lauta Z.
Greaves, Andrew W.
Neuberg, Donna
O'Brien, Susan M.
TI Plasma Alemtuzumab Levels at End of Treatment Correlate with Response
and Response Duration in Patients with CLL Receiving Treatment for
Residual Disease
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Wierda, William G.; Keating, Michael J.; O'Brien, Susan M.] UTMD Anderson Canc Ctr, Houston, TX USA.
[Kipps, Thomas J.; Rassenti, Lauta Z.; Greaves, Andrew W.] Univ Calif San Diego, Moores Canc Ctr, San Diego, CA 92103 USA.
[Brown, Jennifer R.; Neuberg, Donna] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Gribben, John G.] Ctr Med Oncol, Inst Canc, London, England.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 734
EP 734
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702442
ER
PT J
AU Wilson, WH
O'Connor, O
Czuczman, MS
LaCasce, A
Gerecitano, J
Leonard, JP
Tulpule, A
Xiong, H
Chiu, YL
Busman, T
Knight, RA
Enschede, S
Krivoshik, A
Humerickhouse, R
AF Wilson, Wyndham H.
O'Connor, O.
Czuczman, Myron S.
LaCasce, Ann
Gerecitano, J.
Leonard, John P.
Tulpule, Anil
Xiong, Hao
Chiu, Yi-Lin
Busman, Todd
Knight, Raymond A.
Enschede, Sari
Krivoshik, Andrew
Humerickhouse, Rod
TI Phase 1 Study of ABT-263, a Bcl-2 Family Inhibitor, in Relapsed or
Refractory Lymphoid Malignancies
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Wilson, Wyndham H.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[O'Connor, O.] Columbia Univ, Med Ctr, New York, NY USA.
[Czuczman, Myron S.] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[LaCasce, Ann] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Gerecitano, J.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Leonard, John P.] Weill Cornell Med Coll, Div Hem Onc, New York, NY USA.
[Tulpule, Anil] USC, Norris Canc Ctr, Sch Med, Los Angeles, CA USA.
[Xiong, Hao; Chiu, Yi-Lin; Busman, Todd; Knight, Raymond A.; Enschede, Sari; Krivoshik, Andrew; Humerickhouse, Rod] Abbott Labs, Abbott Pk, IL 60064 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 734
EP 734
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702441
ER
PT J
AU Duncan, C
Vrooman, L
Bechard, L
Barry, E
Lehmann, LE
AF Duncan, Christine
Vrooman, Lynda
Bechard, Lori
Barry, Elly
Lehmann, Leslie E.
TI The Prevalence of 25-Hydroxyvitamin D Deficiency in Post-HSCT Pediatric
Patients
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Duncan, Christine; Vrooman, Lynda; Barry, Elly; Lehmann, Leslie E.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Bechard, Lori] Childrens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 745
EP 745
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702472
ER
PT J
AU Sorror, ML
Storer, B
Sandmaier, BM
Maris, M
Chauncey, T
Maziarz, RT
Pulsipher, M
Shizuru, J
Niederwieser, D
Agura, E
Wade, JC
Langston, AA
Storb, RF
Maloney, DG
AF Sorror, Mohamed L.
Storer, Barry
Sandmaier, Brenda M.
Maris, Michael
Chauncey, Thomas
Maziarz, Richard T.
Pulsipher, Michael
Shizuru, Judith
Niederwieser, Dietger
Agura, Edward
Wade, James C.
Langston, Amelia A.
Storb, Rainer F.
Maloney, David G.
TI Sustained Graft-Versus-Lymphoma Effect among Patients (pts) with Mantle
Cell Lymphoma (MCL) Given Nonmyeloablative, Allogeneic Hematopoictic
Cell Transplantation (HCT).
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Chauncey, Thomas] Univ Washington, Fred Hutchinson Canc Res Ctr, VA Puget Sound Hlth Care Syst, Seattle, WA 98195 USA.
[Maziarz, Richard T.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Pulsipher, Michael] Univ Utah, Med Ctr, Salt Lake City, UT USA.
[Shizuru, Judith] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
[Niederwieser, Dietger] Univ Leipzig, Leipzig, Germany.
[Agura, Edward] Baylor Univ, Med Ctr, Dallas, TX USA.
[Wade, James C.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Langston, Amelia A.] Emory Univ, Sch Med, Atlanta, GA USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 747
EP 748
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702480
ER
PT J
AU Sorror, ML
Storer, B
Sandmaier, BM
Maloney, DG
Franke, G
Shizuru, J
Chauncey, T
Agura, E
Maziarz, RT
Sahebi, F
Langston, AA
Wade, JC
Maris, M
Bruno, B
Yeager, AM
Pulsipher, M
Petersen, F
Bethge, WA
McSweeney, PA
Niederwieser, D
Blume, KG
Storb, RF
AF Sorror, Mohamed L.
Storer, Barry
Sandmaier, Brenda M.
Maloney, David G.
Franke, Georg
Shizuru, Judith
Chauncey, Thomas
Agura, Edward
Maziarz, Richard T.
Sahebi, Firoozeh
Langston, Amelia A.
Wade, James C.
Maris, Michael
Bruno, Benedetto
Yeager, Andrew M.
Pulsipher, Michael
Petersen, Finn
Bethge, Wolfgang A.
McSweeney, Peter A.
Niederwieser, Dietger
Blume, Karl G.
Storb, Rainer F.
TI Allogeneic Hematopoietic Cell Transplantation (HCT) after
Nonmyeloablative Conditioning for Patients (pts) Aged >= 60 Years
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Chauncey, Thomas] Univ Washington, Fred Hutchinson Canc Res Ctr, VA Puget Sound Hlth Care Syst, Seattle, WA 98195 USA.
[Agura, Edward] Baylor Univ, Med Ctr, Dallas, TX USA.
[Franke, Georg] Univ Leipzig, Laipzig, Germany.
[Shizuru, Judith; Blume, Karl G.] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
[Maziarz, Richard T.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Sahebi, Firoozeh] City Hope Natl Med Ctr, Duarte, CA 91010 USA.
[Langston, Amelia A.] Emory Univ, Sch Med, Atlanta, GA USA.
[Wade, James C.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Maris, Michael; McSweeney, Peter A.] Rocky Mt Canc Ctr, Denver, CO USA.
[Bruno, Benedetto] Univ Turin, Turin, Italy.
[Yeager, Andrew M.] Univ Arizona, Tucson, AZ USA.
[Pulsipher, Michael] Univ Utah, Med Ctr, Salt Lake City, UT USA.
[Petersen, Finn] LDS Hosp, Salt Lake City, UT USA.
[Bethge, Wolfgang A.] Univ Tubingen, Med Ctr, Tubingen, Germany.
[Niederwieser, Dietger] Univ Leipzig, Leipzig, Germany.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 753
EP 754
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702495
ER
PT J
AU Keating, A
Kukreja, M
da Silva, GT
Gupta, V
Cutler, C
Tallman, MS
Sierra, J
DiPersio, JF
Horowitz, MM
Weisdorf, DJ
AF Keating, Armand
Kukreja, Manisha
da Silva, Gisela Tunes
Gupta, Vikas
Cutler, Corey
Tallman, Martin S.
Sierra, Jorge
DiPersio, John F.
Horowitz, Mary M.
Weisdorf, Daniel J.
TI Similar 5-Year Survival after Peripheral Blood Autotransplants (AutoPB)
Versus HILA Matched Sibling Myeloablative Transplants (AlloBMT) for
Acute Myeloid Leukemia (AML) in First Complete Remission (CRI)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Keating, Armand; Gupta, Vikas] Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
[Kukreja, Manisha; Horowitz, Mary M.] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
[Cutler, Corey] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Tallman, Martin S.] Northwestern Univ, Feinberg Sch Med, Chicago, IL USA.
[Sierra, Jorge] Hosp Santa Creu & Sant Pau, Barcelona, Spain.
[DiPersio, John F.] Washington Univ, Sch Med, St Louis, MO USA.
[Weisdorf, Daniel J.] Univ Minnesota, Minneapolis, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 756
EP 756
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702501
ER
PT J
AU Kao, G
Stevenson, K
Kim, E
Spanjaard, E
Kim, HT
Ritz, J
AF Kao, Grace
Stevenson, Kristen
Kim, Elliot
Spanjaard, Elena
Kim, Haesook T.
Ritz, Jerome
TI Autologous Peripheral Blood Stem Cell Products from Patients with
Hematologic Malignancies Have Increased Frequency of Regulatory T Cells
(CD4+FoxP3+Treg)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Kao, Grace; Stevenson, Kristen; Kim, Elliot; Spanjaard, Elena; Kim, Haesook T.; Ritz, Jerome] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 806
EP 806
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702643
ER
PT J
AU Kirkorian, AY
Collin, MP
Mielcarek, M
Zhang, WD
Neuberg, D
Wu, CJ
Merad, M
AF Kirkorian, A. Yasmine
Collin, Matthew P.
Mielcarek, Marco
Zhang, Wandi
Neuberg, Donna
Wu, Catherine J.
Merad, Miriam
TI A Novel SNP-Based Method for Assessing Langerhans Cell Chimerism
Following Hematopoietic Stem Cell Transplantation in Humans.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Kirkorian, A. Yasmine; Collin, Matthew P.; Merad, Miriam] Mt Sinai Med Ctr, Dept Gene & Cell Med, New York, NY 10029 USA.
[Mielcarek, Marco] Fred Hutchinson Canc Rsch Ctr, Seattle, WA USA.
[Zhang, Wandi] Dana Farber Canc Inst, Canc Vaccine Ctr, Boston, MA 02115 USA.
[Neuberg, Donna] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Wu, Catherine J.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 811
EP 811
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702661
ER
PT J
AU Duran-Struuck, R
Horner, BM
Lutton, BV
Teague, AGS
Ferguson, KK
Summers, JC
Spitzer, T
Jay, F
Houser, S
Sachs, DH
Huang, CA
AF Duran-Struuck, Raimon
Horner, Banjamin M.
Lutton, Bram V.
Teague, Alex G. S.
Ferguson, Kelly K.
Summers, Jonathan C.
Spitzer, Thomas
Jay, Fishman
Houser, Stuart
Sachs, David H.
Huang, Christene A.
TI Conversion to Full Donor Chimerism without Gvhd Using High-Dose DLI in
Minimally Conditioned Miniature Swine Recipients of Haploidentical HCT.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Duran-Struuck, Raimon; Horner, Banjamin M.; Lutton, Bram V.; Teague, Alex G. S.; Ferguson, Kelly K.; Summers, Jonathan C.; Spitzer, Thomas; Jay, Fishman; Houser, Stuart; Sachs, David H.; Huang, Christene A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 814
EP 814
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702669
ER
PT J
AU Li, LQ
Wang, H
Bronson, R
Boussiotis, V
AF Li, Lequn
Wang, Hui
Bronson, Roderick
Boussiotis, Vassiliki
TI Roscovitine Prevents Alloreactive T Cell Expansion and TNF-a-Mediated
Proinflammatory Gene Expression and Protects against GvHD.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Li, Lequn; Boussiotis, Vassiliki] Beth Israel Deaconess Med Ctr, Harvard Inst Med, Boston, MA 02215 USA.
[Wang, Hui] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Bronson, Roderick] Harvard Univ, Sch Med, Dept Rodent Pathol, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 815
EP 816
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702674
ER
PT J
AU Flutter, BR
Fallah-Arani, F
Bennett, C
Sivakumaran, J
Freeman, GJ
Sykes, M
Chakraverty, R
AF Flutter, Barry R.
Fallah-Arani, Farnaz
Bennett, Clare
Sivakumaran, Janani
Freeman, Gordon J.
Sykes, Megan
Chakraverty, Ronjon
TI Peripheral Alloantigen Drives Early Dysfunction and Eventual Exhaustion
of CTL Following Delayed Donor Leukocyte Infusions
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Flutter, Barry R.; Fallah-Arani, Farnaz; Bennett, Clare; Sivakumaran, Janani; Chakraverty, Ronjon] UCL, Transplantat Immunol Grp, London, England.
[Freeman, Gordon J.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Sykes, Megan] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Transplant Biol Res Ctr, Boston, MA USA.
RI bennett, clare/J-5249-2013
OI bennett, clare/0000-0001-9146-2347
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 817
EP 817
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702679
ER
PT J
AU Van Bennekom, CM
Raje, N
Anderson, KC
Anderson, TE
Kaufman, DW
AF Van Bennekom, Carla M.
Raje, Noopur
Anderson, Kenneth C.
Anderson, Theresa E.
Kaufman, David W.
TI Treatment Patterns among Patients with Recently-Diagnosed Multiple
Myeloma in a National Registry
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Van Bennekom, Carla M.; Anderson, Theresa E.; Kaufman, David W.] Boston Univ, Slone Epidemiol Ctr, Boston, MA 02215 USA.
[Raje, Noopur] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Hematol & Oncol, Boston, MA USA.
[Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 827
EP 827
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702707
ER
PT J
AU Friese, CR
Abel, GA
Magazu, LS
Neville, BA
Hevelone, ND
Richardson, LC
Earle, CC
AF Friese, Christopher R.
Abel, Gregory A.
Magazu, Lysa S.
Neville, Bridget A.
Hevelone, Nathanael D.
Richardson, Lisa C.
Earle, Craig C.
TI Diagnostic Patterns of Care and Outcomes for Patients with Chronic.,and
End-Results Lymphocytic Leukemia in the Surveillance, Epidemiology
(SEER)-Medicare Database
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Friese, Christopher R.] Univ Michigan, Sch Nursing, Ann Arbor, MI 48109 USA.
[Abel, Gregory A.; Magazu, Lysa S.; Neville, Bridget A.] Dana Farber Canc Inst, Ctr Outcomes & Policy Res, Dept Med Oncol, Boston, MA 02115 USA.
[Hevelone, Nathanael D.] Univ Calif San Francisco, Dept Surg, San Francisco, CA 94143 USA.
[Richardson, Lisa C.] Ctr Dis Control & Prevent, Div Canc Prevent & Control, Decatur, GA USA.
[Earle, Craig C.] Sunnybrook Hlth Sci Ctr, Inst Clin Evaluat Sci, Toronto, ON M4N 3M5, Canada.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 836
EP 836
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702732
ER
PT J
AU Mizuno, SI
Ozawa, H
Iino, T
Arinobu, Y
Yong, C
Shigematsu, H
Akashi, K
AF Mizuno, Shini-Ichi
Ozawa, Hidetoshi
Iino, Tadafumi
Arinobu, Yojiro
Yong, Chong
Shigematsu, Hirokazu
Akashi, Koichi
TI Notch1 Expression Is Regulated at Post-Transcriptional Level by 3'UTR
Region in Hematopoietic Stem Cell Development.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Mizuno, Shini-Ichi; Ozawa, Hidetoshi; Iino, Tadafumi; Arinobu, Yojiro; Yong, Chong; Shigematsu, Hirokazu; Akashi, Koichi] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 854
EP 854
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702789
ER
PT J
AU Juszczynski, P
Rodig, SJ
Takeyama, K
Ouyang, J
Faber, J
Armstrong, S
Kutok, JL
Shipp, MA
AF Juszczynski, Przemyslaw
Rodig, Scott J.
Takeyama, Kunihiko
Ouyang, Jing
Faber, Jorg
Armstrong, Scott
Kutok, Jeffery L.
Shipp, Margaret A.
TI Selective Expression of the Immunoregulatory Lectin, Galectin-1, in
Precursor B Cell Acute Lymphoblastic Leukemias (ALLs) with MLL
Rearrangements.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Juszczynski, Przemyslaw; Takeyama, Kunihiko; Ouyang, Jing; Shipp, Margaret A.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Rodig, Scott J.; Kutok, Jeffery L.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Faber, Jorg; Armstrong, Scott] Childrens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 882
EP 882
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104702871
ER
PT J
AU Peled, JU
Yu, JJ
Ding, BB
Shaknovich, R
Sicinski, P
Scharff, MD
Ye, BH
AF Peled, Jonathan U.
Yu, J. Jessica
Ding, Beibei Belinda
Shaknovich, Rita
Sicinski, Piotr
Scharff, Matthew D.
Ye, B. Hilda
TI Cyclin D3 Is Required for the Germinal Center Reaction.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Peled, Jonathan U.; Yu, J. Jessica; Ding, Beibei Belinda; Scharff, Matthew D.; Ye, B. Hilda] Albert Einstein Coll Med, Dept Cell Biol, Bronx, NY 10467 USA.
[Shaknovich, Rita] Cornell Med Ctr, Dept Med, New York, NY USA.
[Shaknovich, Rita] Cornell Med Ctr, Dept Pathol, New York, NY USA.
[Sicinski, Piotr] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 895
EP 895
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703022
ER
PT J
AU Canellos, GP
AF Canellos, George P.
TI Chemotherapy Alone for Localized Non-Bulky Hodgkin Lymphoma.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Canellos, George P.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 898
EP 898
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703032
ER
PT J
AU Melhem, MR
Roccaro, AM
Azab, A
Ngo, HT
Sacco, A
Jia, XY
Azab, F
Runnels, J
Burwick, N
Quang, P
Husu, EN
Leleu, X
Anderson, KC
Ghobrial, IM
AF Melhem, Molly R.
Roccaro, Aldo M.
Azab, Abdelkareem
Ngo, Hai T.
Sacco, Antonio
Jia, Xiaoying
Azab, Feda
Runnels, Judith
Burwick, Nicolas
Quang, Phong
Husu, Emanuel N.
Leleu, Xavier
Anderson, Kenneth C.
Ghobrial, Irene M.
TI PKC412, a Small Molecule Tyrosine Kinase Inhibitor, Regulates Survival
and Proliferation Pathways in Waldenstrom Macroglobulinemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Melhem, Molly R.; Roccaro, Aldo M.; Azab, Abdelkareem; Ngo, Hai T.; Sacco, Antonio; Jia, Xiaoying; Azab, Feda; Runnels, Judith; Burwick, Nicolas; Quang, Phong; Husu, Emanuel N.; Leleu, Xavier; Anderson, Kenneth C.; Ghobrial, Irene M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 905
EP 905
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703055
ER
PT J
AU Jia, XY
Roccaro, AM
Azab, AK
Ngo, HT
Sacco, A
Melhem, MR
Azab, F
Runnels, J
Burwick, N
Quang, P
Husu, EN
Leleu, X
Anderson, KC
Bradner, J
Ghobrial, IM
AF Jia, Xiaoying
Roccaro, Aldo M.
Azab, Abdel Kareem
Ngo, Hai T.
Sacco, Antonio
Melhem, Molly R.
Azab, Feda
Runnels, Judith
Burwick, Nicolas
Quang, Phong
Husu, Emanuel N.
Leleu, Xavier
Anderson, Kenneth C.
Bradner, James
Ghobrial, Irene M.
TI Regulation of Histone Deacetylase in Waldenstrom Macroglobulinemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Jia, Xiaoying; Roccaro, Aldo M.; Azab, Abdel Kareem; Ngo, Hai T.; Sacco, Antonio; Melhem, Molly R.; Azab, Feda; Runnels, Judith; Burwick, Nicolas; Quang, Phong; Husu, Emanuel N.; Leleu, Xavier; Anderson, Kenneth C.; Bradner, James; Ghobrial, Irene M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 906
EP 906
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703058
ER
PT J
AU Ngo, HT
Farag, M
Jia, XY
Burwick, N
Methem, MR
Leleu, X
Runnels, J
Azab, AK
Roccaro, AM
Azab, F
Sacco, A
Quang, P
Tai, YT
Anderson, KC
Ghobrial, IM
AF Ngo, Hai T.
Farag, Mena
Jia, Xiaoying
Burwick, Nicolas
Methem, Molly R.
Leleu, Xavier
Runnels, Judith
Azab, Abdel Kareern
Roccaro, Aldo M.
Azab, Feda
Sacco, Antonio
Quang, Phong
Tai, Yu-Tzu
Anderson, Kenneth C.
Ghobrial, Irene M.
TI The Tyrosine Kinase Src Regulates Adhesion and Survival in Waldenstrom
Macroglobulinemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ngo, Hai T.; Farag, Mena; Jia, Xiaoying; Burwick, Nicolas; Methem, Molly R.; Runnels, Judith; Azab, Abdel Kareern; Roccaro, Aldo M.; Azab, Feda; Sacco, Antonio; Quang, Phong; Tai, Yu-Tzu; Anderson, Kenneth C.; Ghobrial, Irene M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Leleu, Xavier] Ctr Hosp Reg & Univ Lille, Hop Huriez, Serv Malad Sang, F-59037 Lille, France.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 906
EP 906
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703056
ER
PT J
AU Bernal, F
Wade, M
Silverstein, AM
Verdine, GL
Wahl, GM
Walensky, LD
AF Bernal, Federico
Wade, Mark
Silverstein, Amy M.
Verdine, Gregory L.
Wahl, Geoffrey M.
Walensky, Loren D.
TI A Stapled p53 Helix Targets HDMX to Overcome Nutlin-3 Resistance and
Reactivate the p53 Tumor Suppressor Pathway in Cancer
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Bernal, Federico; Silverstein, Amy M.; Walensky, Loren D.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Childrens Hosp Boston,Dept Pediat Oncol, Boston, MA USA.
[Wade, Mark; Wahl, Geoffrey M.] Salk Inst Biol Studies, Gene Express Lab, La Jolla, CA 92037 USA.
[Verdine, Gregory L.] Harvard Univ, Dept Chem & Chem Biol, Cambridge, MA 02138 USA.
RI Wade, Mark /B-6719-2009
OI Wade, Mark /0000-0002-2688-5965
NR 0
TC 1
Z9 1
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 NOV 16
PY 2008
VL 112
IS 11
BP 915
EP 915
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703085
ER
PT J
AU Jakubikova, J
Sedlak, J
Klippel, S
Leiba, M
Tai, YT
Hideshima, T
Podar, K
Chauhan, D
Raje, N
Richardson, PG
Anderson, KC
Mitsiades, CS
AF Jakubikova, Jana
Sedlak, Jan
Klippel, Steffen
Leiba, Merav
Tai, Yu-Tzu
Hideshima, Teru
Podar, Klaus
Chauhan, Dharminder
Raje, Noopur
Richardson, Paul G.
Anderson, Kenneth C.
Mitsiades, Constantine S.
TI Sulforaphane and PEITC Augment Activity of Conventional and Novel
Anti-Myeloma Drugs
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Jakubikova, Jana; Klippel, Steffen; Leiba, Merav; Tai, Yu-Tzu; Hideshima, Teru; Podar, Klaus; Chauhan, Dharminder; Raje, Noopur; Richardson, Paul G.; Anderson, Kenneth C.; Mitsiades, Constantine S.] Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA.
[Sedlak, Jan] Slovak Acad Sci, Canc Res Inst, Dept Tumor Immunol, Bratislava, Slovakia.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 916
EP 916
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703088
ER
PT J
AU Ooi, MG
Hayden, PJ
McMillin, DW
Negri, JM
Delmore, J
Raje, NS
Munshi, NC
Chauhan, D
Hideshima, T
Richardson, PG
Mitsiades, CS
Anderson, KC
Mitsiades, N
AF Ooi, Melissa G.
Hayden, Patrick J.
McMillin, Douglas W.
Negri, Joseph M.
Delmore, Jake
Raje, Noopur S.
Munshi, Nikhil C.
Chauhan, Dharminder
Hideshima, Teru
Richardson, Paul G.
Mitsiades, Constantine S.
Anderson, Kenneth C.
Mitsiades, Nicholas
TI Interactions of the Mdm2/p53 and Proteasome Pathways: Implications for
Combination Strategies to Enhance the Anti-Myeloma Activity of
Bortezomib
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ooi, Melissa G.; Hayden, Patrick J.; McMillin, Douglas W.; Negri, Joseph M.; Delmore, Jake; Munshi, Nikhil C.; Chauhan, Dharminder; Hideshima, Teru; Richardson, Paul G.; Mitsiades, Constantine S.; Anderson, Kenneth C.; Mitsiades, Nicholas] Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA.
[Raje, Noopur S.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 917
EP 917
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703091
ER
PT J
AU Ooi, MG
McMillin, DW
Negri, JM
Delmore, J
Munshi, NC
Chauhan, D
Hideshima, T
Richardson, PG
Mitsiades, CS
Anderson, KC
Mitsiades, N
AF Ooi, Melissa G.
McMillin, Douglas W.
Negri, Joseph M.
Delmore, Jake
Munshi, Nikhil C.
Chauhan, Dharminder
Hideshima, Teru
Richardson, Paul G.
Mitsiades, Constantine S.
Anderson, Kenneth C.
Mitsiades, Nicholas
TI The Antidiabetic Biguanide Metformin Induces Growth Arrest in Multiple
Myeloma Cells in Vitro, overcoming the Effect of Stromal Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ooi, Melissa G.; McMillin, Douglas W.; Negri, Joseph M.; Delmore, Jake; Munshi, Nikhil C.; Chauhan, Dharminder; Hideshima, Teru; Richardson, Paul G.; Mitsiades, Constantine S.; Anderson, Kenneth C.; Mitsiades, Nicholas] Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA.
[Munshi, Nikhil C.] VA Bosto Healthcare Syst, Boston, MA USA.
[Mitsiades, Nicholas] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 917
EP 918
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703092
ER
PT J
AU McMillin, DW
Rickes, R
Negri, J
Delmore, J
Ooi, MG
Farwell, M
Crowe, D
Chen, M
Avery, W
Kansra, V
Anderson, KC
Lee, MS
Mitsiades, CS
AF McMillin, Douglas W.
Rickes, Richard
Negri, Joseph
Delmore, Jake
Ooi, Melissa G.
Farwell, Melissa
Crowe, David
Chen, Mei
Avery, William
Kansra, Vikram
Anderson, Kenneth C.
Lee, Margaret S.
Mitsiades, Constantine S.
TI Synergistic Activity of Adenosine A2A and Beta-2 Adrenergic Receptor
Agonists in Myeloma Cells in the Context of Tumor-Stromal Interactions.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [McMillin, Douglas W.; Negri, Joseph; Delmore, Jake; Ooi, Melissa G.; Anderson, Kenneth C.; Mitsiades, Constantine S.] Dana Farber Canc Inst, Dept Med Oncol, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA.
[Rickes, Richard; Farwell, Melissa; Crowe, David; Chen, Mei; Avery, William; Kansra, Vikram; Lee, Margaret S.] CombinatoRx Inc, Cambridge, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 920
EP 921
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703103
ER
PT J
AU Armand, P
Deeg, HJ
Kim, HT
Lee, H
Armistead, P
De Lima, M
Gupta, V
Soiffer, RJ
AF Armand, Philippe
Deeg, H. Joachim
Kim, Haesook T.
Lee, Hun
Armistead, Paul
De Lima, Marcos
Gupta, Vikas
Soiffer, Robert J.
TI Transplantation-Specific Cytogenetics Grouping Scheme for Patients with
Myelodysplastic Syndromes: A Multicenter Validation Study.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Armand, Philippe; Kim, Haesook T.; Soiffer, Robert J.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Deeg, H. Joachim] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Lee, Hun] Long Isl Jewish Med Ctr, New Hyde Pk, NY 11042 USA.
[Armistead, Paul] Univ Texas Houston, MD Anderson Canc Ctr, Houston, TX 77030 USA.
[De Lima, Marcos] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Gupta, Vikas] Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 924
EP 924
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703113
ER
PT J
AU Prabhala, R
Pelluru, D
Fulciniti, M
Nanjappa, P
Prabhala, HK
Prabhala, NS
Mitsiades, C
Tai, YT
Ghobrial, I
Richardson, P
Lefkimmiatis, K
Daley, JF
Efebera, YA
Anderson, KC
Munshi, NC
AF Prabhala, Rao
Pelluru, Dheeraj
Fulciniti, Mariateresa
Nanjappa, Puru
Prabhala, Harsha K.
Prabhala, Nithya S.
Mitsiades, Constantine
Tai, Yu-Tzu
Ghobrial, Irene
Richardson, Paul
Lefkimmiatis, Konstantinos
Daley, John F.
Efebera, Yvonne A.
Anderson, Kenneth C.
Munshi, Nikhil C.
TI TH17 Pathway Promotes Tumor Cell Growth and Suppresses Immune Function
in Myeloma: Potential for Therapeutic Application.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Prabhala, Rao; Pelluru, Dheeraj; Prabhala, Nithya S.; Lefkimmiatis, Konstantinos; Efebera, Yvonne A.] Harvard Univ, Sch Med, VA Boston Healthcare Syst, W Roxbury, MA USA.
[Fulciniti, Mariateresa; Nanjappa, Puru; Mitsiades, Constantine; Tai, Yu-Tzu; Ghobrial, Irene; Richardson, Paul; Daley, John F.; Munshi, Nikhil C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Prabhala, Harsha K.] Univ Virginia, Sch Med, Charlottesville, VA 22908 USA.
[Anderson, Kenneth C.] Dana Farber Canc Inst, Dept Med Oncol, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA.
RI Efebera, Yvonne/E-3012-2011
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 945
EP 946
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703177
ER
PT J
AU Pozzi, S
Yan, H
Vallet, S
Vaghela, N
Fulciniti, M
Cirstea, D
Santo, L
Mukherjee, S
Hideshima, T
Schirtzinger, L
Kuhstoss, S
Munshi, NC
Anderson, KC
Scadden, D
Raje, N
AF Pozzi, Samantha
Yan, Hua
Vallet, Sonia
Vaghela, Nileshwari
Fulciniti, Mariateresa
Cirstea, Diana
Santo, Loredana
Mukherjee, Siddhartha
Hideshima, Teru
Schirtzinger, Linda
Kuhstoss, Stuart
Munshi, Nikhil C.
Anderson, Kenneth C.
Scadden, David
Raje, Noopur
TI Promoting Osteoblastogenesis Using a Novel Dkk-1 Neutralizing Antibody
in the Treatment of Multiple Myeloma Related Bone Disease.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Pozzi, Samantha; Raje, Noopur] Harvard Univ, Massachusetts Gen Hosp, Sch Med,Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA USA.
[Schirtzinger, Linda; Kuhstoss, Stuart] Eli Lilly & Co, Lilly Res Labs, Indianapolis, IN 46285 USA.
RI Pozzi, Samantha/A-7617-2012
OI Pozzi, Samantha/0000-0001-7917-1774
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 946
EP 946
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703179
ER
PT J
AU Pelluru, D
Wang, JY
Prabhala, R
Fulciniti, M
Shammas, MA
Amin, SB
Anderson, KC
Munshi, NC
AF Pelluru, Dheeraj
Wang, Jingyi
Prabhala, Rao
Fulciniti, Mariateresa
Shammas, Masood A.
Amin, Samirkumar B.
Anderson, Kenneth C.
Munshi, Nikhil C.
TI Oncoprotein 18 (Op18) : A Differentially Expressed Gene Is a Novel
Therapeutic Target in Multiple Myeloma.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Pelluru, Dheeraj; Prabhala, Rao; Shammas, Masood A.] R&D, VA Boston Hlth Car Syst, DFCI, HMS, W Roxbury, MA USA.
[Wang, Jingyi] Univ Arkansas, Little Rock, AR 72204 USA.
[Fulciniti, Mariateresa; Amin, Samirkumar B.; Anderson, Kenneth C.; Munshi, Nikhil C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Dis Ctr, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 947
EP 947
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703181
ER
PT J
AU Munshi, NC
Li, C
Minvielle, S
Amin, SB
Moreau, P
Magrangeas, F
Anderson, KC
Avet-Loiseau, H
AF Munshi, Nikhil C.
Li, Cheng
Minvielle, Stepliane
Amin, Samir B.
Moreau, Philippe
Magrangeas, Florence
Anderson, Kenneth C.
Avet-Loiseau, Herve
TI Expression Profile Signature to Predict Response to Bortezomib and
Dexamethasone Combination Therapy in Newly-Diagnosed Myeloma: Moving
towards Prospective Prediction.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Munshi, Nikhil C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, VA Canc Healthcare Syst, Boston, MA 02115 USA.
[Li, Cheng] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Li, Cheng] Harvard Univ, Sch Publ Hlth, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Minvielle, Stepliane; Moreau, Philippe; Magrangeas, Florence; Avet-Loiseau, Herve] Hop Nantes, Dept Hematol, Nantes, France.
[Amin, Samir B.; Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA.
RI Magrangeas, Florence/L-3080-2015; Minvielle, Stephane/K-8251-2015;
richard, chrystelle/K-8595-2015
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 948
EP 948
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703186
ER
PT J
AU Blotta, S
Podar, K
Tai, YT
Roccaro, AM
Gorgun, G
Franco, B
Mitsiades, CS
Venuta, S
Anderson, KC
AF Blotta, Simona
Podar, Klaus
Tai, Yu-Tzu
Roccaro, Aldo M.
Gorgun, Gullu
Franco, Brunella
Mitsiades, Constantine S.
Venuta, Salvatore
Anderson, Kenneth C.
TI Canonical and Non Canonical Activation of Hedgehog Pathway in Multiple
Myeloma.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Blotta, Simona; Podar, Klaus; Tai, Yu-Tzu; Roccaro, Aldo M.; Gorgun, Gullu; Mitsiades, Constantine S.; Anderson, Kenneth C.] Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA.
[Blotta, Simona; Podar, Klaus; Tai, Yu-Tzu; Roccaro, Aldo M.; Gorgun, Gullu; Mitsiades, Constantine S.; Anderson, Kenneth C.] Dana Farber Canc Inst, LeBow Inst Myeloma Therapeut, Boston, MA 02115 USA.
[Franco, Brunella] Telethon Inst Genet & Med TIGEM, Naples, Italy.
[Venuta, Salvatore] Magna Graecia Univ Catanzaro, Catanzaro, Italy.
[Venuta, Salvatore] Ctr Canc, Catanzaro, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 949
EP 949
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703188
ER
PT J
AU Podar, K
Zhang, J
Tonon, G
Grabher, C
Lababidi, S
Raab, MS
Vallet, S
Zhou, YM
Cartron, MA
Sattler, M
Chauhan, D
Anderson, KC
AF Podar, Klaus
Zhang, Jing
Tonon, Giovanni
Grabher, Clemens
Lababidi, Samir
Raab, Marc S.
Vallet, Sonia
Zhou, Yiming
Cartron, Marie-Astrid
Sattler, Martin
Chauhan, Dharminder
Anderson, Kenneth C.
TI C-Myc- Dependent Stabilization of Hif-1alpha in MM: Therapeutic
Implications.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Podar, Klaus] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Lababidi, Samir] US FDA, Div Biostat, Ctr Devices & Radiol Hlth, Rockville, MD 20857 USA.
[Vallet, Sonia] Massachusetts Gen Hosp, Ctr Multiple Myeloma, Boston, MA 02114 USA.
[Zhou, Yiming; Cartron, Marie-Astrid] Univ Arkansas Med Sci, Myeloma Inst Res & Therapy, Little Rock, AR 72205 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 949
EP 949
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703189
ER
PT J
AU Podar, K
Zhang, J
Zimmerhackl, A
Barila, D
Vallet, S
Sattler, M
Tai, YT
Hideshima, T
Chauhan, D
Anderson, KC
AF Podar, Klaus
Zhang, Jing
Zimmerhackl, Alexander
Barila, Daniela
Vallet, Sonia
Sattler, Martin
Tai, Yu-Tzu
Hideshima, Teru
Chauhan, Dharminder
Anderson, Kenneth C.
TI Mcl-1 Fragment Mcl-1(128-350) Induces Inhibition of Multiple Myeloma
Cell Proliferation and Apoptosis Via Both Upregulation of C-Jun as Well
as Modulation of Its Transcriptional Activity.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Barila, Daniela] Univ Roma Tor Vergata, Rome, Italy.
[Barila, Daniela] Dulbecco Telethon Inst, Lab Cell Signaling, Rome, Italy.
[Vallet, Sonia] Massachusetts Gen Hosp, Ctr Multiple Myeloma, Boston, MA 02114 USA.
[Podar, Klaus] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
RI Barila, Daniela/K-8506-2016
OI Barila, Daniela/0000-0002-6192-1562
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 949
EP 950
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703190
ER
PT J
AU Ikeda, H
Hideshima, T
Okawa, Y
Vallet, S
Pozzi, S
Santo, L
Gorgun, G
Fulciniti, M
Raje, NS
Perrone, G
Munshi, N
Richardson, P
Lannutti, BJ
Puri, KD
Giese, NA
Anderson, KC
AF Ikeda, Hiroshi
Hideshima, Teru
Okawa, Yutaka
Vallet, Sonia
Pozzi, Samantha
Santo, Loredana
Gorgun, Gullu
Fulciniti, Mariateresa
Raje, Noopur S.
Perrone, Giulia
Munshi, Nikhil
Richardson, Paul
Lannutti, Brian J.
Puri, Kamal D.
Giese, Neill A.
Anderson, Kenneth C.
TI CAL-101, a Specific Inhibitor of the p110 delta Isoform of
Phosphatidylinositide 3-Kinase Induces Cytotoxicity in Multiple Myeloma
(MM).
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ikeda, Hiroshi; Hideshima, Teru; Okawa, Yutaka; Vallet, Sonia; Pozzi, Samantha; Santo, Loredana; Gorgun, Gullu; Fulciniti, Mariateresa; Raje, Noopur S.; Perrone, Giulia; Munshi, Nikhil; Richardson, Paul; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Lannutti, Brian J.; Puri, Kamal D.; Giese, Neill A.] Calistoga Pharmaceut Inc, Sealle, WA USA.
RI Pozzi, Samantha/A-7617-2012
OI Pozzi, Samantha/0000-0001-7917-1774
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 950
EP 950
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703192
ER
PT J
AU Leiba, M
Jakubikova, J
Klippel, S
Mitsiades, CS
Hideshima, T
Tai, YT
Richardson, P
Kawa, Y
Ikeda, H
Nagler, A
Anderson, KC
AF Leiba, Merav
Jakubikova, Jana
Klippel, Steffen
Mitsiades, Constantine S.
Hideshima, Teru
Tai, Yu-Tzu
Richardson, Paul
Kawa, Yutaka
Ikeda, Hiroshi
Nagler, Amon
Anderson, Kenneth C.
TI Halofuginone, a Novel Antimyeloma Agent, Upregulates C-Jun, JNK and P-53
Protein in vitro, and Inhibits Tumor Growth and Improves Survival in in
vivo Multiple Myeloma(MM) Animal Models.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Leiba, Merav; Jakubikova, Jana; Klippel, Steffen; Mitsiades, Constantine S.; Hideshima, Teru; Tai, Yu-Tzu; Richardson, Paul; Kawa, Yutaka; Ikeda, Hiroshi; Anderson, Kenneth C.] Dana Farber Canc Inst, Dept Med Oncol, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA.
[Nagler, Amon] Chaim Sheba Med Ctr, Div Hematol & Bone Marrow Transplantat, IL-52621 Tel Hashomer, Israel.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 950
EP 951
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703193
ER
PT J
AU Shen, JPYC
Divakaran, S
Ponduru, S
Vogl, DT
Amaravadi, RK
Bradner, JE
AF Shen, John Paul Y. C.
Divakaran, Sanjay
Ponduru, Sridevi
Vogl, Dan T.
Amaravadi, Ravi K.
Bradner, James E.
TI The Rationale for Combined Proteasome and Autophagy Inhibition in
Multiple Myeloma Established Using Novel Translational Platforms.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Shen, John Paul Y. C.] Univ Calif San Diego, Dept Internal Med, San Diego, CA 92103 USA.
[Divakaran, Sanjay; Ponduru, Sridevi; Bradner, James E.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Vogl, Dan T.; Amaravadi, Ravi K.] Univ Penn, Sch Med, Abramson Canc Ctr, Myeloma Program, Philadelphia, PA 19104 USA.
NR 0
TC 1
Z9 1
U1 1
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 NOV 16
PY 2008
VL 112
IS 11
BP 951
EP 951
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703194
ER
PT J
AU Vallet, S
Vaghela, N
Fulciniti, M
Veiby, P
Hideshima, T
Pozzi, S
Santo, L
Mukherjee, S
Cirstea, D
Scadden, DT
Anderson, KC
Raje, N
AF Vallet, Sonia
Vaghela, Nileshwari
Fulciniti, Mariateresa
Veiby, Petter
Hideshima, Tern
Pozzi, Samantha
Santo, Loredana
Mukherjee, Siddhartha
Cirstea, Diana
Scadden, David T.
Anderson, Kenneth C.
Raje, Noopur
TI CCR1 Inhibition Targets Osteoclast-Myeloma Adhesion and Exerts in Vivo
Anti-Osteoclast Activity.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Vallet, Sonia; Vaghela, Nileshwari; Raje, Noopur] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Hematol & Oncol, Boston, MA USA.
[Fulciniti, Mariateresa; Hideshima, Tern; Pozzi, Samantha; Santo, Loredana; Cirstea, Diana; Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Dis Ctr, Boston, MA 02115 USA.
[Veiby, Petter] Millennium Pharmaceut Inc, Cambridge, MA USA.
[Mukherjee, Siddhartha; Scadden, David T.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Regenerat Med, Boston, MA USA.
RI Pozzi, Samantha/A-7617-2012
OI Pozzi, Samantha/0000-0001-7917-1774
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 951
EP 952
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703196
ER
PT J
AU Cirstea, D
Hideshima, T
Pozzi, S
Vallet, S
Ikeda, H
Santo, L
Loferer, H
Vaghela, N
Okawa, Y
Perrone, G
Gorgun, G
Calabrese, E
Munshi, NC
Anderson, KC
Raje, N
AF Cirstea, Diana
Hideshima, Teru
Pozzi, Samantha
Vallet, Sonia
Ikeda, Hiroshi
Santo, Loredana
Loferer, Hannes
Vaghela, Nileshwari
Okawa, Yutaka
Perrone, Giulia
Gorgun, Gullu
Calabrese, Elisabetta
Munshi, Nikhil C.
Anderson, Kenneth C.
Raje, Noopur
TI RGB 286638, a Novel Multi-Targeted Small Molecule Inhibitor, Induces
Multiple Myeloma (MM) Cell Death through Abrogation of CDK-Dependent and
Independent Survival Mechanisms.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Cirstea, Diana; Hideshima, Teru; Ikeda, Hiroshi; Santo, Loredana; Okawa, Yutaka; Perrone, Giulia; Gorgun, Gullu; Calabrese, Elisabetta; Munshi, Nikhil C.; Anderson, Kenneth C.; Raje, Noopur] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Dis Ctr, Boston, MA 02115 USA.
[Pozzi, Samantha; Vallet, Sonia; Vaghela, Nileshwari] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Canc, Boston, MA USA.
[Loferer, Hannes] GPC Biotech AG, Munich, Germany.
RI Pozzi, Samantha/A-7617-2012
OI Pozzi, Samantha/0000-0001-7917-1774
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 952
EP 952
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703198
ER
PT J
AU McMillin, DW
Negri, J
Delmore, J
Ooi, MG
Jakubikova, J
Wright, R
Gray, N
Kung, A
Anderson, KC
Mitsiades, CS
AF McMillin, Douglas W.
Negri, Joseph
Delmore, Jake
Ooi, Melissa G.
Jakubikova, Jana
Wright, Renee
Gray, Nathanael
Kung, Andrew
Anderson, Kenneth C.
Mitsiades, Constantine S.
TI Activity of Plk Inhibitor BI2536 on Myeloma Cells.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [McMillin, Douglas W.; Negri, Joseph; Delmore, Jake; Ooi, Melissa G.; Jakubikova, Jana; Anderson, Kenneth C.; Mitsiades, Constantine S.] Dana Farber Canc Inst, Dept Med Oncol, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA.
[Wright, Renee; Kung, Andrew] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Gray, Nathanael] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 953
EP 954
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703203
ER
PT J
AU Raab, MS
Breitkreutz, I
Tonon, G
Zhang, J
Fruehauf, J
Lin, BK
Chauhan, D
Hideshima, T
Munshi, N
Anderson, KC
Podar, K
AF Raab, Marc S.
Breitkreutz, Iris
Tonon, Giovanni
Zhang, Jing
Fruehauf, Johannes
Lin, Boris K.
Chauhan, Dharminder
Hideshima, Teru
Munshi, Nikhil
Anderson, Kenneth C.
