FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Jacobsohn, DA Mitchell, SA Pavletic, SZ AF Jacobsohn, David A. Mitchell, Sandra A. Pavletic, Steven Z. BE Vogelsang, GB Pavletic, SZ TI EVALUATING THERAPEUTIC RESPONSE IN CHRONIC GRAFT VERSUS HOST DISEASE SO CHRONIC GRAFT VERSUS HOST DISEASE: INTERDISCIPLINARY MANAGEMENT LA English DT Article; Book Chapter ID PATIENT-REPORTED OUTCOMES; CLINICALLY-IMPORTANT-IMPROVEMENT; CONSENSUS DEVELOPMENT PROJECT; WORKING GROUP-REPORT; SYSTEMIC-SCLEROSIS; PINCH STRENGTH; CHRONIC GVHD; CORE SET; TRIALS; VALIDATION C1 [Jacobsohn, David A.] Northwestern Univ, Sch Med, Dept Pediat, Stem Cell Transplant Program,Childrens Mem Hosp, Chicago, IL 60611 USA. [Mitchell, Sandra A.] NIH, Ctr Clin, Bethesda, MD 20892 USA. [Mitchell, Sandra A.] Univ Utah, Coll Nursing, Salt Lake City, UT 84112 USA. [Pavletic, Steven Z.] NCI, Graft Versus Host & Autoimmun Unit, Ctr Canc Res, Bethesda, MD 20892 USA. RP Jacobsohn, DA (reprint author), Northwestern Univ, Sch Med, Dept Pediat, Stem Cell Transplant Program,Childrens Mem Hosp, Chicago, IL 60611 USA. NR 49 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI CAMBRIDGE PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND BN 978-0-521-88423-5 PY 2009 BP 146 EP 156 DI 10.1017/CBO9780511576751.015 D2 10.1017/CBO9780511576751 PG 11 WC Transplantation SC Transplantation GA BDG89 UT WOS:000313180800015 ER PT J AU Cowen, EW Hymes, SR AF Cowen, Edward W. Hymes, Sharon R. BE Vogelsang, GB Pavletic, SZ TI CUTANEOUS MANIFESTATIONS OF CHRONIC GRAFT VERSUS HOST DISEASE SO CHRONIC GRAFT VERSUS HOST DISEASE: INTERDISCIPLINARY MANAGEMENT LA English DT Article; Book Chapter ID CONSENSUS DEVELOPMENT PROJECT; WORKING GROUP-REPORT; STEM-CELL TRANSPLANTATION; EXTRACORPOREAL PHOTOCHEMOTHERAPY; CLINICAL-TRIALS; CHRONIC GVHD; STIMULATORY AUTOANTIBODIES; RADIATION PUVA; PDGF RECEPTOR; UVA1 THERAPY C1 [Cowen, Edward W.] NCI, Dermatol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. [Hymes, Sharon R.] Univ Texas MD Anderson Canc Ctr, Dept Dermatol, Houston, TX 77030 USA. RP Cowen, EW (reprint author), NCI, Dermatol Branch, Ctr Canc Res, NIH, Bldg 10, Bethesda, MD 20892 USA. NR 61 TC 4 Z9 4 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI CAMBRIDGE PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND BN 978-0-521-88423-5 PY 2009 BP 169 EP 181 DI 10.1017/CBO9780511576751.017 D2 10.1017/CBO9780511576751 PG 13 WC Transplantation SC Transplantation GA BDG89 UT WOS:000313180800017 ER PT J AU Treister, NS Schubert, MM Fall-Dickson, JM AF Treister, Nathaniel S. Schubert, Mark M. Fall-Dickson, Jane M. BE Vogelsang, GB Pavletic, SZ TI ORAL CHRONIC GRAFT VERSUS HOST DISEASE SO CHRONIC GRAFT VERSUS HOST DISEASE: INTERDISCIPLINARY MANAGEMENT LA English DT Article; Book Chapter ID BONE-MARROW-TRANSPLANTATION; CONSENSUS DEVELOPMENT PROJECT; STEM-CELL TRANSPLANTATION; WORKING GROUP-REPORT; SALIVARY-GLAND INVOLVEMENT; LONGITUDINAL FOLLOW-UP; TOTAL-BODY IRRADIATION; CLINICAL-TRIALS; CHRONIC GVHD; PILOCARPINE HYDROCHLORIDE C1 [Treister, Nathaniel S.] Harvard Univ, Sch Oral Med, Cambridge, MA 02138 USA. [Treister, Nathaniel S.] Brigham & Womens Hosp, Div Oral Med & Dent, Boston, MA 02115 USA. [Schubert, Mark M.] Univ Washington, Dept Oral Med, Seattle Canc Care Alliance, Seattle, WA 98195 USA. [Fall-Dickson, Jane M.] NINR, Symptom Management Branch, NIH, Bethesda, MD 20892 USA. RP Treister, NS (reprint author), Harvard Univ, Sch Oral Med, Cambridge, MA 02138 USA. NR 107 TC 1 Z9 1 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI CAMBRIDGE PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND BN 978-0-521-88423-5 PY 2009 BP 182 EP 198 DI 10.1017/CBO9780511576751.018 D2 10.1017/CBO9780511576751 PG 17 WC Transplantation SC Transplantation GA BDG89 UT WOS:000313180800018 ER PT J AU Kim, SK Smith, JA Dunn, JP AF Kim, Stella K. Smith, Janine A. Dunn, James P., Jr. BE Vogelsang, GB Pavletic, SZ TI CHRONIC OCULAR GRAFT VERSUS HOST DISEASE SO CHRONIC GRAFT VERSUS HOST DISEASE: INTERDISCIPLINARY MANAGEMENT LA English DT Article; Book Chapter ID BONE-MARROW-TRANSPLANTATION; CONSENSUS DEVELOPMENT PROJECT; WORKING GROUP-REPORT; CENTRAL SEROUS CHORIORETINOPATHY; STEM-CELL TRANSPLANTATION; SERUM EYE DROPS; SEVERE DRY EYE; CLINICAL-TRIALS; SJOGRENS-SYNDROME; ORAL PILOCARPINE C1 [Kim, Stella K.] Univ Texas MD Anderson Canc Ctr, Dept Ophthalmol, Houston, TX 77030 USA. [Kim, Stella K.] Univ Texas MD Anderson Canc Ctr, Dept Radiat Oncol, Houston, TX 77030 USA. [Smith, Janine A.] NEI, Div Epidemiol & Clin Res, NIH, Bethesda, MD 20892 USA. [Dunn, James P., Jr.] Wilmer Ophthalmol Inst, Div Ocular Immunol, Baltimore, MD USA. RP Kim, SK (reprint author), Univ Texas MD Anderson Canc Ctr, Dept Ophthalmol, Houston, TX 77030 USA. NR 71 TC 7 Z9 8 U1 0 U2 1 PU CAMBRIDGE UNIV PRESS PI CAMBRIDGE PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND BN 978-0-521-88423-5 PY 2009 BP 199 EP 206 DI 10.1017/CBO9780511576751.019 D2 10.1017/CBO9780511576751 PG 8 WC Transplantation SC Transplantation GA BDG89 UT WOS:000313180800019 ER PT J AU Turner, ML Stratton, P AF Turner, Maria