Podar, Klaus
TI Targeting PKC: A Novel Role for Beta-catenin in ER Stress and Apoptotic
Signaling.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Raab, Marc S.; Breitkreutz, Iris; Tonon, Giovanni; Zhang, Jing; Chauhan, Dharminder; Hideshima, Teru; Munshi, Nikhil; Anderson, Kenneth C.; Podar, Klaus] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Fruehauf, Johannes] Beth Israel Deaconess Med Ctr, New York, NY 10003 USA.
[Lin, Boris K.] Eli Lilly & Co, Indianapolis, IN 46285 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 953
EP 953
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703202
ER
PT J
AU Breitkreutz, I
Raab, MS
Christensen, O
Zimmerhackl, A
Zhang, J
Blotta, S
Hideshima, T
Chauhan, D
Wilhelm, S
Anderson, KC
Podar, K
AF Breitkreutz, Iris
Raab, Marc S.
Christensen, Olaf
Zimmerhackl, Alexander
Zhang, Jing
Blotta, Simona
Hideshima, Teru
Chauhan, Dharminder
Wilhelm, Scott
Anderson, Kenneth C.
Podar, Klaus
TI The Novel, Orally Available Multi-Kinase Inhibitor BAY 73-4506 in
Multiple Myeloma.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Dis Ctr, Boston, MA 02115 USA.
[Christensen, Olaf; Wilhelm, Scott] Bayer Healthcare Pharmaceut Inc, Montville, NJ USA.
NR 0
TC 0
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 954
EP 954
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703205
ER
PT J
AU Richardson, P
Hofmeister, CC
Zimmerman, TM
Chanan-Khan, AA
Spear, MA
Palladino, MA
Longenecker, AM
Cropp, G
Lloyd, GK
Wear, S
Hannah, AL
Anderson, KC
AF Richardson, Paul
Hofmeister, Craig C.
Zimmerman, Todd M.
Chanan-Khan, Asher Alban
Spear, Matthew A.
Palladino, Michael A.
Longenecker, Angie M.
Cropp, Gillian
Lloyd, G. Kenneth
Wear, Sandra
Hannah, Alison L.
Anderson, Kenneth C.
TI Phase 1 Clinical Trial of NPI-0052, a Novel Proteasome Inhibitor in
Patients with Multiple Myeloma.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Richardson, Paul; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Hofmeister, Craig C.] Ohio State Univ, Columbus, OH 43210 USA.
[Zimmerman, Todd M.] Univ Chicago, Chicago, IL USA.
[Chanan-Khan, Asher Alban] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[Spear, Matthew A.; Palladino, Michael A.; Longenecker, Angie M.; Cropp, Gillian; Lloyd, G. Kenneth; Hannah, Alison L.] Nereus Pharmaceut Inc, San Diego, CA USA.
[Wear, Sandra] Multiple Myeloma Res Consortium, Norwalk, CT USA.
NR 0
TC 1
Z9 2
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 955
EP 956
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703209
ER
PT J
AU Zonder, JA
Singhal, S
Bensinger, W
Mohrbacher, A
Hussein, MA
Munshi, NC
Caras, I
Singhal, A
van Rhee, F
AF Zonder, Jeffrey A.
Singhal, Seema
Bensinger, William
Mohrbacher, Ann
Hussein, Mohamad A.
Munshi, Nikhil C.
Caras, Ingrid
Singhal, Anil
van Rhee, Frits
TI Phase I Study of Elotuzumab (HuLuc63) in Phase I Study of Elotuzumab
(HuLuc63) in Relapsed/Refractory Multiple Myeloma.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Zonder, Jeffrey A.] Wayne State Univ, Karmanos Canc Inst, Detroit, MI USA.
[Singhal, Seema] Northwestern Univ, Sch Med, Chicago, IL USA.
[Bensinger, William] Fred Hutchinson Canc, Seattle, WA USA.
[Mohrbacher, Ann] USC Keck Sch Med, Altadena, CA USA.
[Hussein, Mohamad A.] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Munshi, Nikhil C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Caras, Ingrid; Singhal, Anil] PDL BioPharma Inc, Redwood City, CA USA.
[van Rhee, Frits] Univ Arkansas Med Sci, Myeloma Inst Res & Therapy, Little Rock, AR 72205 USA.
NR 0
TC 2
Z9 3
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 956
EP 957
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703212
ER
PT J
AU Wolf, JL
Siegel, D
Matous, J
Lonial, S
Goldschmidt, H
Schmitt, S
Vij, R
De Malgalhaes-Silverman, M
Abonour, R
Jalaluddin, M
Li, M
Hazell, K
Bourquelot, PM
Mateos, MV
Anderson, KC
Spencer, A
Harousseau, JL
Blade, J
AF Wolf, Jeffrey Lee
Siegel, David
Matous, Jeffrey
Lonial, Sagar
Goldschmidt, Hartmut
Schmitt, Stefan
Vij, Ravi
De Malgalhaes-Silverman, Margarida
Abonour, Rafat
Jalaluddin, Muhammad
Li, Martha
Hazell, Katharine
Bourquelot, Priscille M.
Mateos, Maria-Victoria
Anderson, Kenneth C.
Spencer, Andrew
Harousseau, Jean-Luc
Blade, Joan
TI A Phase II Study of Oral Panobinostat (LBH589) in Adult Patients with
Advanced Refractory Multiple Myeloma.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Wolf, Jeffrey Lee] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Siegel, David] Hackensack Univ, Med Ctr, Hackensack, NJ USA.
[Matous, Jeffrey] Rocky Mt Canc Ctr, Denver, CO USA.
[Lonial, Sagar] Emory Univ, Atlanta, GA 30322 USA.
[Goldschmidt, Hartmut] Natl Ctr Tumorerkrankungen, Heidelberg, Germany.
[Schmitt, Stefan] Univ Hosp, Heidelberg, Germany.
[Vij, Ravi] Washington Univ, Ballwin, MO USA.
[De Malgalhaes-Silverman, Margarida] Univ Iowa, Iowa City, IA USA.
[Abonour, Rafat] Indiana Univ Canc, Indianapolis, IN USA.
[Jalaluddin, Muhammad] Novartis Pharmaceut, Florham Pk, NJ USA.
[Li, Martha] Novartis Pharmaceut, E Hanover, NJ USA.
[Hazell, Katharine; Bourquelot, Priscille M.] Novartis Pharmaceut, Basel, Switzerland.
[Mateos, Maria-Victoria] Hosp Univ Salamanca, Salamanca, Spain.
[Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Spencer, Andrew] Monash Univ, Alfred Hosp, Melbourne, Vic 3181, Australia.
[Harousseau, Jean-Luc] Hop Hotel Dieu, Nantes, France.
[Blade, Joan] IDIBAPS, Hosp Clin, Barcelona, Spain.
NR 0
TC 0
Z9 1
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 957
EP 957
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703213
ER
PT J
AU Harousseau, JL
Palumbo, A
Richardson, P
Schlag, R
Dimopoulos, MA
Shpilberg, O
Kropff, MH
Delforge, M
Schots, R
Cavo, M
Golenkov, A
Komarnicki, M
Mateos, MV
Cakana, A
Liu, K
Deraedt, W
van de Velde, H
Miguel, JFS
AF Harousseau, Jean-Luc
Palumbo, Antonio
Richardson, Paul
Schlag, Rudolf
Dimopoulos, Meletios A.
Shpilberg, Ofer
Kropff, Martin H.
Delforge, Michel
Schots, Rik
Cavo, Michele
Golenkov, Anatoly
Komarnicki, Mieczyslaw
Mateos, Maria-Victoria
Cakana, Andrew
Liu, Kevin
Deraedt, William
van de Velde, Helgi
Miguel, Jesus F. San
TI Superior Outcomes Associated with Complete Response: Analysis of the
Phase III VISTA Study of Bortezomib Plus Melphalan-Prednisone Versus
Melphalan-Prednisone.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Harousseau, Jean-Luc] CHU Hotel Dieu, Serv Hematol, Nantes, France.
[Palumbo, Antonio] Univ Turin, Turin, Italy.
[Richardson, Paul] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Schlag, Rudolf] Praxis Hematol & Oncol, Wurzburg, Germany.
[Dimopoulos, Meletios A.] Univ Athens, Sch Med, GR-10679 Athens, Greece.
[Shpilberg, Ofer] Rabin Med Ctr, Petah Tiqwa, Israel.
[Kropff, Martin H.] Univ Munster, Munster, Germany.
[Delforge, Michel] Univ Hosp Gasthuisberg, B-3000 Louvain, Belgium.
[Schots, Rik] Belgian Hematol Soc, Myeloma Study Grp, Brussels, Belgium.
[Cavo, Michele] Univ Bologna, Bologna, Italy.
[Komarnicki, Mieczyslaw] Karol Marcinkowski Univ Med Sci, Poznan, Poland.
[Miguel, Jesus F. San] CSIC, USAL, IBMCC, Hosp Univ Salamanca,CIC, Salamanca, Spain.
[Cakana, Andrew; Deraedt, William; van de Velde, Helgi] Johnson & Johnson Pharmaceut Res & Dev, Beerse, Belgium.
[Liu, Kevin] Johnson & Johnson Pharmaceut Res & Dev, Raritan, NJ USA.
NR 0
TC 5
Z9 5
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 959
EP 959
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703217
ER
PT J
AU Siegel, D
Sezer, O
Miguel, JFS
Mateos, MV
Prosser, I
Cavo, M
Jalaluddin, M
Hazell, K
Bourquelot, PM
Anderson, KC
AF Siegel, David
Sezer, Orhan
Miguel, Jesus F. San
Mateos, Maria-Victoria
Prosser, Ian
Cavo, Michele
Jalaluddin, Muhammad
Hazell, Katharine
Bourquelot, Priscille M.
Anderson, Kenneth C.
TI A Phase IB, Multicenter, Open-Label, Dose-Escalation Study of Oral
Panobinostat (LBH589) and IV Bortezomib in Patients with Relapsed
Multiple Myeloma.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Siegel, David] Hackensack Univ, Med Ctr, Hackensack, NJ USA.
[Sezer, Orhan] Univ Hosp Charite, Berlin, Germany.
[Miguel, Jesus F. San; Mateos, Maria-Victoria] Hosp Univ Salamanca, Salamanca, Spain.
[Prosser, Ian] Canberra Hosp, Canberra, ACT, Australia.
[Cavo, Michele] Univ Bologna, Bologna, Italy.
[Jalaluddin, Muhammad] Novartis Pharmaceut, Florham Pk, NJ USA.
[Hazell, Katharine; Bourquelot, Priscille M.] Novartis Pharmaceut, Basel, Switzerland.
[Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 960
EP 961
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703220
ER
PT J
AU Alford, KA
Vanes, L
Li, Z
Orkin, SH
Fisher, EMC
Tybulewicz, VLJ
AF Alford, Kate A.
Vanes, Lesley
Li, Zhe
Orkin, Stuart H.
Fisher, Elizabeth M. C.
Tybulewicz, Victor L. J.
TI A Myeloproliferative Disorder in the Tel Mouse Model of Down Syndrome.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Alford, Kate A.; Vanes, Lesley; Tybulewicz, Victor L. J.] Natl Inst Med Res, London NW7 1AA, England.
[Li, Zhe] Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA.
[Orkin, Stuart H.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Fisher, Elizabeth M. C.] UCL, Inst Neurol, London, England.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 964
EP 964
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703229
ER
PT J
AU Bellucci, R
Nguyen, HN
Martin, A
Schinzel, A
Daley, J
Hansen, S
Hahn, WC
Ritz, J
AF Bellucci, Roberto
Nguyen, Hong-Nam
Martin, Allison
Schinzel, Anna
Daley, John
Hansen, Steen
Hahn, William C.
Ritz, Jerome
TI Genetic Screening for Myeloma Cell Susceptibility to NK Cell Mediated
Lysis Using Large Lentiviral shRNA Libraries
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Bellucci, Roberto; Schinzel, Anna; Hahn, William C.; Ritz, Jerome] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Hansen, Steen] Harvard Univ, Childrens Hosp, Sch Med, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 997
EP 998
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703337
ER
PT J
AU Rosenblatt, J
Vasir, B
Wu, ZK
Zarwan, C
Stone, R
Bissonnette, A
Friedman, TM
Neuberg, D
Rozenveyn, N
Glotzbecker, B
Levine, JD
Joyce, R
Boussiotis, V
Tzachanis, D
Spentzos, D
Konstantinopoulos, P
Kufe, D
Avigan, D
AF Rosenblatt, Jacalyn
Vasir, Baldev
Wu, Zekui
Zarwan, Corrine
Stone, Richard
Bissonnette, Adam
Friedman, Thea M.
Neuberg, Donna
Rozenveyn, Natalya
Glotzbecker, Brett
Levine, James D.
Joyce, Robin
Boussiotis, Vassiliki
Tzachanis, Dimitrios
Spentzos, Dimitrios
Konstantinopoulos, Panagiotis
Kufe, Donald
Avigan, David
TI Adoptive T Cell Therapy Using Educated T Cells Generated by the
Sequential Stimulation with DC/Tumor Fusion Cells and Anti-CD3CD28
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Rosenblatt, Jacalyn; Zarwan, Corrine; Rozenveyn, Natalya; Glotzbecker, Brett; Levine, James D.; Joyce, Robin; Boussiotis, Vassiliki; Tzachanis, Dimitrios; Spentzos, Dimitrios; Konstantinopoulos, Panagiotis; Avigan, David] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Vasir, Baldev; Wu, Zekui; Stone, Richard; Bissonnette, Adam; Neuberg, Donna; Kufe, Donald] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Friedman, Thea M.] Hackensack Univ, Med Ctr, Ctr Canc, Hackensack, NJ USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1002
EP 1002
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703350
ER
PT J
AU Huiya, N
Gaynon, PS
Femandez, M
Silverman, LB
Thomson, B
Chu, R
Cooper, T
Kadota, R
Rytting, M
Steinherz, PG
Shen, V
Jeha, S
Barry, E
Carroll, WL
AF Huiya, Nobuko
Gaynon, Paul S.
Femandez, Manuel
Silverman, Lewis B.
Thomson, Blythe
Chu, Roland
Cooper, Todd
Kadota, Richard
Rytting, Michael
Steinherz, Peter G.
Shen, Violet
Jeha, Sima
Barry, Elly
Carroll, William L.
TI Durable Remissions Observed in a Phase I/II Study of Clofarabine in
Combination with Etoposide and Cyclophosphamide in Pediatric Patients
with Refractory or Relapsed Acute Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Huiya, Nobuko] Childrens Mem Hosp, Chicago, IL 60614 USA.
[Gaynon, Paul S.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Femandez, Manuel] Genzyme Corp, San Antonio, TX USA.
[Silverman, Lewis B.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Thomson, Blythe] Childrens Hosp & Med Ctr, Seattle, WA 98105 USA.
[Chu, Roland] Wayne State Univ, Dept Pediat, Detroit, MI 48202 USA.
[Cooper, Todd] Univ Alabama, Birmingham, AL USA.
[Kadota, Richard] Children Hosp San Diego, San Diego, CA USA.
[Rytting, Michael] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Steinherz, Peter G.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Shen, Violet] CHOC Pediat Subspecialty Fac, Orange, CA USA.
[Jeha, Sima] St Jude Childrens Rsch Hosp, Memphis, TN USA.
[Barry, Elly] Genzyme Corp, Boston, MA USA.
[Carroll, William L.] NYU, Inst Canc, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1006
EP 1006
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703362
ER
PT J
AU Kapeller, R
Han, JW
Sun, KM
Gangurde, P
Kawahata, N
Iadanza, M
Guerlevais, V
Horstick, J
Noehre, J
Annis, A
Licklider, L
Nash, HM
Kong, A
Sawyer, TK
AF Kapeller, Rosana
Han, Jiawen
Sun, Kaiming
Gangurde, Pranoti
Kawahata, Nori
Iadanza, Matt
Guerlevais, Vincent
Horstick, Jim
Noehre, Justin
Annis, Allen
Licklider, Larry
Nash, Huw M.
Kong, Andrew
Sawyer, Tomi K.
TI Stapled Peptides: Leveraging the BH3 alpha-Helix to Create a New Class
of Drugs to Treat Hematological Malignancies
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Kapeller, Rosana; Han, Jiawen; Sun, Kaiming; Gangurde, Pranoti; Kawahata, Nori; Iadanza, Matt; Guerlevais, Vincent; Horstick, Jim; Noehre, Justin; Annis, Allen; Licklider, Larry; Nash, Huw M.; Sawyer, Tomi K.] AILERON Therapeut Inc, Cambridge, MA USA.
[Kong, Andrew] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1007
EP 1008
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703366
ER
PT J
AU Rodrigues, MS
Reddy, MM
Walz, C
Salgia, R
Podar, K
Band, H
Reiter, A
Griffin, JD
Sattler, M
AF Rodrigues, Margret S.
Reddy, Mamatha M.
Walz, Christoph
Salgia, Ravi
Podar, Klaus
Band, Hamid
Reiter, Andreas
Griffin, James D.
Sattler, Martin
TI Novel Transforming Mutations of CBL in Human Acute Myeloid Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Rodrigues, Margret S.; Reddy, Mamatha M.; Podar, Klaus; Griffin, James D.; Sattler, Martin] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Walz, Christoph; Reiter, Andreas] Univ Heidelberg, Fak Med, Med Univ Klin 3, D-6800 Mannheim, Germany.
[Salgia, Ravi] Univ Chicago, Med Ctr, Chicago, IL 60637 USA.
[Band, Hamid] Univ Nebraska Med Ctr, Omaha, NE USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1013
EP 1013
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703385
ER
PT J
AU Grant, S
Kolla, S
Sirulnik, LA
Shapiro, G
Supko, J
Cooper, B
Perkins, E
Ramakrishnan, V
Espinoza-Delgado, I
Tombes, MB
Roberts, JD
AF Grant, Steven
Kolla, Sarah
Sirulnik, Leonardo Andres
Shapiro, Geoffrey
Supko, Jeffrey
Cooper, Brenda
Perkins, Edward
Ramakrishnan, Viswanathan
Espinoza-Delgado, Igor
Tombes, M. B.
Roberts, John D.
TI Phase I Trial of Vorinostat (SAHA) in Combination with Alvocidib
(Flavopiridol) in Patients with Relapsed, Refractory or (Selected) Poor
Prognosis Acute Leukemia or Refractor), Anemia with Excess Blasts-2
(RAEB-2)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Grant, Steven; Kolla, Sarah; Perkins, Edward; Ramakrishnan, Viswanathan; Tombes, M. B.; Roberts, John D.] Virginia Commonwealth Univ, Massey Canc Ctr, Richmond, VA 02115 USA.
[Sirulnik, Leonardo Andres; Shapiro, Geoffrey; Supko, Jeffrey] Dana Farber Canc Inst, Boston, MA 44106 USA.
[Cooper, Brenda] Case Western Reserve Univ, Univ Hosp Cleveland, Ireland Canc Ctr, Cleveland, OH 20892 USA.
[Espinoza-Delgado, Igor] NCI, Canc Therapy Evaluat Program, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1026
EP 1026
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703423
ER
PT J
AU Cserti-Gazdewich, C
Dhabangi, A
Musoke, C
Nabukeera-Barungi, N
Ddungu, H
Mpimbaza, A
Ssewanyana, I
Dzik, WH
AF Cserti-Gazdewich, Christine
Dhabangi, Aggrey
Musoke, Charles
Nabukeera-Barungi, Nicolette
Ddungu, Henry
Mpimbaza, Arthur
Ssewanyana, Isaac
Dzik, Walter H.
TI Hematologic Findings and Transfusion Therapy in Severe Pediatric
Plasmodium Falciparum Malaria: Results from a Prospective Observational
Study in Uganda
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Cserti-Gazdewich, Christine] Toronto Gen Hosp, Toronto, ON, Canada.
[Dhabangi, Aggrey; Musoke, Charles; Nabukeera-Barungi, Nicolette; Ddungu, Henry; Mpimbaza, Arthur] Mulago Hosp, Kampala, Uganda.
[Ssewanyana, Isaac] Joint Clin Res Ctr, Kampala, Uganda.
[Dzik, Walter H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1045
EP 1046
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703478
ER
PT J
AU Treon, S
Branagan, A
Ioakimidis, L
Soumerai, J
Patterson, C
Wasi, P
Emmanouilides, C
Frankel, SR
Lister, A
Morel, P
Matous, J
Gregory, SA
Kimby, EK
AF Treon, Steven
Branagan, Andrew
Ioakimidis, Leukothea
Soumerai, Jacob
Patterson, Christopher
Wasi, Parveen
Emmanouilides, Christos
Frankel, Stanley R.
Lister, Andrew
Morel, Pierre
Matous, Jeffrey
Gregory, Stephanie A.
Kimby, Eva K.
TI Long Term Responses to Fludarabine and Rituximab in Waldenstrom's
Macroglobulinemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ioakimidis, Leukothea] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Wasi, Parveen] McMaster Univ, Hamilton, ON, Canada.
[Emmanouilides, Christos] Interbalkan Hosp, Pylaia, Greece.
[Frankel, Stanley R.] Hoffmann La Roche Inc, Nutley, NJ 07110 USA.
[Lister, Andrew] Ctr Med Oncol, London, England.
[Morel, Pierre] Serv Hematol Clin, Lens, France.
[Matous, Jeffrey] Rocky Mt Canc Ctr, Denver, CO USA.
[Gregory, Stephanie A.] Rush Univ, Chicago, IL 60612 USA.
[Kimby, Eva K.] Karolinska Inst, Hematol Ctr, Stockholm, Sweden.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1051
EP 1051
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703494
ER
PT J
AU Novakovic, VA
Baleja, JD
Gilbert, GE
AF Novakovic, Valerie A.
Baleja, James D.
Gilbert, Gary E.
TI The Factor VIIII C2 Domain Shows Stereospecificity for
Phosphatidyl-L-Serine and Increases Factor IXa Activity
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Novakovic, Valerie A.] VA Boston Healthcare Syst, W Roxbury, MA USA.
[Baleja, James D.] Tufts Univ, Sackler Sch Biomed Sci, Boston, MA 02111 USA.
[Gilbert, Gary E.] Harvard Univ, Sch Med, VA Boston Healthcare Syst, W Roxbury, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1061
EP 1061
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703527
ER
PT J
AU Zhou, J
Liu, SC
Ma, M
Hou, JX
Yu, HJ
Lu, CF
Gilbert, G
Shi, JL
AF Zhou, Jin
Liu, Shuchuan
Ma, Ming
Hou, Jinxiao
Yu, Hongjuan
Lu, Chengfang
Gilbert, Gary
Shi, Jialan
TI Procoagulant Activity and Phosphatidylserine of Amniotic Fluid Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Zhou, Jin; Liu, Shuchuan; Ma, Ming; Hou, Jinxiao; Yu, Hongjuan; Lu, Chengfang] Harbin Med Coll, Dept Med, Affiliated Hosp 1, Harbin, Peoples R China.
[Gilbert, Gary; Shi, Jialan] Harvard Univ, Sch Med, Brigham & Womens Hosp, VA Boston Healthcare Syst,Dept Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1061
EP 1061
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703528
ER
PT J
AU Malek, S
Ouillette, P
Wright, W
Dressel, A
Karp, J
Bockenstedt, P
Al-Zoubi, A
Talpaz, M
Kujawski, L
Shedden, K
Shakhan, S
Li, C
Erba, H
Parkin, B
AF Malek, Sami
Ouillette, Peter
Wright, Whitney
Dressel, Amanda
Karp, Judy
Bockenstedt, Paula
Al-Zoubi, Ammar
Talpaz, Moshe
Kujawski, Lisa
Shedden, Kerby
Shakhan, Sajid
Li, Cheng
Erba, Harry
Parkin, Brian
TI Comprehensive Ultra High Resolution Analysis of Copy Number and Allele
Status Including Novel Microdeletions Spanning NF1 in Acute Myelogenous
Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Malek, Sami; Ouillette, Peter; Wright, Whitney; Dressel, Amanda; Bockenstedt, Paula; Al-Zoubi, Ammar; Talpaz, Moshe; Shedden, Kerby; Shakhan, Sajid; Erba, Harry; Parkin, Brian] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Karp, Judy] Johns Hopkins Univ, Sch Med, Johns Hopkins Oncol Ctr, Baltimore, MD 21205 USA.
[Li, Cheng] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Li, Cheng] Harvard Univ, Sch Publ Hlth, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Li, Cheng] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1066
EP 1066
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703544
ER
PT J
AU Malek, S
Wright, W
Li, C
Shakhan, S
Ouillette, P
AF Malek, Sami
Wright, Whitney
Li, Cheng
Shakhan, Sajid
Ouillette, Peter
TI Comparative Genomic Analysis of CLL Genomes Using Affymetrix 50K SNP
Versus SNP 6.0 Arrays
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Malek, Sami; Wright, Whitney; Shakhan, Sajid; Ouillette, Peter] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Li, Cheng] Harvard Univ, Dept Biostat, Sch Publ Hlth, Cambridge, MA 02138 USA.
[Li, Cheng] Harvard Univ, Dept Biostat & Computat Biol, Sch Publ Hlth, Cambridge, MA 02138 USA.
[Li, Cheng] Dana Farber Canc Inst, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1066
EP 1066
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703545
ER
PT J
AU Brown, JR
Rassenti, L
Neuberg, D
Greaves, A
Byrd, JC
Grever, MR
Gribben, JG
Kay, NE
Keating, M
Rai, KR
Wierda, WG
Kipps, TJ
AF Brown, Jennifer R.
Rassenti, Laura
Neuberg, Donna
Greaves, Andrew
Byrd, John C.
Grever, Michael R.
Gribben, John G.
Kay, Neil E.
Keating, Michael
Rai, Kanti R.
Wierda, William G.
Kipps, Thomas J.
TI Characteristics of Familial CLL Evaluated in the CLL Research Consortium
Cohort
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Brown, Jennifer R.; Neuberg, Donna] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Rassenti, Laura; Greaves, Andrew; Kipps, Thomas J.] UCSD, Div Hematol Oncol, Dept Med, Moores Canc Ctr, La Jolla, CA USA.
[Byrd, John C.; Grever, Michael R.] Ohio State Univ, James Canc Inst, Columbus, OH 43210 USA.
[Gribben, John G.] Barts & London Queen Marys Sch Med & Dent, Inst Canc, Ctr Med Oncol, London, England.
[Kay, Neil E.] Mayo Clin, Div Hematol, Rochester, MN USA.
[Keating, Michael; Wierda, William G.] Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Houston, TX 77030 USA.
[Rai, Kanti R.] N Shore Long Isl Jewish Hlth Syst, New Hyde Pk, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1071
EP 1072
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703562
ER
PT J
AU Amrein, PC
Attar, E
Takvorian, T
Hochberg, E
Ballen, KK
Leahy, KM
Neuberg, D
Brown, JR
AF Amrein, Philip C.
Attar, Eyal
Takvorian, Tak
Hochberg, Ephraim
Ballen, Karen K.
Leahy, Kathleen M.
Neuberg, Donna
Brown, Jennifer R.
TI Dasatinib Has Activity in Relapsed/Refractory Chronic Lymphocytic
Leukemia (CLL/SLL), a Phase II Trial
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Amrein, Philip C.; Attar, Eyal; Takvorian, Tak; Hochberg, Ephraim; Ballen, Karen K.; Leahy, Kathleen M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Neuberg, Donna; Brown, Jennifer R.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 4
Z9 4
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1084
EP 1084
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703599
ER
PT J
AU Roberts, AW
Brown, J
Seymour, JF
Wierda, WG
Kipps, TJ
Xiong, H
Chiu, YL
Busman, T
Knight, RA
Enschede, S
Krivoshik, A
Humerickhouse, R
AF Roberts, Andrew W.
Brown, Jennifer
Seymour, John F.
Wierda, William G.
Kipps, Thomas J.
Xiong, Hao
Chiu, Yi-Lin
Busman, Todd
Knight, Raymond A.
Enschede, Sari
Krivoshik, Andrew
Humerickhouse, Rod
TI An Ongoing Phase 1 Study of ABT-263; Pharmacokineties, Safety and
Anti-Tumor Activity in Patients with Relapsed or Refractory Chronic
Lymphocytic Leukemia (CLL).
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Roberts, Andrew W.] Royal Melbourne Hosp, Walter & Eliza Hall Inst Med Res, Div Canc & Haem, Parkville, Vic 3050, Australia.
[Brown, Jennifer] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Seymour, John F.] Peter MacCallum Canc Ctr, Dept Haematol & Med Oncol, Melbourne, Australia.
[Wierda, William G.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Kipps, Thomas J.] CLL Res Consortium, Moores UCSD Canc Ctr, La Jolla, CA USA.
[Xiong, Hao; Chiu, Yi-Lin; Busman, Todd; Knight, Raymond A.; Enschede, Sari; Krivoshik, Andrew; Humerickhouse, Rod] Abbott Labs, Abbott Pk, IL 60064 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1089
EP 1090
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703614
ER
PT J
AU Cutler, C
Aldridge, J
Kim, HT
Ayanian, S
Bradwin, G
Revta, C
Murga, G
Ho, V
Alyea, E
Koreth, J
Armand, P
Richardson, PG
Soiffer, RJ
Ritz, J
Antin, JH
AF Cutler, Corey
Aldridge, J.
Kim, H. T.
Ayanian, S.
Bradwin, G.
Revta, C.
Murga, G.
Ho, V.
Alyea, E.
Koreth, J.
Armand, P.
Richardson, P. G.
Soiffer, R. J.
Ritz, J.
Antin, J. H.
TI Prediction of VOD Using Biomarkers of Endothelial Injury
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Cutler, Corey; Aldridge, J.; Kim, H. T.; Revta, C.; Murga, G.; Ho, V.; Alyea, E.; Koreth, J.; Armand, P.; Richardson, P. G.; Soiffer, R. J.; Ritz, J.; Antin, J. H.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Ayanian, S.; Bradwin, G.] Childrens Hosp, Lab Med, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1122
EP 1122
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703703
ER
PT J
AU Melanson, SE
Antin, JH
Court, MH
Ho, V
Ritz, J
Kim, HT
Kuo, FC
Longtine, JA
Jarolim, P
AF Melanson, Stacy E.
Antin, Joseph H.
Court, Michael H.
Ho, Vincent
Ritz, Jerome
Kim, Haesook T.
Kuo, Frank C.
Longtine, Janina A.
Jarolim, Petr
TI Genetic Variations in CYP2B6 and Risk of Cyclophosphamide Toxicity in
Patients Undergoing Myeloablative Stem Cell Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Antin, Joseph H.] Brigham & Womens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Court, Michael H.] Tufts Univ, Sch Med, Dept Pharmacol & Expt Therapeut, Boston, MA 02111 USA.
[Ritz, Jerome] Dana Farber Canc Inst, Div Hematol Malignancies, Boston, MA 02115 USA.
[Jarolim, Petr] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1129
EP 1130
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104703725
ER
PT J
AU Hursting, MJ
Jang, LK
AF Hursting, Marcie J.
Jang, Lk-Kyung
TI Dosing Patterns and Outcomes in African American, Asian, and Hispanic
Patients with Heparin-Induced Thrombocytopenia Treated with Argatroban
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Hursting, Marcie J.] Clin Sci Consulting, Austin, TX USA.
[Jang, Lk-Kyung] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1167
EP 1168
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704021
ER
PT J
AU Kuter, DJ
Mufti, G
Bain, B
Hasserjian, R
Rutstein, M
AF Kuter, David J.
Mufti, Ghulam
Bain, Barbara
Hasserjian, Robert
Rutstein, Mark
TI Evaluation of Bone Marrow Reticulin Formation in Romiplostim-Treated
Adult Patients with Chronic Immune Thrombocytopenic Purpura (ITP)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology/ASH/ASCO Joint
Symposium
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol (ASH), Sanofi Aventis U.S.
C1 [Kuter, David J.; Hasserjian, Robert] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Mufti, Ghulam] Kings Coll Hosp London, London, England.
[Bain, Barbara] St Marys Hosp, London, England.
[Rutstein, Mark] Amgen Inc, Thousand Oaks, CA 91320 USA.
NR 0
TC 3
Z9 3
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1171
EP 1172
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704034
ER
PT J
AU Zakai, NA
French, B
Arnold, A
Newman, A
Fried, LF
Robbins, J
Chaves, P
Cushman, M
AF Zakai, Neil A.
French, Benjamin
Arnold, Alice
Newman, Anne
Fried, Linda F.
Robbins, John
Chaves, Paolo
Cushman, Mary
TI Hemoglobin Decline and Health Outcomes in the Elderly: the
Cardiovascular Health Study
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Zakai, Neil A.; Cushman, Mary] Univ Vermont, Colchester, VT USA.
[French, Benjamin] Univ Penn, Philadelphia, PA 19104 USA.
[Arnold, Alice] Univ Washington, Seattle, WA 98195 USA.
[Fried, Linda F.] Univ Pittsburgh, VA Pittsburgh Healthcare Syst, Pittsburgh, PA 15260 USA.
[Robbins, John] Univ Calif, David, CA USA.
[Chaves, Paolo] Johns Hopkins Sch Publ Hlth, Baltimore, MD USA.
RI Newman, Anne/C-6408-2013
OI Newman, Anne/0000-0002-0106-1150
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1183
EP 1183
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704066
ER
PT J
AU de Jong, JLO
Burns, CE
Tinmaung, A
Pugach, E
Mayhall, E
Smith, ACH
Feldman, HA
Zhou, Y
Zon, LI
AF de Jong, Jill L. O.
Burns, Caroline E.
Tinmaung, Aye
Pugach, Emily
Mayhall, Elizabeth
Smith, Alexandra C. H.
Feldman, Henry A.
Zhou, Yi
Zon, Leonard I.
TI Development of a Limiting Dilution Assay and MHC-Matched Transplantation
Model to Detect Hematopoietic Stem Cell Activity in Zebrafish.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [de Jong, Jill L. O.; Burns, Caroline E.; Tinmaung, Aye; Pugach, Emily; Mayhall, Elizabeth; Smith, Alexandra C. H.; Zhou, Yi; Zon, Leonard I.] Childrens Hosp, Stem Cell Program, Boston, MA 02115 USA.
[de Jong, Jill L. O.; Burns, Caroline E.; Tinmaung, Aye; Pugach, Emily; Mayhall, Elizabeth; Smith, Alexandra C. H.; Zhou, Yi; Zon, Leonard I.] Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA.
[Feldman, Henry A.] Childrens Hosp, Clin Res Program, Boston, MA 02115 USA.
[Zon, Leonard I.] Harvard Stem Cell Inst, Howard Hughes Med Inst, Dana Farber Canc Inst, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1196
EP 1196
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704107
ER
PT J
AU Andreola, G
Chittenden, M
Sykes, M
AF Andreola, Giovanna
Chittenden, Meredith
Sykes, Megan
TI Lack of "Bystander" Activation and Evidence for Competition for
Resources among Gvh-Reactive CD4 T Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Andreola, Giovanna; Chittenden, Meredith; Sykes, Megan] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Transplantat Biol Res Ctr,Bone Marrow Transplatat, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1202
EP 1202
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704125
ER
PT J
AU Andreola, G
Chittenden, M
Sykes, M
AF Andreola, Giovanna
Chittenden, Meredith
Sykes, Megan
TI Host Environment Determines the Development of Gvhd but Not the Extent
of Activation and Expansion of Gvh-Reactive CD4 T Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Andreola, Giovanna; Chittenden, Meredith; Sykes, Megan] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Transplantat Biol Res Ctr,Marrow Transplantat Sec, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1202
EP 1203
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704126
ER
PT J
AU Iino, T
Chong, Y
Mizuno, S
Ito, K
Tenen, DG
Reizis, B
Akashi, K
AF Iino, Tadafumi
Chong, Yong
Mizuno, Shin-ichi
Ito, Kyoko
Tenen, Daniel G.
Reizis, Boris
Akashi, Koichi
TI PU.1 Plays a Critical Role in Maintenance of Mature Dendritic Cell Pool.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Iino, Tadafumi; Chong, Yong; Mizuno, Shin-ichi; Ito, Kyoko; Akashi, Koichi] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Tenen, Daniel G.] Harvard Univ, Inst Med, Boston, MA 02115 USA.
[Reizis, Boris] Columbia Univ, Dept Microbiol, New York, NY 10032 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1217
EP 1217
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704172
ER
PT J
AU Schepers, K
Mayack, SR
Wagers, AJ
Passegue, E
AF Schepers, Koen
Mayack, Shane R.
Wagers, Amy J.
Passegue, Emmanuelle
TI Investigating the Complex Interplay Between Leukemic Stem Cells, Their
Myeloid Progeny and Cells from the Bone Marrow Microenvironment in
Generating Myeloproliferative Diseases.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Passegue, Emmanuelle] Univ Calif San Francisco, Inst Regenerat Med, Sch Med, San Francisco, CA 94143 USA.
[Mayack, Shane R.; Wagers, Amy J.] Joslin Diabet Ctr, Boston, MA 02215 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1220
EP 1220
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704182
ER
PT J
AU Nombela-Arrieta, C
Harley, B
Levantini, E
Mahoney, JE
Pivarnik, G
Protopopov, A
Tenen, DG
Silberstein, LE
AF Nombela-Arrieta, Cesar
Harley, Brendan
Levantini, Elena
Mahoney, John E.
Pivarnik, Gregory
Protopopov, Alexei
Tenen, Daniel G.
Silberstein, Leslie E.
TI Spatial Analysis of Hematopoietic Stem and Progenitor Cells in the Bone
Marrow
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Nombela-Arrieta, Cesar; Pivarnik, Gregory; Silberstein, Leslie E.] Childrens Hosp, Boston, MA 02115 USA.
[Harley, Brendan] Univ Illinois, Dept Chem & Biomol Engn, Chicago, IL 60680 USA.
[Levantini, Elena; Tenen, Daniel G.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Mahoney, John E.; Protopopov, Alexei] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1222
EP 1222
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704188
ER
PT J
AU Abramson, JS
Barnes, JA
Toomey, CE
Jacobsen, ED
Armand, P
Takvorian, T
Fisher, DC
Reynolds, H
Hochberg, EP
LaCasce, AS
AF Abramson, Jeremy S.
Barnes, Jeffrey A.
Toomey, Christiana E.
Jacobsen, Eric D.
Armand, Philippe
Takvorian, Tak
Fisher, David C.
Reynolds, Hazel
Hochberg, Ephraim P.
LaCasce, Ann S.
TI Rituximab Added to CODOX-M/IVAC Is Highly Effective in HIV-Negative and
hiv-Positive Burkitt Lymphoma.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Abramson, Jeremy S.; Barnes, Jeffrey A.; Toomey, Christiana E.; Takvorian, Tak; Hochberg, Ephraim P.] Massachusetts Gen Hosp, Ctr Canc, Ctr Lymphoma, Boston, MA USA.
[Jacobsen, Eric D.; Armand, Philippe; Fisher, David C.; Reynolds, Hazel; LaCasce, Ann S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1229
EP 1230
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704213
ER
PT J
AU Seymour, JF
Fenaux, P
Silverman, LB
Mufti, GJ
Hellstrom-Lindberg, E
Santini, V
List, AF
Gore, SD
Backstrom, J
McKenzie, D
Beach, CL
AF Seymour, John F.
Fenaux, Pierre
Silverman, Lewis B.
Mufti, Ghulam J.
Hellstroem-Lindberg, Eva
Santini, Valeria
List, Alan F.
Gore, Steven D.
Backstrom, Jay
McKenzie, David
Beach, C. L.
TI Effects of Azacitidine (AZA) Vs Conventional Care Regimens (CCR) in
Elderly (>= 75 years) Patients (Pts) with Myelodysplastic Syndromes
(MDS) from the AZA-001 Survival Trial
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Seymour, John F.] Peter MacCallum Canc Inst, Dept Haematol, Melbourne, Vic, Australia.
[Fenaux, Pierre] Hosp Avicenne, Bobigny, France.
[Silverman, Lewis B.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Mufti, Ghulam J.] Kings Coll London, Dept Haematol Med, London WC2R 2LS, England.
[Hellstroem-Lindberg, Eva] Karolinska Univ Hosp, Stockholm, Sweden.
[Santini, Valeria] Azienda Osped Careggi, Florence, Italy.
[List, Alan F.] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
[Gore, Steven D.] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Baltimore, MD USA.
[Backstrom, Jay; McKenzie, David; Beach, C. L.] Celgene, Overland Pk, KS USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1241
EP 1242
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704247
ER
PT J
AU Fenaux, P
Mufti, GJ
Hellstrom-Lindberg, E
Santini, V
Gattermann, N
Sanz, G
List, AF
Gore, SD
Seymour, JF
Backstrom, J
Zimmerman, L
McKenzie, D
Beach, CL
Silverman, LB
AF Fenaux, Pierre
Mufti, Ghulam J.
Hellstroem-Lindberg, Eva
Santini, Valeria
Gattermann, Norbert
Sanz, Guillermo
List, Alan F.
Gore, Steven D.
Seymour, John F.
Backstrom, Jay
Zimmerman, Linda
McKenzie, David
Beach, C. L.
Silverman, Lewis B.
TI Azacitidine Prolongs Overall Survival (OS) and Reduces Infections and
Hospitalizations in Patients (Pts) with WHO-Defined Acute Myeloid
Leukemia (AML) Compared with Conventional Care Regimens (CCR)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Fenaux, Pierre] Univ Paris 13, Hop Avicenne, Bobigny, France.
[Mufti, Ghulam J.] Kings Coll London, Dept Haematol Med, London WC2R 2LS, England.
[Hellstroem-Lindberg, Eva] Karolinska Univ Hosp, Stockholm, Sweden.
[Santini, Valeria] Azienda Osped Careggi, Florence, Italy.
[Gattermann, Norbert] Univ Dusseldorf, Dusseldorf, Germany.
[Sanz, Guillermo] Hosp Univ La Fe, Dept Hematol, Valencia, Spain.
[List, Alan F.] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Gore, Steven D.] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Baltimore, MD USA.
[Seymour, John F.] Peter MacCallum Canc Inst, Dept Haematol, Melbourne, Vic, Australia.
[Backstrom, Jay; Zimmerman, Linda; McKenzie, David; Beach, C. L.] Celgene, Overland Pk, KS USA.
[Silverman, Lewis B.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1244
EP 1244
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704254
ER
PT J
AU Chauhan, D
Singh, AV
Brahmandam, M
Bianchi, G
Podar, K
Hideshima, T
Munshi, N
Richardson, P
Palladino, MA
Anderson, KC
AF Chauhan, Dhapminder
Singh, Ajita V.
Brahmandam, Mohan
Bianchi, Giada
Podar, Klaus
Hideshima, Teru
Munshi, Nikhil
Richardson, Paul
Palladino, Michael A.
Anderson, Kenneth C.
TI Combination of a Novel Proteasome Inhibitor NPI-0052 and Lenalidomide
Trigger in Vivo Synergistic Cytotoxicity in Multiple Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Chauhan, Dhapminder; Singh, Ajita V.; Brahmandam, Mohan; Bianchi, Giada; Podar, Klaus; Hideshima, Teru; Munshi, Nikhil; Richardson, Paul; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Palladino, Michael A.] Nereus Pharmaceut Inc, San Diego, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1254
EP 1254
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704280
ER
PT J
AU Cirstea, D
Hideshima, T
Pozzi, S
Vallet, S
Ikeda, H
Santo, L
Rodig, S
Vaghela, N
Currie, T
Okawa, Y
Chhetri, G
Patel, CG
Perrone, G
Gorgun, G
Calabrese, E
Trieu, V
Desai, N
Sportelli, P
Munshi, NC
Anderson, KC
Raje, N
AF Cirstea, Diana
Hideshima, Teru
Pozzi, Samantha
Vallet, Sonia
Ikeda, Hiroshi
Santo, Loredana
Rodig, Scott
Vaghela, Nileshwari
Currie, Treeve
Okawa, Yutaka
Chhetri, Gaurav
Patel, Chirayu G.
Perrone, Giulia
Gorgun, Gullu
Calabrese, Elisabetta
Trieu, Voung
Desai, Neil
Sportelli, Peter
Munshi, Nikhil C.
Anderson, Kenneth C.
Raje, Noopur
TI Combination of Nub-Rapamycin and Perifosine Induces Synergistic
Cytotoxicity and Antitumor Activity Via Autophagy. and Apoptosis in
Multiple Myeloma (MM)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Cirstea, Diana; Hideshima, Teru; Ikeda, Hiroshi; Santo, Loredana; Okawa, Yutaka; Chhetri, Gaurav; Patel, Chirayu G.; Perrone, Giulia; Gorgun, Gullu; Calabrese, Elisabetta; Munshi, Nikhil C.; Anderson, Kenneth C.; Raje, Noopur] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Dis Ctr, Boston, MA 02115 USA.
[Rodig, Scott; Currie, Treeve] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Pozzi, Samantha; Vallet, Sonia; Vaghela, Nileshwari] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02115 USA.
[Trieu, Voung; Desai, Neil] Abraxis Biosci LLC, Los Angeles, CA USA.
[Sportelli, Peter] Keryx Biopharmaceut Inc, New York, NY USA.
RI Pozzi, Samantha/A-7617-2012
OI Pozzi, Samantha/0000-0001-7917-1774
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1255
EP 1255
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704281
ER
PT J
AU Fulciniti, M
Tassone, P
Hideshima, T
Nanjappa, P
Podar, K
Adamia, S
Amin, SB
Prabhala, R
Lopez, R
Anderson, KC
Munshi, NC
AF Fulciniti, Mariateresa
Tassone, Pierfrancesco
Hideshima, Teru
Nanjappa, Puru
Podar, Klaus
Adamia, Sophia
Amin, Samir B.
Prabhala, Rao
Lopez, Rocio
Anderson, Kenneth C.
Munshi, Nikhil C.
TI Sp1 Transcription Factor as a Novel Therapeutic Target in Multiple
Myeloma (MM)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Tassone, Pierfrancesco] Magna Graecia Univ Catanzaro, Catanzaro, Italy.
[Amin, Samir B.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA.
[Prabhala, Rao] HMS, DFCI, VA Boston Hlth Care Syst, W Roxbury, MA USA.
[Lopez, Rocio] Erimos Pharmaceut, Raleigh, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1255
EP 1255
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704282
ER
PT J
AU Singh, AV
Lloyd, GK
Palladino, MA
Chauhan, D
Anderson, KC
AF Singh, Ajita V.
Lloyd, G. Kenneth
Palladino, Michael A.
Chauhan, Dharminder
Anderson, Kenneth C.
TI Pharmacodynamic and Efficacy Studies of a Novel Proteasome Inhibitor
NPI-0052 in Human Plasmacytoma Xenograft Mouse Model
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Singh, Ajita V.; Chauhan, Dharminder; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Lloyd, G. Kenneth; Palladino, Michael A.] Nereus Pharmaceut Inc, San Diego, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1255
EP 1255
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704283
ER
PT J
AU Ponduru, S
Moellering, R
Greenberg, E
Shen, JPYC
Stanton, BZ
Bradner, JE
AF Ponduru, Sridevi
Moellering, Raymond
Greenberg, Edward
Shen, John Paul Ying-Ching
Stanton, Benjamin Z.
Bradner, James E.
TI Discovery and Characterization of Macrocyclic Thiopeptide Proteasome
Inhibitors for Hematologic Malignancies
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ponduru, Sridevi; Greenberg, Edward; Bradner, James E.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Moellering, Raymond; Stanton, Benjamin Z.] Harvard Univ, Dept Chem & Chem Biol, Cambridge, MA 02138 USA.
[Shen, John Paul Ying-Ching] Univ Calif San Diego, San Diego, CA 92103 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1257
EP 1257
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704287
ER
PT J
AU Vogl, DT
Stadtmauer, EA
Bradner, JE
Davis, L
Carroll, M
Nichols, CW
Shank, D
Carberry, M
Swider, CR
Mangan, PA
Shelly, BK
Thompson, CB
Amaravadi, RK
AF Vogl, Dan T.
Stadtmauer, Edward A.
Bradner, James E.
Davis, Lisa
Carroll, Martin
Nichols, Charles W.
Shank, Doris
Carberry, Mary
Swider, Cezary R.
Mangan, Patricia A.
Shelly, Brenda K.
Thompson, Craig B.
Amaravadi, Ravi K.
TI Combined Autophagy and Proteasome Inhibition for Multiple Myeloma:
Preliminary Results of a Phase 1/2 Trial of Hydroxychloroquine and
Standard Dose Bortezomib for Relapsed or Refractory Myeloma.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Vogl, Dan T.; Stadtmauer, Edward A.; Carroll, Martin; Shank, Doris; Carberry, Mary; Swider, Cezary R.; Mangan, Patricia A.; Shelly, Brenda K.; Thompson, Craig B.; Amaravadi, Ravi K.] Univ Penn, Sch Med, Myeloma Program, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Bradner, James E.] Dana Farber Canc Inst, Div Hematol Neoplasia, Boston, MA 02115 USA.
[Davis, Lisa] Univ Sci, Philadelphia, PA USA.
[Nichols, Charles W.] Univ Penn, Sch Med, Dept Ophthalmol, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1262
EP 1262
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704302
ER
PT J
AU Chanan-Khan, AA
Munshi, NC
Hussein, MA
Elias, L
Benedetti, F
Smith, J
Khor, SP
Huff, CA
AF Chanan-Khan, Asher Alban
Munshi, Nikhil C.
Hussein, Mohamad A.
Elias, Laurence
Benedetti, Fabio
Smith, Jennifer
Khor, Soo-Peang
Huff, Carol A.
TI Results of a Phase I Study of GRN163L, a Direct Inhibitor of Telomerase,
in Patients with Relapsed and Refractory Multiple Myeloma (MM).
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Chanan-Khan, Asher Alban] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[Munshi, Nikhil C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston VA Canc Healthcare Syst, Boston, MA 02115 USA.
[Hussein, Mohamad A.] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Huff, Carol A.] Johns Hopkins Univ, Baltimore, MD USA.
[Elias, Laurence; Benedetti, Fabio; Smith, Jennifer; Khor, Soo-Peang] Geron Corp, Menlo Pk, CA USA.
NR 0
TC 0
Z9 0
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 NOV 16
PY 2008
VL 112
IS 11
BP 1263
EP 1263
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704306
ER
PT J
AU Chanan-Khan, AA
Gharibo, M
Jagannath, S
Munshi, NC
Anderson, KC
DePaolo, D
Lee, KP
Miller, K
Guild, R
Zildjian, S
Qin, A
AF Chanan-Khan, Asher Alban
Gharibo, Mecide
Jagannath, Sundar
Munshi, Nikhil C.
Anderson, Kenneth C.
DePaolo, Dawn
Lee, Kelvin P.
Miller, Kena
Guild, Robin
Zildjian, Sybil
Qin, Albert
TI Phase I Study of IMGN901 in Patients with Relapsed and
Relapsed/Refractory CD56-Positive Multiple Myeloma.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Chanan-Khan, Asher Alban; DePaolo, Dawn; Lee, Kelvin P.; Miller, Kena] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[Gharibo, Mecide] Canc Inst NJ, Franklin Lakes, NJ USA.
[Jagannath, Sundar] St Vincents Comp Canc Ctr, New York, NY USA.
[Munshi, Nikhil C.; Lee, Kelvin P.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston VA Canc Healthcare Syst, Boston, MA 02115 USA.
[Anderson, Kenneth C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Dis Ctr, Boston, MA 02115 USA.
[Guild, Robin; Zildjian, Sybil] Immunogen Inc, Waltham, MA USA.
[Qin, Albert] Immunogen Inc, Cambridge, MA USA.
NR 0
TC 0
Z9 0
U1 3
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 NOV 16
PY 2008
VL 112
IS 11
BP 1263
EP 1264
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704307
ER
PT J
AU Perrone, G
Hideshima, T
Ikeda, H
Okawa, Y
Cristea, D
Santo, L
Gorgun, G
Calabrese, E
Raje, N
Baccarani, M
Cavo, M
Anderson, KC
AF Perrone, Giulia
Hideshima, Teru
Ikeda, Hiroshi
Okawa, Yutaka
Cristea, Diana
Santo, Loredana
Gorgun, Gullu
Calabrese, Elisabetta
Raje, Noopur
Baccarani, Michele
Cavo, Michele
Anderson, Kenneth C.
TI Dietary Supplement Vitamin C Significantly Abrogates Bortezomib-Induced
Multiple Myeloma (MM) Cell Growth Inhibition.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Perrone, Giulia; Hideshima, Teru; Ikeda, Hiroshi; Okawa, Yutaka; Cristea, Diana; Santo, Loredana; Gorgun, Gullu; Calabrese, Elisabetta; Raje, Noopur; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Baccarani, Michele] Univ Bologna, Dept Hematol & Oncol Sci, Bologna, Italy.
[Cavo, Michele] Univ Bologna, Dept Hematol & Med Oncol, Bologna, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1263
EP 1263
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704305
ER
PT J
AU Jakubowiak, A
Richardson, P
Zimmerman, TM
Alsina, M
Kaufman, JL
Harvey, C
Brozo, C
Kendall, T
McAllister, A
Hideshima, T
Sportelli, P
Gardner, L
Anderson, KC
Giusti, K
AF Jakubowiak, Andrzej
Richardson, Paul
Zimmerman, Todd M.
Alsina, Melissa
Kaufman, Jonathan L.
Harvey, Colleen
Brozo, Christine
Kendall, Tara
McAllister, Amanda
Hideshima, Teru
Sportelli, Peter
Gardner, Lesa
Anderson, Kenneth C.
Giusti, Kathy
TI Phase I Results of Perifosine (KRX-0401) in Combination with
Lenalidomide and Dexamethasone in Patients with Relapsed or Refractory
Multiple Myeloma (MM).
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Jakubowiak, Andrzej; Harvey, Colleen; Brozo, Christine; Kendall, Tara; McAllister, Amanda] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Richardson, Paul; Hideshima, Teru; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Zimmerman, Todd M.] Univ Chicago, Chicago, IL 60637 USA.
[Alsina, Melissa] Univ S Florida, H Lee Moffitt Canc Ctr, Hematol Malignancies Program, Tampa, FL 33682 USA.
[Kaufman, Jonathan L.] Emory Univ, Sch Med, Atlanta, GA USA.
[Sportelli, Peter; Gardner, Lesa] Keryx Biopharmaceut Inc, New York, NY USA.
[Giusti, Kathy] MMRC, Norwalk, CT USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1264
EP 1265
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704309
ER
PT J
AU Ghobrial, IM
Munshi, N
Schlossman, R
Chuma, S
Leduc, R
Nelson, M
Sam, A
O'Connor, K
Harris, B
Warren, D
Dollard, AM
Laubach, J
Vij, R
Campagnaro, E
Birner, A
Dixon-Lipscomb, V
Anderson, KC
Richardson, PG
AF Ghobrial, Irene M.
Munshi, Nikhil
Schlossman, Robert
Chuma, Stacey
Leduc, Renee
Nelson, Marybeth
Sam, Amy
O'Connor, Kelly
Harris, Brianna
Warren, Diane
Dollard, Akari M.
Laubach, Jacob
Vij, Ravi
Campagnaro, Erica
Birner, Ann
Dixon-Lipscomb, Virginia
Anderson, Kenneth C.
Richardson, Paul G.
TI Phase I Trial of CCI-779 (Temsirolimus) and Weekly Bortezomib in
Relapsed and/or Refractory Multiple Myeloma.
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ghobrial, Irene M.; Munshi, Nikhil; Schlossman, Robert; Chuma, Stacey; Leduc, Renee; Nelson, Marybeth; Sam, Amy; O'Connor, Kelly; Harris, Brianna; Warren, Diane; Laubach, Jacob; Anderson, Kenneth C.; Richardson, Paul G.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Dollard, Akari M.] MMRC, Norwalk, CT USA.
[Vij, Ravi] Washington Univ, St Louis, MO USA.
[Campagnaro, Erica] Univ Michigan, Ann Arbor, MI 48109 USA.
[Birner, Ann] Millennium Pharmaceut Inc, Cambridge, MA USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1266
EP 1266
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704314
ER
PT J
AU Mateos, MV
Cibeira, T
Richardson, P
Blade, J
Prosper, F
Oriol, A
de la Rubia, J
Alegre, A
Lahuerta, JJ
Garcia-Sanz, R
Mitsiades, CS
Espinoza, J
Anderson, KC
Miguel, JFS
AF Mateos, Maria-Victoria
Cibeira, Teresa
Richardson, Paul
Blade, Joan
Prosper, Felipe
Oriol, Albert
de la Rubia, Javier
Alegre, Adrian
Lahuerta, Juan Jose
Garcia-Sanz, Ramon
Mitsiades, Constantine S.
Espinoza, Jose
Anderson, Kenneth C.
Miguel, J. F. San
TI Final Results of a Phase II Trial with Plitidepsin (Aplidin) Alone and
in Combination with Dexamethasone in Patients with Relapsed/Refractory
Multiple Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Mateos, Maria-Victoria] Univ Hosp Salamanca, Salamanca, Spain.
[Cibeira, Teresa] Hosp Clin Barcelona, Barcelona, Spain.
[Mitsiades, Constantine S.] Dana Farber Canc Inst, Dept Med Oncol, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA.
[Blade, Joan] IDIBAPS, Hosp Clin, Barcelona, Spain.
[Prosper, Felipe] Univ Navarra Clin, Pamplona, Spain.
[Oriol, Albert] Hosp Germans Trials & Pujol, Badalona, Spain.
[de la Rubia, Javier] Hosp La Fe, E-46009 Valencia, Spain.
[Alegre, Adrian] Hosp La Princesa, Madrid, Spain.
[Lahuerta, Juan Jose] Hosp 12 Octubre, E-28041 Madrid, Spain.
[Garcia-Sanz, Ramon] Hosp Univ Salamanca, Salamanca, Spain.
[Espinoza, Jose] PharmaMar, Madrid, Spain.
[Miguel, J. F. San] CSIC, USAL, IBMCC, CIC, Salamanca, Spain.
NR 0
TC 1
Z9 1
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1268
EP 1268
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704318
ER
PT J
AU Siegel, D
Weber, D
Mitsiades, CS
Rizvi, S
Garcia-Vargas, J
Howe, J
Reiser, D
Anderson, KC
Richardson, P
AF Siegel, David
Weber, Donna
Mitsiades, Constantine S.
Rizvi, Syed
Garcia-Vargas, Jose
Howe, Jason
Reiser, David
Anderson, Kenneth C.
Richardson, Paul
TI A Phase I Study of Vorinostat in Combination with Lenalidomide and
Dexamethasone in Patients with Relapsed or Refractory Multiple Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Siegel, David] Hackensack Univ, Med Ctr, Hackensack, NJ USA.
[Weber, Donna] Univ Texas MD Anderson Canc Ctr, Dept Lymphona & Myeloma, Houston, TX 77030 USA.
[Mitsiades, Constantine S.; Anderson, Kenneth C.] Dana Farber Canc Inst, Dept Med Oncol, Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA.
[Rizvi, Syed; Garcia-Vargas, Jose; Howe, Jason; Reiser, David] Merck & Co Inc, Upper Gwynedd, PA USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1270
EP 1270
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704323
ER
PT J
AU Treon, S
Hunter, Z
Ciccarelli, B
Zhou, YS
Hanzis, C
Manning, R
Ioakimidis, L
Xu, L
Patterson, C
Morra, M
AF Treon, Steven
Hunter, Zachary
Ciccarelli, Bryan
Zhou, Yangsheng
Hanzis, Christina
Manning, Robert
Ioakimidis, Leukothea
Xu, Lian
Patterson, Christopher
Morra, Massimo
TI IgA and IgG Hypogammaglobulinemia Is a Constitutive Feature in Most
Waldenstrom's Macroglobulinemia Patients and May Be Related to Mutations
Associated with Common Variable Immunodeficiency Disorder (CVID)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Zhou, Yangsheng; Manning, Robert; Ioakimidis, Leukothea] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Morra, Massimo] Correlagen Diagnost Inc, Waltham, MA USA.
RI Hunter, Zachary/H-3018-2013
OI Hunter, Zachary/0000-0002-1689-1691
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1284
EP 1285
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704367
ER
PT J
AU Leleu, X
Roccaro, AM
Leduc, R
Poulain, S
Moreau, AS
Gay, J
Dulery, R
Richardson, PG
Ghobrial, IM
AF Leleu, Xavier
Roccaro, Aldo M.
Leduc, Renee
Poulain, Stephanie
Moreau, Anne-Sophie
Gay, Julie
Dulery, Remy
Richardson, Paul G.
Ghobrial, Irene M.
TI Early Response Using Serum Immunoglobulin Free Light Chain (sFLC)
Measurement Predicts Response to Therapy in Waldenstrom
Macroglobulinemia (WM)
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Leleu, Xavier; Poulain, Stephanie; Moreau, Anne-Sophie; Gay, Julie; Dulery, Remy] CHRU, Hop Huriez, Serv Malad Sang, Lille, France.
[Leduc, Renee; Richardson, Paul G.; Ghobrial, Irene M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1286
EP 1286
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704373
ER
PT J
AU Gritsman, K
Kharas, MG
Gilliland, DG
AF Gritsman, Kira
Kharas, Michael G.
Gilliland, D. Gary
TI Constitutively Active AKT Induces Myeloproliferative Disease, Acute
Myeloid Leukemia, and T Cell Lymphoma despite Impaired Engraftment
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Gritsman, Kira] Brigham & Womens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1298
EP 1298
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704411
ER
PT J
AU Gutierrez, A
Sanda, T
Winter, S
Larson, RS
Silverman, LB
Hunger, SP
Sallan, SE
Look, AT
AF Gutierrez, Alejandro
Sanda, Takaomi
Winter, Stuart
Larson, Richard S.
Silverman, Lewis B.
Hunger, Stephen P.
Sallan, Stephen E.
Look, A. Thomas
TI LEF1 Is a Tumor Suppressor in T Cell Acute Lymphoblastic Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Gutierrez, Alejandro] Childrens Hosp, Boston, MA 02115 USA.
[Gutierrez, Alejandro; Sanda, Takaomi; Silverman, Lewis B.; Sallan, Stephen E.; Look, A. Thomas] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Winter, Stuart] Univ New Mexico, Dept Pediat, Albuquerque, NM 87131 USA.
[Larson, Richard S.] Univ New Mexico, Hlth Sci Ctr, Dept Pathol, Albuquerque, NM 87131 USA.
[Hunger, Stephen P.] Childrens Hosp, Aurora, CO USA.
[Hunger, Stephen P.] Univ Colorado, Denver Sch Med, Aurora, CO USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1300
EP 1301
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704420
ER
PT J
AU Mueller, MR
Robbs, BK
Cruz, ALS
Sasaki, Y
Stevanovic, I
Rajewsky, K
Viola, JPB
Rao, A
AF Mueller, Martin R.
Robbs, Bruno K.
Cruz, Andre L. S.
Sasaki, Yoshiteru
Stevanovic, Irena
Rajewsky, Klaus
Viola, Joao P. B.
Rao, Anjana
TI Evidence for NFAT1 as a Tumor Suppressor in T-ALL
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Mueller, Martin R.; Stevanovic, Irena; Rajewsky, Klaus; Rao, Anjana] Harvard Univ, Sch Med, Immune Dis Inst, Boston, MA USA.
[Robbs, Bruno K.; Cruz, Andre L. S.; Viola, Joao P. B.] Brazilian Natl Canc Inst INCA, Div Cell Biol, Rio De Janeiro, Brazil.
[Sasaki, Yoshiteru] RIKEN, Ctr Dev Biol, Lab Stem Cell Biol, Kobe, Hyogo, Japan.
RI Robbs, Bruno/H-5553-2013
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1301
EP 1301
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704422
ER
PT J
AU Scholl, C
Frohling, S
Dunn, IF
Barbie, DA
Schinzel, AC
Kim, SY
Silver, SJ
Bullinger, L
Sandy, P
Boehm, JS
Root, DE
Jacks, T
Hahn, WC
Gilliland, DG
AF Scholl, Claudia
Frohling, Stefan
Dunn, Ian F.
Barbie, David A.
Schinzel, Anna C.
Kim, So Young
Silver, Serena J.
Bullinger, Lars
Sandy, Peter
Boehm, Jesse S.
Root, David E.
Jacks, Tyler
Hahn, William C.
Gilliland, D. Gary
TI High-Throughput RNA Interference Screening Identifies Synthetic
Lethality Between Oncogenic KRAS Dependency and Suppression of STK33
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Scholl, Claudia; Frohling, Stefan; Gilliland, D. Gary] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Dunn, Ian F.; Barbie, David A.; Silver, Serena J.; Sandy, Peter; Boehm, Jesse S.; Root, David E.; Jacks, Tyler] MIT, Cambridge, MA 02139 USA.
[Dunn, Ian F.; Barbie, David A.; Silver, Serena J.; Boehm, Jesse S.; Root, David E.] Broad Inst Harvard, Cambridge, MA USA.
[Schinzel, Anna C.; Kim, So Young; Hahn, William C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Bullinger, Lars] Univ Hosp, Ulm, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1301
EP 1302
PG 2
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704424
ER
PT J
AU Zwicker, J
Liebman, HA
Neuberg, D
Bauer, K
Barbara, F
Bruce, F
AF Zwicker, Jeffrey
Liebman, Howard A.
Neuberg, Donna
Bauer, Kenneth
Barbara, Furie
Bruce, Furie
TI Development of Venous Thromboembolic Events in Cancer Patients with
Elevated Levels of Tissue Factor-Bearing Microparticles
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Zwicker, Jeffrey; Bauer, Kenneth; Barbara, Furie; Bruce, Furie] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Div Hemostasis & Thrombosis, Boston, MA 02215 USA.
[Liebman, Howard A.] Univ So Calif, Los Angeles, CA USA.
[Neuberg, Donna] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1309
EP 1309
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704449
ER
PT J
AU Kwiatkowski, BA
Dong, Z
Richard, RE
AF Kwiatkowski, Boguslaw A.
Dong, ZhaoMing
Richard, Robert E.
TI The Identification of Genes Cooperating with Mpl Signaling Using
Insertional Mutagenesis
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Kwiatkowski, Boguslaw A.] VA Puget Sound Hlth Care Syst, Seattle Inst Biomed & Clin Res, Seattle, WA USA.
[Richard, Robert E.] Univ Washington, Seattle, WA 98195 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1314
EP 1314
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704467
ER
PT J
AU Ho-Tin-Noe, BH
Carbo, C
Demers, M
Cifuni, SM
Goerge, T
Wagner, DD
AF Ho-Tin-Noe, Benoit H.
Carbo, Carla
Demers, Melanie
Cifuni, Stephen M.
Goerge, Tobias
Wagner, Denisa D.
TI Platelets Protect Tumors from Hemorrhage Induced by Stroma-Infiltrating
Leukocytes
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Ho-Tin-Noe, Benoit H.; Carbo, Carla; Demers, Melanie; Cifuni, Stephen M.; Goerge, Tobias; Wagner, Denisa D.] Harvard Univ, Sch Med, Immune Dis Inst, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1335
EP 1335
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704522
ER
PT J
AU Wagers, AJ
Cerletti, M
Mayack, SR
Kim, FS
Shadrach, JL
AF Wagers, Amy J.
Cerletti, Massimiliano
Mayack, Shane R.
Kim, Francis S.
Shadrach, Jennifer L.
TI Age-Related Changes in Tissue-Specific Stem Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Wagers, Amy J.; Cerletti, Massimiliano; Mayack, Shane R.; Kim, Francis S.; Shadrach, Jennifer L.] Joslin Diabet Ctr, Boston, MA 02215 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1343
EP 1343
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704545
ER
PT J
AU Zon, LI
AF Zon, Leonard I.
TI Transcription Factor Integration from Pathways Regulating Adult Blood
Stem Cell Production and Self-Renewal
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Zon, Leonard I.] Childrens Hosp, Stem Cell Program, Boston, MA 02115 USA.
[Zon, Leonard I.] Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA.
[Zon, Leonard I.] Harvard Stem Cell Inst, Howard Hughes Med Inst, Dana Farber Canc Inst, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1346
EP 1346
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704556
ER
PT J
AU Dzik, WH
AF Dzik, Walter H.
TI Nitric Oxide: An Introductory Primer
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Dzik, Walter H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1354
EP 1354
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704588
ER
PT J
AU Golub, TR
AF Golub, Todd R.
TI Genomics and Systems Biology
SO BLOOD
LA English
DT Meeting Abstract
CT 50th Annual Meeting of the American-Society-of-Hematology
CY DEC 06-09, 2008
CL San Francisco, CA
SP Amer Soc Hematol
C1 [Golub, Todd R.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 16
PY 2008
VL 112
IS 11
BP 1355
EP 1355
PG 1
WC Hematology
SC Hematology
GA 389OP
UT WOS:000262104704592
ER
PT J
AU Esrailian, E
Gralnek, IM
Jensen, D
Laine, L
Dulai, GS
Eisen, G
Spiegel, BMR
AF Esrailian, E.
Gralnek, I. M.
Jensen, D.
Laine, L.
Dulai, G. S.
Eisen, G.
Spiegel, B. M. R.
TI Evaluating the process of care in nonvariceal upper gastrointestinal
haemorrhage: a survey of expert vs. non-expert gastroenterologists
SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS
LA English
DT Article
ID ENDOSCOPY; QUALITY; METAANALYSIS; VIGNETTES; TRIAL
AB Background
When faced with the same facts, physicians often make different decisions.
Aim
To perform a survey to measure the process of care and variations in decision-making in nonvariceal upper gastrointestinal tract haemorrhage (NVUGIH) and compare results between experts and non-experts.
Methods
We administered a vignette survey to elicit knowledge and beliefs about NVUGIH, including 13 'best practice' guidelines. We compared guideline compliance between experts and non-experts.
Results
One hundred and eighty-eight gastroenterologists responded (46%). Experts endorsed more 'best practices' than non-experts (93% vs. 85%; P = 0.002). Non-experts were more likely to endorse incorrectly bolus dosing vs. continuous infusion of intravenous proton pump inhibitors (PPIs; 92% vs. 64%; P = 0.005) and to select standard-channel vs. large-channel endoscopes in high-risk bleeding (100% vs. 85%; P = 0.04). There were wide variations within groups regarding the timing of nasogastric lavage, use of promotility agents, use of hemoclips and appropriateness of snaring clots overlying ulcers.
Conclusions
Experts are more likely to comply with NVUGIH guidelines. Non-experts diverge from experts in the dosing of PPIs and choice of endoscope in high-risk bleeding. Moreover, there are wide variations in key practices even within groups. This suggests that best practices have been generally well disseminated, but that persistent disconnects exist that should be further investigated.
C1 [Jensen, D.; Spiegel, B. M. R.] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Esrailian, E.; Jensen, D.; Spiegel, B. M. R.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Esrailian, E.; Spiegel, B. M. R.] Univ Calif Los Angeles, VA Ctr Outcomes Res & Educ CORE, Los Angeles, CA 90095 USA.
[Laine, L.] Univ So Calif, Keck Sch Med, Los Angeles, CA 90033 USA.
[Dulai, G. S.] Kaiser So Calif, Portland, OR USA.
[Eisen, G.] Oregon Hlth & Sci Univ, Portland, OR USA.
[Spiegel, B. M. R.] Univ Calif Los Angeles, Sch Publ Hlth, Los Angeles, CA 90024 USA.
[Gralnek, I. M.] Ramban Med Ctr, Haifa, Israel.
RP Spiegel, BMR (reprint author), 11301 Wilshire Blvd,Bldg 115,Room 215, Los Angeles, CA 90073 USA.
EM bspiegel@mednet.ucla.edu
FU Veteran's Affairs Health Services Research and Development (HSR&D)
Career Development Transition [RCD03-179-2]; CURE Digestive Disease
Research Center [NIH 2P30 DK 041301-17]; NIH K24 [NIH-NIDDK
1K24DK02650]; NIH-NIDDK [AM41301]; AstraZeneca [ESOM0396]
FX Declaration of personal interests: Dr Spiegel is supported by a
Veteran's Affairs Health Services Research and Development (HSR&D)
Career Development Transition Award (RCD03-179-2). Drs. Esrailian,
Jensen and Spiegel are supported by the CURE Digestive Disease Research
Center (NIH 2P30 DK 041301-17). Dr Jensen is supported by an NIH K24
grant (NIH-NIDDK 1K24DK02650), and NIH-NIDDK AM41301. This study was
supported by an investigator-initiated research grant by AstraZeneca.
The authors had complete authority over all aspects of the study,
including development of the hypotheses and analysis plan, development
of data collection instruments, collection of data, analysis and
interpretation of data and writing of the manuscript. Declaration of
funding interests: This investigator-iniated study was funded in full by
AstraZeneca, grant number ESOM0396. All aspects of the study conduct,
interpretation, and writing were performed by the study authors without
influence by the sponsor.
NR 17
TC 13
Z9 13
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0269-2813
J9 ALIMENT PHARM THER
JI Aliment. Pharmacol. Ther.
PD NOV 15
PY 2008
VL 28
IS 10
BP 1199
EP 1208
DI 10.1111/j.1365-2036.2008.03838.x
PG 10
WC Gastroenterology & Hepatology; Pharmacology & Pharmacy
SC Gastroenterology & Hepatology; Pharmacology & Pharmacy
GA 361MK
UT WOS:000260131600003
PM 18729846
ER
PT J
AU Maron, BJ
Bonow, RO
Salberg, L
Roberts, WC
Braunwald, E
AF Maron, Barry J.
Bonow, Robert O.
Salberg, Lisa
Roberts, William C.
Braunwald, Eugene
TI The First Patient Clinically Diagnosed With Hypertrophic Cardiomyopathy
SO AMERICAN JOURNAL OF CARDIOLOGY
LA English
DT Article
ID SURVIVAL; STENOSIS; PROFILE
AB It has now been 50 years since the initial clinical description of hypertrophic cardiomyopathy. In this regard, it is noteworthy that the first patient diagnosed with this disease has survived to date in good health with an active and productive lifestyle-albeit with heart transplantation necessitated by an aggressive disease course with progression to the end-stage phase. (C) 2008 Elsevier Inc. All rights reserved. (Am J Cardiol 2008;102:1418-1420)
C1 [Maron, Barry J.] Minneapolis Heart Inst Fdn, Hypertroph Cardiomyopathy Ctr, Minneapolis, MN USA.
[Bonow, Robert O.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Salberg, Lisa] Hypertroph Cardiomyopathy Assoc, Hibernia, NJ USA.
[Roberts, William C.] Baylor Heart & Vasc Inst, Dallas, TX USA.
[Braunwald, Eugene] Brigham & Womens Hosp, TIMI Study Grp, Boston, MA 02115 USA.
RP Maron, BJ (reprint author), Minneapolis Heart Inst Fdn, Hypertroph Cardiomyopathy Ctr, Minneapolis, MN USA.
EM hcm.maron@mhif.org
NR 13
TC 3
Z9 3
U1 0
U2 1
PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
PI BRIDGEWATER
PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA
SN 0002-9149
J9 AM J CARDIOL
JI Am. J. Cardiol.
PD NOV 15
PY 2008
VL 102
IS 10
BP 1418
EP 1420
DI 10.1016/j.amjcard.2008.08.024
PG 3
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 376OX
UT WOS:000261194000025
PM 18993166
ER
PT J
AU Mergenhagen, KA
Sherman, O
AF Mergenhagen, Kari A.
Sherman, Olga
TI Elevated International Normalized Ratio after concurrent ingestion of
cranberry sauce and warfarin
SO AMERICAN JOURNAL OF HEALTH-SYSTEM PHARMACY
LA English
DT Article
DE Anticoagulants; Drug interactions; Geriatrics; International normalized
ratio; Vaccinium macrocarpon; Warfarin sodium
ID JUICE
AB Purpose. A case of increased International Normalized Ratio (INR) values in a patient receiving warfarin who consumed a large amount of cranberry sauce is reported.
Summary. A 75-year-old Caucasian man with atrial fibrillation was taking 22.5 mg of warfarin weekly for 10 months and had maintained stable INR values between 2 and 3. During a clinic visit one week after Thanksgiving, the patient's INR was 4.8. The patient was extensively questioned about any changes in his diet, medications, and health. The patient reported consuming approximately 113 g of cranberry sauce for seven consecutive days before the clinic visit. He reported no other diet or health changes. The patient denied alcohol consumption, had not taken nutritional supplements, and did not miss or double any medication doses during this time period. There were no dosing changes or discernible compliance issues in the 10 months preceding the change in INR. The patient's complete blood cell count and results of a chemistry panel and liver function tests were within normal limits. He did not have any bleeding or bruising. The only identifiable change was the addition of store-bought cranberry sauce to his diet. The patient's warfarin dose was held for two days. Subsequently, the patient resumed warfarin at a dosage of 20 mg per week. Seven days after the patient discontinued the cranberry sauce, his INR returned to 2.2 and remained stable over the next month.
Conclusion. Consumption of cranberry sauce led to an increase in INR values in a patient receiving warfarin.
C1 [Mergenhagen, Kari A.; Sherman, Olga] James J Peters Vet Affairs Med Ctr, Coagulat Warfarin Lipid Clin, Bronx, NY 10468 USA.
RP Mergenhagen, KA (reprint author), James J Peters Vet Affairs Med Ctr, Coagulat Warfarin Lipid Clin, 130 W Kingsbridge Rd 119, Bronx, NY 10468 USA.
EM kari.mergenhagen2@va.gov
NR 23
TC 4
Z9 6
U1 0
U2 1
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 NOV 15
PY 2008
VL 65
IS 22
BP 2113
EP 2116
DI 10.2146/ajhp080135
PG 4
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 372LG
UT WOS:000260902500012
PM 18997138
ER
PT J
AU Kozora, E
Arciniegas, DB
Filley, CM
West, SG
Brown, M
Miller, D
Grimm, A
Devore, MD
Wingrove, C
Zhang, LN
AF Kozora, Elizabeth
Arciniegas, David B.
Filley, Christopher M.
West, Sterling G.
Brown, Mark
Miller, David
Grimm, Alex
Devore, Maria D.
Wingrove, Christy
Zhang, Lening
TI Cognitive and Neurologic Status in Patients With Systemic Lupus
Erythematosus Without Major Neuropsychiatric Syndromes
SO ARTHRITIS & RHEUMATISM-ARTHRITIS CARE & RESEARCH
LA English
DT Article
ID MULTIPLE-SCLEROSIS; RATING-SCALE; IMPAIRMENT; PREVALENCE; DYSFUNCTION;
MANIFESTATIONS; DEFINITIONS; ANTIBODIES; DEFICITS; FLUENCY
AB Objective. To examine neuropsychological and neurologic functioning in systemic lupus erythematosus (SLE) patients without histories of overt neuropsychiatric disorders (non-NPSLE patients).
Methods. Sixty-seven non-NPSLE patients and 29 healthy controls were administered a standardized neurologic examination and measures of cognition, depression, and self-reported cognitive functioning.
Results. Non-NPSLE patients scored lower than controls on the total score of the neurologic examination (P < 0.0001). Item analysis indicated that the physician's description of mentation and mood was the only item that differed significantly between patients with SLE and controls (P = 0.004). Compared with controls, non-NPSLE patients had significantly higher rates of impairment on logical reasoning (P = 0.012) and verbal memory (P = 0.03), and trends toward greater impairment on visual attention (P = 0.06) and working memory (P = 0.098). There were no significant differences between non-NPSLE patients and controls on a cognitive impairment index (CII): 20.9% of non-NPSLE patients and 13.8% of controls were impaired. Patients with SLE scored higher on depressive symptoms (P < 0.0001) and perceived cognitive difficulties (P = 0.001) compared with controls.
Conclusion. The utility of a standardized neurologic examination in SLE for excluding overt neurologic dysfunction and assuring a non-NPSLE group selection was demonstrated. In contrast to our earlier study, we did not find differences between non-NPSLE patients and controls on the CII Slightly lower CII scores in non-NPSLE patients and higher CII scores in controls may have reduced cognitive differences between these groups. Non-NPSLE patients demonstrate specific decline in the areas of attention, memory, and reasoning; continued studies of associated brain regions are warranted.
C1 [Kozora, Elizabeth; Devore, Maria D.; Wingrove, Christy; Zhang, Lening] Natl Jewish Med & Res Ctr, Denver, CO 80206 USA.
[Kozora, Elizabeth; Arciniegas, David B.; Filley, Christopher M.; West, Sterling G.; Brown, Mark; Miller, David; Grimm, Alex; Zhang, Lening] Univ Colorado Denver, Hlth Sci Ctr, Denver, CO USA.
[Filley, Christopher M.] Denver Vet Affairs Med Ctr, Denver, CO USA.
RP Kozora, E (reprint author), Natl Jewish Med & Res Ctr, 1400 Jackson St, Denver, CO 80206 USA.
EM Kozorae@njc.org
RI Arciniegas, David/A-3792-2009
FU National Institute of Musculoskeletal and Skin Diseases; NIH
[R01-AR04915202]
FX Supported by a grant from National Institute of Musculoskeletal and Skin
Diseases, NIH (R01-AR04915202).
NR 47
TC 29
Z9 30
U1 1
U2 2
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0004-3591
J9 ARTHRIT RHEUM-ARTHR
JI Arthritis Rheum-Arthritis Care Res.
PD NOV 15
PY 2008
VL 59
IS 11
BP 1639
EP 1646
DI 10.1002/art.24189
PG 8
WC Rheumatology
SC Rheumatology
GA 371TC
UT WOS:000260853200015
PM 18975359
ER
PT J
AU Hur, W
Velentza, A
Kim, S
Flatauer, L
Jiang, XN
Valente, D
Mason, DE
Suzuki, M
Larson, B
Zhang, JM
Zagorska, A
DiDonato, M
Nagle, A
Warmuth, M
Balk, SP
Peters, EC
Gray, NS
AF Hur, Wooyoung
Velentza, Anastasia
Kim, Sungjoon
Flatauer, Laura
Jiang, Xinnong
Valente, David
Mason, Daniel E.
Suzuki, Melissa
Larson, Brad
Zhang, Jianming
Zagorska, Anna
DiDonato, Michael
Nagle, Advait
Warmuth, Markus
Balk, Steven P.
Peters, Eric C.
Gray, Nathanael S.
TI Clinical stage EGFR inhibitors irreversibly alkylate Bmx kinase
SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS
LA English
DT Article
DE Irreversible inhibitors; Quinazoline scaffold; EFGR; Tec-family kinase;
Bmx; Reactive cysteine
ID GROWTH-FACTOR RECEPTOR; TYROSINE KINASE; PROSTATE-CANCER; ETK/BMX;
DOMAIN
AB Irreversible HER/erbB inhibitors selectively inhibit HER-family kinases by targeting a unique cysteine residue located within the ATP-binding pocket. Sequence alignment reveals that this rare cysteine is also present in ten other protein kinases including all five Tec-family members. We demonstrate that the Tec-family kinase Bmx is potently inhibited by irreversible modi. cation at Cys496 by clinical stage EGFR inhibitors such as CI-1033. This cross-reactivity may have significant clinical implications. (C) 2008 Elsevier Ltd. All rights reserved.
C1 [Zhang, Jianming; Gray, Nathanael S.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Hur, Wooyoung] Scripps Res Inst, Dept Chem, La Jolla, CA 92037 USA.
[Velentza, Anastasia; Kim, Sungjoon; Flatauer, Laura; Valente, David; Mason, Daniel E.; DiDonato, Michael; Nagle, Advait; Warmuth, Markus; Peters, Eric C.] Genom Inst Novartis Res Fdn, San Diego, CA 92121 USA.
[Jiang, Xinnong; Balk, Steven P.] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA.
[Suzuki, Melissa; Larson, Brad] Invitrogen Corp, Madison, WI 53719 USA.
[Zagorska, Anna] Univ Dundee, Coll Life Sci, MRC, Prot Phosphorylat Unit, Dundee, Scotland.
RP Gray, NS (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Biol Chem & Mol Pharmacol, Seeley G Mudd Bldg,Room 628A,250 Longwood Ave, Boston, MA 02115 USA.
EM nathanael_gray@dfci.harvard.edu
FU NCI NIH HHS [R01 CA130876, R01 CA130876-01A1]; NIGMS NIH HHS [P41
GM079575, P41 GM079575-01]
NR 13
TC 23
Z9 24
U1 0
U2 8
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-894X
EI 1464-3405
J9 BIOORG MED CHEM LETT
JI Bioorg. Med. Chem. Lett.
PD NOV 15
PY 2008
VL 18
IS 22
BP 5916
EP 5919
DI 10.1016/j.bmcl.2008.07.062
PG 4
WC Chemistry, Medicinal; Chemistry, Organic
SC Pharmacology & Pharmacy; Chemistry
GA 373JB
UT WOS:000260966800021
PM 18667312
ER
PT J
AU Westerberg, LS
de la Fuente, MA
Wermeling, F
Ochs, HD
Karlsson, MCI
Snapper, SB
Notarangelo, LD
AF Westerberg, Lisa S.
de la Fuente, Miguel A.
Wermeling, Fredrik
Ochs, Hans D.
Karlsson, Mikael C. I.
Snapper, Scott B.
Notarangelo, Luigi D.
TI WASP confers selective advantage for specific hematopoietic cell
populations and serves a unique role in marginal zone B-cell homeostasis
and function
SO BLOOD
LA English
DT Article
ID WISKOTT-ALDRICH-SYNDROME; SOCIETY-FOR-IMMUNODEFICIENCIES; REGULATORY
T-CELLS; SYNDROME PROTEIN; IN-VIVO; MARROW TRANSPLANTATION; DEFICIENCY
LEADS; APOPTOTIC CELLS; GENE-TRANSFER; X-CHROMOSOME
AB Development of hematopoietic cells depends on a dynamic actin cytoskeleton. Here we demonstrate that expression of the cytoskeletal regulator WASP, mutated in the Wiskott-Aldrich syndrome, provides selective advantage for the development of naturally occurring regulatory T cells, natural killer T cells, CD4(+) and CD8(+) T lymphocytes, marginal zone (MZ) B cells, MZ macrophages, and platelets. To define the relative contribution of MZ B cells and MZ macrophages for MZ development, we generated wild-type and WASP-deficient bone marrow chimeric mice, with full restoration of the MZ. However, even in the presence of MZ macrophages, only 10% of MZ B cells were of WASP-deficient origin. We show that WASP-deficient MZ B cells hyperproliferate in vivo and fail to respond to sphingosine-1-phosphate, a crucial chemoattractant for MZ B-cell positioning. Abnormalities of the MZ compartment in WASP(-/-) mice lead to aberrant uptake of Staphylococcus aureus and to a reduced immune response to TNP-Ficoll. Moreover, WASP-deficient mice have increased levels of "natural" IgM antibodies. Our findings reveal that WASP regulates both development and function of hematopoietic cells. We demonstrate that WASP deficiency leads to an aberrant MZ that may affect responses to blood-borne pathogens and peripheral B-cell tolerance. (Blood. 2008; 112: 4139-4147)
C1 [Westerberg, Lisa S.; Snapper, Scott B.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[Westerberg, Lisa S.; Snapper, Scott B.] Massachusetts Gen Hosp, Ctr Study Inflammatory Bowel Dis, Boston, MA 02114 USA.
[Westerberg, Lisa S.; Snapper, Scott B.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[de la Fuente, Miguel A.; Notarangelo, Luigi D.] Childrens Hosp, Div Immunol, Boston, MA 02115 USA.
[de la Fuente, Miguel A.; Notarangelo, Luigi D.] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
[Wermeling, Fredrik; Karlsson, Mikael C. I.] Karolinska Inst, Dept Med, Unit Clin Allergy Res, Stockholm, Sweden.
[Ochs, Hans D.] Univ Washington, Sch Med, Dept Pediat, Seattle, WA 98195 USA.
RP Snapper, SB (reprint author), Massachusetts Gen Hosp, Gastrointestinal Unit, Jackson 825C,55 Fruit St, Boston, MA 02114 USA.
EM ssnapper@hms.harvard.edu; Luigi.Notarangelo@childrens.harvard.edu
RI de la Fuente, Miiguel /C-7478-2013; Notarangelo, Luigi/F-9718-2016;
OI de la Fuente, Miiguel /0000-0003-4619-8756; Notarangelo,
Luigi/0000-0002-8335-0262; Wermeling, Fredrik/0000-0001-9633-677X;
Westerberg, Lisa/0000-0003-2943-2192
FU Swedish Society for Medical Research; National Institutes of Health
[HL59561, AI50950, P01HL059561-A11]
FX This work was supported by a postdoctoral fellowship from the Swedish
Society for Medical Research (L. W.) and National Institutes of Health
grants HL59561 and AI50950 (S. B. S.) and grant P01HL059561-A11 (S. B.