L. Stratton, Pamela BE Vogelsang, GB Pavletic, SZ TI GYNECOLOGICAL MANIFESTATIONS OF CHRONIC GRAFT VERSUS HOST DISEASE SO CHRONIC GRAFT VERSUS HOST DISEASE: INTERDISCIPLINARY MANAGEMENT LA English DT Article; Book Chapter ID BONE-MARROW-TRANSPLANTATION; CONSENSUS DEVELOPMENT PROJECT; WORKING GROUP-REPORT; HEMATOPOIETIC-CELL TRANSPLANTATION; OUTFLOW TRACT OBSTRUCTION; CLINICAL-TRIALS; STEM-CELL; VAGINAL STENOSIS; RECIPIENTS; DIAGNOSIS C1 [Turner, Maria L.] NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA. [Stratton, Pamela] NICHHD, Reprod Biol & Med Branch, NIH, Bethesda, MD 20892 USA. RP Turner, ML (reprint author), NCI, Dermatol Branch, NIH, Bldg 10, Bethesda, MD 20892 USA. NR 30 TC 2 Z9 2 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI CAMBRIDGE PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND BN 978-0-521-88423-5 PY 2009 BP 207 EP 215 DI 10.1017/CBO9780511576751.020 D2 10.1017/CBO9780511576751 PG 9 WC Transplantation SC Transplantation GA BDG89 UT WOS:000313180800020 ER PT J AU Li, L Chan, L Gerber, LH AF Li, Li Chan, Leighton Gerber, Lynn H. BE Vogelsang, GB Pavletic, SZ TI REHABILITATION EVALUATION AND TREATMENT OF PATIENTS WITH CHRONIC GRAFT VERSUS HOST DISEASE SO CHRONIC GRAFT VERSUS HOST DISEASE: INTERDISCIPLINARY MANAGEMENT LA English DT Article; Book Chapter ID STEM-CELL TRANSPLANTATION; BONE-MARROW-TRANSPLANTATION; LONG-TERM SURVIVORS; AVASCULAR NECROSIS; MYASTHENIA-GRAVIS; CANCER SURVIVORS; AEROBIC EXERCISE; CLINICAL-TRIALS; FATIGUE; MANIFESTATION C1 [Li, Li; Chan, Leighton] NIH, Dept Rehabil Med, Warren G Magnuson Clin Res Ctr, Bethesda, MD 20892 USA. [Gerber, Lynn H.] George Mason Univ, Coll Hlth & Human Serv, Ctr Study Chron Illness & Disabil, Fairfax, VA 22030 USA. RP Li, L (reprint author), NIH, Dept Rehabil Med, Warren G Magnuson Clin Res Ctr, Bethesda, MD 20892 USA. NR 63 TC 2 Z9 2 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI CAMBRIDGE PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND BN 978-0-521-88423-5 PY 2009 BP 252 EP 267 DI 10.1017/CBO9780511576751.025 D2 10.1017/CBO9780511576751 PG 16 WC Transplantation SC Transplantation GA BDG89 UT WOS:000313180800025 ER PT J AU Gea-Banacloche, J Boeckh, M AF Gea-Banacloche, Juan Boeckh, Michael BE Vogelsang, GB Pavletic, SZ TI INFECTIONS SO CHRONIC GRAFT VERSUS HOST DISEASE: INTERDISCIPLINARY MANAGEMENT LA English DT Article; Book Chapter ID VERSUS-HOST-DISEASE; STEM-CELL TRANSPLANTATION; BONE-MARROW-TRANSPLANTATION; INVASIVE FUNGAL-INFECTIONS; VARICELLA-ZOSTER-VIRUS; NONINFECTIOUS PULMONARY COMPLICATIONS; PNEUMOCYSTIS-CARINII-PNEUMONIA; BRONCHOALVEOLAR LAVAGE FLUID; RESPIRATORY SYNCYTIAL VIRUS; HIGH-RESOLUTION CT C1 [Gea-Banacloche, Juan] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA. [Boeckh, Michael] Univ Washington, Fred Hutchinson Canc Res Ctr, Dept Med, Seattle, WA 98195 USA. RP Gea-Banacloche, J (reprint author), NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA. NR 185 TC 1 Z9 1 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI CAMBRIDGE PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND BN 978-0-521-88423-5 PY 2009 BP 268 EP 288 DI 10.1017/CBO9780511576751.026 D2 10.1017/CBO9780511576751 PG 21 WC Transplantation SC Transplantation GA BDG89 UT WOS:000313180800026 ER PT J AU Baird, K Gilman, AL AF Baird, Kristin Gilman, Andrew L. BE Vogelsang, GB Pavletic, SZ TI OTHER MANIFESTATIONS OF CHRONIC GRAFT VERSUS HOST DISEASE SO CHRONIC GRAFT VERSUS HOST DISEASE: INTERDISCIPLINARY MANAGEMENT LA English DT Article; Book Chapter ID BONE-MARROW-TRANSPLANTATION; STEM-CELL TRANSPLANTATION; CORONARY-ARTERY-DISEASE; CENTRAL-NERVOUS-SYSTEM; MYASTHENIA-GRAVIS; NEPHROTIC SYNDROME; RETROPERITONEAL FIBROSIS; T-CELLS; PERICARDIAL-EFFUSION; CLINICAL-MANIFESTATION C1 [Baird, Kristin] NCI, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA. [Gilman, Andrew L.] Univ N Carolina, Dept Pediat Pediat Blood & Marrow Transplantat, Chapel Hill, NC USA. RP Baird, K (reprint author), NCI, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA. NR 70 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI CAMBRIDGE PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND BN 978-0-521-88423-5 PY 2009 BP 302 EP 313 DI 10.1017/CBO9780511576751.028 D2 10.1017/CBO9780511576751 PG 12 WC Transplantation SC Transplantation GA BDG89 UT WOS:000313180800028 ER PT J AU Mitchell, SA Reeve, BB AF Mitchell, Sandra A. Reeve, Bryce B. BE Vogelsang, GB Pavletic, SZ TI HEALTH-RELATED QUALITY OF LIFE (HRQOL) IN CHRONIC GRAFT VERSUS HOST DISEASE SO CHRONIC GRAFT VERSUS HOST DISEASE: INTERDISCIPLINARY MANAGEMENT LA English DT Article; Book Chapter ID BONE-MARROW-TRANSPLANTATION; STEM-CELL TRANSPLANTATION; PATIENT-REPORTED OUTCOMES; LONG-TERM SURVIVORS; CHRONIC MYELOID-LEUKEMIA; INFORMATION-SYSTEM PROMIS; CANCER CLINICAL-TRIALS; FUNCTIONAL STATUS; RESPONSE SHIFT; SYMPTOM ASSESSMENT C1 [Mitchell, Sandra A.] NCI, Ctr Clin, NIH, Bethesda, MD 20892 USA. [Mitchell, Sandra A.] Univ Utah, Coll Nursing, Salt Lake City, UT 84112 USA. RP Mitchell, SA (reprint author), NCI, Ctr Clin, NIH, Bethesda, MD 20892 USA. NR 123 TC 2 