S. and L. S. N.).
NR 49
TC 60
Z9 64
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 15
PY 2008
VL 112
IS 10
BP 4139
EP 4147
DI 10.1182/blood-2008-02-140715
PG 9
WC Hematology
SC Hematology
GA 369JU
UT WOS:000260691300034
PM 18772454
ER
PT J
AU Kurtzberg, J
Prasad, VK
Carter, SL
Wagner, JE
Baxter-Lowe, LA
Wall, D
Kapoor, N
Guinan, EC
Feig, SA
Wagner, EL
Kernan, NA
AF Kurtzberg, Joanne
Prasad, Vinod K.
Carter, Shelly L.
Wagner, John E.
Baxter-Lowe, Lee Ann
Wall, Donna
Kapoor, Neena
Guinan, Eva C.
Feig, Stephen A.
Wagner, Elizabeth L.
Kernan, Nancy A.
CA COBLT Steering Comm
TI Results of the Cord Blood Transplantation Study (COBLT): clinical
outcomes of unrelated donor umbilical cord blood transplantation in
pediatric patients with hematologic malignancies
SO BLOOD
LA English
DT Article
ID STEM-CELL TRANSPLANTATION; BONE-MARROW; ACUTE-LEUKEMIA; CHILDREN;
RECONSTITUTION; RECIPIENTS; ADULTS
AB Outcomes of unrelated donor cord blood transplantation in 191 hematologic malignancy children (median age, 7.7 years; median weight, 25.9 kg) enrolled between 1999 and 2003 were studied (median follow-up, 27.4 months) in a prospective phase 2 multicenter trial. Human leukocyte antigen (HLA) matching at enrollment was 6/6 (n = 17), 5/6 (n = 58), 4/6 (n = 111), or 3/6 (n = 5) by low-resolution HLA-A, -B, and high-resolution (HR) DRB1. Retrospectively, 179 pairs were HLA typed by HR. The median precryopreservation total nucleated cell (TNC) dose was 5.1 x 107 TNC/kg (range, 1.5-23.7) with 3.9 x 107 TNC/kg (range, 0.8-22.8) infused. The median time to engraftment (absolute neutrophil count > 500/mm(3) and platelets 50 000/mu L) was 27 and 174 days. The cumulative incidence of neutrophil engraftment by day 42 was 79.9% (95% confidence interval [CI], 75.1%-85.2%); acute grades III/IV GVHD by day 100 was 19.5% ( 95% CI, 13.9%-25.5%); and chronic GVHD at 2 years was 20.8% (95% CI, 14.8%-27.7%). HR matching decreased the probability of severe acute GVHD. The cumulative incidence of relapse at 2 years was 19.9% (95% CI, 14.8%-25.7%). The probabilities of 6-month and 2-year survivals were 67.4% and 49.5%. Unrelated donor cord blood transplantation from partially HLA-mismatched units can cure many children with leukemias. The study was registered at www. clinicaltrials. gov as #NCT00000603. (Blood. 2008; 112: 4318-4327)
C1 [Kurtzberg, Joanne; Prasad, Vinod K.] Duke Univ, Med Ctr, Durham, NC 27710 USA.
[Carter, Shelly L.] EMMES Corp, Rockville, MD USA.
[Wagner, John E.] Univ Minnesota, Minneapolis, MN USA.
[Baxter-Lowe, Lee Ann] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Wall, Donna] Texas Transplant Inst, San Antonio, TX USA.
[Kapoor, Neena] Childrens Hosp, Los Angeles, CA 90027 USA.
[Guinan, Eva C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Feig, Stephen A.] Mattel Childrens Hosp, Los Angeles, CA USA.
[Wagner, Elizabeth L.] NHLBI, Bethesda, MD 20892 USA.
[Kernan, Nancy A.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
RP Kurtzberg, J (reprint author), Duke Univ, Med Ctr, Box 3350, Durham, NC 27710 USA.
EM kurtz001@mc.duke.edu
OI Kernan, Nancy/0000-0003-1417-1823
FU NHLBI NIH HHS [N01-HB 67135, N01-HB 67139, N01-HB-67132, N01HB67132,
N01HB67135, N01HB67138, N01HB67139]
NR 25
TC 178
Z9 188
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 15
PY 2008
VL 112
IS 10
BP 4318
EP 4327
DI 10.1182/blood-2007-06-098020
PG 10
WC Hematology
SC Hematology
GA 369JU
UT WOS:000260691300056
PM 18723429
ER
PT J
AU Benimetskaya, L
Wu, S
Voskresenskiy, AM
Echart, C
Zhou, JF
Shin, J
Iacobelli, M
Richardson, P
Ayyanar, K
Stein, CA
AF Benimetskaya, Luba
Wu, Sijian
Voskresenskiy, Anatoliy M.
Echart, Cinara
Zhou, Jin-Feng
Shin, Joongho
Iacobelli, Massimo
Richardson, Paul
Ayyanar, Kanyalakshmi
Stein, C. A.
TI Angiogenesis alteration by defibrotide: implications for its mechanism
of action in severe hepatic veno-occlusive disease
SO BLOOD
LA English
DT Article
ID FIBROBLAST-GROWTH-FACTOR; SUBENDOTHELIAL EXTRACELLULAR-MATRIX;
SINUSOIDAL OBSTRUCTION SYNDROME; BONE-MARROW-TRANSPLANTATION;
HEPARIN-LIKE MOLECULES; HIGH-RISK POPULATION; ENDOTHELIAL-CELLS;
SIGNIFICANT TOXICITY; COMPASSIONATE-USE; RECEPTOR
AB Defibrotide (DF) is a mixture of porcine-derived single-stranded phosphodiester oligonucleotides (9-80-mer; average, 50-mer) that has been successfully used to treat severe hepatic veno-occlusive disease (sVOD) with multiorgan failure (MOF) in patients who have received cytotoxic chemotherapy in preparation for bone marrow transplantation. However, its mechanism of action is unknown. Herein, we show that DF and phosphodiester oligonucleotides can bind to heparin-binding proteins (eg, basic fibroblast growth factor [bFGF] but not vascular endothelial growth factor [VEGF] 165) with low nanomolar affinity. This binding occurred in a length- and concentration-dependent manner. DF can mobilize proangiogenic factors such as bFGF from their depot or storage sites on bovine corneal endothelial matrix. However, these molecules do not interfere with high-affinity binding of bFGF to FGFR1 IIIc but can replace heparin as a required cofactor for binding and hence cellular mitogenesis. DF also protects bFGF against digestion by trypsin and chymotrypsin and from air oxidation. In addition, DF binds to collagen I with low nanomolar affinity and can promote human microvascular endothelial cell-1 (HMEC-1) cell mitogenesis and tubular morphogenesis in three-dimensional collagen I gels. Thus, our data suggest that DF may provide a stimulus to the sinusoidal endothelium of a liver that has suffered a severe angiotoxic event, thus helping to ameliorate the clinical sVOD/MOF syndrome. (Blood. 2008; 112: 4343-4352)
C1 [Benimetskaya, Luba; Wu, Sijian; Voskresenskiy, Anatoliy M.; Zhou, Jin-Feng; Shin, Joongho; Ayyanar, Kanyalakshmi; Stein, C. A.] Montefiore Med Ctr, Albert Einstein Montefiore Canc Ctr, Dept Oncol, Bronx, NY 10467 USA.
[Echart, Cinara; Iacobelli, Massimo] Gentium SpA, Villa Guardia, Italy.
[Richardson, Paul] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Stein, CA (reprint author), Montefiore Med Ctr, Albert Einstein Montefiore Canc Ctr, Dept Oncol, 111 E 210th St, Bronx, NY 10467 USA.
EM cstein@montefiore.org
FU Gentium S. p. A (Como, Italy; C.S.); Rick Corman Foundation
FX This work was supported by funding from Gentium S. p. A. (Como, Italy;
C.S.), and from the Rick Corman Foundation (P.R. and C.S.).
NR 58
TC 22
Z9 25
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 15
PY 2008
VL 112
IS 10
BP 4343
EP 4352
DI 10.1182/blood-2008-04-149682
PG 10
WC Hematology
SC Hematology
GA 369JU
UT WOS:000260691300059
PM 18711003
ER
PT J
AU Schwartz, GF
Hughes, KS
Lynch, HT
Fabian, CJ
Fentiman, IS
Robson, ME
Domchek, SM
Hartmann, LC
Holland, R
Winchester, DJ
AF Schwartz, Gordon F.
Hughes, Kevin S.
Lynch, Henry T.
Fabian, Carol J.
Fentiman, Ian S.
Robson, Mark E.
Domchek, Susan M.
Hartmann, Lynn C.
Holland, Roland
Winchester, David J.
CA Consensus Conference Comm
TI Proceedings of the International Consensus Conference on Breast Cancer
Risk, Genetics, & Risk Management, April, 2007
SO CANCER
LA English
DT Editorial Material
DE breast cancer; risk factors; BRCA mutations; international conference;
patient management guidelines
AB A consensus conference including 30 experts was held in April, 2007, to discuss risk factors for breast cancer and their management. Four categories of risk were outlined, from "average" through "very high" risk, the latter including individuals with high penetrance BRCA1/2 gene mutations. Guidelines for management of patients in each of these categories were discussed, with the major portion of the conference devoted to individuals with BRCA1/2 mutations. Prevalence of these mutations in the general population was estimated to be 1 in 250-500 individuals, with an increased prevalence in Ashkenazi Jews and other founder groups. Risk-reduction strategies for these individuals included surveillance, with or without chemoprevention drugs, or surgical procedures to remove the organs at risk, ie, bilateral mastectomy and/or bilateral salpingo-oophorectomy. These risk reduction strategies were evaluated fully, and recommendations were made for the care of patients in each risk category. These guidelines for patient care were approved by the entire group of experts. Cancer 2008;113:2627-37. (C) 2008 American Cancer Society.
C1 [Schwartz, Gordon F.] Thomas Jefferson Univ, Jefferson Med Coll, Dept Surg, Philadelphia, PA 19107 USA.
[Hughes, Kevin S.] Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA.
[Hughes, Kevin S.] Massachusetts Gen Hosp, Avon Comprehens Breast Ctr, Boston, MA 02114 USA.
[Lynch, Henry T.] Creighton Univ, Sch Med, Dept Prevent Med, Omaha, NE 68178 USA.
[Fabian, Carol J.] Univ Kansas, Med Ctr, Dept Med, Breast Canc Prevent Ctr, Kansas City, KS 66103 USA.
[Fentiman, Ian S.] Guys & St Thomas NHS Trust, Dept Surg Oncol, London, England.
[Robson, Mark E.] Mem Sloan Kettering Canc Ctr, Clin Genet Serv, New York, NY 10021 USA.
[Domchek, Susan M.] Univ Penn, Med Ctr, Dept Canc Res, Philadelphia, PA 19104 USA.
[Hartmann, Lynn C.] Mayo Clin, Ctr Canc, Dept Oncol, Rochester, MN USA.
[Holland, Roland] Univ Nijmegen Hosp, Ctr Breast Canc Screening, NL-6500 HB Nijmegen, Netherlands.
[Winchester, David J.] Northwestern Univ, Feinberg Sch Med, Dept Surg, Chicago, IL 60611 USA.
RP Schwartz, GF (reprint author), Thomas Jefferson Univ, Jefferson Med Coll, Dept Surg, 1015 Chestnut St,Suite 510, Philadelphia, PA 19107 USA.
EM gordonschwartz@yahoo.com
OI Hughes, Kevin/0000-0003-4084-6484; Howell, Anthony/0000-0002-6233-719X;
Robson, Mark/0000-0002-3109-1692
NR 0
TC 47
Z9 48
U1 0
U2 2
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 15
PY 2008
VL 113
IS 10
BP 2627
EP 2637
DI 10.1002/cncr.23903
PG 11
WC Oncology
SC Oncology
GA 372PV
UT WOS:000260914400003
PM 18853415
ER
PT J
AU Lin, NU
Claus, E
Sohl, J
Razzak, AR
Arnaout, A
Winer, EP
AF Lin, Nancy U.
Claus, Elizabeth
Sohl, Jessica
Razzak, Abdul R.
Arnaout, Amal
Winer, Eric P.
TI Sites of Distant Recurrence and Clinical Outcomes in Patients With
Metastatic Triple-negative Breast Cancer High Incidence of Central
Nervous System Metastases
SO CANCER
LA English
DT Article
DE triple-negative breast cancer; basal-like breast cancer; brain
metastases; survival; central nervous system recurrence
ID TRASTUZUMAB-BASED THERAPY; BRAIN METASTASES; GENE-EXPRESSION; CNS
METASTASES; PHASE-II; SURVIVAL; CARCINOMA; SUBTYPES; WOMEN; PATTERNS
AB BACKGROUND. The purpose of the current study was to characterize the Outcomes of patients with metastatic triple-negative breast cancers, including the risk and clinical consequences of central nervous system (CNS) recurrence.
METHODS. Using pharmacy and pathology records, a study group of 116 patients who were treated for metastatic triple-negative breast cancer at Dana-Farber Cancer Institute between January 2000 and June 2006 was identified.
RESULTS. The median survival front time of metastatic diagnosis was 13.3 months. Sixteen patients (14%) were diagnosed with CNS involvement at the time of initial metastatic diagnosis; overall, 46% of patients were diagnosed with CNS metastases before death. The median survival after a diagnosis of CNS metastasis was 4.9 months. The age-adjusted and race-adjusted rate of death for patients whose first presentation included a CNS metastasis was 3.4 times (95% confidence interval, 1.9-6.1 times) that of patients without a CNS lesion at the time of first metastatic presentation. Of the 53 patients who developed brain metastases, only 3 patients were judged to have stable or responsive systemic disease in the face of progressive CNS disease at the last follow-up before death.
CONCLUSIONS. Triple-negative breast cancer is associated with poor survival after recurrence. CNS recurrence is common, but death as a direct consequence of CNS progression in the setting of controlled systemic disease is uncommon. Thus, it does not appear that the high rate of CNS involvement is because of a sanctuary effect, but rather is due to the lack of effective therapies in general for this aggressive subtype of breast cancer. New treatment strategies are needed. Cancer 2008; 113:2638-45. (C) 2008 American Cancer Society.
C1 [Lin, Nancy U.; Sohl, Jessica; Razzak, Abdul R.; Arnaout, Amal; Winer, Eric P.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Claus, Elizabeth] Brigham & Womens Hosp, Dept Neurosurg, Boston, MA 02115 USA.
[Claus, Elizabeth] Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA.
RP Lin, NU (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA.
EM nlin@partners.org
FU Breast Cancer Research Foundation; Hurricane Voices Junior Faculty
Award; American Society of Clinical Oncology Career Development Award;
Karen Webster and David Evans Research Fund; National Cancer Institute
Specialized Program in Research Excellence in Breast Cancer at DF/HCC
[CA89393]; Susan G. Komen Breast Cancer Foundation; NIH [R01-CA81393]
FX Supported by the Breast Cancer Research Foundation, the Hurricane Voices
Junior Faculty Award, the American Society of Clinical Oncology Career
Development Award, the Karen Webster and David Evans Research Fund, the
National Cancer Institute Specialized Program in Research Excellence in
Breast Cancer at DF/HCC (CA89393), the Susan G. Komen Breast Cancer
Foundation, and NIH R01-CA81393 (to E.C.).
NR 39
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U1 2
U2 13
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 15
PY 2008
VL 113
IS 10
BP 2638
EP 2645
DI 10.1002/cncr.23930
PG 8
WC Oncology
SC Oncology
GA 372PV
UT WOS:000260914400004
PM 18833576
ER
PT J
AU Elting, LS
Keefe, DM
Sonis, ST
Garden, AS
Spijkervet, FKL
Barasch, A
Tishler, RB
Canty, TP
Kudrimoti, MK
Vera-Lionch, M
AF Elting, Linda S.
Keefe, Dorothy M.
Sonis, Stephen T.
Garden, Adam S.
Spijkervet, F. K. L.
Barasch, Andrei
Tishler, Roy B.
Canty, Thomas P.
Kudrimoti, Mahesh K.
Vera-Lionch, Montserrat
CA Burden Illness Head & Neck Writing
TI Patient-reported Measurements of Oral Mucositis in Head and Neck Cancer
Patients Treated With Radiotherapy With or Without Chemotherapy
Demonstration of Increased Frequency, Severity, Resistance to
Palliation, and Impact on Quality of Life
SO CANCER
LA English
DT Article; Proceedings Paper
CT 49th Annual Meeting of the
American-Society-for-Therapeutic-Radiology-and-Oncology (ASTRO)
CY OCT 27-NOV 01, 2007
CL Los Angeles, CA
SP Amer Soc Therapeut Radiol & Oncol (ASTRO)
DE mucositis; radiation therapy; head and neck cancer; patient-reported
outcomes; quality of life
ID MODULATED RADIATION-THERAPY; FUNCTIONAL ASSESSMENT; OROPHARYNGEAL
CARCINOMA; MEANINGFUL CHANGE; QUESTIONNAIRE; OUTCOMES; TRIAL;
CONSEQUENCES; FLUOROURACIL; DOCETAXEL
AB BACKGROUND. I-lie risk, severity, and patient-reported outcomes of radiation-induced mucositis among head and neck cancer patients were prospectively estimated.
METHODS. A validated, patient-reported questionnaire (OMDQ), the FACT quality of life (QOL), and the Functional Assessment of Chronic Illness Therapy (FACIT) fatigue scales Were used to measure mucositis (reported as mouth and throat Soreness), daily functioning, and Use of analgesics. Patients were studied before radiotherapy (RT), daily during RT, and for 4 weeks after RT.
RESULTS. contrary to previous reports, the risk of mucositis was virtually identical in the 126 patients with oral cavity or oropharynx tumors (99% overall; 85% grade 3-4) compared with 65 patients with tumors of the larynx or hypopharynx (98% overall; 77% grade 3-4). The mean QOL score decreased significantly during RT, from 85.1 at baseline to 69.0 at Week 6, corresponding with the peak of mucositis severity The mean functional status score decreased by 33% from 18.3 at baseline to 12.3 at week 6. The impact of mucositis on QOL was proportional to its severity, although even a score of I or 2 (mild or moderate) was associated with a significant reduction in QOL (from 93.6 at baseline to 74.7 at Week 6). Despite increases in analgesic use from 34% at baseline to 80% at Week 6, mean mucositis scores exceeded 2.5 at Week 6.
CONCLUSIONS. Mucositis occurs among virtually all patients who are Undergoing radiation treatment of head and neck cancers. The detrimental effects on QOL and functional status are significant, and opioid analgesia provides inadequate relief. Preventive rather than symptom palliation measures are needed. Cancer 2008;113:2704-13. (C) 2008 American Cancer Society.
C1 [Elting, Linda S.] Univ Texas MD Anderson Canc Ctr, Dept Biostat, Houston, TX 77030 USA.
[Keefe, Dorothy M.] Royal Adelaide Hosp, Ctr Canc, Dept Oncol, Adelaide, SA 5000, Australia.
[Sonis, Stephen T.] Harvard Univ, Sch Med, Dept Oral Med Infect & Immun, Boston, MA USA.
[Sonis, Stephen T.] Dana Farber Canc Inst, Dept Surg, Div Oral Med, Boston, MA 02115 USA.
[Garden, Adam S.] Univ Texas MD Anderson Canc Ctr, Dept Radiat Oncol, Houston, TX 77030 USA.
[Spijkervet, F. K. L.] Univ Groningen, Univ Med Ctr Groningen, Dept Maxillofacial Surg, NL-9713 AV Groningen, Netherlands.
[Barasch, Andrei] Univ Alabama, Med Ctr, Birmingham, AL 35294 USA.
[Tishler, Roy B.] Harvard Univ, Sch Med, Dept Radiat Oncol, Boston, MA USA.
[Tishler, Roy B.] Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA.
[Canty, Thomas P.] Arizona Oncol Serv Fdn, Phoenix, AZ USA.
[Kudrimoti, Mahesh K.] Univ Kentucky, Coll Med, Chandler Med Ctr, Lexington, KY USA.
[Vera-Lionch, Montserrat] Policy Anal Inc, Brookline, MA USA.
RP Elting, LS (reprint author), Univ Texas MD Anderson Canc Ctr, Dept Biostat, 1515 Holcombe Blvd,Unit 1411, Houston, TX 77030 USA.
EM lelting@mdanderson.org
NR 29
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U1 1
U2 10
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0008-543X
J9 CANCER-AM CANCER SOC
JI Cancer
PD NOV 15
PY 2008
VL 113
IS 10
BP 2704
EP 2713
DI 10.1002/cncr.23898
PG 10
WC Oncology
SC Oncology
GA 372PV
UT WOS:000260914400012
PM 18973181
ER
PT J
AU Tu, C
Ortega-Cava, CF
Chen, GS
Fernandes, ND
Cavallo-Medved, D
Sloane, BF
Band, V
Band, H
AF Tu, Chun
Ortega-Cava, Cesar F.
Chen, Gengsheng
Fernandes, Norvin D.
Cavallo-Medved, Dora
Sloane, Bonnie F.
Band, Vimla
Band, Hamid
TI Lysosomal Cathepsin B Participates in the Podosome-Mediated
Extracellular Matrix Degradation and Invasion via Secreted Lysosomes in
v-Src Fibroblasts
SO CANCER RESEARCH
LA English
DT Article
ID OSTEOCLASTIC BONE-RESORPTION; PLASMINOGEN-ACTIVATOR; CYSTEINE
CATHEPSINS; PLASMA-MEMBRANE; TRANSFORMED-CELLS; CARCINOMA-CELLS;
MELANOMA-CELLS; CANCER-CELLS; H+-ATPASE; C-SRC
AB Podosomes mediate cell migration and invasion by coordinating the reorganization of actin cytoskeleton and focal matrix degradation. MMP and serine proteases have been found to function at podosomes. The lysosomal cysteine cathepsins, a third major class of matrix-degrading enzymes involved in tumor invasion and tissue remodeling, have yet to be linked to podosomes with the exception of cathepsin K in osteoclasts. Using inhibitors and shRNA-mediated depletion, we show that cathepsin B participates in podosomes-mediated focal matrix degradation and invasion in v-Src-transformed fibroblasts. We observed that lysosomal marker LAMP-1 localized at the center of podosome rosettes protruding into extracellular matrix using confocal microscopy. Time-lapse live-cell imaging revealed that lysosomal vesicles moved to and fused with podosomes. Disruption of lysosomal pH gradient with Bafilomycin A1, chloroquine, or ammonium chloride greatly enhanced the formation of podosomes and increased the matrix degradation. Live-cell imaging showed that actin structures, induced shortly after Bafilomycin A1 treatment, were closely associated with lysosomes. Overall, our results suggest that cathepsin B, delivered by lysosomal vesicles, is involved in the matrix degradtion of podosomes. [Cancer Res 2008;68(22):9147-56]
C1 [Tu, Chun; Ortega-Cava, Cesar F.; Band, Hamid] Univ Nebraska, Med Ctr, Eppley Inst Res Canc & Allied Dis, Omaha, NE 68198 USA.
[Tu, Chun; Ortega-Cava, Cesar F.; Band, Vimla; Band, Hamid] Univ Nebraska, Med Ctr, UNMC Eppley Canc Ctr, Omaha, NE 68198 USA.
[Band, Hamid] Univ Nebraska, Med Ctr, Coll Med, Dept Biochem & Mol Biol, Omaha, NE 68198 USA.
[Band, Vimla] Univ Nebraska, Med Ctr, Coll Med, Dept Genet Coll Biol & Anat, Omaha, NE 68198 USA.
[Cavallo-Medved, Dora; Sloane, Bonnie F.] Wayne State Univ, Sch Med, Dept Pharmacol, Detroit, MI 48201 USA.
[Cavallo-Medved, Dora; Sloane, Bonnie F.] Wayne State Univ, Sch Med, Barbara Ann Karmanos Canc Inst, Detroit, MI USA.
[Tu, Chun; Ortega-Cava, Cesar F.; Chen, Gengsheng; Band, Vimla; Band, Hamid] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston NW Healthcare Res Inst, Dept Med,Div Mol Oncol,Feinberg Sch Med, Evanston, IL USA.
[Tu, Chun; Ortega-Cava, Cesar F.; Chen, Gengsheng; Band, Vimla; Band, Hamid] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston NW Healthcare Res Inst, Dept Med,Div Canc Biol,Feinberg Sch Med, Evanston, IL USA.
[Tu, Chun; Ortega-Cava, Cesar F.; Chen, Gengsheng; Band, Vimla; Band, Hamid] Northwestern Univ, Dept Biochem Mol Biol & Cell Biol, Evanston, IL USA.
[Fernandes, Norvin D.] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Band, H (reprint author), Univ Nebraska, Med Ctr, Eppley Inst, 986805 Nebraska Med Ctr, Omaha, NE 68198 USA.
EM hband@unmc.edu
FU NIH [CA 87986, CA 76118, CA 99900, CA 116552, CA99163, CA94143, CA96844,
CA81076]; Department of Defense Breast Cancer Research
[DAMD17-02-1-0508]; National Cancer Institute (NCI) Cancer Center of
Nanotechnology Excellence [NCI IU54, CA119341-01]; NCI Breast, Cancer
Specialized programs of Research Excellence; AVON Breast Cancer Fund at
Robert H. Luric Cancer Center, Northwestern University; H Foundation,
Chicago, IL; Jean Ruggles-Romoser Chair of Cancer Research; Duckworth
Family Chair of Breast Cancer Research; Nebraska Research Initiative;
Eppley Cancer center
FX Grant support: the NIH grants CA 87986, CA 76118, CA 99900, CA 116552,
and CA99163 (H. Band), and CA94143, CA96844, and CA81076 (V. Band):
Department of Defense Breast Cancer Research Grants DAMD17-02-1-0508 (V.
Band); the National Cancer Institute (NCI) Cancer Center of
Nanotechnology Excellence Grant NCI IU54 CA119341-01 (H. Band and V.
Band); the NCI Breast, Cancer Specialized programs of Research
Excellence and AVON Breast Cancer Fund at Robert H. Luric Cancer Center,
Northwestern University; the H Foundation, Chicago, IL; and the Jean
Ruggles-Romoser Chair of Cancer Research (H. Band) and the Duckworth
Family Chair of Breast Cancer Research (V. Band).; The costs of
publication of this article were defrayed in part by the payment of page
charges. This article must therefore be hereby marked advertisement in
accordance with 18 U.S.C. Section 1734 solely to indicate this fact.; We
thank Dr. Joan Brugge for v-Src, plasmid, Dr. Qingshen Gao, Janice
Taylor, and James Talaska of the Confocal laser Scanning microscope Core
Facility at the University of Nebraska Medical Center; the latter is
supported by the Nebraska Research Initiative and the Eppley Cancer
center, and the members of the Band laboratories for helpful suggestions
and discussion.
NR 50
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U1 0
U2 7
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD NOV 15
PY 2008
VL 68
IS 22
BP 9147
EP 9156
DI 10.1158/0008-5472.CAN-07-5127
PG 10
WC Oncology
SC Oncology
GA 375TQ
UT WOS:000261136600009
PM 19010886
ER
PT J
AU Minkis, K
Kavanagh, DG
Alter, G
Bogunovic, D
O'Neill, D
Adams, S
Pavlick, A
Walker, BD
Brockman, MA
Gandhi, RT
Bhardwaj, N
AF Minkis, Kira
Kavanagh, Daniel G.
Alter, Galit
Bogunovic, Dusan
O'Neill, David
Adams, Sylvia
Pavlick, Anna
Walker, Bruce D.
Brockman, Mark A.
Gandhi, Rajesh T.
Bhardwaj, Nina
TI Type 2 Bias of T Cells Expanded from the Blood of Melanoma Patients
Switched to Type 1 by IL-12p70 mRNA-Transfected Dendritic Cells
SO CANCER RESEARCH
LA English
DT Article
ID RECOMBINANT HUMAN INTERLEUKIN-12; ANTITUMOR IMMUNITY; IN-VITRO;
METASTATIC MELANOMA; MALIGNANT-MELANOMA; TUMOR; IMMUNOTHERAPY;
RESPONSES; CANCER; LYMPHOCYTES
AB Melanoma patients may exhibit a T(H)2-skewed cytokine profile within blood and tumor-infiltrating lymphocytes. Therapies that induce beneficial T(H)1-type tumor-specific immune responses, therefore, are highly desirable. Dendritic cells (DC) are widely used as immune adjuvants for cancer. Before their administration, DC are generally induced to mature with a cocktail of recombinant cytokines [interleukin (IL)-1 beta, tumor necrosis factor alpha, and IL-6] and prostaglandin E-2 (PGE(2)), which is added to preserve the ability of DC to migrate to draining lymph nodes. However, PGE(2) suppresses the production of IL-12p70, a cytokine essential for differentiation of T(H)1 responses. In this study, human DC were transfected with IL-12p70 mRNA and tested for their ability to alter the T(H)2 type bias manifested by blood T cells of patients with melanoma. Transfected DC secreted high levels of bioactive IL-12p70, as indicated by their capacity to enhance natural killer cell activity, skew T(H)1 responses in allogeneic mixed lymphocyte reactions through reduction of IL-4 and IL-5, and prime CD8(+) T cells to the melanoma-associated antigen Melan A/MART-1. Furthermore, T-cell lines primed in vitro from the blood of melanoma patients showed strong type 2 skewing that was dramatically reversed by IL-12p70 transfection of autologons DC. Thus, IL-12p70 transfection of clinical DC preparations may enhance type 1 antitumor responses and may thereby contribute to effective immune-based therapy. [Cancer Res 2008;68(22):9441-50]
C1 [Bhardwaj, Nina] NYU, Med Ctr, Sch Med, New York, NY 10016 USA.
[Walker, Bruce D.; Brockman, Mark A.] Howard Hughes Med Inst, Boston, MA 02115 USA.
[Kavanagh, Daniel G.; Alter, Galit; Walker, Bruce D.; Brockman, Mark A.; Gandhi, Rajesh T.; Bhardwaj, Nina] Massachusetts Gen Hosp, Partners AIDS Res Ctr, Boston, MA 02114 USA.
[Kavanagh, Daniel G.; Alter, Galit; Walker, Bruce D.; Brockman, Mark A.; Gandhi, Rajesh T.; Bhardwaj, Nina] Harvard Univ, Sch Med, Boston, MA USA.
RP Bhardwaj, N (reprint author), NYU, Med Ctr, Sch Med, 550 1st Ave, New York, NY 10016 USA.
EM Nina.Bhardwaj@nyumc.org
OI Brockman, Mark/0000-0001-6432-1426
FU NIH [F32 AI058457-03, R01 AI066992-01AI, R01 044628]; Burroughs Wellcome
Foundations; Elizabeth Glaser Pediatric AIDS Foundation; Howard Hughes
Medical Institute
FX Grant support: NIH grants F32 AI058457-03 (D.G. Kavanagh), R01
AI066992-01AI (R.T. Gandhi), R01 044628 (N. Bhardwaj), and R01 1061684
(N. Bhardwaj); the Doris Duke, Emerald, and Burroughs Wellcome
Foundations and the Elizabeth Glaser Pediatric AIDS Foundation (N.
Bhardwaj); and the Howard Hughes Medical Institute (M.A. Brockman and
B.D. Walker).
NR 49
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U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD NOV 15
PY 2008
VL 68
IS 22
BP 9441
EP 9450
DI 10.1158/0008-5472.CAN-08-0900
PG 10
WC Oncology
SC Oncology
GA 375TQ
UT WOS:000261136600042
PM 19010919
ER
PT J
AU Nikolsky, Y
Sviridov, E
Yao, J
Dosymbekov, D
Ustyansky, V
Kaznacheev, V
Dezso, Z
Mulvey, L
Macconaill, LE
Winckler, W
Serebryiskaya, T
Nikolskaya, T
Polyak, K
AF Nikolsky, Yuri
Sviridov, Evgeny
Yao, Jun
Dosymbekov, Damir
Ustyansky, Vadirn
Kaznacheev, Valery
Dezso, Zoltan
Mulvey, Laura
Macconaill, Laura E.
Winckler, Wendy
Serebryiskaya, Tatiana
Nikolskaya, Tatiana
Polyak, Kornelia
TI Genome-Wide Functional Synergy between Amplified and Mutated Genes in
Human Breast Cancer
SO CANCER RESEARCH
LA English
DT Article
ID COLORECTAL CANCERS; HYBRIDIZATION; PATTERNS; FREQUENT
AB A single cancer cell contains large numbers of genetic alterations that in combination create the malignant phenotype. However, whether amplified and mutated genes form functional and physical interaction networks that could explain the selection for cells with combined alterations is unknown. To investigate this issue, we characterized copy number alterations in 191 breast tumors using dense single nucleotide polymorphism arrays and identified 1,747 genes with copy number gain organized into 30 amplicons. Amplicons were distributed unequally throughout the genome. Each amplicon had distinct enrichment pattern in pathways, networks, and molecular functions, but genes within individual amplicons did not form coherent functional units. Genes in amplicons included all major tumorigenic pathways and were highly enriched in breast cancer-causative genes. In contrast, 1,188 genes with somatic mutations in breast cancer were distributed randomly over the genome, did not represent a functionally cohesive gene set, and were relatively less enriched in breast cancer marker genes. Mutated and gained genes did not show statisticalty signifiicant overlap but were highly synergistic in populating key tumorigenic pathways including transforming growth factor beta, WNT, fibroblast growth factor, and PIP3 signaling. In general, mutated genes were more frequently upstream of gained genes in transcription regulation signaling than vice versa, suggesting that mutated genes are mainly regulators, whereas gained genes are mostly regulated. ESR1 was the major transcription factor regulating amplified but not mutated genes. Our results support the hypothesis that multiple genetic events, including copy number gains and somatic mutations, are necessary for establishing the malignant cell phenotype. [Cancer Res 2008;68(22):9532-40]
C1 [Macconaill, Laura E.; Winckler, Wendy; Polyak, Kornelia] Dana Farber Canc Inst, Ctr Canc Genome Discovery, Boston, MA 02115 USA.
[Nikolsky, Yuri; Ustyansky, Vadirn; Dezso, Zoltan; Nikolskaya, Tatiana] GeneGo Inc, St Joseph, MI USA.
[Yao, Jun; Mulvey, Laura; Polyak, Kornelia] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Sviridov, Evgeny; Dosymbekov, Damir; Kaznacheev, Valery; Serebryiskaya, Tatiana; Nikolskaya, Tatiana] NI Vavilov Gen Genet Res Inst, Moscow 117809, Russia.
[Yao, Jun; Polyak, Kornelia] Harvard Univ, Sch Med, Boston, MA USA.
[Mulvey, Laura] Harvard Univ, Cambridge, MA 02138 USA.
[Macconaill, Laura E.; Winckler, Wendy] Broad Inst, Cambridge, MA USA.
RP Polyak, K (reprint author), Dana Farber Canc Inst, Ctr Canc Genome Discovery, 44 Binney St D740C, Boston, MA 02115 USA.
EM Kornelia_Polyak@dfci.harvard.edu
RI Nikolskaya, Tatiana/M-5008-2013
FU National Cancer Institute [CA89393, CA94074]; NCI [CA134175, CA112828];
GeneGo, Inc
FX Grant support: National Cancer Institute (CA89393 and CA94074) grants
(K. Polyak). NCI (CA134175) to Y. Nikolsky, and NCI (CA112828) to T.
Nikolskaya, and by GeneGo, Inc.
NR 26
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U1 0
U2 6
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD NOV 15
PY 2008
VL 68
IS 22
BP 9532
EP 9540
DI 10.1158/0008-5472.CAN-08-3082
PG 9
WC Oncology
SC Oncology
GA 375TQ
UT WOS:000261136600053
PM 19010930
ER
PT J
AU Rocha-Singh, K
Jaff, MR
Kelley, EL
AF Rocha-Singh, Krishna
Jaff, Michael R.
Kelley, E. Lynne
CA RENAISSANCE Trial Investigators
TI Renal Artery Stenting With Noninvasive Duplex Ultrasound Follow-up:
3-Year Results From the RENAISSANCE Renal Stent Trial
SO CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS
LA English
DT Article
DE atherosclerosis; kidney disease; percutaneous intervention
ID BALLOON ANGIOPLASTY; STENOSIS; ULTRASONOGRAPHY; HYPERTENSION;
RESTENOSIS; DIAGNOSIS; INDEX
AB Objective: The multicenter, single-arm RENAISSANCE trial evaluated outcomes in patients with progressive atherosclerotic renal artery stenosis (ARAS) treated with the Express (TM) Renal Premounted Stent System (Boston Scientific, Natick, MA). Background: Renal artery stenting may prevent the morbidity and mortality of surgical revascularization and high restenosis rates of percutaneous renal angioplasty (PTRA). Renal artery duplex ultrasonography (DUS) offers an alternative to traditional invasive poststenting angiographic surveillance, though concordance with angiography for in-stent restenosis has yet to be validated independently. Methods: RENAISSANCE enrolled 100 patients (117 lesions) with de novo or restenotic ostial atherosclerotic lesions <= 15 mm long in vessels >= 4.0 and <= 7.0 mm diameter with diameter stenosis >= 70%. The primary endpoint, 9-month binary restenosis, was compared to an objective performance criterion (OPC) of 40% for published PTRA results. Follow-up was conducted through 3 years. Results: Technical and procedural success was both 99%. Follow-up angiography, triggered clinically or by ultrasonography, revealed 21.3% binary restenosis at 9 months, which was superior to the OPC (P < 0.0001). Concordance between ultrasonography and angiography for detection of binary restenosis at 9 months was 87%. Peak systolic velocity and renal-to-aortic ratio were both significantly improved compared to baseline at 9 months and 2 years. The major adverse event (defined as device- or procedure-related death, target lesion revascularization or significant embolic event) rate was 10.5% at 9 months and 20.9% at 3 years. Conclusions: RENAISSANCE demonstrates that renal artery stenting is superior to the prespecified OPC at 9 months, and also shows that DUS can accurately identify in-stent restenosis. (C) 2008 Wiley-Liss, Inc.
C1 [Rocha-Singh, Krishna] Prairie Vasc Inst, Springfield, IL 62719 USA.
[Jaff, Michael R.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Kelley, E. Lynne] Boston Sci Corp, Natick, MA USA.
RP Rocha-Singh, K (reprint author), Prairie Vasc Inst, 619 E Mason St, Springfield, IL 62719 USA.
EM ksingh@prairieheart.com
NR 24
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U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1522-1946
J9 CATHETER CARDIO INTE
JI Catheter. Cardiovasc. Interv.
PD NOV 15
PY 2008
VL 72
IS 6
BP 853
EP 862
DI 10.1002/ccd.21749
PG 10
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 373QZ
UT WOS:000260988400020
PM 19006254
ER
PT J
AU Schainfeld, RM
AF Schainfeld, Robert M.
TI IVUS: Cracking the "Code" in the Wall
SO CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS
LA English
DT Editorial Material
ID INTRAVASCULAR ULTRASOUND; ANGIOPLASTY
C1 Massachusetts Gen Hosp, Sect Vasc Med, Div Cardiol, Boston, MA 02114 USA.
RP Schainfeld, RM (reprint author), Massachusetts Gen Hosp, Sect Vasc Med, Div Cardiol, Boston, MA 02114 USA.
EM rschainfeld@partners.org
NR 6
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1522-1946
J9 CATHETER CARDIO INTE
JI Catheter. Cardiovasc. Interv.
PD NOV 15
PY 2008
VL 72
IS 6
BP 871
EP 872
DI 10.1002/ccd.21862
PG 2
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 373QZ
UT WOS:000260988400023
PM 19009631
ER
PT J
AU Bazzaro, M
Lin, ZH
Santillan, A
Lee, MK
Wang, MC
Chan, KC
Bristow, RE
Mazitschek, R
Bradner, J
Roden, RBS
AF Bazzaro, Martina
Lin, Zhenhua
Santillan, Antonio
Lee, Michael K.
Wang, Mei-Cheng
Chan, Kwun C.
Bristow, Robert E.
Mazitschek, Ralph
Bradner, James
Roden, Richard B. S.
TI Ubiquitin Proteasome System Stress Underlies Synergistic Killing of
Ovarian Cancer Cells by Bortezomib and a Novel HDAC6 Inhibitor
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID HISTONE DEACETYLASE INHIBITORS; PROTEIN-DEGRADATION; INDUCED APOPTOSIS;
NEURODEGENERATION; TRANSFORMATION; EXPRESSION; AUTOPHAGY; DOMAIN; LAQ824
AB Purpose: Elevated metabolic activity of ovarian cancer cells causes increased ubiquitin-proteasome -system (UPS) stress, resulting in their greater sensitivity to the toxic effects of proteasomal inhibition. The proteasomes and a potentially compensatory histone deacetylase 6 (HDAC6)-dependent lysosomal pathway mediate eukaryotic protein turnover. We hypothesized that up-regulation of the HDAC6-dependent lysosomal pathway occurs in response to UPS stress and proteasomal inhibition, and thus, ovarian cancer cell death can be triggered most effectively by coinhibition of both the proteasome- and HDAC6-dependent protein degradation pathways.
Experimental Design: To address this hypothesis, we examined HDAC6 expression patterns in normal and cancerous ovarian tissues and used a novel HDAC6-specific inhibitor, NK84, to address HDAC6 function in ovarian cancer.
Results: Abnormally high levels of HDAC6 are expressed by ovarian cancer cells in situ and in culture relative to benign epithelium and immortalized ovarian surface epithelium, respectively. Specific HDAC6 inhibition acts in synergy with the proteasome inhibitor Bortezomib (PS-341) to cause selective apoptotic cell death of ovarian cancer cells at doses that do not cause significant toxicity when used individually. Levels of UPS stress regulate the sensitivity of ovarian cancer cells to proteasome/HDAC6 inhibition. Pharmacologic inhibition of HDAC6 also reduces ovarian cancer cell spreading and migration consistent with its known function in regulating microtubule polymerization via deacetylation of alpha-tubulin.
Conclusion: Our results suggest the elevation of both the proteasomal and alternate HDAC6-dependent proteolytic pathways in ovarian cancer and the potential of combined inhibition of proteasome and HDAC6 as a therapy for ovarian cancer.
C1 [Bazzaro, Martina; Lin, Zhenhua; Santillan, Antonio; Lee, Michael K.; Roden, Richard B. S.] Johns Hopkins Univ, Dept Pathol, Baltimore, MD 21231 USA.
[Santillan, Antonio; Bristow, Robert E.; Roden, Richard B. S.] Johns Hopkins Univ, Dept Oncol Obstet & Gynecol, Baltimore, MD 21231 USA.
[Wang, Mei-Cheng; Chan, Kwun C.] Johns Hopkins Univ, Dept Biostat, Baltimore, MD 21231 USA.
[Mazitschek, Ralph; Bradner, James] Harvard Univ, Broad Inst, Cambridge, MA 02138 USA.
[Mazitschek, Ralph; Bradner, James] MIT, Cambridge, MA 02139 USA.
[Bradner, James] Dana Farber Canc Inst, Div Hematol Neoplasia, Boston, MA 02115 USA.
RP Roden, RBS (reprint author), Johns Hopkins Univ, Dept Pathol, Canc Res Bldg 2,Room 308,1550 Orleans St, Baltimore, MD 21231 USA.
EM roden@jhmi.edu
RI Lee, Michael/D-9491-2013; Mazitschek, Ralph/E-3741-2013
OI Lee, Michael/0000-0001-5865-9682; Mazitschek, Ralph/0000-0002-1105-689X
FU US Public Health Service [R01CA122581, P50 CA098252]; HERA foundation
FX US Public Health Service grants R01CA122581 (R.B.S. Roden), P50 CA098252
(R. B.S. Roden, R.E. Bristow, and M.C. Wang), and the HERA foundation
(M. Bazzaro, Z. Lin, and A. Santillan).
NR 32
TC 52
Z9 60
U1 0
U2 10
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 15
PY 2008
VL 14
IS 22
BP 7340
EP 7347
DI 10.1158/1078-0432.CCR-08-0642
PG 8
WC Oncology
SC Oncology
GA 374AL
UT WOS:000261014500022
PM 19010849
ER
PT J
AU Shimazaki, K
Lepin, EJ
Wei, B
Nagy, AK
Coulam, CP
Mareninov, S
Fu, MY
Wu, AM
Marks, JD
Braun, J
Gordon, LK
Wadehra, M
AF Shimazaki, Kaori
Lepin, Eric J.
Wei, Bo
Nagy, Agnes K.
Coulam, Catherine P.
Mareninov, Sergey
Fu, Maoyong
Wu, Anna M.
Marks, James D.
Braun, Jonathan
Gordon, Lynn K.
Wadehra, Madhuri
TI Diabodies Targeting Epithelial Membrane Protein 2 Reduce Tumorigenicity
of Human Endometrial Cancer Cell Lines
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID SINGLE-CHAIN FV; FOCAL ADHESION KINASE; ANTIBODY FRAGMENTS; SURFACE
EXPRESSION; GYNECOLOGIC MALIGNANCIES; INTEGRIN FUNCTION; LIPID RAFTS;
EMP2; GENE; CARCINOGENESIS
AB Purpose: Endometrial cancer is the most common gynecologic malignancy. One promising biomarker is epithelial membrane protein 2 (EMP2), and its expression is an independent prognostic indicator for tumors with poor clinical outcome expression. The present study assesses the suitability of EMP2 as a therapeutic target.
Experimental Design: Human monovalent anti-EMP2 antibody fragments were isolated from a human phage display library and engineered as bivalent antibody fragments (diabodies) with specificity and avidity to both EMP2 peptides and native cell-surface EMP2 protein. Diabodies were assessed using cell death and apoptosis assays. In addition, the efficacy of EMP2 diabodies on endometrial cancer tumors was determined using mouse xenograft models.
Results: Treatment of human endometrial adenocarcinoma cell lines with anti-EMP2 diabodies induced significant cell death and caspase-3 cleavage in vitro. These responses correlated with cellular EMP2 expression and were augmented by progesterone, which physiologically induces EMP2 expression. In vivo, treatment of subcutaneous human xenografts of HEC-1A cell lines with anti-EMP2 diabodies suppressed tumor growth and induced cell death in the xenograft.
Conclusions: These findings suggest that EMP2 may be a potential pharmacologic target for human endometrial cancer.
C1 [Wei, Bo; Nagy, Agnes K.; Coulam, Catherine P.; Mareninov, Sergey; Fu, Maoyong; Braun, Jonathan; Wadehra, Madhuri] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab, Los Angeles, CA 90095 USA.
[Shimazaki, Kaori; Braun, Jonathan] Univ Calif Los Angeles, Inst Mol Biol, Los Angeles, CA 90095 USA.
[Gordon, Lynn K.] Univ Calif Los Angeles, Jules Stein Eye Inst, Los Angeles, CA 90095 USA.
[Gordon, Lynn K.] Greater Los Angeles Vet Affairs Healthcare Syst, Dept Surg, Los Angeles, CA USA.
[Marks, James D.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RP Wadehra, M (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab, 14-127 Ctr Hlth Sci, Los Angeles, CA 90095 USA.
EM mwadehra@mednet.ucla.edu
RI Fu, Maoyong/E-9201-2010
FU NIH [HD48540, CA86306, CA009120, 2-T32-Al-07323]; University of
California at Los Angeles Jonsson Comprehensive Cancer Center flow
cytometry core [CA016042]; Iris Cantor Seed Grant, Giannini Family
Foundation [U54 CA119367]; Oppenheimer Family Foundation; Center for the
Prevention of Eye Disease
FX NIH grants HD48540 (J. Braun), CA86306 (A.M. Wu and J. Braun), CA009120
(M. Wadehra), 2-T32-Al-07323 (K. Shimazaki), and CA016042 (University of
California at Los Angeles Jonsson Comprehensive Cancer Center flow
cytometry core); Iris Cantor Seed Grant, Giannini Family Foundation, and
U54 CA119367 (M.Wadehra), unrestricted gift of Dr. Richard and Barbara
Braun (J. Braun); and Oppenheimer Family Foundation Grant Center for the
Prevention of Eye Disease (L.K. Gordon).
NR 50
TC 15
Z9 16
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 15
PY 2008
VL 14
IS 22
BP 7367
EP 7377
DI 10.1158/1078-0432.CCR-08-1016
PG 11
WC Oncology
SC Oncology
GA 374AL
UT WOS:000261014500025
PM 19010852
ER
PT J
AU Jackson, LA
Janoff, EN
AF Jackson, Lisa A.
Janoff, Edward N.
TI Pneumococcal Vaccination of Elderly Adults: New Paradigms for Protection
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID COMMUNITY-ACQUIRED PNEUMONIA; POLYSACCHARIDE VACCINE; CONJUGATE VACCINE;
HIGH-RISK; UNITED-STATES; OLDER-ADULTS; CLINICAL-EFFICACY; PHASE-1
TRIAL; DISEASE; POPULATION
AB Pneumococcal polysaccharide vaccine has been licensed for use in the United States for 130 years, and two-thirds of the elderly population in the United States have received this vaccine. Observational studies have demonstrated that pneumococcal polysaccharide vaccine reduces the risk of invasive pneumococcal disease in immunocompetent elderly individuals, but neither observational studies nor clinical trials have demonstrated consistent evidence for a reduction in the incidence of pneumonia in vaccinated older adults. The introduction of pneumococcal protein conjugate vaccine among children has led to a herd immunity effect that has resulted in a 38% decrease in the rate of invasive pneumococcal disease among elderly adults. The high efficacy of pneumococcal protein conjugate vaccine in children has renewed interest in evaluating pneumococcal protein conjugate vaccines in adults for prevention of invasive pneumococcal disease and pneumonia. Moreover, the recognition of the presence and function of noncapsular pneumococcal protein antigens and the increasing availability of adjuvants highlight the promise of new vaccination strategies to decrease the burden of pneumococcal infection in this high-risk population.
C1 [Jackson, Lisa A.] Grp Hlth Ctr Hlth Studies, Seattle, WA 98101 USA.
[Janoff, Edward N.] Univ Colorado, Denver Sch Med, Mucosal & Vaccine Res Program Colorado, Div Infect Dis,Denver Vet Affairs Med Ctr, Denver, CO USA.
RP Jackson, LA (reprint author), Grp Hlth Ctr Hlth Studies, 1730 Minor Ave,Ste 1600, Seattle, WA 98101 USA.
EM Jackson.L@ghc.org
FU Veterans Affairs Research Service; Mucosal and Vaccine Research Program
Colorado; National Institutes of Health [R21-AI077069, R01-AI48796]
FX Financial support. Veterans Affairs Research Service, Mucosal and
Vaccine Research Program Colorado ( to E.N.J.), and the National
Institutes of Health (R21-AI077069 and R01-AI48796 to E.N.J.).
NR 63
TC 73
Z9 74
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD NOV 15
PY 2008
VL 47
IS 10
BP 1328
EP 1338
DI 10.1086/592691
PG 11
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 360ST
UT WOS:000260078800014
PM 18844484
ER
PT J
AU Kamiya, N
Ye, L
Kobayashi, T
Mochida, Y
Yamauchi, M
Kronenberg, HM
Feng, JQ
Mishina, Y
AF Kamiya, Nobuhiro
Ye, Ling
Kobayashi, Tatsuya
Mochida, Yoshiyuki
Yamauchi, Mitsuo
Kronenberg, Henry M.
Feng, Jian Q.
Mishina, Yuji
TI BMP signaling negatively regulates bone mass through sclerostin by
inhibiting the canonical Wnt pathway
SO DEVELOPMENT
LA English
DT Article
DE BMP receptor IA; Bone mass; Canonical Wnt signaling; Osteoblast;
Osteoclastogenesis; Sclerostin; Mouse
ID RECEPTOR-RELATED PROTEIN-5; TAMOXIFEN-INDUCIBLE FORM;
VAN-BUCHEM-DISEASE; MORPHOGENETIC PROTEIN; BETA-CATENIN; OSTEOBLAST
LINEAGE; OSTEOCLAST DIFFERENTIATION; CELL-DIFFERENTIATION; SOST GENE;
LRP5 GENE
AB Bone morphogenetic proteins (BMPs) are known to induce ectopic bone. However, it is largely unknown how BMP signaling in osteoblasts directly regulates endogenous bone. This study investigated the mechanism by which BMP signaling through the type IA receptor (BMPR1A) regulates endogenous bone mass using an inducible Cre-loxP system. When BMPR1A in osteoblasts was conditionally disrupted during embryonic bone development, bone mass surprisingly was increased with upregulation of canonical Wnt signaling. Although levels of bone formation markers were modestly reduced, levels of resorption markers representing osteoclastogenesis were severely reduced, resulting in a net increase in bone mass. The reduction of osteoclastogenesis was primarily caused by Bmpr1a-deficiency in osteoblasts, at least through the RANKL-OPG pathway. Sclerostin (Sost) expression was downregulated by about 90% and SOST protein was undetectable in osteoblasts and osteocytes, whereas the Wnt signaling was upregulated. Treatment of Bmpr1a-deficient calvariae with sclerostin repressed the Wnt signaling and restored normal bone morphology. By gain of Smad-dependent BMPR1A signaling in mice, Sost expression was upregulated and osteoclastogenesis was increased. Finally, the Bmpr1a-deficient bone phenotype was rescued by enhancing BMPR1A signaling, with restoration of osteoclastogenesis. These findings demonstrate that BMPR1A signaling in osteoblasts restrain endogenous bone mass directly by upregulating osteoclastogenesis through the RANKL-OPG pathway, or indirectly by downregulating canonical Wnt signaling through sclerostin, a Wnt inhibitor and a bone mass mediator.
C1 [Kamiya, Nobuhiro; Mishina, Yuji] NIEHS, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Mishina, Yuji] Univ Michigan, Sch Dent, Ann Arbor, MI 48109 USA.
[Ye, Ling; Feng, Jian Q.] Univ Missouri, Sch Dent, Kansas City, MO 64108 USA.
[Kobayashi, Tatsuya; Kronenberg, Henry M.] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
[Kobayashi, Tatsuya; Kronenberg, Henry M.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Mochida, Yoshiyuki; Yamauchi, Mitsuo] Univ N Carolina, Dent Res Ctr, Chapel Hill, NC 27599 USA.
RP Mishina, Y (reprint author), NIEHS, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
EM mishina@umich.edu
OI Mochida, Yoshiyuki/0000-0002-2115-4303
FU NIH [P01 DK56246, R01 AR051587, R21 AR052824, ES071003- 11]; RIKEN Brain
Science Institute; Lilly Fellowship Foundation
FX We gratefully thank Tomokazu Fukuda and Greg Scott for generation of
caBmpr1a mouse line and Donald Lucas for critical reading of this
manuscript. This work was supported by NIH grants P01 DK56246 (H. K.),
R01 AR051587 (J. F.), R21 AR052824 (M. Y.), ES071003- 11 and a
conditional gift from RIKEN Brain Science Institute (Y. M.) and Lilly
Fellowship Foundation (N. K.).
NR 74
TC 130
Z9 136
U1 0
U2 10
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0950-1991
J9 DEVELOPMENT
JI Development
PD NOV 15
PY 2008
VL 135
IS 22
BP 3801
EP 3811
DI 10.1242/dev.025825
PG 11
WC Developmental Biology
SC Developmental Biology
GA 364MV
UT WOS:000260340700016
PM 18927151
ER
PT J
AU Ozsolak, F
Poling, LL
Wang, ZX
Liu, H
Liu, XS
Roeder, RG
Zhang, XM
Song, JS
Fisher, DE
AF Ozsolak, Fatih
Poling, Laura L.
Wang, Zhengxin
Liu, Hui
Liu, X. Shirley
Roeder, Robert G.
Zhang, Xinmin
Song, Jun S.
Fisher, David E.
TI Chromatin structure analyses identify miRNA promoters
SO GENES & DEVELOPMENT
LA English
DT Article
DE Transcription; microRNA; promoter; chromatin
ID RNA-POLYMERASE-III; GENOME-WIDE ANALYSIS; MICRORNA EXPRESSION;
GENE-EXPRESSION; ALPHA-AMANITIN; C-MYC; CAENORHABDITIS-ELEGANS; HISTONE
MODIFICATIONS; ANIMAL DEVELOPMENT; TRANSCRIPTION
AB Although microRNAs (miRNAs) are key regulators of gene expression in normal human physiology and disease, transcriptional regulation of miRNAs is poorly understood, because most miRNA promoters have not yet been characterized. We identified the proximal promoters of 175 human miRNAs by combining nucleosome mapping with chromatin signatures for promoters. We observe that one-third of intronic miRNAs have transcription initiation regions independent from their host promoters and present a list of RNA polymerase II- and III-occupied miRNAs. Nucleosome mapping and linker sequence analyses in miRNA promoters permitted accurate prediction of transcription factors regulating miRNA expression, thus identifying nine miRNAs regulated by the MITF transcription factor/oncoprotein in melanoma cells. Furthermore, DNA sequences encoding mature miRNAs were found to be preferentially occupied by positioned-nucleosomes, and the 3' end sites of known genes exhibited nucleosome depletion. The high-throughput identification of miRNA promoter and enhancer regulatory elements sheds light on evolution of miRNA transcription and permits rapid identification of transcriptional networks of miRNAs.
C1 [Song, Jun S.] Inst Adv Study, Simons Ctr Syst Biol, Princeton, NJ 08540 USA.
[Ozsolak, Fatih; Poling, Laura L.; Fisher, David E.] Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA.
[Ozsolak, Fatih; Poling, Laura L.; Fisher, David E.] Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Boston, MA 02114 USA.
[Ozsolak, Fatih; Poling, Laura L.; Fisher, David E.] Harvard Univ, Sch Med, Childrens Hosp Boston, Dana Farber Canc Inst,Dept Pediat Oncol, Boston, MA 02114 USA.
[Wang, Zhengxin] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Liu, Hui; Zhang, Xinmin] Roche NimbleGen Inc, Madison, WI 53719 USA.
[Liu, X. Shirley] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Liu, X. Shirley] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Roeder, Robert G.] Rockefeller Univ, Biochem & Mol Biol Lab, New York, NY 10021 USA.
RP Song, JS (reprint author), Inst Adv Study, Simons Ctr Syst Biol, Einstein Dr, Princeton, NJ 08540 USA.
EM jssong@ias.edu; dfisher3@partners.org
FU NIH; Doris Duke Medical Foundation
FX We thank C. S. Chan, R. Cui, V. Igras, A. Kawakami, M. Khaled, A. J.
Levine, E. Makino, V. Nanda, and S. Yokoyama for discussions and
support. This work was supported by a grant from NIH to D. E. F. D. E.
F. is a Distinguished Clinical Scholar of the Doris Duke Medical
Foundation. H. L. and X. Z. are employees of Roche NimbleGen, Inc. D. E.
F. wishes to disclose consulting relationships with Novartis
Pharmaceuticals, Magen BioSciences, and Source MDx.
NR 80
TC 330
Z9 344
U1 2
U2 27
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
J9 GENE DEV
JI Genes Dev.
PD NOV 15
PY 2008
VL 22
IS 22
BP 3172
EP 3183
DI 10.1101/gad.1706508
PG 12
WC Cell Biology; Developmental Biology; Genetics & Heredity
SC Cell Biology; Developmental Biology; Genetics & Heredity
GA 378UJ
UT WOS:000261349400009
PM 19056895
ER
PT J
AU Kundu, ST
Gosavi, P
Khapare, N
Patel, R
Hosing, AS
Maru, GB
Ingle, A
DeCaprio, JA
Dalal, SN
AF Kundu, Samrat T.
Gosavi, Prajakta
Khapare, Nileema
Patel, Rachana
Hosing, Amol S.
Maru, Girish B.
Ingle, Arvind
DeCaprio, James A.
Dalal, Sorab N.
TI Plakophilin3 downregulation leads to a decrease in cell adhesion and
promotes metastasis
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE plakophilin3; cell adhesion; desmosome; transformation; metastasis
ID LARGE-T-ANTIGEN; PLAQUE PROTEIN; MEDIATED TRANSFORMATION; DESMOSOMAL
CADHERINS; EPITHELIAL-CELLS; LUNG-CANCER; BINDING; GENE; MICE;
LOCALIZATION
AB Plakophilin3 is a desmosomal plaque protein whose levels are reduced in poorly differentiated tumors of the oropharyngeal cavity and in invasive colon carcinomas. To test the hypothesis that plakophilin3 loss stimulates neoplastic progression, plakophilin3 expression was inhibited by DNA vector driven RNA interference in 3 epithelial cell lines, HCT116, HaCaT and fetal buccal mucosa. The plakophilin3-knockdown clones showed a decrease in cell-cell adhesion as assessed in a hanging drop assay, which was accompanied by an increase in cell migration. The HCT116 plakophilin3-knockdown clones showed a decrease in desmosome size as revealed by electron microscopy. These altered desmosomal properties were accompanied by colony formation in soft agar and growth to high density in culture. The HCT116-derived clones showed accelerated tumor formation in nude mice and increased metastasis to the lung, a phenotype consistent with the increased migration observed in vitro and is consistent with data from human tumors that suggests that plakophililn3 is lost in invasive and metastatic tumors. These data indicate that plakophilin3 loss leads to a decrease in cell-cell adhesion leading to the stimulation of neoplastic progression and metastasis. (C) 2008 Wiley-Liss, Inc.
C1 [Kundu, Samrat T.; Gosavi, Prajakta; Khapare, Nileema; Patel, Rachana; Hosing, Amol S.; Maru, Girish B.; Ingle, Arvind; Dalal, Sorab N.] ACTREC, Tata Mem Ctr, Kharghar Node 410210, Navi Mumbai, India.
[DeCaprio, James A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Dalal, SN (reprint author), ACTREC, Tata Mem Ctr, Kharghar Node 410210, Navi Mumbai, India.
EM sdalal@actrec.gov.in
RI Patel, Rachana/G-2274-2010
FU University Grants Commission; Council for Scientific and Industrial
Research; Lady Tata Memorial Trust; Department of Science and Technology
(DST); ACTREC
FX Grant sponsors: University Grants Commission, Council for Scientific and
Industrial Research, Lady Tata Memorial Trust, Department of Science and
Technology (DST) and ACTREC.
NR 40
TC 38
Z9 39
U1 0
U2 2
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD NOV 15
PY 2008
VL 123
IS 10
BP 2303
EP 2314
DI 10.1002/ijc.23797
PG 12
WC Oncology
SC Oncology
GA 365XQ
UT WOS:000260443300010
PM 18729189
ER
PT J
AU Caglar, HB
Tishler, RB
Othus, M
Burke, E
Li, Y
Goguen, L
Wirth, LJ
Haddad, RI
Norris, CM
Court, LE
Aninno, DJ
Posner, MR
Allen, AM
AF Caglar, Hale B.
Tishler, Roy B.
Othus, Megan
Burke, Elaine
Li, Yi
Goguen, Laura
Wirth, Lori J.
Haddad, Robert I.
Norris, Carl M.
Court, Laurence E.
Aninno, Donald J.
Posner, Marshall R.
Allen, Aaron M.
TI DOSE TO LARYNX PREDICTS FOR SWALLOWING COMPLICATIONS AFTER
INTENSITY-MODULATED RADIOTHERAPY
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE Aspiration; Intensity-modulated radiotherapy; Head and neck cancer
ID QUALITY-OF-LIFE; SQUAMOUS-CELL CARCINOMA; FLUOROURACIL INDUCTION
CHEMOTHERAPY; TRIAL COMPARING RADIOTHERAPY; STAGE OROPHARYNX CARCINOMA;
RADIATION-THERAPY IMRT; NECK-CANCER; ORGAN PRESERVATION; ADVANCED HEAD;
CONCOMITANT CHEMORADIOTHERAPY
AB Purpose: To evaluate early swallowing after intensity-modulated radiotherapy for head and neck squamous cell carcinoma and determine factors correlating with aspiration and/or stricture.
Methods and Materials: Consecutive patients treated with intensity-modulated radiotherapy with or without chemotherapy between September 2004 and August 2006 at the Dana Farber Cancer Institute/Brigham and Women's Hospital were evaluated with institutional review board approval. Patients underwent swallowing evaluation after completion of therapy; including video swallow studies. The clinical- and treatment-related variables were examined for correlation with aspiration or strictures, as well as doses to the larynx, pharyngeal constrictor muscles, and cervical esophagus. The correlation was assessed with logistic regression analysis.
Results: A total of 96 patients were evaluated. Their median age was 55 years, and 79 (82%) were men. The primary site of cancer was the oropharynx in 43, hypopharynx/larynx in 17, oral cavity in 13, nasopharynx in 11, maxillary sinus in 2, and unknown primary in 10. Of the 96 patients, 85% underwent definitive RT and 15% postoperative RT. Also, 28 patients underwent induction chemotherapy followed by concurrent chemotherapy, 59 received concurrent chemotherapy, and 9 patients underwent RT alone. The median follow-up was 10 months. Of the 96 patients, 31 (32%) had clinically significant aspiration and 36 (37%) developed a stricture. The radiation dose-volume metrics, including the volume of the larynx receiving >= 50 Gy (p = 0.04 and p = 0.03, respectively) and volume of the inferior constrictor receiving >= 50 Gy (p = 0.05 and p = 0.02, respectively) were significantly associated with both aspiration and stricture. The mean larynx dose correlated with aspiration (p = 0.003). Smoking history was the only clinical factor to correlate with stricture (P = 0.05) but not aspiration.
Conclusion: Aspiration and stricture are common side effects after intensity-modulated radiotherapy for head-and-neck squamous cell carcinoma. The dose given to the larynx and inferior constrictors correlated with these side effects. (C) 2008 Elsevier Inc.
C1 [Caglar, Hale B.; Tishler, Roy B.; Court, Laurence E.; Allen, Aaron M.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dana Farber Canc Inst,Dept Radiat Oncol, Boston, MA 02115 USA.
[Goguen, Laura; Norris, Carl M.; Aninno, Donald J.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dana Farber Canc Inst,Dept Otolaryngol, Boston, MA 02115 USA.
[Othus, Megan; Li, Yi] Dana Farber Canc Inst, Dept Biostat, Boston, MA 02115 USA.
[Burke, Elaine; Wirth, Lori J.; Haddad, Robert I.; Posner, Marshall R.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Allen, AM (reprint author), Dana Farber Canc Inst, Dept Radiat Oncol, 44 Binney St, Boston, MA 02115 USA.
EM aallen@lroc.harvard.edu
FU NCI NIH HHS [T32 CA009337]
NR 43
TC 116
Z9 117
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD NOV 15
PY 2008
VL 72
IS 4
BP 1110
EP 1118
DI 10.1016/j.ijrobp.2008.02.048
PG 9
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 368AB
UT WOS:000260592600021
PM 18468812
ER
PT J
AU Hong, TS
Craft, DL
Carlsson, F
Bortfeld, TR
AF Hong, Theodore S.
Craft, David L.
Carlsson, Fredrik
Bortfeld, Thomas R.
TI MULTICRITERIA OPTIMIZATION IN INTENSITY-MODULATED RADIATION THERAPY
TREATMENT PLANNING FOR LOCALLY ADVANCED CANCER OF THE PANCREATIC HEAD
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE Pancreatic cancer; Multicriteria optimization; IMRT
ID PENCIL BEAM; IMRT; RADIOTHERAPY; CONCURRENT
AB Purpose: Intensity-modulated radiation therapy (IMRT) affords the potential to decrease radiation therapy-associated toxicity by creating highly conformal dose distributions. However, the inverse planning process can create a suboptimal plan despite meeting all constraints. Multicriteria optimization (MCO) may reduce the time-consuming iteration loop necessary to develop a satisfactory plan while providing information regarding trade-offs between different treatment planning goals. In this exploratory study, we examine the feasibility and utility of MCO in physician plan selection in patients with locally advanced pancreatic cancer (LAPC).
Methods and Materials: The first 10 consecutive patients with LAPC treated with IMRT were evaluated. A database of plans (Pareto surface) was created that met the inverse planning goals. The physician then navigated to an "optimal" plan from the point on the Pareto surface at which kidney dose was minimized.
Results: Pareto surfaces were created for all 10 patients. A physician was able to select a plan from the Pareto surface within 10 minutes for all cases. Compared with the original (treated) IMRT plans, the plan selected from the Pareto surface had a lower stomach mean dose in 9 of 10 patients, although often at the expense of higher kidney dose than with the treated plan.
Conclusion: The MCO is feasible in patients with LAPC and allows the physician to choose a satisfactory plan quickly. Generally, when given the opportunity, the physician will choose a plan with a lower stomach dose. The MCO enables a physician to provide greater active clinical input into the IMRT planning process. (c) 2008 Elsevier Inc.
C1 [Hong, Theodore S.; Craft, David L.; Bortfeld, Thomas R.] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
[Hong, Theodore S.; Craft, David L.; Bortfeld, Thomas R.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Carlsson, Fredrik] RaySearch Labs, Stockholm, Sweden.
RP Hong, TS (reprint author), Massachusetts Gen Hosp, Dept Radiat Oncol, 100 Blossom St,Cox 3, Boston, MA 02114 USA.
EM tshong1@partners.org
FU National Cancer Institute [CA103904-01A1]
FX Supported by 1 RO1 CA103904-01A1 from the National Cancer Institute.
NR 14
TC 31
Z9 34
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD NOV 15
PY 2008
VL 72
IS 4
BP 1208
EP 1214
DI 10.1016/j.ijrobp.2008.07.015
PG 7
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 368AB
UT WOS:000260592600034
PM 18954714
ER
PT J
AU Chakraverty, R
Flutter, B
Fallah-Arani, F
Eom, HS
Means, T
Andreola, G
Schwarte, S
Buchli, J
Cotter, P
Zhao, GL
Sykes, M
AF Chakraverty, Ronjon
Flutter, Barry
Fallah-Arani, Farnaz
Eom, Hyeon-Seok
Means, Terry
Andreola, Giovanna
Schwarte, Sebastian
Buchli, Jennifer
Cotter, Pete
Zhao, Guiling
Sykes, Megan
TI The Host Environment Regulates the Function of CD8(+)
Graft-versus-Host-Reactive Effector Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID BONE-MARROW-TRANSPLANTATION; DONOR LYMPHOCYTE INFUSION;
ANTIGEN-PRESENTING CELLS; TOTAL-BODY IRRADIATION; T-CELLS; CUTTING EDGE;
ALLOGENEIC CHIMERAS; LEUKOCYTE INFUSIONS; LEUKEMIA RESPONSES; DENDRITIC
CELLS
AB We have examined how the host environment influences the graft-vs-leukemia (GVL) response following transfer of donor T cells to allogeneic chimeras. Donor T cells induce significant GVL when administered in large numbers to established mixed chimeras (MC). However, when using limiting numbers of T cells, we found that late transfer to MC induced less GVL than did early transfer to freshly irradiated allogeneic recipients. Late donor T cell transfer to MC was associated with marked accumulation of anti-host CD8 cells within the spleen, but delayed kinetics of differentiation, reduced expression of effector molecules including IFN-gamma, impaired cytotoxicity, and higher rates of sustained apoptosis. Furthermore, in contrast to the spleen, we observed a significant delay in donor CD8 cell recruitment to the bone marrow, a key location for hematopoietic tumors. Increasing the numbers of T cells transferred to MC led to the enhancement of CTL activity and detectable increases in absolute numbers of IFN-gamma(+) cells without inducing graft-vs-host disease (GVHD). TLR-induced systemic inflammation accelerated differentiation of functional CTL in MC but was associated with severe GVHD. In the absence of inflammation, both recipient T and non-T cell populations impeded the full development of GVHD-inducing effector function. We conclude that per-cell deficits in the function of donor CD8 cells activated in MC may be overcome by transferring larger numbers of T cells without inducing GVHD. The Journal of Immunology, 2008, 181: 6820-6828.
C1 [Andreola, Giovanna; Schwarte, Sebastian; Cotter, Pete; Zhao, Guiling; Sykes, Megan] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Transplantat Biol Res Ctr,Bone Marrow Transplatat, Boston, MA 02129 USA.
[Eom, Hyeon-Seok; Means, Terry] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Immunol & Inflammatory Dis, Boston, MA 02129 USA.
[Chakraverty, Ronjon; Flutter, Barry; Fallah-Arani, Farnaz; Buchli, Jennifer] UCL, Transplantat Immunol Grp, Dept Hematol, London, England.
RP Sykes, M (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Transplantat Biol Res Ctr,Bone Marrow Transplatat, MGH East,Bldg 149-5102,13th St, Boston, MA 02129 USA.
EM Megan.Sykes@tbrc.mgh.harvard.edu
FU Leukemia Research, U.K; National Institutes of Health [PO1 CA111519, RO1
CA79989]; Multiple Myeloma Foundation
FX This work was supported by the Leukemia Research, U.K., and by National
Institutes of Health Grants PO1 CA111519 and RO1 CA79989, and by a
Senior Research Award from the Multiple Myeloma Foundation.
NR 45
TC 23
Z9 24
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD NOV 15
PY 2008
VL 181
IS 10
BP 6820
EP 6828
PG 9
WC Immunology
SC Immunology
GA 372PQ
UT WOS:000260913900019
PM 18981100
ER
PT J
AU Divangahi, M
Mostowy, S
Coulombe, F
Kozak, R
Guillot, L
Veyrier, F
Kobayashi, KS
Flavell, RA
Gros, P
Behr, MA
AF Divangahi, Maziar
Mostowy, Serge
Coulombe, Francois
Kozak, Robert
Guillot, Loic
Veyrier, Frederic
Kobayashi, Koichi S.
Flavell, Richard A.
Gros, Philippe
Behr, Marcel A.
TI NOD2-Deficient Mice Have Impaired Resistance to Mycobacterium
tuberculosis Infection through Defective Innate and Adaptive Immunity
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID AVIUM SUBSPECIES PARATUBERCULOSIS; INTERFERON-GAMMA; DENDRITIC CELLS;
CROHNS-DISEASE; NOD2; RESPONSES; RECOGNITION; SUSCEPTIBILITY;
PEPTIDOGLYCAN; ACTIVATION
AB NOD2/CARD15 mediates innate immune responses to mycobacterial infection. However, its role in the regulation of adaptive immunity has remained unknown. In this study, we examined host defense, T cell responses, and tissue pathology in two models of pulmonary mycobacterial infection, using wild-type and Nod2-deficient mice. During the early phase of aerosol infection with Mycobacterium tuberculosis, Nod2(-/-) mice had similar bacterial counts but reduced inflammatory response on histopathology at 4 and 8 wk postchallenge compared with wild-type animals. These findings were confirmed upon intratracheal infection of mice with attenuated Mycobacterium bovis bacillus Calmette-Guerin. Analysis of the lungs 4 wk after bacillus Calmette-Guerin infection demonstrated that Nod2(-/-) mice had decreased production of type 1 cytokines; and reduced recruitment of CD8(+) and CD4(+) T cells. Ag-specific T cell responses in both the spleens and thoracic lymph nodes were diminished in Nod2(-/-) mice, indicating impaired adaptive antimycobacterial immunity. The immune regulatory role of NOD2 was not restricted to the lung since Nod2 disruption also led to reduced type 1 T cell activation following i.m. bacillus Calmette-Guerin infection. To determine the importance of diminished innate and adaptive immunity, we measured bacterial burden 6 mo after aerosol infection with M. tuberculosis and followed a second infected group for assessment of survival. Nod2(-/-) mice had a higher bacterial burden in the lungs 6 mo after infection and succumbed sooner than did wild-type controls. Taken together, these data indicate that NOD2 mediates resistance to mycobacterial infection via both innate and adaptive immunity. The Journal of Immunology, 2008, 181: 7157-7165.
C1 [Divangahi, Maziar; Mostowy, Serge; Coulombe, Francois; Kozak, Robert; Guillot, Loic; Veyrier, Frederic; Behr, Marcel A.] McGill Univ, Dept Med, Ctr Hlth, Montreal, PQ H3G 1A4, Canada.
[Kobayashi, Koichi S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Kobayashi, Koichi S.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Flavell, Richard A.] Howard Hughes Med Inst, New Haven, CT 06510 USA.
[Flavell, Richard A.] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT 06510 USA.
[Gros, Philippe] McGill Univ, Dept Biochem, Montreal, PQ H3G 1A4, Canada.
RP Behr, MA (reprint author), McGill Univ, Dept Med, Ctr Hlth, A5-156,1650 Cedar Ave, Montreal, PQ H3G 1A4, Canada.
EM marcel.behr@mcgill.ca
RI Guillot, Loic/D-8893-2011;
OI Guillot, Loic/0000-0001-6853-7945; Mostowy, Serge/0000-0002-7286-6503
FU Canadian Genetic Diseases Network; Canadian Institutes for Health
Research [MOP-86536]; Fonds de la Recherche en Sante du Quebec (FRSQ)
FX This work was funded by a group grant from the Canadian Genetic Diseases
Network to P.G. and M.B. and an operating grant (MOP-86536) from the
Canadian Institutes for Health Research to M.B. F.C. was supported by a
studentship award of the Fonds de la Recherche en Sante du Quebec
(FRSQ). R.A.F. is an investigator of the Howard Hughes Medical
Institute. P.G. is a James McGill Professor of McGill University. M.B.
is a William Dawson Scholar of McGill University and a
Chercheur-Boursier Senior of the FRSQ.
NR 42
TC 116
Z9 120
U1 0
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD NOV 15
PY 2008
VL 181
IS 10
BP 7157
EP 7165
PG 9
WC Immunology
SC Immunology
GA 372PQ
UT WOS:000260913900056
PM 18981137
ER
PT J
AU Purdon, PL
Millan, H
Fuller, PL
Bonmassar, G
AF Purdon, Patrick L.
Millan, Hernan
Fuller, Peter L.
Bonmassar, Giorgio
TI An open-source hardware and software system for acquisition and
real-time processing of electrophysiology during high field MRI
SO JOURNAL OF NEUROSCIENCE METHODS
LA English
DT Article
DE EEG; Local field potentials; fMRI; Multimodal imaging; Real-time signal
processing; Sleep; Anesthesia; Hyperbaric medicine; Neuropharmacology;
Learning; Attention
ID SIMULTANEOUS EEG; EXPERT-SYSTEM; SLEEP EXPERIMENT; FUNCTIONAL MRI; FMRI;
ARTIFACT; CLASSIFICATION; ELECTRODES; REMOVAL; SIGNAL
AB Simultaneous recording of electrophysiology and functional magnetic resonance imaging (fMRI) is a technique of growing importance in neuroscience. Rapidly evolving clinical and scientific requirements have created a need for hardware and software that can be customized for specific applications. Hardware may require customization to enable a variety of recording types (e.g., electroencephalogram, local field potentials, or multi-unit activity) while meeting the stringent and costly requirements of MRI safety and compatibility. Real-time signal processing tools are an enabling technology for studies of learning, attention, sleep, epilepsy, neurofeedback, and neuropharmacology, yet real-time signal processing tools are difficult to develop. We describe an open-source system for simultaneous electrophysiology and fMRI featuring low-noise (< 0.6 mu V p-p input noise), electromagnetic compatibility for MRI (tested up to 7T), and user-programmable real-time signal processing. The hardware distribution provides the complete specifications required to build an MRI-compatible electrophysiological data acquisition system, including circuit schematics, print circuit board (PCB) layouts, Gerber files for PCB fabrication and robotic assembly, a bill of materials with part numbers, data sheets, and vendor information, and test procedures. The software facilitates rapid implementation of real-time signal processing algorithms. This system has been used in human EEG/fMRI studies at 3 and 7T examining the auditory system, visual system, sleep physiology, and anesthesia, as well as in intracranial electrophysiological studies of the non-human primate visual system during 3T fMRI, and in human hyperbaric physiology studies at depths of up to 300 feet below sea level. Published by Elsevier B.V.
C1 [Purdon, Patrick L.] Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Neurosci Stat Res Lab, Boston, MA 02129 USA.
[Millan, Hernan; Bonmassar, Giorgio] MGH MIT HMS Athinoula A Martinos Ctr Biomed Imagi, Boston, MA 02129 USA.
[Fuller, Peter L.] PLF Consulting, Brookline, MA 02446 USA.
RP Purdon, PL (reprint author), Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Neurosci Stat Res Lab, 149 13th St,Room 4005, Boston, MA 02129 USA.
EM patrickp@nmr.mgh.harvard.edu
FU NIH/NINDS [K25-NS05758]; NIH/NCRR [M01-RR-01066, P41-RR14075]; NIH/NIBIB
[R01-EB006385]; NIH/NEI [R03-EY16047]; Naval Submarine Medical Research
Laboratory [N66596-07-IPA-001]
FX This work was supported by grants from the United Stated Department of
Health and Human Services, grant numbers NIH/NINDS K25-NS05758
(Purclon), NIH/NCRR M01-RR-01066 (Bonmassar), P41-RR14075 (Bonmassar),
NIH/NIBIB R01-EB006385 (Bonmassar), NIH/NEI R03-EY16047 (Bonmassar), and
Naval Submarine Medical Research Laboratory Grant N66596-07-IPA-001
(Bonmassar). The technologies described in this manuscript are protected
by two patents: Bonmassar G, Belliveau JW, inventors.
Electroencephalograph sensor for use with magnetic resonance imaging and
methods using such arrangements. US patent PCT/US03/05614,2 February
2003; Bonmassar G, Purdon PL, inventors. Apparatuses and methods for
electrophysiological signal delivery and recording during MRI.
PCT/US2005/042401.
NR 60
TC 12
Z9 12
U1 4
U2 18
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0270
J9 J NEUROSCI METH
JI J. Neurosci. Methods
PD NOV 15
PY 2008
VL 175
IS 2
BP 165
EP 186
DI 10.1016/j.jneumeth.2008.07.017
PG 22
WC Biochemical Research Methods; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 374XJ
UT WOS:000261076700001
PM 18761038
ER
PT J
AU Tan, AT
Loggi, E
Boni, C
Chia, A
Gehring, AJ
Sastry, KSR
Goh, V
Fisicaro, P
Andreone, P
Brander, C
Lim, SG
Ferrari, C
Bihl, F
Bertoletti, A
AF Tan, Anthony Tanoto
Loggi, Elisabetta
Boni, Carolina
Chia, Adeline
Gehring, Adam J.
Sastry, Konduru S. R.
Goh, Vera
Fisicaro, Paola
Andreone, Pietro
Brander, Christian
Lim, Seng Gee
Ferrari, Carlo
Bihl, Florian
Bertoletti, Antonio
TI Host Ethnicity and Virus Genotype Shape the Hepatitis B Virus-Specific
T-Cell Repertoire
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; CLASS-I SUPERTYPES; LYMPHOCYTE RESPONSES;
NUCLEOCAPSID ANTIGEN; IMMUNE-RESPONSE; HLA-A2 SUBTYPES; HBV INFECTION;
CTL EPITOPES; IMMUNOGENICITY; DISTINCT
AB Repertoire composition, quantity, and qualitative functional ability are the parameters that define virus-specific T-cell responses and are linked with their potential to control infection. We took advantage of the segregation of different hepatitis B virus (HBV) genotypes in geographically and genetically distinct host populations to directly analyze the impact that host and virus variables exert on these virus-specific T-cell parameters. T-cell responses against the entire HBV proteome were analyzed in a total of 109 HBV-infected subjects of distinct ethnicities (47 of Chinese origin and 62 of Caucasian origin). We demonstrate that HBV-specific T-cell quantity is determined by the virological and clinical profiles of the patients, which outweigh any influence of race or viral diversity. In contrast, HBV-specific T-cell repertoires are divergent in the two ethnic groups, with T-cell epitopes frequently found in Caucasian patients seldom detected in Chinese patients. In conclusion, we provide a direct biological evaluation of the impact that host and virus variables exert on virus-specific T-cell responses. The discordance between HBV-specific CD8 T-cell repertoires present in Caucasian and Chinese subjects shows the ability of HLA micropolymorphisms to diversify T-cell responses and has implications for the rational development of therapeutic and prophylactic vaccines for worldwide use.
C1 [Bertoletti, Antonio] ASTAR, Singapore Inst Clin Sci, Brenner Ctr Mol Med, Singapore 117609, Singapore.
[Tan, Anthony Tanoto; Lim, Seng Gee; Bertoletti, Antonio] Natl Univ Singapore, Yong Loo Lin Sch Med, Singapore 117595, Singapore.
[Loggi, Elisabetta; Andreone, Pietro] Univ Bologna, Osped S Orsola Malpighi, Dept Internal Med Cardioangiol & Hepatol, Bologna, Italy.
[Boni, Carolina; Fisicaro, Paola; Ferrari, Carlo] Univ Parma, Azienda Osped, Unit Infect Dis & Hepatol, I-43100 Parma, Italy.
[Brander, Christian; Bihl, Florian] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Partner AIDS Res Ctr, Boston, MA USA.
[Brander, Christian] Hosp Badalona Germans Trias & Pujol, IrsiCaixa Fdn, Badalona, Spain.
[Brander, Christian] ICREA, Barcelona, Spain.
[Bihl, Florian] Univ Hosp Geneva, Div Gastroenterol & Hepatol, Geneva, Switzerland.
[Bertoletti, Antonio] ASTAR, Singapore Immunol Network, Singapore, Singapore.
RP Bertoletti, A (reprint author), ASTAR, Singapore Inst Clin Sci, Brenner Ctr Mol Med, 30 Med Dr, Singapore 117609, Singapore.
EM antonio_bertoletti@sics.a-star.edu.sg
RI Boni, Carolina/J-5249-2016; Ferrari, Carlo/D-5663-2017; Loggi,
Elisabetta/K-7848-2016;
OI Boni, Carolina/0000-0002-7630-5180; Ferrari, Carlo/0000-0002-7843-4963;
Brander, Christian/0000-0002-0548-5778; Loggi,
Elisabetta/0000-0003-4985-9783; Bertoletti, Antonio/0000-0002-2942-0485;
ANDREONE, PIETRO/0000-0002-4794-9809
NR 48
TC 49
Z9 51
U1 1
U2 9
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 NOV 15
PY 2008
VL 82
IS 22
BP 10986
EP 10997
DI 10.1128/JVI.01124-08
PG 12
WC Virology
SC Virology
GA 364XD
UT WOS:000260368000003
PM 18799575
ER
PT J
AU Richardson, MW
Carroll, RG
Stremlau, M
Korokhov, N
Humeau, LM
Silvestri, G
Sodroski, J
Riley, JL
AF Richardson, Max W.
Carroll, Richard G.
Stremlau, Matthew
Korokhov, Nikolay
Humeau, Laurent M.
Silvestri, Guido
Sodroski, Joseph
Riley, James L.
TI Mode of Transmission Affects the Sensitivity of Human Immunodeficiency
Virus Type 1 to Restriction by Rhesus TRIM5 alpha
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID CD4(+) T-CELLS; HIV-1 INFECTION; RETROVIRUS RESTRICTION; VIROLOGICAL
SYNAPSE; LENTIVIRAL VECTOR; IN-VITRO; EXPRESSION; PROTEIN; DOMAIN; ENTRY
AB Rhesus TRIM5 alpha (rhTRIM5 alpha), but not human TRIM5 alpha (huTRIM5 alpha), potently inhibits human immunodeficiency virus (HIV) infection and is thus a potentially valuable therapeutic tool. Primary human CD4 T cells engineered to express rhTRIM5 alpha were highly resistant to cell-free HIV type 1 (HIV-1) infection. However, when cocultured with unmodified T cells, rhTRIM5 alpha-expressing cells became highly permissive to HIV-1 infection. Physical separation of rhTRIM5 alpha-expressing cells and unmodified cells revealed that rhTRIM5 alpha efficiently restricts cell-free but not cell-associated HIV transmission. Furthermore, we observed that HIV-infected human cells could infect rhesus CD4 T cells by cell-to-cell contact, but the infection was self-limiting. Subsequently, we noted that a spreading infection ensued when HIV-1-infected rhTRIM5 alpha-expressing human cells were cultured with huTRIM5 alpha- but not rhTRIM5 alpha-expressing cells. Our results suggest that cell-associated HIV transmission in humans is blocked only when both donor and recipient cells express rhTRIM5 alpha. These studies further define the role of rhTRIM5 alpha in cell-free and cell-associated HIV transmission and delineate the utility of rhTRIM5 alpha in anti-HIV therapy.