Z9 2 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI CAMBRIDGE PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND BN 978-0-521-88423-5 PY 2009 BP 335 EP 348 DI 10.1017/CBO9780511576751.031 D2 10.1017/CBO9780511576751 PG 14 WC Transplantation SC Transplantation GA BDG89 UT WOS:000313180800031 ER PT J AU Baird, K Wayne, AS Jacobsohn, DA AF Baird, Kristin Wayne, Alan S. Jacobsohn, David A. BE Vogelsang, GB Pavletic, SZ TI PEDIATRIC CHRONIC GRAFT VERSUS HOST DISEASE SO CHRONIC GRAFT VERSUS HOST DISEASE: INTERDISCIPLINARY MANAGEMENT LA English DT Article; Book Chapter ID STEM-CELL TRANSPLANTATION; BONE-MARROW-TRANSPLANTATION; ACUTE LYMPHOBLASTIC-LEUKEMIA; UMBILICAL-CORD-BLOOD; CONSENSUS DEVELOPMENT PROJECT; WORKING GROUP-REPORT; MATCHED UNRELATED DONORS; CHILDRENS ONCOLOGY GROUP; EXTRACORPOREAL PHOTOCHEMOTHERAPY; APLASTIC-ANEMIA C1 [Baird, Kristin; Wayne, Alan S.] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. [Jacobsohn, David A.] Northwestern Univ, Childrens Mem Hosp, Stem Cell Transplant Program, Dept Pediat,Sch Med, Chicago, IL 60614 USA. RP Baird, K (reprint author), NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. NR 145 TC 1 Z9 1 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI CAMBRIDGE PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND BN 978-0-521-88423-5 PY 2009 BP 369 EP 385 DI 10.1017/CBO9780511576751.034 D2 10.1017/CBO9780511576751 PG 17 WC Transplantation SC Transplantation GA BDG89 UT WOS:000313180800034 ER PT J AU Anders, V Moravec, C Mitchell, SA AF Anders, Viki Moravec, Carina Mitchell, Sandra A. BE Vogelsang, GB Pavletic, SZ TI PRINCIPLES OF INTERDISCIPLINARY PRACTICE IN THE CARE OF PATIENTS WITH CHRONIC GRAFT VERSUS HOST DISEASE SO CHRONIC GRAFT VERSUS HOST DISEASE: INTERDISCIPLINARY MANAGEMENT LA English DT Article; Book Chapter ID CONSENSUS DEVELOPMENT PROJECT; WORKING GROUP-REPORT; RANDOMIZED CONTROLLED-TRIAL; TERM FOLLOW-UP; CHILDHOOD-CANCER; CLINICAL-TRIALS; MARROW-TRANSPLANTATION; CELL TRANSPLANTATION; BONE-MARROW; COLLABORATION C1 [Anders, Viki] Johns Hopkins, Sidney Kimmel Comprehens Canc Ctr, Graft Versus Host Dis Clin, Baltimore, MD 21218 USA. [Moravec, Carina] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. [Mitchell, Sandra A.] NIH, Ctr Clin, Bethesda, MD 20892 USA. [Mitchell, Sandra A.] NCI, Bethesda, MD 20892 USA. [Mitchell, Sandra A.] Univ Utah, Coll Nursing, Salt Lake City, UT 84112 USA. RP Anders, V (reprint author), Johns Hopkins, Sidney Kimmel Comprehens Canc Ctr, Graft Versus Host Dis Clin, Baltimore, MD 21218 USA. NR 48 TC 0 Z9 0 U1 2 U2 3 PU CAMBRIDGE UNIV PRESS PI CAMBRIDGE PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND BN 978-0-521-88423-5 PY 2009 BP 386 EP 395 DI 10.1017/CBO9780511576751.035 D2 10.1017/CBO9780511576751 PG 10 WC Transplantation SC Transplantation GA BDG89 UT WOS:000313180800035 ER PT J AU Castro, KM Stewart, S Jacobs, MJ Kim, P AF Castro, Kathleen M. Stewart, Susan Jacobs, Myra J. Kim, Paula BE Vogelsang, GB Pavletic, SZ TI PATIENT ADVOCACY, EDUCATION AND PSYCHOSOCIAL SUPPORT SO CHRONIC GRAFT VERSUS HOST DISEASE: INTERDISCIPLINARY MANAGEMENT LA English DT Article; Book Chapter ID STEM-CELL TRANSPLANTATION; NATIONAL TRENDS SURVEY; VERSUS-HOST-DISEASE; QUALITY-OF-LIFE; HEALTH INFORMATION; CANCER SURVIVORS; INTERNET; MAIL C1 [Castro, Kathleen M.] NIH, Ctr Clin, Bethesda, MD 20892 USA. [Stewart, Susan] BMT InfoNet, Highland Pk, IL USA. [Jacobs, Myra J.] Natl Bone Marrow Transplant Link, Southfield, MI USA. RP Castro, KM (reprint author), NIH, Ctr Clin, Bethesda, MD 20892 USA. NR 39 TC 0 Z9 0 U1 2 U2 2 PU CAMBRIDGE UNIV PRESS PI CAMBRIDGE PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND BN 978-0-521-88423-5 PY 2009 BP 396 EP 405 DI 10.1017/CBO9780511576751.036 D2 10.1017/CBO9780511576751 PG 10 WC Transplantation SC Transplantation GA BDG89 UT WOS:000313180800036 ER PT B AU Ahlenstiel, G Rehermann, B AF Ahlenstiel, G. Rehermann, B. BE Adler, G Jia, JD Owyang, C Fan, DM LaRusso, NF TI State-of-the-Art Lecture: The liver as an immune organ SO CHRONIC INFLAMMATION OF LIVER AND GUT SE Falk Symposium LA English DT Proceedings Paper CT Falk Symposium 163 on Chronic Inflammatory Diseases of Liver and Gut CY MAR 14-15, 2008 CL Hangzhou, PEOPLES R CHINA ID HEPATITIS-C-VIRUS; NATURAL-KILLER-CELLS; CD8(+) T-CELLS; MURINE CYTOMEGALOVIRUS-INFECTION; IMMUNOGLOBULIN-LIKE RECEPTORS; NKT CELLS; B-VIRUS; HLA-C; CUTTING EDGE; PSORIATIC-ARTHRITIS C1 [Ahlenstiel, G.] NIDDK, Immunol Sect, Liver Dis Branch, NIH,DHHS, 10 Ctr Dr,Rm 9B11, Bethesda, MD 20892 USA. RP Ahlenstiel, G (reprint author), NIDDK, Immunol Sect, Liver Dis Branch, NIH,DHHS, 10 Ctr Dr,Rm 9B11, Bethesda, MD 20892 USA. OI Ahlenstiel, Golo/0000-0003-0026-1457 NR 78 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS BN 978-1-4020-9352-4 J9 FALK SYMP PY 2009 VL 163 BP 77 EP + DI 10.1007/978-1-4020-9353-1_11 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA BJD52 UT WOS:000265018500011 ER PT J AU Doo, E Ghany, M AF Doo, Edward Ghany, Marc BE Shetty, K Wu, GY TI Management of Patients Co-Infected with Chronic Hepatitis B (CHB) and