C1 [Richardson, Max W.; Silvestri, Guido; Riley, James L.] Univ Penn, Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
[Richardson, Max W.; Carroll, Richard G.; Riley, James L.] Univ Penn, Sch Med, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA.
[Stremlau, Matthew; Sodroski, Joseph] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS,Div AIDS, Boston, MA 02115 USA.
[Korokhov, Nikolay; Humeau, Laurent M.] VIRxSYS Corp, Gaithersburg, MD 20877 USA.
[Sodroski, Joseph] Harvard Univ, Sch Med, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
RP Riley, JL (reprint author), Univ Penn, Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
EM rileyj@mail.med.upenn.edu
OI Riley, James/0000-0002-1057-576X
FU NIH/NIAID [U19AI066290, AI63987]; National Defense Science and
Engineering Fellowship; Ryan Foundation
FX This work was supported by NIH/NIAID grant U19AI066290. M. S. and J. S.
were funded by a grant (AI63987) from the National Institutes of Health.
M. S. was supported by a National Defense Science and Engineering
Fellowship and was a Fellow of the Ryan Foundation.; We thank Tatiana
Golovina, Tatiana Mikheeva, and Chanelle Case from the Penn-CFAR
Immunology Core for providing primary human T cells and Farida Shaheen
from Penn-CFAR Virology Core for p24 analysis; Paul Hallberg from the
BSL3 Cell Sorting Facility for sorting the HIV-1-infected T cells; James
Blanchard and Andrew Lackner from the Tulane National Primate Center for
reagents and expertise pertaining to the use of rhesus T cells; and
Angel Varela-Rohena, Carl June, Gwen Binder, Bob Doms, and Jim Hoxie for
helpful suggestions and discussions.
NR 43
TC 41
Z9 42
U1 0
U2 1
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 NOV 15
PY 2008
VL 82
IS 22
BP 11117
EP 11128
DI 10.1128/JVI.01046-08
PG 12
WC Virology
SC Virology
GA 364XD
UT WOS:000260368000015
PM 18768965
ER
PT J
AU Rodrigues, GGR
Walker, RH
Brice, A
Cazeneuve, C
Russaouen, O
Teive, HAG
Munhoz, RP
Becker, N
Raskin, S
Werneck, LC
Marques, W
Tumas, V
AF Rodrigues, Guilherme G. Riccioppo
Walker, Ruth H.
Brice, Alexis
Cazeneuve, Cecile
Russaouen, Odile
Teive, Helio A. G.
Munhoz, Renato Puppi
Becker, Nilson
Raskin, Salino
Werneck, Lineu Cesar
Marques, Wilson Junior
Tumas, Vitor
TI Huntington's Disease-Like 2 in Brazil-Report of 4 Patients
SO MOVEMENT DISORDERS
LA English
DT Article
DE Huntington's disease; junctophilin 3; Huntington's disease like
ID REPEAT EXPANSION; CAG EXPANSION; HUNTINGTON-DISEASE-LIKE-2; FEATURES;
HUNTINGTONS-DISEASE-LIKE-2; PHENOCOPIES; ANCESTRY; FAMILY
AB Huntington's disease-like 2 (HDL2) is a neurodegenerative disorder found in people of African ancestry with clinical, radiological, and neuropathological manifestations similar to Huntington's disease (HD). HDL2 is caused by a pathological expansion of CAG/CTG triplets in exon 2A of the JPH3 gene. We describe four cases of HDL2 from four unrelated families, and discuss their clinical findings. HDL2 should be considered in every patient with an HD-like phenotype who tests negative for the HD mutation, even if African ancestry is not immediately apparent. (C) 2008 Movement Disorder Society
C1 [Rodrigues, Guilherme G. Riccioppo; Marques, Wilson Junior; Tumas, Vitor] Univ Sao Paulo, Ribeirao Preto Sch Med, Dept Neurol, Ribeirao Preto, SP, Brazil.
[Walker, Ruth H.] James J Peters Vet Affairs Med Ctr, Dept Neurol, Bronx, NY USA.
[Walker, Ruth H.] Mt Sinai Sch Med, Dept Neurol, New York, NY USA.
[Brice, Alexis; Cazeneuve, Cecile; Russaouen, Odile] Grp Hosp Pitie Salpetriere, Neurogenet Unit, Dept Genet & Cytogenet, AP HP, F-75634 Paris, France.
[Teive, Helio A. G.; Munhoz, Renato Puppi; Becker, Nilson; Raskin, Salino; Werneck, Lineu Cesar] Univ Fed Parana, Hosp Clin, Neurol Serv, Movement Disorders Unit, BR-80060000 Curitiba, Parana, Brazil.
RP Tumas, V (reprint author), Univ Sao Paulo, Ribeirao Preto Sch Med, Dept Neurol, Ribeirao Preto, SP, Brazil.
EM tumasv@rnp.fmrp.usp.br
RI Rodrigues, Guilherme/D-3547-2009; Marques, Wilson/G-4240-2012; Tumas,
Vitor/C-9949-2014
OI Rodrigues, Guilherme/0000-0002-4296-1016; Marques,
Wilson/0000-0002-4589-2749;
NR 17
TC 12
Z9 12
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0885-3185
J9 MOVEMENT DISORD
JI Mov. Disord.
PD NOV 15
PY 2008
VL 23
IS 15
BP 2244
EP 2247
DI 10.1002/mds.22223
PG 4
WC Clinical Neurology
SC Neurosciences & Neurology
GA 380CF
UT WOS:000261442600015
PM 18816802
ER
PT J
AU Gow, DW
Segawa, JA
Ahlfors, SP
Lin, FH
AF Gow, David W., Jr.
Segawa, Jennifer A.
Ahlfors, Seppo P.
Lin, Fa-Hsuan
TI Lexical influences on speech perception: A Granger causality analysis of
MEG and EEG source estimates
SO NEUROIMAGE
LA English
DT Article
ID SURFACE-BASED ANALYSIS; EVENT-RELATED FMRI; CORTICAL SURFACE; HUMAN
BRAIN; COORDINATE SYSTEM; CEREBRAL-CORTEX; WORD; LOCALIZATION;
ACTIVATION; MODEL
AB Behavioral and functional imaging studies have demonstrated that lexical knowledge influences the categorization of perceptually ambiguous speech sounds. However, methodological and inferential constraints have so far been unable to resolve the question of whether this interaction takes the form of direct top-down influences on perceptual processing, or feedforward convergence during a decision process. We examined top-down lexical influences on the categorization of segments in a/s/-/integral/ continuum presented in different lexical contexts to produce a robust Ganong effect. Using integrated MEG/EEG and MRI data we found that, within a network identified by 40 Hz gamma phase locking, activation in the supramarginal gyrus associated with wordform representation influences phonetic processing in the posterior superior temporal gyrus during a period of time associated with lexical processing. This result provides direct evidence that lexical processes influence lower level phonetic perception, and demonstrates the potential value of combining Granger causality analyses and high spatiotemporal resolution multimodal imaging data to explore the functional architecture of cognition. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Gow, David W., Jr.; Segawa, Jennifer A.] Massachusetts Gen Hosp, Neuropsychol Lab, Boston, MA 02114 USA.
[Gow, David W., Jr.] Salem State Coll, Dept Psychol, Salem, MA 01970 USA.
[Gow, David W., Jr.; Segawa, Jennifer A.; Ahlfors, Seppo P.; Lin, Fa-Hsuan] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Cambridge, MA 02129 USA.
[Gow, David W., Jr.; Ahlfors, Seppo P.] Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
[Lin, Fa-Hsuan] Natl Taiwan Univ, Inst Biomed Engn, Taipei 106, Taiwan.
RP Gow, DW (reprint author), Cognit Behav Neurol Grp, 175 Cambridge St,Suite S340, Boston, MA 02114 USA.
EM gow@helix.mgh.harvard.edu
RI Lin, Fa-Hsuan/G-6988-2012; Ahlfors, Seppo/P-3644-2016
OI Lin, Fa-Hsuan/0000-0002-9539-1731;
FU NIDCD [R013108]; MIND Institute; NCRR [P41RR14075, R21EB007298]
FX This work was supported by NIDCD grant R013108 and also benefited from
funding from the MIND Institute and NCRR grants P41RR14075 and
R21EB007298 which support the development of technology and analysis
tools at the Athinoula A. Martinos Center for Biomedical Imaging. We
thank Eric Halgren, Matti H m l inen, Deirdre von Pechman, and Christina
Congleton for their assistance in implementing the experiment and Gina
Kuperberg, Steven Stufflebeam, Catherine Stoodley, David Cohen and David
Caplan for their comments on earlier versions of the manuscript.
NR 63
TC 64
Z9 64
U1 0
U2 14
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 NOV 15
PY 2008
VL 43
IS 3
BP 614
EP 623
DI 10.1016/j.neuroimage.2008.07.027
PG 10
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 392JY
UT WOS:000262300200020
PM 18703146
ER
PT J
AU Gold, JM
Burstein, HJ
AF Gold, Julie M.
Burstein, Harold J.
TI Aromatase Inhibitor-Associated Musculoskeletal Symptoms: Etiology and
Strategies for Management The Henry/Giles/Stearns Article Reviewed
SO ONCOLOGY-NEW YORK
LA English
DT Editorial Material
ID POSITIVE BREAST-CANCER; ADJUVANT THERAPY
C1 [Gold, Julie M.; Burstein, Harold J.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Gold, JM (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA.
NR 8
TC 1
Z9 1
U1 0
U2 0
PU P R R INC
PI MELVILLE
PA 48 SOUTH SERVICE RD, MELVILLE, NY 11747 USA
SN 0890-9091
J9 ONCOLOGY-NY
JI Oncology-NY
PD NOV 15
PY 2008
VL 22
IS 12
BP 1416
EP +
PG 2
WC Oncology
SC Oncology
GA 395NP
UT WOS:000262531100009
PM 19322949
ER
PT J
AU Medarova, Z
Kumar, M
Ng, SW
Yang, JZ
Barteneva, N
Evgenov, NV
Petkova, V
Moore, A
AF Medarova, Zdravka
Kumar, Mohanraja
Ng, Shu-wing
Yang, Junzheng
Barteneva, Natasha
Evgenov, Natalia V.
Petkova, Victoria
Moore, Anna
TI Multifunctional Magnetic Nanocarriers for Image-Tagged SiRNA Delivery to
Intact Pancreatic Islets
SO TRANSPLANTATION
LA English
DT Article
DE Magnetic resonance imaging; Optical imaging; RNA interference;
Pancreatic islets
ID IN-VIVO; BETA-CELLS; GENE-EXPRESSION; ADENOASSOCIATED VIRUS; HIGH
GLUCOSE; TRANSDUCTION; INSULIN; EFFICIENT; VECTORS; TRANSPLANTATION
AB Background. With the ultimate hope of finding a cure for diabetes, researches are looking into altering the genetic profile of the beta cell as a way to manage metabolic dysregulation. One of the most powerful new approaches for the directed regulation of gene expression uses the phenomenon of RNA interference.
Methods. Here, we establish the feasibility of a novel technology centered around multifunctional magnetic nanocarriers, which concurrently deliver siRNA to intact pancreatic islets and can be detected by magnetic resonance and optical imaging.
Results. In the proof-of-principle studies described here, we demonstrate that, after in vitro incubation, magnetic nanoparticles carrying siRNA designed to target the model gene for enhanced green fluorescent protein are efficiently taken up by murine pancreatic islets, derived from egfp transgenic animals. This uptake can be visualized by magnetic resonance imaging and near-infrared fluorescence optical imaging and results in suppression of the target gene.
Conclusions. These results illustrate the value of our approach in overcoming the challenges associated with genetic modification of intact pancreatic islets in a clinically acceptable manner. Furthermore, an added advantage of our technology derives from the combined capability of our magnetic nanoparticles for siRNA delivery and magnetic labeling of pancreatic islets.
C1 [Medarova, Zdravka; Kumar, Mohanraja; Evgenov, Natalia V.; Moore, Anna] Harvard Univ, Massachusetts Gen Hosp, Sch Med,Mol Imaging Lab, MGH MIT HMS,Athinoula A Martinos Ctr Biomed Imagi, Charlestown, MA 02129 USA.
[Ng, Shu-wing; Yang, Junzheng] Brigham & Womens Hosp, Dept Obstet Gynecol & Reprod Biol, Div Gynecol Oncol, Boston, MA 02115 USA.
[Barteneva, Natasha] Harvard Univ, Sch Med, Immune Dis Inst, Boston, MA USA.
[Barteneva, Natasha] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Petkova, Victoria] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Boston, MA 02215 USA.
RP Moore, A (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med,Mol Imaging Lab, MGH MIT HMS,Athinoula A Martinos Ctr Biomed Imagi, Bldg 75,13th St, Charlestown, MA 02129 USA.
EM amoore@helix.mgh.harvard.edu
FU NIDDK NIH HHS [R01 DK080784, R01 DK064850, 5R01DK080784, R01
DK080784-01A1, R01 DK064850-01]
NR 41
TC 25
Z9 26
U1 1
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0041-1337
J9 TRANSPLANTATION
JI Transplantation
PD NOV 15
PY 2008
VL 86
IS 9
BP 1170
EP 1177
DI 10.1097/TP.0b013e31818a81b2
PG 8
WC Immunology; Surgery; Transplantation
SC Immunology; Surgery; Transplantation
GA 373BI
UT WOS:000260945600004
PM 19005396
ER
PT J
AU Xu, CQ
Gagnon, E
Call, ME
Schnell, JR
Schwieters, CD
Carman, CV
Chou, JJ
Wucherpfennig, KW
AF Xu, Chenqi
Gagnon, Etienne
Call, Matthew E.
Schnell, Jason R.
Schwieters, Charles D.
Carman, Christopher V.
Chou, James J.
Wucherpfennig, Kai W.
TI Regulation of T Cell Receptor Activation by Dynamic Membrane Binding of
the CD3 epsilon Cytoplasmic Tyrosine-Based Motif
SO CELL
LA English
DT Article
ID EFFECTOR DOMAIN; PROTEIN; PHOSPHORYLATION; BICELLES; BILAYER; COMPLEX;
ZAP-70; ZETA
AB Many immune system receptors signal through cytoplasmic tyrosine-based motifs (ITAMs), but how receptor ligation results in ITAM phosphorylation remains unknown. Live-cell imaging studies showed a close interaction of the CD3 epsilon cytoplasmic domain of the T cell receptor (TCR) with the plasma membrane through fluorescence resonance energy transfer between a C-terminal fluorescent protein and a membrane fluorophore. Electrostatic interactions between basic CD3 epsilon residues and acidic phospholipids enriched in the inner leaflet of the plasma membrane were required for binding. The nuclear magnetic resonance structure of the lipid-bound state of this cytoplasmic domain revealed deep insertion of the two key tyrosines into the hydrophobic core of the lipid bilayer. Receptor ligation thus needs to result in unbinding of the CD3 epsilon ITAM from the membrane to render these tyrosines accessible to Src kinases. Sequestration of key tyrosines into the lipid bilayer represents a previously unrecognized mechanism for control of receptor activation.
C1 [Call, Matthew E.; Schnell, Jason R.; Chou, James J.] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Xu, Chenqi; Gagnon, Etienne; Wucherpfennig, Kai W.] Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA.
[Carman, Christopher V.] Harvard Univ, Sch Med, Dept Med, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA.
[Wucherpfennig, Kai W.] Harvard Univ, Sch Med, Dept Neurol, Boston, MA 02115 USA.
[Wucherpfennig, Kai W.] Harvard Univ, Sch Med, Program Immunol, Boston, MA 02115 USA.
[Schwieters, Charles D.] Natl Inst Hlth, Imaging Sci Lab, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA.
RP Chou, JJ (reprint author), Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
EM james_chou@hms.harvard.edu; kai_wucherpfennig@dfci.harvard.edu
RI Carman, Christopher/L-8108-2016; Chou, James/N-9840-2013
OI Carman, Christopher/0000-0001-7358-2548;
FU Intramural NIH HHS; NIAID NIH HHS [AI054520, R01 AI054520, R01
AI054520-05]
NR 33
TC 182
Z9 188
U1 0
U2 24
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD NOV 14
PY 2008
VL 135
IS 4
BP 702
EP 713
DI 10.1016/j.cell.2008.09.044
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 372FG
UT WOS:000260886900020
PM 19013279
ER
PT J
AU Hill, JA
Hall, JA
Sun, CM
Cai, Q
Ghyselinck, N
Chambon, P
Belkaid, Y
Mathis, D
Benoist, C
AF Hill, Jonathan A.
Hall, Jason A.
Sun, Cheng-Ming
Cai, Qi
Ghyselinck, Norbert
Chambon, Pierre
Belkaid, Yasmine
Mathis, Diane
Benoist, Christophe
TI Retinoic Acid Enhances Foxp3 Induction Indirectly by Relieving
Inhibition from CD4(+)CD44(hi) Cells
SO IMMUNITY
LA English
DT Article
ID REGULATORY T-CELLS; IOXP-FLANKED ALLELE; TRANSCRIPTION FACTOR FOXP3;
TGF-BETA; SIGNALING PATHWAY; NUCLEAR RECEPTORS; DENDRITIC CELLS; ORAL
TOLERANCE; RAR-GAMMA; DIFFERENTIATION
AB CD4(+)Foxp3(+) regulatory T (Treg) cells originate primarily from thymic differentiation, but conversion of mature T lymphocytes to Foxp3 positivity can be elicited by several means, including in vitro activation in the presence of TGF-beta. Retinoic acid (RA) increases TGF-beta-induced expression of Foxp3, through unknown molecular mechanisms. We showed here that, rather than enhancing TGF-beta signaling directly in naive CD4(+) T cells, RA negatively regulated an accompanying population of CD4(+) T cells with a CD44(hi) memory and effector phenotype. These memory cells actively inhibited the TGF-beta-induced conversion of naive CD4(+) T cells through the synthesis of a set of cytokines (IL-4, IL-21, IFN-gamma) whose expression was coordinately curtailed by RA. This indirect effect was evident in vivo and required the expression of the RA receptor alpha. Thus, cytokine-producing CD44(hi) cells actively restrain TGF-beta-mediated Foxp3 expression in naive T cells, and this balance can be shifted or fine-tuned by RA.
C1 [Hill, Jonathan A.; Mathis, Diane; Benoist, Christophe] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med,Joslin Diabet Ctr,Sect Immunol & Immunog, Boston, MA 02215 USA.
[Hall, Jason A.; Sun, Cheng-Ming; Belkaid, Yasmine] NIAID, Mucosal Immunol Unit, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Hall, Jason A.] Univ Penn, Immunol Grad Grp, Philadelphia, PA 19104 USA.
[Cai, Qi; Ghyselinck, Norbert; Chambon, Pierre] Univ Strasbourg 1, INSERM, CNRS, Inst Genet & Biol Mol & Cellulaire, F-67404 Illkirch Graffenstaden, France.
RP Mathis, D (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med,Joslin Diabet Ctr,Sect Immunol & Immunog, Boston, MA 02215 USA.
EM cbdm@joslin.harvard.edu; cbdm@joslin.harvard.edu
RI Cai, Qi/E-4357-2014; GHYSELINCK, Norbert/I-6999-2015
OI Cai, Qi/0000-0002-2598-542X; GHYSELINCK, Norbert/0000-0003-4042-6818
FU Juvenile Diabetes Research Foundation [4-2007-1057]; National Institutes
of Health (NIH) [1R01A151530-5]; Young Chair; National Institute of
Diabetes and Digestive and Kidney Diseases; Canadian Institutes of
Health Research; Division of Intramural Research of the National
Institute of Allergy and Infectious Diseases, NIH
FX We thank S. Vitolo and K. Hattori for assistance with mice, J. LaVecchio
and G. Buruzala for help with cytometry, J. Perez and K. Leatherbee for
microarrays, and C. Laplace for graphics. This work was supported by
grants from the Juvenile Diabetes Research Foundation (4-2007-1057) and
the National Institutes of Health (NIH) (1R01A151530-5), by Young Chair
funds to D.M. and C.B., and by the National Institute of Diabetes and
Digestive and Kidney Diseases-funded Joslin Diabetes and Endocrinology
Research Center core facilities. J.A. Hill was supported by a
postdoctoral fellowship from the Canadian Institutes of Health Research,
and C.M.S. and J.A. Hall were supported by the Division of Intramural
Research of the National Institute of Allergy and Infectious Diseases,
NIH.
NR 54
TC 204
Z9 208
U1 0
U2 6
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
J9 IMMUNITY
JI Immunity
PD NOV 14
PY 2008
VL 29
IS 5
BP 758
EP 770
DI 10.1016/j.immuni.2008.09.018
PG 13
WC Immunology
SC Immunology
GA 374IC
UT WOS:000261036000013
PM 19006694
ER
PT J
AU Shi, W
Ma, ZF
Willers, H
Akhtar, K
Scott, SP
Zhang, JQ
Powell, S
Zhang, JR
AF Shi, Wei
Ma, Zhefu
Willers, Henning
Akhtar, Kamal
Scott, Shaun P.
Zhang, Jiuqin
Powell, Simon
Zhang, Junran
TI Disassembly of MDC1 Foci Is Controlled by Ubiquitin-Proteasome-dependent
Degradation
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID DNA-DAMAGE RESPONSE; DOUBLE-STRAND BREAKS; REPAIR PROTEINS; HOMOLOGOUS
RECOMBINATION; CONJUGATED UBIQUITIN; SIGNALING PATHWAYS;
MAMMALIAN-CELLS; HISTONE H2AX; REPLICATION; CHECKPOINT
AB The orderly recruitment, retention, and disassembly of DNA damage response proteins at sites of damaged DNA is a conserved process throughout eukaryotic evolution. The recruitment and retention of DNA repair factors in foci is mediated by a complex network of protein-protein interactions; however, the mechanisms of focus disassembly remain to be defined. Mediator of DNA damage checkpoint protein 1 (MDC1) is an early and key component of the genome surveillance network activated by DNA double-strand breaks (DSBs). Here, we investigated the disassembly of MDC1 foci. First, we show that ubiquitylation directs the MDC1 protein for proteasome-dependent degradation. Ubiquitylated MDC1 associates with chromatin before and after exposure of cells to ionizing radiation (IR). In addition, increased MDC1 ubiquitylation in the chromatin fraction is observed in response to IR, which is correlated with a reduction in total MDC1 protein levels. We demonstrate that blocking MDC1 degradation by proteasome inhibitors leads to a persistence of MDC1 foci. Consistent with this observation, chromatin immunoprecipitation experiments reveal increased MDC1 protein at site-specific DSBs. Interestingly, we show that the persistence of MDC1 foci is associated with an abrogated recruitment of the downstream factor BRCA1 in a manner that is RNF8 independent. Collectively, the evidence presented here supports a novel mechanism for the disassembly of MDC1 foci via ubiquitin-proteasome dependent degradation, which appears to be a key step for the efficient assembly of BRCA1 foci.
C1 [Shi, Wei; Akhtar, Kamal; Scott, Shaun P.; Zhang, Jiuqin; Zhang, Junran] Washington Univ, Sch Med, Dept Radiat Oncol, St Louis, MO 63108 USA.
[Ma, Zhefu] Nanchang Univ, Affiliated Hosp 1, Dept Surg, Breast Ctr, Nanchang 330006, Peoples R China.
[Willers, Henning] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
[Powell, Simon] Mem Sloan Kettering Canc Ctr, Dept Radiat Oncol, New York, NY 10065 USA.
RP Zhang, JR (reprint author), Washington Univ, Sch Med, Dept Radiat Oncol, 4511 Forest Pk Blvd, St Louis, MO 63108 USA.
EM jzhang@radonc.wustl.edu
FU Department of Radiation Oncology, Washington University School of
Medicine; Dr. Joseph Roti Roti and Stephanie Pagano Fund for
Mesothelioma Research [IRG-58-010-51]; American Cancer Society
FX This work was supported by a seed grant and startup fund from the
Department of Radiation Oncology, Washington University School of
Medicine, by the Dr. Joseph Roti Roti and Stephanie Pagano Fund for
Mesothelioma Research, and by Grant IRG-58-010-51 from the American
Cancer Society (to J. Z.). The costs of publication of this article were
defrayed in part by the payment of page charges. This article must
therefore be hereby marked "advertisement" in accordance with 18 U. S.
C. Section 1734 solely to indicate this fact.
NR 63
TC 37
Z9 38
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 NOV 14
PY 2008
VL 283
IS 46
BP 31608
EP 31616
DI 10.1074/jbc.M801082200
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 370KJ
UT WOS:000260760800041
PM 18757370
ER
PT J
AU Mckee, CJ
Kessl, JJ
Shkriabai, N
Dar, MJ
Engelman, A
Kvaratskhelia, M
AF McKee, Christopher J.
Kessl, Jacques J.
Shkriabai, Nikolozi
Dar, Mohd Jamal
Engelman, Alan
Kvaratskhelia, Mamuka
TI Dynamic Modulation of HIV-1 Integrase Structure and Function by Cellular
Lens Epithelium-derived Growth Factor (LEDGF) Protein
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; DNA-BINDING-DOMAIN; IN-VITRO; TYPE-1
INTEGRASE; PREINTEGRATION COMPLEXES; ENZYMATIC-ACTIVITY;
MASS-SPECTROMETRY; CRYSTAL-STRUCTURE; TERMINAL DOMAINS; CDNA INTEGRATION
AB The mandatory integration of the reverse-transcribed HIV-1 genome into host chromatin is catalyzed by the viral protein integrase (IN), and IN activity can be regulated by numerous viral and cellular proteins. Among these, LEDGF has been identified as a cellular cofactor critical for effective HIV-1 integration. The x-ray crystal structure of the catalytic core domain (CCD) of IN in complex with the IN binding domain (IBD) of LEDGF has furthermore revealed essential protein-protein contacts. However, mutagenic studies indicated that interactions between the full-length proteins were more extensive than the contacts observed in the co-crystal structure of the isolated domains. Therefore, we have conducted detailed biochemical characterization of the interactions between full-length IN and LEDGF. Our results reveal a highly dynamic nature of IN subunit-subunit interactions. LEDGF strongly stabilized these interactions and promoted IN tetramerization. Mass spectrometric protein footprinting and molecular modeling experiments uncovered novel intra- and inter-protein-protein contacts in the full-length IN-LEDGF complex that lay outside of the observable IBD-CCD structure. In particular, our studies defined the IN tetramer interface important for enzymatic activities and high affinity LEDGF binding. These findings provide new insight into how LEDGF modulates HIV-1 IN structure and function, and highlight the potential for exploiting the highly dynamic structure of multimeric IN as a novel therapeutic target.
C1 [McKee, Christopher J.; Kessl, Jacques J.; Shkriabai, Nikolozi; Kvaratskhelia, Mamuka] Ohio State Univ, Ctr Retrovirus Res, Coll Pharm, Columbus, OH 43210 USA.
[McKee, Christopher J.; Kessl, Jacques J.; Shkriabai, Nikolozi; Kvaratskhelia, Mamuka] Ohio State Univ, Ctr Comprehens Canc, Coll Pharm, Columbus, OH 43210 USA.
[Dar, Mohd Jamal; Engelman, Alan] Harvard Univ, Sch Med, Dept Canc Immunol & AIDS, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Dar, Mohd Jamal; Engelman, Alan] Harvard Univ, Sch Med, Div Aids, Boston, MA 02115 USA.
RP Kvaratskhelia, M (reprint author), Ohio State Univ, Ctr Retrovirus Res, Coll Pharm, 500 W 12th Ave,238 LM Pk Hall, Columbus, OH 43210 USA.
EM kvaratskhelia.1@osu.edu
RI Kessl, Jacques/J-6073-2015
FU National Institutes of Health AIDS Research [118-D-24]; Reference
Reagent Program; Division of AIDS; NIAID; National Institutes of Health
FX We thank Jocelyn Norris for help with purifying LEDGF proteins. The
integrase strand transfer inhibitor (118-D-24) was obtained through the
National Institutes of Health AIDS Research and Reference Reagent
Program, Division of AIDS, NIAID, National Institutes of Health.
NR 76
TC 76
Z9 77
U1 0
U2 2
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 14
PY 2008
VL 283
IS 46
BP 31802
EP 31812
DI 10.1074/jbc.M805843200
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 370KJ
UT WOS:000260760800063
PM 18801737
ER
PT J
AU Cooper, MP
Uldry, M
Kajimura, S
Arany, Z
Spiegelman, BM
AF Cooper, Marcus P.
Uldry, Marc
Kajimura, Shingo
Arany, Zoltan
Spiegelman, Bruce M.
TI Modulation of PGC-1 Coactivator Pathways in Brown Fat Differentiation
through LRP130
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID MITOCHONDRIAL UNCOUPLING PROTEIN; C-OXIDASE DEFICIENCY; ADIPOSE CELL
LINE; MESSENGER-RNA; ADIPOCYTE DIFFERENTIATION; TRANSGENIC MICE;
IN-VIVO; ADAPTIVE THERMOGENESIS; INDUCIBLE COACTIVATOR;
ENERGY-METABOLISM
AB The PGC-1 coactivators are important regulators of oxidative metabolism. We previously demonstrated that LRP130 is a binding partner of PGC-1 alpha, required for hepatic gluconeogenesis. LRP130 is the gene mutated in Leigh syndrome French Canadian variant, a rare neurodegenerative disease. The importance of LRP130 in other, non-hepatocyte biology remains obscure. To better understand PGC-1 coactivator function in brown fat development, we explored the metabolic role of LRP130 in brown adipocyte differentiation. We show that LRP130 is preferentially enriched in brown fat compared with white, and induced in a PGC-1-dependent manner during differentiation. Despite intact PGC-1 coactivator expression, brown fat cells deficient for LRP130 exhibit attenuated expression of several genes characteristic of brown fat, including uncoupling protein 1. Oxygen consumption studies support a specific defect in proton leak due to attenuated uncoupling protein 1 expression. Notably, brown fat cell development common to both PGC-1 coactivators is governed by LRP130. Conversely, the cAMP response controlled by PGC-1 alpha is not regulated by LRP130. These data implicate LRP130 in brown fat cell development and differentiation.
C1 [Spiegelman, Bruce M.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
RP Spiegelman, BM (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, 1 Jimmy Fund Way, Boston, MA 02115 USA.
EM marcus.cooper@umassmed.edu; bruce_spiegelman@dfci.harvard.edu
FU National Institutes of Health [R01DK61562, K08DK071017]
FX This work was supported, in whole or in part, by National Institutes of
Health Grants R01DK61562 (to B. M. S.) and K08DK071017 (to M. P. C.).
The costs of publication of this article were defrayed in part by the
payment of page charges. This article must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section 1734 solely to
indicate this fact.
NR 50
TC 22
Z9 24
U1 0
U2 2
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 14
PY 2008
VL 283
IS 46
BP 31960
EP 31967
DI 10.1074/jbc.M805431200
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 370KJ
UT WOS:000260760800078
PM 18728005
ER
PT J
AU Orsi, RH
Borowsky, ML
Lauer, P
Young, SK
Nusbaum, C
Galagan, JE
Birren, BW
Ivy, RA
Sun, Q
Graves, LM
Swaminathan, B
Wiedmann, M
AF Orsi, Renato H.
Borowsky, Mark L.
Lauer, Peter
Young, Sarah K.
Nusbaum, Chad
Galagan, James E.
Birren, Bruce W.
Ivy, Reid A.
Sun, Qi
Graves, Lewis M.
Swaminathan, Bala
Wiedmann, Martin
TI Short-term genome evolution of Listeria monocytogenes in a
non-controlled environment
SO BMC GENOMICS
LA English
DT Article
ID FIELD GEL-ELECTROPHORESIS; ENCODING CHOLERA-TOXIN; GROUP-A
STREPTOCOCCUS; ESCHERICHIA-COLI; PROCESSING PLANTS; BACILLUS-SUBTILIS;
VIBRIO-CHOLERAE; UNITED-STATES; EXPERIMENTAL POPULATIONS; CONTAMINATION
PATTERNS
AB Background: While increasing data on bacterial evolution in controlled environments are available, our understanding of bacterial genome evolution in natural environments is limited. We thus performed full genome analyses on four Listeria monocytogenes, including human and food isolates from both a 1988 case of sporadic listeriosis and a 2000 listeriosis outbreak, which had been linked to contaminated food from a single processing facility. All four isolates had been shown to have identical subtypes, suggesting that a specific L. monocytogenes strain persisted in this processing plant over at least 12 years. While a genome sequence for the 1988 food isolate has been reported, we sequenced the genomes of the 1988 human isolate as well as a human and a food isolate from the 2000 outbreak to allow for comparative genome analyses.
Results: The two L. monocytogenes isolates from 1988 and the two isolates from 2000 had highly similar genome backbone sequences with very few single nucleotide (nt) polymorphisms (1-8 SNPs/isolate; confirmed by re-sequencing). While no genome rearrangements were identified in the backbone genome of the four isolates, a 42 kb prophage inserted in the chromosomal comK gene showed evidence for major genome rearrangements. The human-food isolate pair from each 1988 and 2000 had identical prophage sequence; however, there were significant differences in the prophage sequences between the 1988 and 2000 isolates. Diversification of this prophage appears to have been caused by multiple homologous recombination events or possibly prophage replacement. In addition, only the 2000 human isolate contained a plasmid, suggesting plasmid loss or acquisition events. Surprisingly, besides the polymorphisms found in the comK prophage, a single SNP in the tRNA Thr-4 prophage represents the only SNP that differentiates the 1988 isolates from the 2000 isolates.
Conclusion: Our data support the hypothesis that the 2000 human listeriosis outbreak was caused by a L. monocytogenes strain that persisted in a food processing facility over 12 years and show that genome sequencing is a valuable and feasible tool for retrospective epidemiological analyses. Short-term evolution of L. monocytogenes in non-controlled environments appears to involve limited diversification beyond plasmid gain or loss and prophage diversification, highlighting the importance of phages in bacterial evolution.
C1 [Orsi, Renato H.; Ivy, Reid A.; Wiedmann, Martin] Cornell Univ, Dept Food Sci, Ithaca, NY 14853 USA.
[Borowsky, Mark L.; Young, Sarah K.; Nusbaum, Chad; Galagan, James E.; Birren, Bruce W.] MIT, Broad Inst, Genome Sequencing & Anal Program, Cambridge, MA 02139 USA.
[Galagan, James E.] Boston Univ, Dept Biomed Engn & Microbiol, Boston, MA 02215 USA.
[Sun, Qi] Cornell Univ, Ctr Adv Comp, Computat Biol Serv Unit, Ithaca, NY 14853 USA.
[Graves, Lewis M.; Swaminathan, Bala] Ctr Dis Control & Prevent, Enter Dis Lab Branch, Div Foodborne Bacterial & Mycot Dis, Atlanta, GA USA.
[Borowsky, Mark L.] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
[Lauer, Peter] Anza Therapeut, Concord, MA USA.
[Borowsky, Mark L.; Young, Sarah K.; Nusbaum, Chad; Galagan, James E.; Birren, Bruce W.] Harvard Univ, Cambridge, MA 02138 USA.
RP Wiedmann, M (reprint author), Cornell Univ, Dept Food Sci, Ithaca, NY 14853 USA.
EM rho2@cornell.edu; borowsky@molbio.mgh.harvard.edu;
plauer@anzatherapeutics.com; stowey@broad.mit.edu; chad@broad.mit.edu;
jgalag@mit.edu; bwb@broad.mit.edu; rai6@cornell.edu;
qisun@tc.cornell.edu; lmg2@cdc.gov; balas7780@gmail.com;
mw16@cornell.edu
RI Wiedmann, Martin/A-9683-2008;
OI Wiedmann, Martin/0000-0002-4168-5662; Galagan, James/0000-0003-0542-3291
FU USDA Special Research [2005-34459-15625, 34459-16952-06]
FX This work was partially supported by USDA Special Research Grants
2005-34459-15625 and 34459-16952-06 (to MW). We thank USDA FSIS and
Kitty Pupedis for providing isolate J2818 and for providing information
on the history of this isolate. We also thank Yesim Soyer for help with
PFGE analyses and Barbara Bowen for help with the rhamnose tests.
NR 77
TC 80
Z9 80
U1 5
U2 20
PU BIOMED CENTRAL LTD
PI LONDON
PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T
4LB, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PD NOV 13
PY 2008
VL 9
AR 539
DI 10.1186/1471-2164-9-539
PG 17
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 417VE
UT WOS:000264105800001
PM 19014550
ER
PT J
AU Zhang, Y
Shin, H
Song, JS
Lei, Y
Liu, XS
AF Zhang, Yong
Shin, Hyunjin
Song, Jun S.
Lei, Ying
Liu, X. Shirley
TI Identifying Positioned Nucleosomes with Epigenetic Marks in Human from
ChIP-Seq
SO BMC GENOMICS
LA English
DT Article
ID HUMAN GENOME; HISTONE MODIFICATIONS; SACCHAROMYCES-CEREVISIAE;
GENE-EXPRESSION; HUMAN PROMOTERS; ACTIVE GENES; CHROMATIN; METHYLATION;
RESOLUTION; PATTERNS
AB Background: In vivo positioning and covalent modifications of nucleosomes play an important role in epigenetic regulation, but genome-wide studies of positioned nucleosomes and their modifications in human still remain limited.
Results: This paper describes a novel computational framework to efficiently identify positioned nucleosomes and their histone modification profiles from nucleosome-resolution histone modification ChIP-Seq data. We applied the algorithm to histone methylation ChIP-Seq data in human CD4(+) T cells and identified over 438,000 positioned nucleosomes, which appear predominantly at functionally important regions such as genes, promoters, DNase I hypersensitive regions, and transcription factor binding sites. Our analysis shows the identified nucleosomes play a key role in epigenetic gene regulation within those functionally important regions via their positioning and histone modifications.
Conclusion: Our method provides an effective framework for studying nucleosome positioning and epigenetic marks in mammalian genomes. The algorithm is open source and available at http://liulab.dfci.harvard.edu/NPS/.
C1 [Zhang, Yong; Shin, Hyunjin; Lei, Ying; Liu, X. Shirley] Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Song, Jun S.] Inst Adv Study, Simons Ctr Syst Biol, Princeton, NJ 08540 USA.
RP Liu, XS (reprint author), Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Dept Biostat & Computat Biol, 44 Binney St, Boston, MA 02115 USA.
EM zy@jimmy.harvard.edu; shin@jimmy.harvard.edu; jssong@ias.edu;
ylei@jimmy.harvard.edu; xsliu@jimmy.harvard.edu
RI Zhang, Yong/B-4838-2011
OI Zhang, Yong/0000-0001-6316-2734
FU NIH [HG004069-02]; Martin A. and Helen Chooljian Membership in Biology
FX We thank Myles Brown, Kevin Struhl, Keji Zhao, Jerome Eeckhoute, Mathieu
Lupien, Dustin Schones and Wei Li for their insightful discussions and
critical readings of this manuscript. The project was partially funded
by NIH grant HG004069-02. JSS was supported in part by the Martin A. and
Helen Chooljian Membership in Biology.
NR 37
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U1 2
U2 12
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PD NOV 13
PY 2008
VL 9
AR 537
DI 10.1186/1471-2164-9-537
PG 11
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 382MB
UT WOS:000261609000001
PM 19014516
ER
PT J
AU Fish, KN
Sweet, RA
Deo, AJ
Lewis, DA
AF Fish, Kenneth N.
Sweet, Robert A.
Deo, Anthony J.
Lewis, David A.
TI An automated segmentation methodology for quantifying immunoreactive
puncta number and fluorescence intensity in tissue sections
SO BRAIN RESEARCH
LA English
DT Article
DE Quantitative fluorescence microscopy; Immunoreactive puncta;
Segmentation; Synaptic structure; Fluorescent immunohistochemistry
ID MONKEY PREFRONTAL CORTEX; GAD(67) MESSENGER-RNAS; POSTNATAL-DEVELOPMENT;
AXON TERMINALS; LOCALIZATION; MICROSCOPY; PERFORMANCE; SYNAPSES;
PROTEINS; SUPPORTS
AB A number of human brain diseases have been associated with disturbances in the structure and function of cortical synapses. Answering fundamental questions about the synaptic machinery in these disease states requires the ability to image and quantify small synaptic structures in tissue sections and to evaluate protein levels at these major sites of function. We developed a new automated segmentation imaging method specifically to answer such fundamental questions. The method takes advantage of advances in spinning disk confocal microscopy, and combines information from multiple iterations of a fluorescence intensity/morphological segmentation protocol to construct three-dimensional object masks of immunoreactive (IR) puncta. This new methodology is unique in that high- and low-fluorescing IR puncta are equally masked, allowing for quantification of the number of fluorescently-labeled puncta in tissue sections. In addition, the shape of the final object masks highly represents their corresponding original data. Thus, the object masks can be used to extract information about the IR puncta (e.g., average fluorescence intensity of proteins of interest). Importantly, the segmentation method presented can be easily adapted for use with most existing microscopy analysis packages. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Fish, Kenneth N.] Univ Pittsburgh, Sch Med, Dept Psychiat, Western Psychiat Inst & Clin, Pittsburgh, PA 15213 USA.
[Lewis, David A.] Univ Pittsburgh, Sch Med, Dept Neurosci, Pittsburgh, PA 15213 USA.
[Sweet, Robert A.] Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15213 USA.
[Sweet, Robert A.] VA Pittsburgh Healthcare Syst, VISN Mental Illness Res Educ & Clin Ctr MIRECC 4, Pittsburgh, PA USA.
[Deo, Anthony J.] Univ Pittsburgh, Sch Med, Phys Sci Training Program, Pittsburgh, PA 15213 USA.
RP Fish, KN (reprint author), Univ Pittsburgh, Sch Med, Dept Psychiat, Western Psychiat Inst & Clin, Biomed Sci Tower,Room W165, Pittsburgh, PA 15213 USA.
EM fishkn@upmc.edu
RI Lewis, David/G-4053-2014
OI Lewis, David/0000-0002-3225-6778
FU NIH [MHOS1234, MH071533]; University of Pittsburgh
FX Supported by NIH grant MHOS1234 (DAL), MH071533 (RAS), and University of
Pittsburgh CMRF award (KNF). The content is solely the responsibility of
the authors and does not necessarily represent the official views of the
National Institute of Mental Health or the National Institutes of
Health. We are extremely grateful to Mrs. Kelly Rogers and Heidi Scriven
for their technical assistance. We are also grateful to Olympus American
and B and B Microscopes for their advice.
NR 25
TC 20
Z9 20
U1 0
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD NOV 13
PY 2008
VL 1240
BP 62
EP 72
DI 10.1016/j.brainres.2008.08.060
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 379SD
UT WOS:000261415600008
PM 18793619
ER
PT J
AU Ford, AC
Talley, NJ
Spiegel, BMR
Foxx-Orenstein, AE
Schiller, L
Quigley, EMM
Moayyedi, P
AF Ford, Alexander C.
Talley, Nicholas J.
Spiegel, Brennan M. R.
Foxx-Orenstein, Amy E.
Schiller, Lawrence
Quigley, Eamonn M. M.
Moayyedi, Paul
TI Effect of fibre, antispasmodics, and peppermint oil in the treatment of
irritable bowel syndrome: systematic review and meta-analysis
SO BRITISH MEDICAL JOURNAL
LA English
DT Review
ID CLINICAL-TRIALS; VISCERAL SENSATION; NATURAL-HISTORY; SMOOTH-MUSCLE;
PREVALENCE; DISORDERS; QUALITY; POPULATION; MANAGEMENT; TRANSIT
AB Objective To determine the effect of fibre, antispasmodics, and peppermint oil in the treatment of irritable bowel syndrome.
Design Systematic review and meta- analysis of randomised controlled trials.
Data sources Medline, Embase, and the Cochrane controlled trials register up to April 2008.
Review methods Randomised controlled trials comparing fibre, antispasmodics, and peppermint oil with placebo or no treatment in adults with irritable bowel syndrome were eligible for inclusion. The minimum duration of therapy considered was one week, and studies had to report either a global assessment of cure or improvement in symptoms, or cure of or improvement in abdominal pain, after treatment. A random effects model was used to pool data on symptoms, and the effect of therapy compared with placebo or no treatment was reported as the relative risk (95% confidence interval) of symptoms persisting.