the Human Immunodeficiency Virus (HIV) SO CHRONIC VIRAL HEPATITIS: DIAGNOSIS AND THERAPEUTICS, SECOND EDITION SE Clinical Gastroenterology LA English DT Article; Book Chapter ID ADEFOVIR DIPIVOXIL; COINFECTED PATIENTS; HOMOSEXUAL-MEN; NATURAL-HISTORY; LIVER-TRANSPLANTATION; VIROLOGICAL RESPONSE; LAMIVUDINE TREATMENT; HBV INFECTION; UNITED-STATES; RESISTANCE C1 [Doo, Edward; Ghany, Marc] NIH, Bethesda, MD 20892 USA. RP Doo, E (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA. NR 52 TC 0 Z9 0 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA BN 978-1-59745-565-7 J9 CLIN GASTROENT-SER PY 2009 BP 259 EP 272 DI 10.1007/978-1-59745-565-7_9 D2 10.1007/978-1-59745-565-7 PG 14 WC Medicine, General & Internal SC General & Internal Medicine GA BLX05 UT WOS:000271248100010 ER PT J AU Doo, E Ghany, M AF Doo, Edward Ghany, Marc BE Shetty, K Wu, GY TI Management of Antiviral Resistance in Chronic Hepatitis B SO CHRONIC VIRAL HEPATITIS: DIAGNOSIS AND THERAPEUTICS, SECOND EDITION SE Clinical Gastroenterology LA English DT Article; Book Chapter ID ADEFOVIR DIPIVOXIL ADV; LAMIVUDINE THERAPY; VIRUS; HBV; ENTECAVIR; TENOFOVIR; SELECTION; PATIENT; POLYMERASE; MUTATIONS C1 [Doo, Edward; Ghany, Marc] NIH, Bethesda, MD 20892 USA. RP Doo, E (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA. NR 34 TC 0 Z9 0 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA BN 978-1-59745-565-7 J9 CLIN GASTROENT-SER PY 2009 BP 273 EP 287 DI 10.1007/978-1-59745-565-7_10 D2 10.1007/978-1-59745-565-7 PG 15 WC Medicine, General & Internal SC General & Internal Medicine GA BLX05 UT WOS:000271248100011 ER PT J AU Benbrahim-Tallaa, L Waalkes, M AF Benbrahim-Tallaa, Lamia Waalkes, Michael TI Inorganic arsenic and human prostate cancer SO CIENCIA & SAUDE COLETIVA LA English DT Review DE Androgen-independent; Arsenic; Carcinogenesis; Human malignant transformation; Prostate; Ras ID INDUCED MALIGNANT-TRANSFORMATION; CELL LINES CHARACTERISTICS; EPITHELIAL-CELLS; DRINKING-WATER; WELL WATER; ANDROGEN INDEPENDENCE; ACTIVATION; GENE; TRANSPORT; MORTALITY AB We critically evaluated the etiologic role of inorganic arsenic in human prostate cancer. We assessed data from relevant epidemiologic studies concerning environmental inorganic arsenic exposure. Whole animal studies were evaluated as were in vitro model systems of inorganic arsenic carcinogenesis in the prostate. Multiple studies in humans reveal an association between environmental inorganic arsenic exposure and prostate cancer mortality or incidence. Many of these human studies provide clear evidence of a dose-response relationship. Relevant whole animal models showing a relationship between inorganic arsenic and prostate cancer are not available. However, cellular model systems indicate arsenic can induce malignant transformation of human prostate epithelial cells in vitro. Arsenic also appears to impact prostate cancer cell progression by precipitating events leading to androgen independence in vitro. Available evidence in human populations and human cells in vitro indicates that the prostate is a target for inorganic arsenic carcinogenesis. A role for this common environmental contaminant in human prostate cancer initiation and/or progression would be very important. C1 [Benbrahim-Tallaa, Lamia; Waalkes, Michael] Natl Inst Environm Hlth Sci, Inorgan Carcinogenesis Sect, Comparat Carcinogenesis Lab, NCI,NIH,Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. RP Benbrahim-Tallaa, L (reprint author), Natl Inst Environm Hlth Sci, Inorgan Carcinogenesis Sect, Comparat Carcinogenesis Lab, NCI,NIH,Dept Hlth & Human Serv, MD F0-09,111 Alexander Dr, Res Triangle Pk, NC 27709 USA. EM waalkes@niehs.nih.gov NR 78 TC 1 Z9 1 U1 1 U2 6 PU ABRASCO PI RIO DE JANEIRO PA RUA HESPERIA, 16-PARTE MANGUINHOS, RIO DE JANEIRO, 21050-040, BRAZIL SN 1413-8123 J9 CIENC SAUDE COLETIVA JI Cienc. Saude Coletiva PD JAN-FEB PY 2009 VL 14 IS 1 BP 307 EP 318 PG 12 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 544AF UT WOS:000273622700037 ER PT J AU Lauer, MS AF Lauer, Michael S. TI CT Angiography First Things First SO CIRCULATION-CARDIOVASCULAR IMAGING LA English DT Editorial Material DE angiography; tomography ID COMPUTED-TOMOGRAPHY; RANDOMIZED-TRIALS; MORTALITY; BENEFIT; DISEASE C1 [Lauer, Michael S.] NHLBI, Div Prevent & Populat Sci, Bethesda, MD 20892 USA. RP Lauer, MS (reprint author), 6701 Rock Ledge Dr,Room 10122, Bethesda, MD 20892 USA. EM lauerm@nhlbi.nih.gov RI Lauer, Michael/L-9656-2013 OI Lauer, Michael/0000-0002-9217-8177 NR 20 TC 7 Z9 7 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1941-9651 J9 CIRC-CARDIOVASC IMAG JI Circ.-Cardiovasc. Imaging PD JAN PY 2009 VL 2 IS 1 BP 1 EP 3 DI 10.1161/CIRCIMAGING.108.841429 PG 3 WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical Imaging SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine & Medical Imaging GA 446NT UT WOS:000266129000001 PM 19808556 ER PT J AU Hsu, DT Pearson, GD AF Hsu, Daphne T. Pearson, Gail D. TI Heart Failure in Children Part I: History, Etiology, and Pathophysiology SO CIRCULATION-HEART FAILURE LA English DT Article DE heart failure; pediatrics ID BRAIN NATRIURETIC PEPTIDE; PEDIATRIC CARDIOMYOPATHY; INTERNATIONAL-SOCIETY; DEVELOPMENTAL-CHANGES; LUNG-TRANSPLANTATION; CARDIAC FAILURE; GREAT-ARTERIES; DISEASE; CHILDHOOD; INFANTS C1 [Pearson, Gail D.] NHLBI, Heart Dev & Struct Dis Branch, NIH, Bethesda, MD 20892 USA. [Hsu, Daphne T.] Childrens Hosp Montefiore, Dept Pediat, Albert Einstein Coll Med, New York, NY USA. RP Pearson, GD (reprint author), NHLBI, Heart Dev & Struct Dis Branch, NIH, 6701 Rockledge Dr,Room 8104, Bethesda, MD 20892 USA. EM pearsong@nhlbi.nih.gov OI Hsu, Daphne/0000-0002-2654-0430 NR 75 TC 36 Z9 39 U1 1 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1941-3289 J9 CIRC-HEART FAIL JI Circ.-Heart Fail. PD JAN PY 2009 VL 2 IS 1 BP 63 EP 70 DI 10.1161/CIRCHEARTFAILURE.108.820217 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 446NL UT WOS:000266128200010 PM 19808316 ER PT B AU Udey, MC AF Udey, Mark C. BE Gaspari, AA Tyring, SK TI Cutaneous Dendritic Cells in Health and Disease SO CLINICAL AND BASIC IMMUNODERMATOLOGY LA English DT Article; Book Chapter ID EPIDERMAL LANGERHANS CELLS; IN-VIVO; CONTACT HYPERSENSITIVITY; ADAPTIVE IMMUNITY; LYMPHOID ORGANS; STEADY-STATE; MOUSE SPLEEN; BONE-MARROW; SKIN; ANTIGEN C1 NCI, Dermatol Branch, Ctr Canc Res, Bethesda, MD 20892 USA. RP Udey, MC (reprint author), NCI, Dermatol Branch, Ctr Canc Res, Bldg 10, Bethesda, MD 20892 USA. NR 49 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER-VERLAG LONDON LTD PI GODALMING PA SWEETAPPLE HOUSE CATTESHALL RD FARNCOMBE, GODALMING GU7 1NH, SURREY, ENGLAND BN 978-1-84882-851-3 PY 2009 BP 119 EP 130 PG 12 WC Dermatology SC Dermatology GA BMD46 UT WOS:000271919100008 ER PT B AU Cowen, EW AF Cowen, Edward W. BE Gaspari, AA Tyring, SK TI Graft-Versus-Host Disease SO CLINICAL AND BASIC IMMUNODERMATOLOGY LA English DT Article; Book Chapter ID BONE-MARROW-TRANSPLANTATION; STEM-CELL TRANSPLANTATION; CONSENSUS DEVELOPMENT PROJECT; WORKING GROUP-REPORT; ANTI-THYMOCYTE GLOBULIN; EXTRACORPOREAL PHOTOCHEMOTHERAPY; CLINICAL-TRIALS; CHRONIC GVHD; ULTRAVIOLET-IRRADIATION; MYCOPHENOLATE-MOFETIL C1 NCI, Dermatol Branch, Ctr Canc Res, Bethesda, MD 20892 USA. RP Cowen, EW (reprint author), NCI, Dermatol Branch, Ctr Canc Res, Bldg 10, Bethesda, MD 20892 USA. NR 114 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER-VERLAG LONDON LTD PI GODALMING PA SWEETAPPLE HOUSE CATTESHALL RD FARNCOMBE, GODALMING GU7 1NH, SURREY, ENGLAND BN 978-1-84882-851-3 PY 2009 BP 439 EP 457 PG 19 WC Dermatology SC Dermatology GA BMD46 UT WOS:000271919100026 ER PT B AU Studenski, S Ferrucci, L Resnick, NM AF Studenski, Stephanie Ferrucci, Luigi Resnick, Neil M. BE Robertson, D Williams, GH TI Geriatrics SO CLINICAL AND TRANSLATIONAL SCIENCE: PRINCIPLES OF HUMAN RESEARCH LA English DT Article; Book Chapter ID LOWER-EXTREMITY FUNCTION; SUBCLINICAL CARDIOVASCULAR-DISEASE; FUNCTIONAL INDEPENDENCE MEASURE; PHYSICAL PERFORMANCE-MEASURES; PERIPHERAL ARTERIAL-DISEASE; MILD COGNITIVE IMPAIRMENT; LIFE-STYLE INTERVENTIONS; NURSING-HOME ADMISSION; LIVING OLDER PERSONS; MINI-MENTAL STATE C1 [Studenski, Stephanie] Univ Pittsburgh, Div Geriatr & Gerontol, Pittsburgh, PA 15213 USA. [Studenski, Stephanie] VA Pittsburgh GRECC, Pittsburgh, PA 15213 USA. [Ferrucci, Luigi] NIH, Baltimore Longitudinal Study Aging, Baltimore, MD 20892 USA. [Resnick, Neil M.] Univ Pittsburgh, Inst Aging, Pittsburgh, PA 15213 USA. [Resnick, Neil M.] Univ Pittsburgh, Inst Aging, Div Geriatr & Gerontol, Pittsburgh, PA 15213 USA. RP Studenski, S (reprint author), Univ Pittsburgh, Div Geriatr & Gerontol, Pittsburgh, PA 15213 USA. NR 120 TC 0 Z9 0 U1 1 U2 2 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA BN 978-0-08-092019-1; 978-0-12-373639-0 PY 2009 BP 477 EP 495 DI 10.1016/B978-0-12-373639-0.00032-7 PG 19 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA BHL23 UT WOS:000325772400034 ER PT J AU Parkhurst, MR Joo, J Riley, JP Yu, ZY Li, Y Robbins, PF Rosenberg, SA AF Parkhurst, Maria R. Joo, Jayne Riley, John P. Yu, Zhiya Li, Yong Robbins, Paul F. Rosenberg, Steven A. TI Characterization of Genetically Modified T-Cell Receptors that Recognize the CEA:691-699 Peptide in the Context of HLA-A2.1 on Human Colorectal Cancer Cells SO CLINICAL CANCER RESEARCH LA English DT Article ID CARCINOEMBRYONIC ANTIGEN FAMILY; VACCINIA-CEA VACCINE; STIMULATING FACTOR; IMMUNE-RESPONSES; EPITHELIAL-CELLS; DENDRITIC CELLS; TUMOR-ANTIGEN; HUMAN-TISSUES; IN-VIVO; PHASE-I AB Purpose: Carcinoembryonic antigen (CEA) is a tumor-associated protein expressed on a variety of adenocarcinomas. To develop an immunotherapy for patients with cancers that overexpress CEA, we isolated and genetically modified a T-cell receptors (TCRs) that specifically bound a CEA peptide on human cancer cells. Experimental Design: HLA-A2.1 transgenic mice were immunized with CEA:691-699. A CEA-reactive TCR was isolated from splenocytes of these mice and was genetically introduced into human peripheral blood lymphocytes via RNA electroporation or retroviral transduction. Amino acid substitutions were introduced