Results 12 studies compared fibre with placebo or no treatment in 591 patients (relative risk of persistent symptoms 0.87, 95% confidence interval 0.76 to 1.00). This effect was limited to ispaghula (0.78, 0.63 to 0.96). Twenty two trials compared antispasmodics with placebo in 1778 patients (0.68, 0.57 to 0.81). Various antispasmodics were studied, but otilonium (four trials, 435 patients, relative risk of persistent symptoms 0.55, 0.31 to 0.97) and hyoscine (three trials, 426 patients, 0.63, 0.51 to 0.78) showed consistent evidence of efficacy. Four trials compared peppermint oil with placebo in 392 patients ( 0.43, 0.32 to 0.59).
Conclusion Fibre, antispasmodics, and peppermint oil were all more effective than placebo in the treatment of irritable bowel syndrome.
C1 [Ford, Alexander C.; Moayyedi, Paul] McMaster Univ, Hlth Sci Ctr, Div Gastroenterol, Hamilton, ON L8N 3Z5, Canada.
[Talley, Nicholas J.] Mayo Clin, Dept Med, Jacksonville, FL 32224 USA.
[Spiegel, Brennan M. R.] Univ Calif Los Angeles, VA Ctr Outcomes Res & Educ, Los Angeles, CA USA.
[Spiegel, Brennan M. R.] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Foxx-Orenstein, Amy E.] Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN USA.
[Schiller, Lawrence] Baylor Univ, Med Ctr, Digest Hlth Assoc Texas, Dallas, TX USA.
[Quigley, Eamonn M. M.] Cork Univ Hosp, Dept Med, Cork, Ireland.
RP Ford, AC (reprint author), McMaster Univ, Hlth Sci Ctr, Div Gastroenterol, 1200 Main St W, Hamilton, ON L8N 3Z5, Canada.
EM alexf12399@yahoo.com
RI Ford, Alexander/K-5491-2012; Talley, nicholas/D-5399-2013; Moayyedi,
Paul/M-6178-2014
OI Ford, Alexander/0000-0001-6371-4359; Talley,
nicholas/0000-0003-2537-3092; Moayyedi, Paul/0000-0002-3616-9292
FU American College of Gastroenterology
FX This study was funded by the American College of Gastroenterology. The
authors' work was independent of the funders.
NR 32
TC 167
Z9 170
U1 4
U2 25
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0959-535X
J9 BRIT MED J
JI Br. Med. J.
PD NOV 13
PY 2008
VL 337
AR a2313
DI 10.1136/bmj.a2313
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 385AE
UT WOS:000261784500003
PM 19008265
ER
PT J
AU Rosolowsky, ET
Niewczas, MA
Ficociello, LH
Perkins, BA
Warram, JH
Krolewski, AS
AF Rosolowsky, Elizabeth T.
Niewczas, Monika A.
Ficociello, Linda H.
Perkins, Bruce A.
Warram, James H.
Krolewski, Andrzej S.
TI Between hyperfiltration and impairment: Demystifying early renal
functional changes in diabetic nephropathy
SO DIABETES RESEARCH AND CLINICAL PRACTICE
LA English
DT Article; Proceedings Paper
CT International Symposium on Diabetic Nephropathy
CY 2008
CL Shiga, JAPAN
DE Type 1 Diabetes; Microalbuminuria; Early renal function decline;
Cystatin C
ID GLOMERULAR-FILTRATION-RATE; URINARY ALBUMIN EXCRETION; CREATININE-BASED
METHODS; SERUM CYSTATIN-C; URIC-ACID; SERIAL MEASUREMENTS; FUNCTION
DECLINE; BLOOD-PRESSURE; MELLITUS; MICROALBUMINURIA
AB Renal functional changes in diabetic nephropathy conventionally have been linked to progression of urinary albumin excretion. This paradigm was based on historic evidence noting that hyperfiltration occurred in the setting of normoalbuminuria and microalbuminuria and that loss of renal function began in the context of proteinuria. More contemporaneous research findings, using serum cystatin-C-based estimates of glomerular filtration rate (cC-GFR), have challenged this paradigm. Rather, the process of renal function loss appears to begin prior to the onset of proteinuria. In the 2nd Joslin Kidney Study on the Natural History of Microalbuminuria, over one-third of type I diabetes (T1DM) patients with microalbuminuria at the time of enrollment already had evidence of mild (cC-GFR < 90) or moderate (cC-GFR < 60 ml/min) renal function impairment. Understanding the mechanisms underlying this phenomenon of early renal function impairment may allow for interventions directed at altering or retarding early renal function decline. To date, serum uric acid and components of the TNF alpha pathway appear to be involved. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
C1 [Krolewski, Andrzej S.] Joslin Diabet Ctr, Sect Genet & Epidemiol, Div Res, Boston, MA 02215 USA.
[Rosolowsky, Elizabeth T.] Childrens Hosp Boston, Div Endocrinol, Boston, MA USA.
[Niewczas, Monika A.; Krolewski, Andrzej S.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med, Boston, MA USA.
[Perkins, Bruce A.] Univ Toronto, Div Endocrinol & Metab, Toronto, ON, Canada.
[Niewczas, Monika A.] Warsaw Med Univ, Dept Immunol Transplant Med & Internal Dis, Warsaw, Poland.
RP Krolewski, AS (reprint author), Joslin Diabet Ctr, Sect Genet & Epidemiol, Div Res, 1 Joslin Pl, Boston, MA 02215 USA.
EM Andrzej.Krolewski@joslin.harvard.edu
FU AHRQ HHS [T32 HS00063]; NIDDK NIH HHS [DK41526]
NR 54
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U1 0
U2 1
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0168-8227
J9 DIABETES RES CLIN PR
JI Diabetes Res. Clin. Pract.
PD NOV 13
PY 2008
VL 82
SU 1
BP S46
EP S53
DI 10.1016/j.diabres.2008.09.018
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 381RM
UT WOS:000261553600010
PM 18849087
ER
PT J
AU Cadwell, K
Liu, JY
Brown, SL
Miyoshi, H
Loh, J
Lennerz, JK
Kishi, C
Kc, W
Carrero, JA
Hunt, S
Stone, CD
Brunt, EM
Xavier, RJ
Sleckman, BP
Li, E
Mizushima, N
Stappenbeck, TS
Virgin, HW
AF Cadwell, Ken
Liu, John Y.
Brown, Sarah L.
Miyoshi, Hiroyuki
Loh, Joy
Lennerz, Jochen K.
Kishi, Chieko
Kc, Wumesh
Carrero, Javier A.
Hunt, Steven
Stone, Christian D.
Brunt, Elizabeth M.
Xavier, Ramnik J.
Sleckman, Barry P.
Li, Ellen
Mizushima, Noboru
Stappenbeck, Thaddeus S.
Virgin, Herbert W.
TI A key role for autophagy and the autophagy gene Atg16l1 in mouse and
human intestinal Paneth cells
SO NATURE
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; INFLAMMATORY-BOWEL-DISEASE; MESENTERIC
ADIPOSE-TISSUE; CROHNS-DISEASE; SUSCEPTIBILITY LOCI; PATHOGENESIS;
PROTEIN; PROLIFERATION; EXPRESSION; MEMBRANE
AB Susceptibility to Crohn's disease, a complex inflammatory disease involving the small intestine, is controlled by over 30 loci(1). One Crohn's disease risk allele is in ATG16L1, a gene homologous to the essential yeast autophagy gene ATG16 ( ref. 2). It is not known how ATG16L1 or autophagy contributes to intestinal biology or Crohn's disease pathogenesis. To address these questions, we generated and characterized mice that are hypomorphic for ATG16L1 protein expression, and validated conclusions on the basis of studies in these mice by analysing intestinal tissues that we collected from Crohn's disease patients carrying the Crohn's disease risk allele of ATG16L1. Here we show that ATG16L1 is a bona fide autophagy protein. Within the ileal epithelium, both ATG16L1 and a second essential autophagy protein ATG5 are selectively important for the biology of the Paneth cell, a specialized epithelial cell that functions in part by secretion of granule contents containing antimicrobial peptides and other proteins that alter the intestinal environment(3). ATG16L1- andATG5- deficient Paneth cells exhibited notable abnormalities in the granule exocytosis pathway. In addition, transcriptional analysis revealed an unexpected gain of function specific to ATG16L1- deficient Paneth cells including increased expression of genes involved in peroxisome proliferator- activated receptor ( PPAR) signalling and lipid metabolism, of acute phase reactants and of two adipocytokines, leptin and adiponectin, known to directly influence intestinal injury responses. Importantly, Crohn's disease patients homozygous for the ATG16L1 Crohn's disease risk allele displayed Paneth cell granule abnormalities similar to those observed in autophagy- protein- deficient mice and expressed increased levels of leptin protein. Thus, ATG16L1, and probably the process of autophagy, have a role within the intestinal epithelium of mice and Crohn's disease patients by selective effects on the cell biology and specialized regulatory properties of Paneth cells.
C1 [Cadwell, Ken; Liu, John Y.; Brown, Sarah L.; Miyoshi, Hiroyuki; Loh, Joy; Lennerz, Jochen K.; Kc, Wumesh; Carrero, Javier A.; Brunt, Elizabeth M.; Sleckman, Barry P.; Stappenbeck, Thaddeus S.; Virgin, Herbert W.] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA.
[Hunt, Steven] Washington Univ, Sch Med, Dept Surg, St Louis, MO 63110 USA.
[Stone, Christian D.; Li, Ellen] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA.
[Virgin, Herbert W.] Washington Univ, Sch Med, Dept Mol Microbiol, St Louis, MO 63110 USA.
[Kishi, Chieko; Mizushima, Noboru] Tokyo Med & Dent Univ, Grad Sch, Dept Physiol & Cell Biol, Tokyo 1138519, Japan.
[Kishi, Chieko; Mizushima, Noboru] Tokyo Med & Dent Univ, Fac Med, Dept Physiol & Cell Biol, Tokyo 1138519, Japan.
[Xavier, Ramnik J.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Boston, MA 02114 USA.
[Xavier, Ramnik J.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
RP Virgin, HW (reprint author), Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA.
EM stappenb@wustl.edu; virgin@wustl.edu
RI Mizushima, Noboru/C-3635-2009;
OI Mizushima, Noboru/0000-0002-6258-6444; Cadwell, Ken/0000-0002-5860-0661
FU Broad Foundation; NIH [T32 AR07279, R01 AI062832, AI062773, DK43351];
Lallage Feazel Wall Fellowship [DRG-1972-08]; Damon Runyon Cancer
Research Foundation; Pew Foundation; Washington University Digestive
Diseases Research Core Center [P30 DK52574]; Barnes Jewish Foundation;
Johnson and Johnson Translational Seed Award; Crohn's Colitis Foundation
of America; Scientific Research from the Ministry of Education, Culture,
Sports, Science and Technology of Japan; Toray Science Foundation; [U54
AI057160 Project 6]
FX We thank N. Abe for technical assistance with fluorescence microscopy,
V. Cavalli for microscope use, J. Eisenberg and A. Ng for help with
bioinformatics analysis, A. J. Ouellette for technical advice, and I.
Mysorekar and J. Mills for help with antibodies. This research was
supported by grant U54 AI057160 Project 6 and the Broad Foundation
(K.C., J. Loh and H.W.V.), training grant NIH T32 AR07279 (K.C.), the
Lallage Feazel Wall Fellowship DRG-1972-08 (K.C.) from the Damon Runyon
Cancer Research Foundation; the Pew Foundation (J. Liu, S.L.B., H.M.,
W.K. and T.S.S.); the Washington University Digestive Diseases Research
Core Center P30 DK52574, Barnes Jewish Foundation, Johnson and Johnson
Translational Seed Award, and the Crohn's Colitis Foundation of America
(E.L., S.H. and C.S.); grants-in-aid for Scientific Research from the
Ministry of Education, Culture, Sports, Science and Technology of Japan,
and the Toray Science Foundation (C.K. and N.M.); NIH R01 AI062832
(J.A.C.); and NIH AI062773 and DK43351 (R.J.X.).
NR 29
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Z9 704
U1 13
U2 65
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 13
PY 2008
VL 456
IS 7219
BP 259
EP U62
DI 10.1038/nature07416
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 374JJ
UT WOS:000261039300044
PM 18849966
ER
PT J
AU Treadway, K
AF Treadway, Katharine
TI The Future of Primary Care: Sustaining Relationships
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
C1 [Treadway, Katharine] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Treadway, Katharine] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Treadway, K (reprint author), Harvard Univ, Sch Med, Boston, MA 02115 USA.
NR 0
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 NOV 13
PY 2008
VL 359
IS 20
BP 2086
EP +
DI 10.1056/NEJMp0805762
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 371IB
UT WOS:000260823900002
PM 19005191
ER
PT J
AU Goroll, AH
AF Goroll, Allan H.
TI The Future of Primary Care: Reforming Physician Payment
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
ID PERFORMANCE; QUALITY; HEALTH; PAY
C1 [Goroll, Allan H.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Goroll, Allan H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Goroll, AH (reprint author), Harvard Univ, Sch Med, Boston, MA 02115 USA.
NR 5
TC 9
Z9 11
U1 1
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 NOV 13
PY 2008
VL 359
IS 20
BP 2087
EP +
DI 10.1056/NEJMp0805765
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 371IB
UT WOS:000260823900004
PM 19005194
ER
PT J
AU Daffner, KR
Sherman, JC
Gonzalez, RG
Hasserjian, RP
Alcalay, RN
Cole, AJ
Hedley-Whyte, ET
AF Daffner, Kirk R.
Sherman, Janet C.
Gonzalez, R. Gilberto
Hasserjian, Robert P.
Alcalay, Roy N.
Cole, Andrew J.
Hedley-Whyte, E. Tessa
TI A Man with Confusion and Memory Loss Atypical carcinoid tumor
(well-differentiated neuroendocrine carcinoma) of the thymus, associated
with paraneoplastic limbic encephalitis
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID HERPES-SIMPLEX ENCEPHALITIS; POTASSIUM CHANNEL ANTIBODIES; LUNG-CANCER;
NERVOUS-SYSTEM; TEMPORAL-LOBE; AUTOIMMUNITY; MRI; PATIENT;
ENCEPHALOMYELITIS; DIAGNOSIS
C1 [Daffner, Kirk R.] Brigham & Womens Hosp, Div Cognit & Behav Neurol, Boston, MA 02115 USA.
[Sherman, Janet C.] Massachusetts Gen Hosp, Psychol Assessment Ctr, Boston, MA 02114 USA.
[Sherman, Janet C.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Gonzalez, R. Gilberto] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Hasserjian, Robert P.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Daffner, Kirk R.; Sherman, Janet C.] Harvard Univ, Sch Med, Dept Neurol, Boston, MA 02115 USA.
[Gonzalez, R. Gilberto] Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02115 USA.
[Hasserjian, Robert P.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
RP Daffner, KR (reprint author), Brigham & Womens Hosp, Div Cognit & Behav Neurol, 75 Francis St, Boston, MA 02115 USA.
FU Bayer; General Electric
FX Dr. Gonzalez reports receiving lecture fees from Bayer and General
Electric. No other potential conflict of interest relevant to this
article was reported.
NR 42
TC 5
Z9 7
U1 0
U2 2
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 13
PY 2008
VL 359
IS 20
BP 2155
EP 2164
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 371IB
UT WOS:000260823900015
PM 19005200
ER
PT J
AU Ciaranello, AL
Seage, GR
Freedberg, KA
Weinstein, MC
Lockman, S
Walensky, RP
AF Ciaranello, Andrea L.
Seage, George R., III
Freedberg, Kenneth A.
Weinstein, Milton C.
Lockman, Shahin
Walensky, Rochelle P.
TI Antiretroviral drugs for preventing mother-to-child transmission of HIV
in sub-Saharan Africa: balancing efficacy and infant toxicity
SO AIDS
LA English
DT Article
DE antiretroviral therapy; decision analysis; HIV/AIDS; mitochondrial
toxicity; pediatric HIV; PMTCT; sub-Saharan Africa
ID IMMUNODEFICIENCY-VIRUS TYPE-1; RANDOMIZED CONTROLLED-TRIAL; SINGLE-DOSE
NEVIRAPINE; PERSISTENT MITOCHONDRIAL DYSFUNCTION; LATE POSTNATAL
TRANSMISSION; PLACEBO-CONTROLLED TRIAL; SHORT-COURSE ZIDOVUDINE;
BREAST-FED CHILDREN; IN-UTERO EXPOSURE; UNINFECTED CHILDREN
AB Objective: Antiretroviral drugs can prevent mother-to-child transmission of HIV infection, but in-utero antiretroviral exposure may be associated with neurologic symptoms due to mitochondrial toxicity. We sought to identify the currently recommended regimen to prevent mother-to-child transmission that optimally balances risks of pediatric HIV infection and neurologic mitochondrial toxicity.
Design: Published MTCT and mitochondrial toxicity data were used in a decision analytic model of MTCT among women in sub-Saharan Africa.
Methods: We investigated the HIV and mitochondrial toxicity risks associated with no antiretroviral prophylaxis and five recommended regimens ranging from single-dose nevirapine to three-drug antiretroviral therapy (ART). Sensitivity analyses varied all parameters, including infant feeding strategy and the disability of mitochondrial toxicity relative to HIV. Results: Provision of no antiretroviral drugs is the least effective and least toxic strategy, with 18-month HIV risk of 30.4% and mitochondrial toxicity risk of 0.2% (breastfed infants). With increasing drug number and duration, HIV risk decreases markedly (to 4.9% with three-drug ART), but mitochondrial toxicity risk also increases (to 2.2%, also with three-drug ART). Despite increased toxicity, three-drug ART minimizes total adverse pediatric outcomes (HIV plus mitochondrial toxicity), unless the highest published risks are true for both HIV and mitochondrial toxicity, or the disability from mitochondrial toxicity exceeds 6.4 times that of HIV infection.
Conclusion: The risk of pediatric mitochondrial toxicity from effective regimens to prevent mother-to-child transmission is at least an order of magnitude lower than the risk of HIV infection associated with less-effective regimens. Concern regarding mitochondrial toxicity should not currently limit the use of three-drug ART to prevent mother-to-child transmission where it is available. (C) 2008 Wolters Kluwer Health | Lippincott Williams & Wilkins
C1 [Ciaranello, Andrea L.; Freedberg, Kenneth A.; Walensky, Rochelle P.] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
[Freedberg, Kenneth A.; Walensky, Rochelle P.] Massachusetts Gen Hosp, Div Gen Med, Dept Med, Boston, MA 02114 USA.
[Lockman, Shahin; Walensky, Rochelle P.] Brigham & Womens Hosp, Div Infect Dis, Boston, MA 02115 USA.
[Freedberg, Kenneth A.; Walensky, Rochelle P.] Harvard Univ, Sch Med, Ctr AIDS Res, Boston, MA USA.
[Seage, George R., III] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Freedberg, Kenneth A.; Weinstein, Milton C.] Harvard Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA 02115 USA.
[Lockman, Shahin] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
RP Ciaranello, AL (reprint author), Massachusetts Gen Hosp, Div Infect Dis, 50 Staniford St,9th Floor, Boston, MA 02114 USA.
EM aciaranello@partners.org
OI Walensky, Rochelle P./0000-0002-8795-379X
FU National Institute of Allergy and Infectious Disease [T32 A107433, R01
A1058736, 11-37 A142006-10A1, U01 Al 069456-01]; National Institute of
Child Health and Human Development [U01 HD052102-03, K01 HD044391];
Doris Duke Charitable Foundation
FX The authors gratefully acknowledge Jennifer Chu, BS, and Brandon Morris,
BA, for assistance with manuscript preparation. Funding for this work
was provided by the National Institute of Allergy and Infectious Disease
[T32 A107433 (A.L.C.; PI: K.A.F.); R01 A1058736 and 11-37 A142006-10A1
(K.A.E, M.C.W, R.P.W); and U01 Al 069456-01 (S.L.)]; the National
Institute of Child Health and Human Development [Cooperative Agreement
U01 HD052102-03 (G.R.S.); K01 HD044391 (S.L.)]; and the Doris Duke
Charitable Foundation [Clinical Scientist Development Award (R.P.W)].
NR 95
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U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0269-9370
J9 AIDS
JI Aids
PD NOV 12
PY 2008
VL 22
IS 17
BP 2359
EP 2369
DI 10.1097/QAD.0b013e3283189bd7
PG 11
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 377SH
UT WOS:000261270400016
PM 18981776
ER
PT J
AU Sesso, HD
Buring, JE
Christen, WG
Kurth, T
Belanger, C
MacFadyen, J
Bubes, V
Manson, JE
Glynn, RJ
Gaziano, JM
AF Sesso, Howard D.
Buring, Julie E.
Christen, William G.
Kurth, Tobias
Belanger, Charlene
MacFadyen, Jean
Bubes, Vadim
Manson, Joann E.
Glynn, Robert J.
Gaziano, J. Michael
TI Vitamins E and C in the Prevention of Cardiovascular Disease in Men The
Physicians' Health Study II Randomized Controlled Trial
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID CORONARY-HEART-DISEASE; PLACEBO-CONTROLLED TRIAL; NUTRITION EXAMINATION
SURVEY; LONG-TERM SUPPLEMENTATION; BETA-CAROTENE; ANTIOXIDANT VITAMINS;
MYOCARDIAL-INFARCTION; POSTMENOPAUSAL WOMEN; SECONDARY PREVENTION;
ALPHA-TOCOPHEROL
AB Context Basic research and observational studies suggest vitamin E or vitamin C may reduce the risk of cardiovascular disease. However, few long- term trials have evaluated men at initially low risk of cardiovascular disease, and no previous trial in men has examined vitamin C alone in the prevention of cardiovascular disease.
Objective To evaluate whether long- term vitamin E or vitamin C supplementation decreases the risk of major cardiovascular events among men.
Design, Setting, and Participants The Physicians' Health Study II was a randomized, double- blind, placebo- controlled factorial trial of vitamin E and vitamin C that began in 1997 and continued until its scheduled completion on August 31, 2007. There were 14 641 US male physicians enrolled, who were initially aged 50 years or older, including 754 men ( 5.1%) with prevalent cardiovascular disease at randomization.
Intervention Individual supplements of 400 IU of vitamin E every other day and 500 mg of vitamin C daily.
Main Outcome Measures A composite end point of major cardiovascular events ( nonfatal myocardial infarction, nonfatal stroke, and cardiovascular disease death).
Results During a mean follow- up of 8 years, there were 1245 confirmed major cardiovascular events. Compared with placebo, vitamin E had no effect on the incidence of major cardiovascular events ( both active and placebo vitamin E groups, 10.9 events per 1000 person- years; hazard ratio [ HR], 1.01 [ 95% confidence interval {CI}, 0.90- 1.13]; P=. 86), as well as total myocardial infarction ( HR, 0.90 [ 95% CI, 0.75- 1.07]; P=. 22), total stroke ( HR, 1.07 [ 95% CI, 0.89- 1.29]; P=. 45), and cardiovascular mortality ( HR, 1.07 [ 95% CI, 0.90- 1.28]; P=. 43). There also was no significant effect of vitamin C on major cardiovascular events ( active and placebo vitamin E groups, 10.8 and 10.9 events per 1000 person-years, respectively; HR, 0.99 [ 95% CI, 0.89- 1.11]; P=. 91), as well as total myocardial infarction ( HR, 1.04[ 95% CI, 0.87- 1.24]; P=. 65), total stroke ( HR, 0.89[ 95% CI, 0.74- 1.07]; P=. 21), and cardiovascular mortality ( HR, 1.02 [ 95% CI, 0.85- 1.21]; P=. 86). Neither vitamin E ( HR, 1.07 [ 95% CI, 0.97- 1.18]; P=. 15) nor vitamin C ( HR, 1.07 [ 95% CI, 0.97-1.18]; P=. 16) had a significant effect on total mortality but vitamin E was associated with an increased risk of hemorrhagic stroke ( HR, 1.74 [ 95% CI, 1.04- 2.91]; P=. 04).
Conclusions In this large, long- term trial of male physicians, neither vitamin E nor vitamin C supplementation reduced the risk of major cardiovascular events. These data provide no support for the use of these supplements for the prevention of cardiovascular disease in middle- aged and older men.
Trial Registration clinicaltrials. gov Identifier: NCT00270647.
C1 [Sesso, Howard D.; Buring, Julie E.; Christen, William G.; Kurth, Tobias; Belanger, Charlene; MacFadyen, Jean; Bubes, Vadim; Manson, Joann E.; Glynn, Robert J.; Gaziano, J. Michael] Brigham & Womens Hosp, Dept Med, Div Prevent Med, Boston, MA 02215 USA.
[Sesso, Howard D.; Buring, Julie E.; Kurth, Tobias; Gaziano, J. Michael] Brigham & Womens Hosp, Dept Med, Div Aging, Boston, MA 02215 USA.
[Gaziano, J. Michael] Brigham & Womens Hosp, Dept Med, Div Cardiovasc Dis, Boston, MA 02215 USA.
[Buring, Julie E.] Harvard Univ, Sch Med, Dept Ambulatory Care & Prevent, Boston, MA USA.
[Sesso, Howard D.; Buring, Julie E.; Kurth, Tobias; Manson, Joann E.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Gaziano, J. Michael] VA Boston Healthcare Syst, Boston, MA USA.
RP Sesso, HD (reprint author), Brigham & Womens Hosp, Dept Med, Div Prevent Med, 900 Commonwealth Ave E, Boston, MA 02215 USA.
EM hsesso@hsph.harvard.edu
RI Kurth, Tobias/A-9243-2012
OI Kurth, Tobias/0000-0001-7169-2620
FU National Institutes of Health (Bethesda, Maryland) [CA 97193, CA 34944,
CA 40360, HL 26490, HL 34595]; BASF Corporation (Florham Park, New
Jersey)
FX This work was supported by grants CA 97193, CA 34944, CA 40360, HL
26490, and HL 34595 from the National Institutes of Health (Bethesda,
Maryland), and an investigator-initiated grant from BASF Corporation
(Florham Park, New Jersey). Study agents and packaging were provided by
BASF Corporation, Wyeth Pharmaceuticals (Madison, New Jersey), and DSM
Nutritional Products Inc (formerly Roche Vitamins) (Parsippany, New
Jersey).
NR 59
TC 368
Z9 385
U1 3
U2 42
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 12
PY 2008
VL 300
IS 18
BP 2123
EP 2133
DI 10.1001/jama.2008.600
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 370WM
UT WOS:000260793800022
PM 18997197
ER
PT J
AU Metin, C
Vallee, RB
Rakic, P
Bhide, PG
AF Metin, Christine
Vallee, Richard B.
Rakic, Pasko
Bhide, Pradeep G.
TI Modes and Mishaps of Neuronal Migration in the Mammalian Brain
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID LATERAL GANGLIONIC EMINENCE; NERVOUS-SYSTEM DEVELOPMENT; LISSENCEPHALY
GENE LIS1; ONSET TORSION DYSTONIA; CYTOPLASMIC DYNEIN; CEREBRAL-CORTEX;
CELL-MIGRATION; PRENATAL EXPOSURE; CORTICAL DEVELOPMENT; GABAERGIC
NEURONS
AB The ability of neurons to migrate to their appropriate positions in the developing brain is critical to brain architecture and function. Recent research has elucidated different modes of neuronal migration and the involvement of a host of signaling factors in orchestrating the migration, as well as vulnerabilities of this process to environmental and genetic factors. Here we discuss the role of cytoskeleton, motor proteins, and mechanisms of nuclear translocation in radial and tangential migration of neurons. We will also discuss how these and other events essential for normal migration of neurons can be disrupted by genetic and environmental factors that contribute to neurological disease in humans.
C1 [Metin, Christine] INSERM, Inst Fer Moulin, UMR S 839, F-75005 Paris, France.
[Vallee, Richard B.] Columbia Univ, Dept Pathol, New York, NY 10032 USA.
[Rakic, Pasko] Yale Univ, Sch Med, Dept Neurobiol, New Haven, CT 06520 USA.
[Bhide, Pradeep G.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, Boston, MA 02129 USA.
RP Bhide, PG (reprint author), Massachusetts Gen Hosp, 149 13th St, Charlestown, MA 02129 USA.
EM bhide@helix.mgh.harvard.edu
RI Metin, Christine/E-4995-2017
FU NIDA NIH HHS [R01 DA020796-03, R01 DA020796]; NINDS NIH HHS [P01
NS037409, P01 NS037409-08, P30 NS045776, P30 NS045776-05, R01 NS043426,
R01 NS043426-05]
NR 78
TC 75
Z9 75
U1 1
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 NOV 12
PY 2008
VL 28
IS 46
BP 11746
EP 11752
DI 10.1523/JNEUROSCI.3860-08.2008
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 371JM
UT WOS:000260827600002
PM 19005035
ER
PT J
AU Kuznetsova, MS
Higgs, MH
Spain, WJ
AF Kuznetsova, Marina S.
Higgs, Matthew H.
Spain, William J.
TI Adaptation of Firing Rate and Spike-Timing Precision in the Avian
Cochlear Nucleus
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE sound localization; nucleus magnocellularis; potassium channel;
phase-locking; spike-timing precision; coincidence detection
ID INTERAURAL TIME DIFFERENCES; STEM AUDITORY NUCLEI; INACTIVATING
POTASSIUM CURRENT; NEOCORTICAL PYRAMIDAL NEURONS; BRAIN-STEM;
COINCIDENCE DETECTION; TEMPORAL INTEGRATION; MEMBRANE-PROPERTIES; BARN
OWL; FEEDFORWARD INHIBITION
AB Adaptation is commonly defined as a decrease in response to a constant stimulus. In the auditory system such adaptation is seen at multiple levels. However, the first-order central neurons of the interaural time difference detection circuit encode information in the timing of spikes rather than the overall firing rate. We investigated adaptation during in vitro whole-cell recordings from chick nucleus magnocellularis neurons. Injection of noisy, depolarizing current caused an increase in firing rate and a decrease in spike time precision that developed over similar to 20 s. This adaptation depends on sustained depolarization, is independent of firing, and is eliminated by alpha-dendrotoxin (0.1 mu M), implicating slow inactivation of low-threshold voltage-activated K+ channels as its mechanism. This process may alter both firing rate and spike-timing precision of phase-locked inputs to coincidence detector neurons in nucleus laminaris and thereby adjust the precision of sound localization.
C1 [Kuznetsova, Marina S.; Higgs, Matthew H.; Spain, William J.] Univ Washington, Dept Physiol & Biophys, Seattle, WA 98105 USA.
[Kuznetsova, Marina S.] Univ Washington, Interdisciplinary Grad Program Neurobiol & Behav, Seattle, WA 98105 USA.
[Spain, William J.] Univ Washington, Dept Neurol, Seattle, WA 98105 USA.
[Spain, William J.] Vet Affairs Puget Sound Hlth Care Syst, Neurol Sect, Seattle, WA 98108 USA.
RP Spain, WJ (reprint author), Neurol 127,1660 S Columbian Way, Seattle, WA 98108 USA.
EM spain@u.washington.edu
FU Veterans Affairs Merit Review; National Institute on Deafness and Other
Communication Disorders [5F31DC009176]
FX This work was supported by a Veterans Affairs Merit Review (W.J.S.) and
by National Research Service Award 5F31DC009176 from the National
Institute on Deafness and Other Communication Disorders (M.S.K.). We
thank Sean Slee, Adrienne Fairhall, Marc Binder, David Perkel, and Ed
Rubel for helpful discussions, Carol Robbins, and Sue Usher for
excellent technical assistance.
NR 79
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U1 1
U2 3
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 12
PY 2008
VL 28
IS 46
BP 11906
EP 11915
DI 10.1523/JNEUROSCI.3827-08.2008
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 371JM
UT WOS:000260827600023
PM 19005056
ER
PT J
AU Lee, PS
Patel, SR
Christiani, DC
Bajwa, E
Stossel, TP
Waxman, AB
AF Lee, Po-Shun
Patel, Sanjay R.
Christiani, David C.
Bajwa, Ednan
Stossel, Thomas P.
Waxman, Aaron B.
TI Plasma Gelsolin Depletion and Circulating Actin in Sepsis-A Pilot Study
SO PLOS ONE
LA English
DT Article
AB Background: Depletion of the circulating actin-binding protein, plasma gelsolin (pGSN) has been described in septic patients and animals. We hypothesized that the extent of pGSN reduction correlates with outcomes of septic patients and that circulating actin is a manifestation of sepsis.
Methodology/Principal Findings: We assayed pGSN in plasma samples from non-surgical septic patients identified from a pre-existing database which prospectively enrolled patients admitted to adult intensive care units at an academic hospital. We identified 21 non-surgical septic patients for the study. Actinemia was detected in 17 of the 21 patients, suggesting actin released into circulation from injured tissues is a manifestation of sepsis. Furthermore, we documented the depletion of pGSN in human clinical sepsis, and that the survivors had significantly higher pGSN levels than the non-survivors (163 +/- 47 mg/L vs. 89 +/- 48 mg/L, p = 0.01). pGSN levels were more strongly predictive of 28-day mortality than APACHE III scores. For every quartile reduction in pGSN, the odds of death increased 3.4-fold.
Conclusion: We conclude that circulating actin and pGSN deficiency are associated with early sepsis. The degree of pGSN deficiency correlates with sepsis mortality. Reversing pGSN deficiency may be an effective treatment for sepsis.
C1 [Lee, Po-Shun] Brigham & Womens Hosp, Div Pulm & Crit Care, Boston, MA 02115 USA.
[Lee, Po-Shun; Christiani, David C.; Bajwa, Ednan; Stossel, Thomas P.; Waxman, Aaron B.] Harvard Univ, Sch Med, Boston, MA USA.
[Lee, Po-Shun; Stossel, Thomas P.] Brigham & Womens Hosp, Translat Med Div, Boston, MA USA.
[Patel, Sanjay R.] Case Western Reserve Univ, Univ Hosp Cleveland, Div Pulmonary & Critical Care Med, Cleveland, OH USA.
[Christiani, David C.; Bajwa, Ednan; Waxman, Aaron B.] Mass Gen Hosp, Pulmonary & Critical Care Unit, Boston, MA USA.
RP Lee, PS (reprint author), Brigham & Womens Hosp, Div Pulm & Crit Care, 75 Francis St, Boston, MA 02115 USA.
EM plee4@partners.org
OI Patel, Sanjay/0000-0002-9142-5172
FU NIH [5R01HL074859-04]; AHA [0735620N]
FX NIH 5R01HL074859-04, AHA Scientist Development Grant 0735620N. The
funding institutions played no role in the designed of the study or in
the preparation of this manuscript.
NR 28
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Z9 37
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 NOV 12
PY 2008
VL 3
IS 11
AR e3712
DI 10.1371/journal.pone.0003712
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 432WW
UT WOS:000265166000012
PM 19002257
ER
PT J
AU Nosho, K
Irahara, N
Shima, K
Kure, S
Kirkner, GJ
Schernhammer, ES
Hazra, A
Hunter, DJ
Quackenbush, J
Spiegelman, D
Giovannucci, EL
Fuchs, CS
Ogino, S
AF Nosho, Katsuhiko
Irahara, Natsumi
Shima, Kaori
Kure, Shoko
Kirkner, Gregory J.
Schernhammer, Eva S.
Hazra, Aditi
Hunter, David J.
Quackenbush, John
Spiegelman, Donna
Giovannucci, Edward L.
Fuchs, Charles S.
Ogino, Shuji
TI Comprehensive Biostatistical Analysis of CpG Island Methylator Phenotype
in Colorectal Cancer Using a Large Population-Based Sample
SO PLOS ONE
LA English
DT Article
AB Background: The CpG island methylator phenotype (CIMP) is a distinct phenotype associated with microsatellite instability (MSI) and BRAF mutation in colon cancer. Recent investigations have selected 5 promoters (CACNA1G, IGF2, NEUROG1, RUNX3 and SOCS1) as surrogate markers for CIMP-high. However, no study has comprehensively evaluated an expanded set of methylation markers (including these 5 markers) using a large number of tumors, or deciphered the complex clinical and molecular associations with CIMP-high determined by the validated marker panel.
Metholodology/Principal Findings: DNA methylation at 16 CpG islands [the above 5 plus CDKN2A (p16), CHFR, CRABP1, HIC1, IGFBP3, MGMT, MINT1, MINT31, MLH1, p14 (CDKN2A/ARF) and WRN] was quantified in 904 colorectal cancers by real-time PCR (MethyLight). In unsupervised hierarchical clustering analysis, the 5 markers (CACNA1G, IGF2, NEUROG1, RUNX3 and SOCS1), CDKN2A, CRABP1, MINT31, MLH1, p14 and WRN were generally clustered with each other and with MSI and BRAF mutation. KRAS mutation was not clustered with any methylation marker, suggesting its association with a random methylation pattern in CIMP-low tumors. Utilizing the validated CIMP marker panel ( including the 5 markers), multivariate logistic regression demonstrated that CIMP-high was independently associated with older age, proximal location, poor differentiation, MSI-high, BRAF mutation, and inversely with LINE-1 hypomethylation and beta-catenin (CTNNB1) activation. Mucinous feature, signet ring cells, and p53-negativity were associated with CIMP-high in only univariate analysis. In stratified analyses, the relations of CIMP-high with poor differentiation, KRAS mutation and LINE-1 hypomethylation significantly differed according to MSI status.
Conclusions: Our study provides valuable data for standardization of the use of CIMP-high-specific methylation markers. CIMP-high is independently associated with clinical and key molecular features in colorectal cancer. Our data also suggest that KRAS mutation is related with a random CpG island methylation pattern which may lead to CIMP-low tumors.
C1 [Nosho, Katsuhiko; Irahara, Natsumi; Shima, Kaori; Kure, Shoko; Fuchs, Charles S.; Ogino, Shuji] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Kirkner, Gregory J.; Schernhammer, Eva S.; Hazra, Aditi; Hunter, David J.; Spiegelman, Donna; Giovannucci, Edward L.; Fuchs, Charles S.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Schernhammer, Eva S.] Applied Canc Res Inst Translat Res, Ludwig Boltzmann Inst Applied Canc Res, Vienna, Austria.
[Schernhammer, Eva S.; Hazra, Aditi; Hunter, David J.; Spiegelman, Donna; Giovannucci, Edward L.; Ogino, Shuji] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Quackenbush, John] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Biostat, Boston, MA USA.
[Quackenbush, John; Spiegelman, Donna] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Ogino, Shuji] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Pathol, Boston, MA USA.
RP Nosho, K (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
EM shuji_ogino@dfci.harvard.edu
FU U.S. National Institute of Health (NIH) [P01 CA87969, P01 CA55075, P50
CA127003, K07 CA122826]; Bennett Family Fund; Entertainment Industry
Foundation (EIF) through the EIF National Colorectal Cancer Research
Alliance (NCCRA); Japanese Society for Promotion of Science
FX This work was supported by U.S. National Institute of Health (NIH)
grants P01 CA87969, P01 CA55075, P50 CA127003 and K07 CA122826 (to
S.O.), and in part by grants from the Bennett Family Fund and from the
Entertainment Industry Foundation (EIF) through the EIF National
Colorectal Cancer Research Alliance (NCCRA). K.N. was supported by a
fellowship grant from the Japanese Society for Promotion of Science. The
content is solely the responsibility of the authors and does not
necessarily represent the official views of NCI or NIH. The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 50
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Z9 177
U1 2
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 12
PY 2008
VL 3
IS 11
AR e3698
DI 10.1371/journal.pone.0003698
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 432WW
UT WOS:000265166000004
PM 19002263
ER
PT J
AU Madani, N
Schon, A
Princiotto, AM
LaLonde, JM
Courter, JR
Soeta, T
Ng, D
Wang, LP
Brower, ET
Xiang, SH
Do Kwon, Y
Huang, CC
Wyatt, R
Kwong, PD
Freire, E
Smith, AB
Sodroski, J
AF Madani, Navid
Schoen, Arne
Princiotto, Amy M.
LaLonde, Judith M.
Courter, Joel R.
Soeta, Takahiro
Ng, Danny
Wang, Liping
Brower, Evan T.
Xiang, Shi-Hua
Do Kwon, Young
Huang, Chih-Chin
Wyatt, Richard
Kwong, Peter D.
Freire, Ernesto
Smith, Amos B., III
Sodroski, Joseph
TI Small-Molecule CD4 Mimics Interact with a Highly Conserved Pocket on
HIV-1 gp120
SO STRUCTURE
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; ENVELOPE GLYCOPROTEIN; RECEPTOR-BINDING;
MONOCLONAL-ANTIBODY; ACCURATE DOCKING; SITE; NEUTRALIZATION; DESIGN;
CCR5; MINIPROTEIN
AB Human immunodeficiency virus (HIV-1) interaction with the primary receptor, CD4, induces conformational changes in the viral envelope glycoproteins that allow binding to the CCR5 second receptor and virus entry into the host cell. The small molecule NBD-556 mimics CD4 by binding the gp120 exterior envelope glycoprotein, moderately inhibiting virus entry into CD4-expressing target cells and enhancing CCR5 binding and virus entry into CCR5-expressing cells lacking CD4. Studies of NBD-556 analogs and gp120 mutants suggest that (1) NBD-556 binds within the Phe 43 cavity, a highly conserved, functionally important pocket formed as gp120 assumes the CD4-bound conformation; (2) the NBD-556 phenyl ring projects into the Phe 43 cavity; (3) enhancement of CD4-independent infection by NBD-556 requires the induction of conformational changes in gp120; and (4) increased affinity of NBD-556 analogs for gp120 improves antiviral potency during infection of CD4-expressing cells.
C1 [Madani, Navid; Princiotto, Amy M.; Wang, Liping; Xiang, Shi-Hua; Sodroski, Joseph] Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA.
[Madani, Navid; Sodroski, Joseph] Harvard Univ, Sch Med, Dept Pathol, Div AIDS, Boston, MA 02115 USA.
[Schoen, Arne; Brower, Evan T.; Freire, Ernesto] Johns Hopkins Univ, Dept Biol, Baltimore, MD 21218 USA.
[LaLonde, Judith M.] Bryn Mawr Coll, Dept Chem, Bryn Mawr, PA 19010 USA.
[Courter, Joel R.; Soeta, Takahiro; Ng, Danny; Smith, Amos B., III] Univ Penn, Dept Chem, Philadelphia, PA 19104 USA.
[Do Kwon, Young; Huang, Chih-Chin; Wyatt, Richard; Kwong, Peter D.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Sodroski, Joseph] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
RP Sodroski, J (reprint author), Dana Farber Canc Inst, Dept Canc Immunol & AIDS, 44 Binney St,JFB 824, Boston, MA 02115 USA.
EM joseph_sodroski@dfci.harvard.edu
RI Kwon, Young Do/A-6957-2010; SOETA, Takahiro/E-7060-2015
OI SOETA, Takahiro/0000-0001-9883-4772
FU National Institutes of Health [GM56550, AI24755I60354]; International
AIDS Vaccine Initiative; William F. McCarty-Cooper
FX We thank Wayne Hendrickson and Irwin Chaiken for valuable discussion. We
thank Yvette McLaughlin and Elizabeth Carpelan for manuscript
preparation, and Jonathan Stuckey for preparation of figures. This study
was supported by the National Institutes of Health (Grants GM56550,
AI24755, and AI60354), the International AIDS Vaccine Initiative, and
William F. McCarty-Cooper.
NR 39
TC 100
Z9 102
U1 0
U2 19
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0969-2126
J9 STRUCTURE
JI Structure
PD NOV 12
PY 2008
VL 16
IS 11
BP 1689
EP 1701
DI 10.1016/j.str.2008.09.005
PG 13
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 374GQ
UT WOS:000261032200012
PM 19000821
ER
PT J
AU Becker, V
Sengupta, D
Ketteler, R
Ullmann, GM
Smith, JC
Klingmuller, U
AF Becker, Verena
Sengupta, Durba
Ketteler, Robin
Ullmann, G. Matthias
Smith, Jeremy C.