throughout the complementarity determining regions (CDR1, CDR2, and CDR3) of both TCR alpha and beta chains to improve recognition of CEA. Results: Murine lymphocytes bearing the CEA-reactive TCR specifically recognized peptide-loaded T2 cells and HLA-A2.1(+) CEA(+) human colon cancer cells, Both CD8(+) and CD4(+) human lymphocytes expressing the murine TCR specifically recognized peptide-loaded T2 cells. However, only gene-modified CD8(+) lymphocytes specifically recognized HLA-A2.1(+) CEA(+) colon cancer cell lines, and tumor cell recognition was weak and variable. We identified two substitutions in the CDR3 of the alpha chain that significantly influenced tumor cell recognition by human peripheral blood lymphocytes. One substitution,T for S at position 112 (S112T), enhanced tumor cell recognition by CD8(+) lymphocytes, and a second dually substituted receptor (S112T L110F) enhanced tumor cell recognition by CD4(+) T cells. Conclusions: The modified CEA-reactive TCRs are good candidates for future gene therapy clinical trials and show the power of selected amino acid substitutions in the antigen-binding regions of the TCR to enhance desired reactivities, C1 [Parkhurst, Maria R.; Riley, John P.; Yu, Zhiya; Li, Yong; Robbins, Paul F.; Rosenberg, Steven A.] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA. [Joo, Jayne] Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA. RP Parkhurst, MR (reprint author), NCI, Surg Branch, NIH, Bldg CRC,Room 4-5744,9000 Rockville Pike, Bethesda, MD 20892 USA. EM Maria_Parkhurst@nih.gov FU Intramural NIH HHS [Z01 SC003811-33] NR 48 TC 46 Z9 47 U1 1 U2 3 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD JAN 1 PY 2009 VL 15 IS 1 BP 169 EP 180 DI 10.1158/1078-0432.CCR-08-1638 PG 12 WC Oncology SC Oncology GA 391JO UT WOS:000262229800020 PM 19118044 ER PT J AU Roepman, P Jassem, J Smit, EF Muley, T Niklinski, J van de Velde, T Witteveen, AT Rzyman, W Floore, A Burgers, S Giaccone, G Meister, M Dienemann, H Skrzypski, M Kozlowski, M Mooi, WJ van Zandwijk, N AF Roepman, Paul Jassem, Jacek Smit, Egbert F. Muley, Thomas Niklinski, Jacek van de Velde, Tony Witteveen, Anke T. Rzyman, Witold Floore, Arno Burgers, Sjaak Giaccone, Giuseppe Meister, Michael Dienemann, Hendrik Skrzypski, Marcin Kozlowski, Miroslaw Mooi, Wolter J. van Zandwijk, Nico TI An Immune Response Enriched 72-Gene Prognostic Profile for Early-Stage Non-Small-Cell Lung Cancer SO CLINICAL CANCER RESEARCH LA English DT Article ID BREAST-CANCER; SQUAMOUS-CELL; SIGNATURE; ADENOCARCINOMA; CLASSIFICATION; VALIDATION; CARCINOMAS; STRATEGY; HEAD AB Purpose: Current staging methods are imprecise for predicting prognosis of early-stage non small-cell lung cancer (NSCLC). We aimed to develop a gene expression profile for stage I and stage II NSCLC, allowing identification of patients with a high risk of disease recurrence within 2 to 3 years after initial diagnosis. Experimental Design: We used whole-genome gene expression microarrays to analyze frozen tumor samples from 172 NSCLC patients (pT1-2, N0-1, M0) from five European institutions, who had undergone complete surgical resection. Median follow-up was 89 months (range, 1.2-389) and 64 patients developed a recurrence. A random two thirds of the samples were assigned as the training cohort with the remaining samples set aside for independent validation. Cox proportional hazards models were used to evaluate the association between expression levels of individual genes and patient recurrence-free survival. A nearest mean analysis was used to develop a gene-expression classifier for disease recurrence. Results: We have developed a 72-gene expression prognostic NSCLC classifier. Based on the classifier score, patients were classified as either high or low risk of disease recurrence. Patients classified as low risk showed a significantly better recurrence-free survival both in the training set (P < 0.001; n = 103) and in the independent validation set (P < 0.01; n = 69). Genes in our prognostic signature were strongly enriched for genes associated with immune response. Conclusions: Our 72-gene signature is closely associated with recurrence-free and overall survival in early-stage NSCLC patients and may become a tool for patient selection for adjuvant therapy. C1 [van de Velde, Tony; Burgers, Sjaak; van Zandwijk, Nico] Netherlands Canc Inst, Dept Thorac Oncol, NL-1066 CX Amsterdam, Netherlands. [Smit, Egbert F.; Mooi, Wolter J.] Vrije Univ Med Ctr, Dept Pulm Dis, Amsterdam, Netherlands. [Jassem, Jacek; Rzyman, Witold; Skrzypski, Marcin] Med Univ Gdansk, Dept Oncol & Radiotherapy, Gdansk, Poland. [Muley, Thomas; Meister, Michael; Dienemann, Hendrik] Thoraxklin Univ Heidelberg, Dept Translat Res, Heidelberg, Germany. [Niklinski, Jacek; Kozlowski, Miroslaw] Med Univ Bialystok, Dept Thorac Surg, Bialystok, Poland. [Giaccone, Giuseppe] NCI, Med Oncol Branch, CCR, NIH, Bethesda, MD 20892 USA. RP van Zandwijk, N (reprint author), Netherlands Canc Inst, Dept Thorac Oncol, Plesmanlaan 121, NL-1066 CX Amsterdam, Netherlands. EM n.v.zandwijk@nki.nl RI van Zandwijk, Nico/E-4177-2012; Giaccone, Giuseppe/E-8297-2017 OI van Zandwijk, Nico/0000-0002-8405-9688; Giaccone, Giuseppe/0000-0002-5023-7562 FU Eli Lilly FX Grant support: Eli Lilly. NR 24 TC 84 Z9 84 U1 0 U2 1 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 JAN 1 PY 2009 VL 15 IS 1 BP 284 EP 290 DI 10.1158/1078-0432.CCR-08-1258 PG 7 WC Oncology SC Oncology GA 391JO UT WOS:000262229800032 PM 19118056 ER PT J AU Yang, SX Swain, SM AF Yang, Sherry X. Swain, Sandra M. TI Biomarkers and Response to Therapy in Breast Cancer Reply SO CLINICAL CANCER RESEARCH LA English DT Letter ID METASTATIC COLORECTAL-CANCER; PACLITAXEL PLUS BEVACIZUMAB C1 [Yang, Sherry X.] NCI, Natl Clin Target Validat Lab, Div Canc Treatment & Diag, Bethesda, MD 20892 USA. [Swain, Sandra M.] Washington Hosp Ctr, Washington Canc Inst, Washington, DC 20010 USA. RP Yang, SX (reprint author), NCI, Natl Clin Target Validat Lab, Div Canc Treatment & Diag, Bethesda, MD 20892 USA. NR 6 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD JAN 1 PY 2009 VL 15 IS 1 BP 414 EP 415 DI 10.1158/1078-0432.CCR-08-2602 PG 2 WC Oncology SC Oncology GA 391JO UT WOS:000262229800052 ER PT J AU Miller, WG Bruns, DE Hortin, GL Sandberg, S Aakre, KM McQueen, MJ Itoh, Y Lieske, JC Seccombe, DW Jones, G Bunk, DM Curhan, GC Narva, AS AF Miller, W. Greg Bruns, David E. Hortin, Glen L. Sandberg, Sverre Aakre, Kristin M. McQueen, Matthew J. Itoh, Yoshihisa Lieske, John C. Seccombe, David W. Jones, Graham Bunk, David M. Curhan, Gary C. Narva, Andrew S. CA Natl Kidney Dis Educ Program-IFCC Working Grp Std Albumin Urine TI Current Issues in Measurement and Reporting of Urinary Albumin Excretion SO CLINICAL CHEMISTRY LA English DT Review ID HUMAN-SERUM-ALBUMIN; CHROMATOGRAPHY-MASS-SPECTROMETRY; EXERCISE-INDUCED PROTEINURIA; DEPENDENT DIABETES-MELLITUS; LIQUID-CHROMATOGRAPHY; PROTEOMIC ANALYSIS; FROZEN STORAGE; ORTHOSTATIC PROTEINURIA; FANCONI-SYNDROME; TRACT-INFECTION AB BACKGROUND: Urinary excretion of albumin indicates kidney damage and is recognized as a risk factor for progression of kidney disease and cardiovascular disease. The role of urinary albumin measurements has focused attention on the clinical need for accurate and clearly reported results. The National Kidney Disease Education Program and the IFCC converted a conference to assess the current state of preanalytical, analytical, and postanalytical issues affecting urine albumin measurements and to identify areas needing improvement. CONTENT: The chemistry of albumin in urine is incompletely understood. Current guidelines recommend the use of the albumin/creatinine ratio (ACR) as a surrogate for the error-prone collection of timed urine samples. Although ACR results are affected by patient preparation and time of day of sample collection, neither is standardized. Considerable intermethod differences have been reported for both albumin and creatinine measurement, but trueness is unknown because there are no reference measurement procedures for albumin and no reference materials for either analyte in urine. The recommended reference intervals for the ACR do not take into account the large intergroup differences in creatinine excretion (e.g., related to differences in age, sex, and ethnicity) nor the continuous increase in risk related to albumin excretion. DISCUSSION: Clinical needs have been identified for standardization of (a) urine collection methods, (b) urine albumin and creatinine measurements based on a complete reference system, (c) reporting of test results, and (d) reference intervals for the ACR. (C) 2008 American Association for Clinical Chemistry C1 [Miller, W. Greg] Virginia Commonwealth Univ, Dept Pathol, Richmond, VA USA. [Bruns, David E.] Univ Virginia, Sch Med, Dept Pathol, Charlottesville, VA 22908 USA. [Hortin, Glen L.] NIH, Dept Lab Med, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA. [Sandberg, Sverre; Aakre, Kristin M.] Norwegian Qual Improvement Lab Serv Primary Care, NOKLUS, Bergen, Norway. [Sandberg, Sverre; Aakre, Kristin M.] Haukeland Hosp, Lab Clin Biochem, Bergen, Norway. [McQueen, Matthew J.] McMaster Univ, Dept Pathol & Mol Med, Hamilton Reg Lab, Program Med, Hamilton, ON, Canada. [Itoh, Yoshihisa] Asahikawa Med Coll, Dept Lab Med, Asahikawa, Hokkaido 078, Japan. [Lieske, John C.] Mayo Clin, Renal Funct Lab, Dept Lab Med & Pathol, Div Nephrol & Hypertens,Dept Internal Med, Rochester, MN USA. [Seccombe, David W.] Univ British Columbia, Canadian External Qual Assessment Lab, Vancouver, BC V5Z 1M9, Canada. [Seccombe, David W.] Univ British Columbia, Dept Pathol & Lab Med, Vancouver, BC V5Z 1M9, Canada. [Jones, Graham] St Vincents Hosp Sydney, Dept Chem Pathol, Sydney, NSW, Australia. [Bunk, David M.] Natl Inst Stand & Technol, Div Analyt Chem, Gaithersburg, MD 20899 USA. [Curhan, Gary C.