Klingmueller, Ursula
TI Packing Density of the Erythropoietin Receptor Transmembrane Domain
Correlates with Amplification of Biological Responses
SO BIOCHEMISTRY
LA English
DT Article
ID PRIMARY FAMILIAL POLYCYTHEMIA; SIGNAL-TRANSDUCTION; MEMBRANE-PROTEINS;
PROGENITOR CELLS; POINT MUTATION; DIMERIZATION; ACTIVATION;
OLIGOMERIZATION; GENE; ERYTHROCYTOSIS
AB The formation of signal-promoting dimeric or oligomeric receptor complexes at the cell surface is modulated by self-interaction of their transmembrane (TM) domains. To address the importance of TM domain packing density for receptor functionality, we examined a set of asparagine mutants in the TM domain of the erythropoietin receptor (EpoR). We identified EpoR-T242N as a receptor variant that is present at the cell surface similar to wild-type EpoR but lacks visible localization in vesicle-like structures and is impaired in efficient activation of specific signaling cascades. Analysis by a molecular modeling approach indicated an increased interhelical distance for the EpoR-T242N TM dimer. By employing the model, we designed additional mutants with increased or decreased packing volume and confirmed a correlation between packing volume and biological responsiveness. These results propose that the packing density of the TM domain provides a novel layer for fine-tuned regulation of signal transduction and cellular decisions.
C1 [Becker, Verena; Klingmueller, Ursula] German Canc Res Ctr, DKFZ ZMBH Alliance, Div Syst Biol Signal Transduct, D-6900 Heidelberg, Germany.
[Sengupta, Durba; Smith, Jeremy C.] Univ Heidelberg, Interdisciplinary Ctr Sci Comp, Heidelberg, Germany.
[Ketteler, Robin] Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Boston, MA 02114 USA.
[Ullmann, G. Matthias] Univ Bayreuth, Bayreuth, Germany.
[Smith, Jeremy C.] Univ Tennessee, ORNL Ctr Mol Biophys, Oak Ridge Natl Lab, Oak Ridge, TN 37831 USA.
RP Klingmuller, U (reprint author), German Canc Res Ctr, DKFZ ZMBH Alliance, Div Syst Biol Signal Transduct, D-6900 Heidelberg, Germany.
EM u.klingmueller@dkfz-heidelberg.de
RI smith, jeremy/B-7287-2012; Klingmuller, Ursula/G-8477-2013; Ullmann,
Matthias/H-1361-2014;
OI smith, jeremy/0000-0002-2978-3227; Klingmuller,
Ursula/0000-0001-9845-3099; Ullmann, Matthias/0000-0002-6350-798X;
Ketteler, Robin/0000-0002-2786-7291
FU European Commission Sixth Framework Programme COSBICS
[LSHG-CT-2004-512060]; Deutsche Forschungsgemeinschaft [DFG/Ke904]
FX This work was supported by the European Commission Sixth Framework
Programme COSBICS project (LSHG-CT-2004-512060) (to V.B.) and by the
Deutsche Forschungsgemeinschaft (DFG/Ke904) (to R. K.).
NR 49
TC 11
Z9 11
U1 0
U2 0
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD NOV 11
PY 2008
VL 47
IS 45
BP 11771
EP 11782
DI 10.1021/bi801425e
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 368JH
UT WOS:000260616900009
PM 18855427
ER
PT J
AU Jesser, C
Mucci, L
Farmer, D
Moon, C
Li, H
Gaziano, JM
Stampfer, M
Ma, J
Kantoff, P
AF Jesser, C.
Mucci, L.
Farmer, D.
Moon, C.
Li, H.
Gaziano, J. M.
Stampfer, M.
Ma, J.
Kantoff, P.
TI Effects of G/A polymorphism, rs266882, in the androgen response element
I of the PSA gene on prostate cancer risk, survival and circulating PSA
levels
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE prostate cancer; PSA gene; AREI-158 G/A polymorphism (rs266882);
androgen receptor; Physicians' Health Study
ID GROWTH-FACTOR-I; ANTIGEN LEVELS; RECEPTOR GENE; SUSCEPTIBILITY; BINDING;
PSA/KLK3; REPEATS; REGION; CELLS
AB Prostate-specific antigen (PSA) is a protease produced in the prostate that cleaves insulin-like growth factor binding protein-3 and other proteins. Production is mediated by the androgen receptor (AR) binding to the androgen response elements (ARE) in the promoter region of the PSA gene. Studies of a single nucleotide polymorphism (PSA - 158 G/A, rs266882) in AREI of the PSA gene have been conflicting for risk of prostate cancer and effect on plasma PSA levels. In this nested case - control analysis of 500 white cases and 676 age- and smoking-matched white controls in the Physicians' Health Study we evaluated the association of rs266882 with risk and survival of prostate cancer and prediagnostic total and free PSA plasma levels, alone or in combination with AR CAG repeats. We used conditional logistic regression, linear regression and Cox regression, and found no significant associations between rs266882 (GG allele vs AA allele) and overall prostate cancer risk (RR = 1.21, 95% confidence intervals (CI): 0.88 - 1.67) or prostate cancer-specific survival (RR = 0.94, 95% CI: 0.56 - 1.58). Similarly, no associations were found among high grade or advanced stage tumours, or by calendar year of diagnosis. There was no significant association between rs266882 and baseline total or free PSA levels or the AR CAG repeats, nor any interaction associated with prostate cancer risk. Meta-analysis of 12 studies of rs266882 and overall prostate cancer risk was null.
C1 [Jesser, C.; Mucci, L.; Gaziano, J. M.; Stampfer, M.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Mucci, L.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA.
[Farmer, D.; Moon, C.; Kantoff, P.] Dana Farber Canc Inst, Div Solid Tumor Oncol, Lank Ctr Genitourinary Oncol, Boston, MA 02115 USA.
[Gaziano, J. M.] Brigham & Womens Hosp, Div Aging, Boston, MA 02115 USA.
RP Mucci, L (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Channing Lab, 181 Longwood Ave,3rd Floor, Boston, MA 02115 USA.
EM lorelei.mucci@channing.harvard.edu
FU National Cancer Institute [CA-34944, CA-40360, CA-097193]; National
Heart, Lung and Blood Institute, Bethesda, MD [HL-26490, HL-34595];
Cancer Epidemiology [T32 CA 09001]; NCI/NIH [R01 CA 090598]
FX We thank the participants of the Physicians' Health Study for their
longstanding commitment and participation in the study. The Physicians'
Health Study is supported by grants CA-34944, CA-40360 and CA-097193
from the National Cancer Institute and grants HL-26490 and HL-34595 from
the National Heart, Lung and Blood Institute, Bethesda, MD. Ms Jesser
was supported by the National Research Service Award Training Program in
Cancer Epidemiology (T32 CA 09001). Project supported by R01 CA 090598
(NCI/NIH).
NR 28
TC 17
Z9 17
U1 0
U2 2
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 NOV 11
PY 2008
VL 99
IS 10
BP 1743
EP 1747
DI 10.1038/sj.bjc.6604690
PG 5
WC Oncology
SC Oncology
GA 371LI
UT WOS:000260832400026
PM 18827812
ER
PT J
AU Velagaleti, RS
Pencina, MJ
Murabito, JM
Wang, TJ
Parikh, NI
D'Agostino, RB
Levy, D
Kannel, WB
Vasan, RS
AF Velagaleti, Raghava S.
Pencina, Michael J.
Murabito, Joanne M.
Wang, Thomas J.
Parikh, Nisha I.
D'Agostino, Ralph B.
Levy, Daniel
Kannel, William B.
Vasan, Ramachandran S.
TI Long-Term Trends in the Incidence of Heart Failure After Myocardial
Infarction
SO CIRCULATION
LA English
DT Article
DE heart failure; myocardial infarction; prognosis; risk factors;
epidemiology
ID LEFT-VENTRICULAR DYSFUNCTION; TEMPORAL TRENDS; FRAMINGHAM; DISEASE;
EPIDEMIOLOGY; PERSPECTIVE; MORTALITY; SURVIVAL; RATES; DEATH
AB Background - Although mortality after myocardial infarction (MI) has declined in the United States in recent decades, there have been few community-based investigations of the long-term trends in the incidence of heart failure after MI, and their results appear to be conflicting.
Methods and Results - We evaluated 676 Framingham Heart Study participants between 45 and 85 years of age (mean age 67 years, 34% women) who developed a first MI between 1970 and 1999. We assessed the incidence rates of heart failure and of death without heart failure in each of 3 decades (1970 to 1979, 1980 to 1989, and 1990 to 1999). We estimated the multivariable-adjusted risk of events in the latter 2 decades, with the period 1970 to 1979 serving as the referent. The 30-day incidence of heart failure after MI rose from 10% in 1970 to 1979 to 23.1% in 1990 to 1999 (P for trend 0.003), whereas 30-day mortality after MI declined from 12.2% (1970 to 1979) to 4.1% (1990 to 1999). The 5-year incidence of heart failure after MI rose from 27.6% in 1970 to 1979 to 31.9% in 1990 to 1999 (P for trend 0.02), whereas 5-year mortality after MI declined from 41.1% (1970 to 1979) to 17.3% (1990 to 1999). In multivariable analyses, compared with the period 1970 to 1979, we observed higher 30-day (risk ratio 2.05, 95% confidence interval 1.25 to 3.36) and 5-year (risk ratio 1.74, 95% confidence interval 1.07 to 2.84) risks of heart failure in the decade 1990 to 1999. These trends were accompanied by lower 30-day (risk ratio 0.21, 95% confidence interval 0.09 to 0.47) and 5-year (risk ratio 0.31, 95% confidence interval 0.18 to 0.54) mortality rates in 1990 to 1999.
Conclusions - In the present community-based sample, we observed an increase in the incidence of heart failure in recent decades that paralleled the decrease in mortality after MI. (Circulation. 2008; 118: 2057-2062.)
C1 [Velagaleti, Raghava S.; Pencina, Michael J.; Murabito, Joanne M.; Wang, Thomas J.; Parikh, Nisha I.; D'Agostino, Ralph B.; Levy, Daniel; Kannel, William B.; Vasan, Ramachandran S.] NHLBI, Framingham Heart Study, Framingham, MA 01702 USA.
[Wang, Thomas J.] Harvard Univ, Sch Med, Dept Med, Massachusetts Gen Hosp,Div Cardiol, Boston, MA USA.
[Pencina, Michael J.; D'Agostino, Ralph B.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
[Levy, Daniel] NHLBI, Ctr Populat Studies, Bethesda, MD 20892 USA.
[Levy, Daniel; Vasan, Ramachandran S.] Boston Univ, Sch Med, Prevent Med Sect, Boston Med Ctr, Boston, MA 02118 USA.
[Levy, Daniel; Vasan, Ramachandran S.] Boston Univ, Sch Med, Cardiol Sect, Boston Med Ctr, Boston, MA 02118 USA.
[Murabito, Joanne M.] Boston Univ, Sch Med, Gen Internal Med Sect, Boston Med Ctr, Boston, MA 02118 USA.
RP Vasan, RS (reprint author), NHLBI, Framingham Heart Study, 73 Mt Wayte Ave, Framingham, MA 01702 USA.
EM vasan@bu.edu
OI Murabito, Joanne/0000-0002-0192-7516; Ramachandran,
Vasan/0000-0001-7357-5970
FU National Institutes of Health/National Heart, Lung, and Blood Institute
[N01-HC-25195, 2K24HL4334]
FX This work was supported by National Institutes of Health/National Heart,
Lung, and Blood Institute contract No. N01-HC-25195 and 2K24HL4334 (Dr
Vasan).
NR 23
TC 187
Z9 196
U1 1
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 11
PY 2008
VL 118
IS 20
BP 2057
EP 2062
DI 10.1161/CIRCULATIONAHA.108.784215
PG 6
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 370XG
UT WOS:000260795800007
PM 18955667
ER
PT J
AU Terranova, R
Yokobayashi, S
Stadler, MB
Otte, AP
van Lohuizen, M
Orkin, SH
Peters, AHFM
AF Terranova, Rrni
Yokobayashi, Shihori
Stadler, Michael B.
Otte, Arie P.
van Lohuizen, Maarten
Orkin, Stuart H.
Peters, Antoine H. F. M.
TI Polycomb Group Proteins Ezh2 and Rnf2 Direct Genomic Contraction and
Imprinted Repression in Early Mouse Embryos
SO DEVELOPMENTAL CELL
LA English
DT Article
ID NONCODING RNAS; EPIGENETIC DYNAMICS; HISTONE METHYLATION; DNA
METHYLATION; X-INACTIVATION; CONTROL REGION; STEM-CELLS; GENES;
RECRUITMENT; COMPLEXES
AB Genomic imprinting regulates parental-specific expression of particular genes and is required for normal mammalian development. How imprinting is established during development is, however, largely unknown. To address this question, we studied the mouse Kcnq1 imprinted cluster at which paternal-specific silencing depends on expression of the non-coding RNA Kcnq1ot1. We show that Kcnq1ot1 is expressed from the zygote stage onward and rapidly associates with chromatin marked by Polycomb group (PcG) proteins and repressive histone modifications, forming a discrete repressive nuclear compartment devoid of RNA polymerase II, a configuration also observed at the Igf2r imprinted cluster. In this compartment, the paternal Kcnq1 cluster exists in a three-dimensionally contracted state. In vivo the PcG proteins Ezh2 and Rnf2 are independently required for genomic contraction and imprinted silencing. We propose that the formation of a parental-specific higher-order chromatin organization renders imprint clusters competent for monoallelic silencing and assign a central role to PcG proteins in this process.
C1 [Terranova, Rrni; Yokobayashi, Shihori; Stadler, Michael B.; Peters, Antoine H. F. M.] Friedrich Miescher Inst Biomed Res, CH-4058 Basel, Switzerland.
[Otte, Arie P.] Univ Amsterdam, Swammerdam Inst Life Sci, NL-1098 SM Amsterdam, Netherlands.
[van Lohuizen, Maarten] Netherlands Canc Inst, Div Mol Genet, NL-1066 CX Amsterdam, Netherlands.
[van Lohuizen, Maarten] Netherlands Canc Inst, Ctr Biomed Genet, NL-1066 CX Amsterdam, Netherlands.
[Orkin, Stuart H.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat,Div Hematol Oncol,Childrens Hosp, Boston, MA 02115 USA.
RP Peters, AHFM (reprint author), Friedrich Miescher Inst Biomed Res, Maulbeerstr 66, CH-4058 Basel, Switzerland.
EM antoine.peters@fmi.ch
FU HFSP; Novartis Research Foundation; NoE network
FX We thank Miguel Vidal, Haruhiko Koseki, Christian Seiser, and Thomas
Jenu-wein for providing antisera; Barbara Knowles and Robert Fell for
making available Zp3-Cre transgenic mice and SD7P11 congenic mice,
respectively. We thank Edith Heard and Julie Chaumeil for helpful
technical advice. We acknowledge FMI colleagues Laurent Gelman. Jens
Rietdorf, and Patrick Schwarb for excellent microscopy and imaging
assistance; Aaron Ponti for generating the random-spot algorithms Fred
Zilbermann and Carolin Kolb for technical assistance and the FMI animal
facility. We thank Ruth Williams, Philip Hublitz, and Dirk Schblbeler
for critical reading of the manuscript and all members of the Peters lab
for fruitful discussions. R.T., S.Y., and A.H.F.M.P. conceived and
designed the experiments. R.T. and S.Y. performed the experiments. R.T.,
S.Y., M.B.S., and A.H.F.M.P. analyzed the data. A.P.O. provided
antibodies; NI and S.H.O provided Rnf2 and Ezh2 conditionally deficient
mice, respectively. R.T. and A.H.F.M.P. wrote the manuscript. S.Y. is a
recipient of a HFSP fellowship. Research in the Peters lab is supported
by the Novartis Research Foundation and the NoE network "The Epigenome."
NR 37
TC 181
Z9 197
U1 1
U2 2
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1534-5807
J9 DEV CELL
JI Dev. Cell
PD NOV 11
PY 2008
VL 15
IS 5
BP 668
EP 679
DI 10.1016/j.devcel.2008.08.015
PG 12
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA 371XW
UT WOS:000260867000008
PM 18848501
ER
PT J
AU Kalinchuk, AV
McCarley, RW
Stenberg, D
Porkka-Heiskanen, T
Basheer, R
AF Kalinchuk, A. V.
McCarley, R. W.
Stenberg, D.
Porkka-Heiskanen, T.
Basheer, R.
TI THE ROLE OF CHOLINERGIC BASAL FOREBRAIN NEURONS IN ADENOSINE-MEDIATED
HOMEOSTATIC CONTROL OF SLEEP: LESSONS FROM 192 IGG-SAPORIN LESIONS
SO NEUROSCIENCE
LA English
DT Article
DE sleep deprivation; cholinergic lesion; delta activity; stereology; rat;
immunotoxin
ID BEHAVIORAL STATE; RECOVERY SLEEP; NGF RECEPTOR; TIME-COURSE; WAKE CYCLE;
C-FOS; RAT; MICRODIALYSIS; DEPRIVATION; WAKEFULNESS
AB A topic of high current interest and controversy is the basis of the homeostatic sleep response, the increase in non-rapid-eye-movement (NREM) sleep and NREM-delta activity following sleep deprivation (SD). Adenosine, which accumulates in the cholinergic basal forebrain (BF) during SD, has been proposed as one of the important homeostatic sleep factors. It is suggested that sleep-inducing effects of adenosine are mediated by inhibiting the wake-active neurons of the BF, including cholinergic neurons. Here we examined the association between SD-induced adenosine release, the homeostatic sleep response and the survival of cholinergic neurons in the BF after injections of the immunotoxin 192 immunoglobulin G (IgG)-saporin (saporin) in rats. We correlated SD-induced adenosine level in the BF and the homeostatic sleep response with the cholinergic cell loss 2 weeks after local saporin injections into the BF, as well as 2 and 3 weeks after i.c.v. saporin injections.
Two weeks after local saporin injection there was an 88% cholinergic cell loss, coupled with nearly complete abolition of the SD-induced adenosine increase in the BF, the homeostatic sleep response, and the sleep-inducing effects of BF adenosine infusion.
Two weeks after i.c.v. saporin injection there was a 59% cholinergic cell loss, correlated with significant increase in SD-induced adenosine level in the BF and an intact sleep response. Three weeks after i.c.v. saporin injection there was an 87% cholinergic cell loss, nearly complete abolition of the SD-induced adenosine increase in the BF and the homeostatic response, implying that the time course of i.c.v. saporin lesions is a key variable in interpreting experimental results.
Taken together, these results strongly suggest that cholinergic neurons in the BF are important for the SD-induced increase in adenosine as well as for its sleep-inducing effects and play a major, although not exclusive, role in sleep homeostasis. (C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.
C1 [Kalinchuk, A. V.; McCarley, R. W.; Basheer, R.] Harvard Univ, Sch Med, Dept Psychiat, Neurosci Lab, Boston, MA 02132 USA.
[Kalinchuk, A. V.; McCarley, R. W.; Basheer, R.] VA Boston Healthcare Syst, Boston, MA 02132 USA.
[Stenberg, D.; Porkka-Heiskanen, T.] Univ Helsinki, Inst Biomed, Helsinki, Finland.
RP Kalinchuk, AV (reprint author), Harvard Univ, Sch Med, Dept Psychiat, Neurosci Lab, 1400 VFW Pkwy, Boston, MA 02132 USA.
EM anna_kalinchuk@hms.harvard.edu
RI McCarley, Robert/N-5562-2014
OI McCarley, Robert/0000-0001-5705-7495
FU Department of Veterans Affairs Medical Research Service; ESRS
Sanoff-Synthelabo Research; National Institute of Mental Health
[NIMH39683]; Academy of Finland, European Union [LSHM-CT-2005-518189];
European Union [MCRTN-CT-2004-512362]; Finska Lakaresallskapet, the
Sigrid Juselius Foundation
FX We dedicate this paper to the late Dr. Dag Stenberg. This work was
supported by the Department of Veterans Affairs Medical Research Service
Award to R.B., the ESRS Sanoff-Synthelabo Research Award to A. V. K.,
the National Institute of Mental Health (NIMH39683) to R. W.M., and the
Academy of Finland, European Union grant LSHM-CT-2005-518189, European
Union grant MCRTN-CT-2004-512362, Finska Lakaresallskapet, the Sigrid
Juselius Foundation to T.P.-H. We thank Drs. James T. McKenna and Robert
E. Strecker for helpful discussion. We thank Dr. rer. Nat. Ernst Mecke,
Mrs. Pirjo Saarelainen and Mrs. Sari Levo-Siitari for excellent
technical assistance and Peter Hirsch and Dewayne Williams for help with
animal care.
NR 60
TC 42
Z9 43
U1 0
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4522
J9 NEUROSCIENCE
JI Neuroscience
PD NOV 11
PY 2008
VL 157
IS 1
BP 238
EP 253
DI 10.1016/j.neuroscience.2008.08.040
PG 16
WC Neurosciences
SC Neurosciences & Neurology
GA 369UE
UT WOS:000260718600024
PM 18805464
ER
PT J
AU Irazoqui, JE
Ng, A
Xavier, RJ
Ausubel, FM
AF Irazoqui, Javier E.
Ng, Aylwin
Xavier, Ramnik J.
Ausubel, Frederick M.
TI Role for beta-catenin and HOX transcription factors in Caenorhabditis
elegans and mammalian host epithelial-pathogen interactions
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE homeobox protein; host-pathogen interactions; Staphylococcus aureus
ID NF-KAPPA-B; INNATE IMMUNITY; C-ELEGANS; STAPHYLOCOCCUS-AUREUS; GENES;
PATHWAY; WNT; CELLS; MODEL; DIFFERENTIATION
AB We used the model nematode Caenorhabditis elegans infected with the human pathogen Staphylococcus aureus to identify components of epithelial immunity. Transcriptional profiling and reverse genetic analysis revealed that mutation of the C elegans beta-catenin homolog bar-1 or the downstream homeobox gene egl-5 results in a defective response and hypersensitivity to S. aureus infection. Epistasis analysis showed that bar-1 and egi-5 function in parallel to previously described C elegans immune-response pathways. Overexpression of human homologs of egl-5 modulated NF-kappa B-dependent TLR2 signaling in epithelial cells. These data suggest that beta-catenin and homeobox genes play an important and conserved role in innate immune defense.
C1 [Irazoqui, Javier E.; Ausubel, Frederick M.] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
[Irazoqui, Javier E.; Ausubel, Frederick M.] Massachusetts Gen Hosp, Dept Genet, Boston, MA 02114 USA.
[Irazoqui, Javier E.; Ng, Aylwin; Xavier, Ramnik J.; Ausubel, Frederick M.] Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Boston, MA 02114 USA.
RP Ausubel, FM (reprint author), Massachusetts Gen Hosp, Dept Mol Biol, Simches Res Bldg,185 Cambridge St CPZN7250, Boston, MA 02114 USA.
EM ausubel@molbio.mgh.harvard.edu
RI Irazoqui, Javier/A-8028-2013;
OI Irazoqui, Javier/0000-0001-6553-1329
FU National Institutes of Health [DK43351, DK57521, AI062773, AI064332];
National Center for Research Resources; Jane Coffin Childs Memorial
FX We thank E. Troemel, L. Stanek, S. Margolis, and D. Colon-Ramos for
critical reading of the manuscript and J.Powell for help designing
qRT-PCR primers. TEM was performed by M. McKee in the Microscopy Core of
the Center for Systems Biology supported by National Institutes of
Health Grants DK43351 and DK57521. Nematode strains were provided by the
Caenorhabditis Genetics Center funded by the National Institutes of
Health National Center for Research Resources. This work was funded by
National Institutes of Health Grants A1062773 (to RAX) and AI064332 (to
F.M.A.) and by postdoctoral fellowships from the Jane Coffin Childs
Memorial Fund for Medical Research and the Charles A. King Trust, Bank
of America, Co-Trustee (Boston, MA) (to J.E.I.), and from the Crohn's
and Colitis Foundation of America (to A.N.).
NR 39
TC 52
Z9 77
U1 3
U2 12
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 11
PY 2008
VL 105
IS 45
BP 17469
EP 17474
DI 10.1073/pnas.0809527105
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 373OP
UT WOS:000260981800056
PM 18981407
ER
PT J
AU Kita, T
Hata, Y
Arita, R
Kawahara, S
Miura, M
Nakao, S
Mochizuki, Y
Enaida, H
Goto, Y
Shimokawa, H
Hafezi-Moghadam, A
Ishibashi, T
AF Kita, Takeshi
Hata, Yasuaki
Arita, Ryoichi
Kawahara, Shuhei
Miura, Muneki
Nakao, Shintaro
Mochizuki, Yasutaka
Enaida, Hiroshi
Goto, Yoshinobu
Shimokawa, Hiroaki
Hafezi-Moghadam, Ali
Ishibashi, Tatsuro
TI Role of TGF-beta in proliferative vitreoretinal diseases and ROCK as a
therapeutic target
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE proliferative diabetic retinopathy; proliferative vitreoretinopathy;
fibrosis; wound healing
ID GROWTH-FACTOR-BETA; COLLAGEN GEL CONTRACTION; RHO-KINASE PATHWAY;
SMOOTH-MUSCLE; CELLS; EYE; HYALOCYTES; MIGRATION; MYOFIBROBLAST;
INVOLVEMENT
AB Cicatricial contraction of preretinal fibrous membrane is a cause of severe vision loss in proliferative vitreoretinal diseases such as proliferative diabetic retinopathy (PDR) and proliferative vitreoretinopathy (PVR). TGF-beta is overexpressed in the vitreous of patients with proliferative vitreoretinal diseases and is also detectable in the contractile membranes. Therefore, TGF-beta is presumed to contribute to the cicatricial contraction of the membranes, however, the underlying mechanisms and TGF-beta's importance among various other factors remain to be elucidated. Vitreous samples from PDR or PVR patients caused significantly larger contraction of hyalocyte-containing collagen gels, compared with nonproliferative controls. The contractile effect was strongly correlated with the vitreal concentration of activated TGF-beta 2 (r = 0.82, P < 0.0001). PDR or PVR vitreous promoted expression of a-smooth muscle actin (a-SMA) and phosphorylation of myosin light chain (MLC), a downstream mediator of Rho-kinase (ROCK), both of which were dramatically but incompletely suppressed by TGF-beta blockade. In contrast, fasudil, a potent and selective ROCK inhibitor, almost completely blocked the vitreous-induced MLC phosphorylation and collagen gel contraction. Fasudil disrupted a-SMA organization, but it did not affect its vitreal expression. in vivo, fasudil significantly inhibited the progression of experimental PVR in rabbit eyes without affecting the viability of retinal cells by electroretinographic and histological analyses. These results elucidate the critical role of TGF-beta in mediating cicatricial contraction in proliferative vitreoretinal diseases. ROCK, a key downstream mediator of TGF-beta and other factors might become a unique therapeutic target in the treatment of proliferative vitreoretinal diseases.
C1 [Kita, Takeshi; Hata, Yasuaki; Arita, Ryoichi; Kawahara, Shuhei; Miura, Muneki; Nakao, Shintaro; Mochizuki, Yasutaka; Enaida, Hiroshi; Ishibashi, Tatsuro] Kyushu Univ, Grad Sch Med Sci, Dept Ophthalmol, Higashi Ku, Fukuoka 8128582, Japan.
[Nakao, Shintaro; Hafezi-Moghadam, Ali] Harvard Univ, Sch Med, Angiogenesis Lab, Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
[Nakao, Shintaro; Hafezi-Moghadam, Ali] Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA 02114 USA.
[Goto, Yoshinobu] Int Univ Hlth & Welf, Fac Rehabil, Dept Occupat Therapy, Fukuoka 8318501, Japan.
[Shimokawa, Hiroaki] Tohoku Univ, Grad Sch Med, Dept Cardiol, Aoba Ku, Sendai, Miyagi 9808575, Japan.
RP Hata, Y (reprint author), Kyushu Univ, Grad Sch Med Sci, Dept Ophthalmol, Higashi Ku, 3-1-1 Maidashi, Fukuoka 8128582, Japan.
EM hatachan@med.kyushu-u.ac.jp
RI U-ID, Kyushu/C-5291-2016;
OI Hafezi-Moghadam, Ali/0000-0002-5336-0697
FU Asahi Kasei Pharma Corporation, Tokyo, Japan; Ministry of Education,
Science, Sports and Culture, Japan [19592026, 18791283, 18591925];
National Institutes of Health [Al-050775, EY-14104, HL-086933]
FX We thank Marion W. Knight and Edward F. Knight and Research to Prevent
Blindness. We acknowledge Asahi Kasei Pharma Corporation, Tokyo, Japan
for its generous provision of fasudil. This study was supported in part
by grants from the Ministry of Education, Science, Sports and Culture,
Japan (Grant-in-Aid for Scientific Research nos. 19592026, 18791283, and
18591925). This work was supported by National Institutes of Health
Grants Al-050775, EY-14104, and HL-086933, a Research Fellowship Award
from Bausch & Lomb, and a Fellowship Award from the Japan Eye Bank
Association (to S.N.).
NR 38
TC 63
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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 NOV 11
PY 2008
VL 105
IS 45
BP 17504
EP 17509
DI 10.1073/pnas.0804054105
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 373OP
UT WOS:000260981800062
PM 18952846
ER
PT J
AU Roffman, JL
Gollub, RL
Calhoun, VD
Wassink, TH
Weiss, AP
Ho, BC
White, T
Clark, VP
Fries, J
Andreasen, NC
Goff, DC
Manoach, DS
AF Roffman, Joshua L.
Gollub, Randy L.
Calhoun, Vince D.
Wassink, Thomas H.
Weiss, Anthony P.
Ho, Beng C.
White, Tonya
Clark, Vincent P.
Fries, Jill
Andreasen, Nancy C.
Goff, Donald C.
Manoach, Dara S.
TI MTHFR 677C -> T genotype disrupts prefrontal function in schizophrenia
through an interaction with COMT 158Val -> Met
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE dopamine; folate; functional MRI; genetics; methylation
ID CATECHOL-O-METHYLTRANSFERASE; WORKING-MEMORY PERFORMANCE; EXECUTIVE
FUNCTION; VAL(108/158) MET; CORTEX; BRAIN; GENE; VAL(158)MET;
METHYLATION; DYSFUNCTION
AB Understanding how risk genes cumulatively impair brain function in schizophrenia could provide critical insights into its pathophysiology. Working memory impairment in schizophrenia has been associated with abnormal dopamine signaling in the prefrontal cortex, which is likely under complex genetic control. The catechol-O-methyltransferase (COMT) 158Val -> Met polymorphism (rs4680), which affects the availability of prefrontal dopamine signaling, consistently stratifies prefrontal activation during working memory performance. However, the low-dopamine COMT 158Val allele does not confer increased risk for schizophrenia, and its effects on prefrontal function are not specific to the disorder. In the setting of other genetic variants influencing prefrontal dopamine signaling, COMT 158Val -> Met genotype may exert disease-specific effects. A second polymorphism, methylenetetrahydrofolate reductase (MTHFR) 677C -> T (rs1801133), has been associated with overall schizophrenia risk and executive function impairment in patients, and may influence dopamine signaling through mechanisms upstream of COMT effects. We found that the hypofunctional 677T variant was associated with decreased working memory load-dependent activation in the prefrontal and insular cortices in 79 schizophrenia patients, but not in 75 demographically matched healthy controls. Further, significant MTHFR x COMT genotype interactions were observed, which differed by diagnostic group: Reduced prefrontal activation was associated with the 677T and 158Val alleles in patients, but with 677C/C and 158Met/Met genotype in controls. These findings are consistent with epistatic effects of the COMT and MTHFR polymorphisms on prefrontal dopamine signaling, and suggest that in schizophrenia patients, the MTHFR 677T allele exacerbates prefrontal dopamine deficiency. The findings also suggest the importance of weighing COMT effects on prefrontal function within the context of MTHFR genotype.
C1 [Roffman, Joshua L.; Gollub, Randy L.; Weiss, Anthony P.; Goff, Donald C.; Manoach, Dara S.] Massachusetts Gen Hosp, Dept Psychiat, Charlestown, MA 02129 USA.
[Roffman, Joshua L.; Gollub, Randy L.; Weiss, Anthony P.; Goff, Donald C.; Manoach, Dara S.] Harvard Univ, Sch Med, Charlestown, MA 02129 USA.
[Calhoun, Vince D.] Univ New Mexico, Dept Elect & Comp Engn, Albuquerque, NM 87131 USA.
[Calhoun, Vince D.; Clark, Vincent P.; Fries, Jill] MIND Res Network, Albuquerque, NM 87131 USA.
[Wassink, Thomas H.; Ho, Beng C.; Andreasen, Nancy C.] Univ Iowa, Dept Psychiat, Iowa City, IA 52242 USA.
[White, Tonya] Univ Minnesota, Dept Psychiat, Minneapolis, MN 55455 USA.
[Clark, Vincent P.] Univ New Mexico, Dept Psychol, Albuquerque, NM 87131 USA.
RP Roffman, JL (reprint author), Massachusetts Gen Hosp, Dept Psychiat, 149 13th St,Room 2656, Charlestown, MA 02129 USA.
EM jroffman@partners.org
RI Ho, Beng-Choon/D-6959-2011; Calhoun, Vince/H-7146-2013; Clark,
Vincent/B-3343-2010
OI Ho, Beng-Choon/0000-0003-3976-1555; Calhoun, Vince/0000-0001-9058-0747;
Clark, Vincent/0000-0002-9151-2102
FU MIND Institute; SFNR; Department of Energy [DE-F02-99ER62764-AO12]; MIND
Research Network; National Institutes of Health [EB001 632-04]
FX The authors thank all of the participants as well as the investigators
and support staff of the MIND Institute who made this study possible. we
also thank Dr. Doug Greve for his assistance with the SFNR analysis.
This research was supported by a grant from the Department of Energy
(DE-F02-99ER62764-AO12) to the MIND Research Network and National
Institutes of Health Grant EB001 632-04 (to J.L.R.).
NR 38
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U1 1
U2 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 11
PY 2008
VL 105
IS 45
BP 17573
EP 17578
DI 10.1073/pnas.0803727105
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 373OP
UT WOS:000260981800074
PM 18988738
ER
PT J
AU Rifkin, DE
Shlipak, MG
Katz, R
Fried, LF
Siscovick, D
Chonchol, M
Newman, AB
Sarnak, MJ
AF Rifkin, Dena E.
Shlipak, Michael G.
Katz, Ronit
Fried, Linda F.
Siscovick, David
Chonchol, Michel
Newman, Anne B.
Sarnak, Mark J.
TI Rapid Kidney Function Decline and Mortality Risk in Older Adults
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Article
ID SERUM CYSTATIN-C; GLOMERULAR-FILTRATION-RATE; BODY-COMPOSITION; ELDERLY
PERSONS; CARDIOVASCULAR-DISEASE; RENAL-INSUFFICIENCY; POOLED ANALYSIS;
CREATININE; INDIVIDUALS; PROGNOSIS
AB Background: Impaired kidney function is associated with increased mortality risk in older adults. It remains unknown, however, whether longitudinal declines in kidney function are independently associated with increased cardiovascular and all-cause mortality in older adults.
Methods: The Cardiovascular Health Study evaluated a cohort of community-dwelling older adults enrolled from 1989 to 1993 in 4 US communities with follow-up through 2005. Among 4380 participants, the slope of annual decline in estimated glomerular filtration rate (eGFR) was estimated using both serum creatinine (eGFR(creat)) and cystatin C (eGFR(cys)) rates, which were measured at baseline, year 3, and year 7 of follow-up. Rapid decline in eGFR was defined as a loss greater than 3 mL/min/1.73 m(2) per year, and cardiovascular and all-cause mortality were assessed over a mean of 9.9 years of follow-up.
Results: Mean (SD) levels of creatinine and cystatin C were 0.93 (0.30) mg/dL and 1.03 (0.25) mg/L, respectively; mean (SD) eGFR(creat) and eGFR(cys) were 79 (23) mL/min/1.73 m(2) and 79 (19) mL/min/1.73m(2), respectively. Individuals with rapid decline measured by eGFR(creat) (n = 714; 16%) had increased risk of cardiovascular (adjusted hazard ratio [AHR], 1.70; 95% confidence interval [CI], 1.40-2.06) and all-cause (AHR, 1.73; 95% CI, 1.54-1.94) mortality. Individuals with rapid decline measured by eGFR(cys) (n = 1083; 25%) also had increased risk of cardiovascular (AHR, 1.53; 95% CI, 1.29-1.80) and all-cause (AHR, 1.53; 95% CI, 1.38-1.69) mortality. The association of rapid decline in eGFR with elevated mortality risk did not differ across subgroups based on baseline kidney function, age, sex, race, or prevalent coronary heart disease.
Conclusion: Rapid decline in eGFR is associated with an increased risk of cardiovascular and all-cause mortality in older adults, independent of baseline eGFR and other demographic variables.
C1 [Rifkin, Dena E.; Sarnak, Mark J.] Tufts Med Ctr, Div Nephrol, Boston, MA 02111 USA.
[Shlipak, Michael G.] Univ Calif San Francisco, Gen Internal Med Sect, San Francisco Vet Affairs Med Ctr, San Francisco, CA 94143 USA.
[Shlipak, Michael G.] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA.
[Shlipak, Michael G.] Univ Calif San Francisco, Dept Epidemiol, San Francisco, CA 94143 USA.
[Shlipak, Michael G.] Univ Calif San Francisco, Dept Biostat, San Francisco, CA 94143 USA.
[Katz, Ronit] Univ Washington, Collaborat Hlth Studies Coordinating Ctr, Seattle, WA 98195 USA.
[Fried, Linda F.] Vet Affairs Pittsburgh Healthcare Syst, Renal Sect, Med Serv, Pittsburgh, PA USA.
[Fried, Linda F.; Newman, Anne B.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
[Fried, Linda F.; Newman, Anne B.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Med, Pittsburgh, PA USA.
[Siscovick, David] Univ Washington, Dept Med, Seattle, WA USA.
[Siscovick, David] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Chonchol, Michel] Univ Colorado, Hlth Sci Ctr, Div Renal Dis & Hypertens, Denver, CO USA.
RP Rifkin, DE (reprint author), Tufts Med Ctr, Div Nephrol, 750 Washington St,Box 391, Boston, MA 02111 USA.
EM drifkin@tuftsmedicalcenter.org
RI Newman, Anne/C-6408-2013
OI Newman, Anne/0000-0002-0106-1150
FU National Heart, Lung, and Blood Institute (NHLBI), Bethesda, Maryland
[R01-AG-027002, K24DK078204, N01-HC-35129, N01-HC-45133, N01HC-75150,
N01-HC-85079, N01-HC-85086, N01-HC-15103, N01-HC-55222, U01 HL080295];
National Institute of Neurological Disorders and Stroke, Bethesda
FX The research reported in this article was supported by contracts
R01-AG-027002, K24DK078204, N01-HC-35129, N01-HC-45133, N01HC-75150,
N01-HC-85079 through N01-HC-85086, N01-HC-15103, N01-HC-55222, and U01
HL080295 from the National Heart, Lung, and Blood Institute (NHLBI),
Bethesda, Maryland, with additional contribution from the National
Institute of Neurological Disorders and Stroke, Bethesda.
NR 25
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Z9 166
U1 0
U2 4
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 NOV 10
PY 2008
VL 168
IS 20
BP 2212
EP 2218
DI 10.1001/archinte.168.20.2212
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA 370XS
UT WOS:000260797000005
PM 19001197
ER
PT J
AU Levanon, K
Crum, C
Drapkin, R
AF Levanon, Keren
Crum, Christopher
Drapkin, Ronny
TI New Insights Into the Pathogenesis of Serous Ovarian Cancer and Its
Clinical Impact
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Review
ID PROPHYLACTIC OOPHORECTOMY SPECIMENS; HUMAN FALLOPIAN-TUBE; REDUCING
SALPINGO-OOPHORECTOMY; NECROSIS-FACTOR-ALPHA; GERMLINE MUTATION
CARRIERS; EPITHELIAL-CELLS; SURFACE EPITHELIUM; FOLLOW-UP; LOW-GRADE;
INTRAEPITHELIAL CARCINOMA
AB There are only a handful of concepts concerning cancer and carcinogenesis that are currently beyond dispute. One such dogma is the adenoma-carcinoma sequence and that a multistep accumulation of genetic alterations is required for transformation from a benign to a neoplastic tissue. The inevitable derivative of this dogma is that every invasive carcinoma is in fact a missed intraepithelial tumor, and furthermore, a late evolutionary stage in the sequence of development from a precursor lesion. Until fairly recently, high-grade serous ovarian carcinoma seemed to be one of the only known deviants of these concepts. In this article, we discuss the emergence of the fallopian tube fimbria as a field of origin for high-grade serous carcinomas and present a binary model of ovarian cancer pathogenesis that takes into consideration prior epidemiologic, morphologic, and genetic data. With the rise of the fallopian tube secretory epithelial cell as a cell of origin for high-grade pelvic serous carcinomas, the need to develop tools and model systems to characterize the biology and physiology of this cell is recognized.
C1 [Drapkin, Ronny] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
RP Drapkin, R (reprint author), Dana Farber Canc Inst, Dept Med Oncol, JF215D,44 Binney St, Boston, MA 02115 USA.
EM ronny_drapkin@dfci.harvard.edu
RI Drapkin, Ronny/E-9944-2016
OI Drapkin, Ronny/0000-0002-6912-6977
FU National Cancer Institute [P50 CA105009, K08 CA108748, R21 CA12468];
Ovarian Cancer Research Fund; Phi Beta Psi Sorority Charitable Trust;
Fannie E. Ripple Foundation; Robert and Deborah First Fund; Randi and
Joei Cutler Ovarian Cancer Research Fund; Columbia Hospital for Women
Research Foundation
FX Supported by Grants No. P50 CA105009, K08 CA108748, R21 CA12468 from the
National Cancer Institute, Ovarian Cancer Research Fund (individual
investigator award and program project development award), Phi Beta Psi
Sorority Charitable Trust, Fannie E. Ripple Foundation, Robert and
Deborah First Fund, Randi and Joei Cutler Ovarian Cancer Research Fund,
and the Columbia Hospital for Women Research Foundation.
NR 119
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U1 0
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 NOV 10
PY 2008
VL 26
IS 32
BP 5284
EP 5293
DI 10.1200/JCO.2008.18.1107
PG 10
WC Oncology
SC Oncology
GA 369MK
UT WOS:000260698400023
PM 18854563
ER
PT J
AU Zhou, XH
Lin, HZ
AF Zhou, Xiao-Hua
Lin, Huazhen
TI Semi-parametric maximum likelihood estimates for ROC curves of
continuous-scale tests
SO STATISTICS IN MEDICINE
LA English
DT Article
DE ROC curves; sensitivity and specificity; semi-parametric maximum
likelihood estimators
ID COMPARING DIAGNOSTIC MARKERS; TRANSFORMATION MODELS
AB In this paper, we propose a new semi-parametric maximum likelihood (ML) estimate of a receiver operating characteristic (ROC) curve that satisfies the property of invariance of the ROC curve and is easy to compute. We show that our new estimator is root n-consistent and has an asymptotically normal distribution. Our extensive Simulation studies show that the proposed method is efficient and robust. Finally, we illustrate the application of the proposed estimator in a real data set. Copyright (C) 2008 John Wiley & Sons, Ltd.
C1 [Zhou, Xiao-Hua; Lin, Huazhen] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Zhou, Xiao-Hua] VA Puget Sound Hlth Care Syst, HSR&D Ctr Excellence, Seattle, WA 98108 USA.
[Lin, Huazhen] Sichuan Univ, Sch Math, Chengdu 610064, Sichuan, Peoples R China.
RP Zhou, XH (reprint author), Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
EM azhou@u.washington.edu
FU NIH [R01EB005829]; NSF [DMS 0603913]; Fund of National Natural Science
[10771148]
FX Contract/grant sponsor: NIH; contract/grant number: R01EB005829;
Contract/grant sponsor: NSF; contract/grant number: DMS 0603913;
Contract/grant sponsor: Fund of National Natural Science; contract/grant
number: 10771148
NR 17
TC 5
Z9 5
U1 0
U2 3
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD NOV 10
PY 2008
VL 27
IS 25
BP 5271
EP 5290
DI 10.1002/sim.3349
PG 20
WC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Medicine, Research &
Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Research & Experimental
Medicine; Mathematics
GA 368RS
UT WOS:000260640800010
PM 18613272
ER
EF