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Renal Div, Boston, MA 02115 USA. [Narva, Andrew S.] Natl Inst Diabet & Digest Dis, Natl Kidney Dis Educ Program, NIH, Bethesda, MD USA. RP Miller, WG (reprint author), POB 980286, Richmond, VA 23298 USA. EM gmiller@vcu.edu NR 128 TC 144 Z9 166 U1 0 U2 17 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD JAN PY 2009 VL 55 IS 1 BP 24 EP 38 DI 10.1373/clinchem.2008.106567 PG 15 WC Medical Laboratory Technology SC Medical Laboratory Technology GA 392LJ UT WOS:000262303900008 PM 19028824 ER PT J AU Kamrava, M Tsang, KY Madan, RA Kaushal, A Coleman, CN Gulley, J AF Kamrava, M. Tsang, Kwong Y. Madan, R. A. Kaushal, A. Coleman, C. N. Gulley, J. TI Long-Term Survival and PSA Control with Radiation and Immunotherapy for Node Positive Prostate Cancer SO CLINICAL & DEVELOPMENTAL IMMUNOLOGY LA English DT Article ID THERAPY; VACCINE AB We describe a patient with node positive prostate cancer treated with radiation, androgen deprivation, and immunotherapy with long-term overall survival and PSA control. ELISPOT immunoassay studies demonstrated PSA specific T-cells prior to starting vaccine therapy suggesting that this positive response may be related to an improved antitumor immune response of the patient, increased immunogenicity of the tumor, or decreased activation of immune escape pathways. Further evaluation of therapeutic cancer vaccines in combination with radiation and hormonal therapy in the definitive management of prostate cancer is warranted. Copyright (C) 2009 National Cancer Institute, National Institutes of Health (NIH/NCI). C1 [Tsang, Kwong Y.; Madan, R. A.; Gulley, J.] NCI, Tumor Immunol & Biol Lab, Ctr Canc Res, Bethesda, MD 20892 USA. [Kamrava, M.; Kaushal, A.; Coleman, C. N.] NCI, Radiat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA. RP Gulley, J (reprint author), NCI, Tumor Immunol & Biol Lab, Ctr Canc Res, Bldg 10, Bethesda, MD 20892 USA. EM gulleyj@mail.nih.gov NR 10 TC 2 Z9 2 U1 1 U2 3 PU HINDAWI PUBLISHING CORPORATION PI NEW YORK PA 410 PARK AVENUE, 15TH FLOOR, #287 PMB, NEW YORK, NY 10022 USA SN 1740-2522 J9 CLIN DEV IMMUNOL JI Clin. Dev. Immunol. PY 2009 AR 363914 DI 10.1155/2009/363914 PG 4 WC Immunology SC Immunology GA 575KN UT WOS:000276066000001 ER PT J AU Herning, RI AF Herning, Ronald I. TI Brain Imaging in Substance Abusers SO CLINICAL EEG AND NEUROSCIENCE LA English DT Editorial Material C1 Biomed Res Ctr, Neuroimaging Res Branch Natl Inst Drug Abuse IRP, Baltimore, MD USA. RP Herning, RI (reprint author), Biomed Res Ctr, Neuroimaging Res Branch Natl Inst Drug Abuse IRP, Baltimore, MD USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU EEG & CLINICAL NEUROSCIENCE SOC (E C N S) PI WHEATON PA 805 W LIBERTY DR, PO BOX 725, WHEATON, IL 60187 USA SN 1550-0594 J9 CLIN EEG NEUROSCI JI Clin. EEG Neurosci. PD JAN PY 2009 VL 40 IS 1 BP VI EP VI PG 1 WC Clinical Neurology; Neurosciences; Neuroimaging; Psychiatry; Psychology SC Neurosciences & Neurology; Psychiatry; Psychology GA 410NV UT WOS:000263585400001 PM 19278125 ER PT J AU Copersino, ML Herning, RI Better, W Cadet, JL Gorelick, DA AF Copersino, Marc L. Herning, Ronald I. Better, Warren Cadet, Jean-Lud Gorelick, David A. TI EEG and Cerebral Blood Flow Velocity Abnormalities in Chronic Cocaine Users SO CLINICAL EEG AND NEUROSCIENCE LA English DT Article; Proceedings Paper CT 4th Joint Meeting of the EEG-and-Clinical-Neuroscience-Society/International-Society-for-NeuroIma ging-in-Psychiatry (ECNS-ISNIP) CY SEP 19-23, 2007 CL Montreal, CANADA SP EEG & Clin Neurosci Soc, Int Soc Neuro Imaging Psychiat DE Cerebral Blood FLow Velocity; Cocaine; Electroencephalography; Pulsatility Index; Transcranial Doppler Sonography ID ANEURYSMAL SUBARACHNOID HEMORRHAGE; POLYSUBSTANCE ABUSERS; ALZHEIMERS-DISEASE; GENDER-DIFFERENCES; DEPENDENCE; PERFUSION; STROKE; ALCOHOL; YOUNG; TECHNETIUM-99M-HMPAO AB EEG and cerebral blood flow abnormalities have been documented in chronic cocaine abusers, To identify possible relationships between EEG and blood flow changes and their relationship to the intensity of cocaine use, we recorded the resting eyes-closed EEG and anterior (ACA) and middle (MCA) cerebral artery blood flow velocity during systole (V(S)) and diastole (V(D)) by transcranial Doppler (TCD) sonography of 99 (76 male, 23 females mean [SD] age 34.3 [5.2] years, 8.6 [5.5] years of cocaine use, 17.8 [7,7] days of cocaine use in month prior to screening) cocaine users within 5 days of admission to a closed research unit, Forty-two non-drug-using, age-matched control subjects (22 male, 20 female) were tested as outpatients. A 3-minute period of resting EEG was recorded from 16 standard scalp electrodes. Artifact-free EEG was converted to six frequency bands (delta, theta, alphal, alpha2, betal and beta2) using a Fast Fourier Transform. Pulsatility index (PI) was calculated as a measure of small vessel resistance. Cocaine users had decreased VD and increased PI in the MCA, with no difference in VS, and reduced EEG theta, betal and beta2 absolute power in posterior brain regions, Recent cocaine use was positively associated with MCA PI (r = 0.27, p < 0.001) and negatively associated with low frequency EEG power (delta power: r = -0.25, p < 0,002; theta power: r = -0.29, p< 0.001). EEG betal (r = -0.211, p < 0.05) and beta2 (r = -0.176, p < 0.05) power measures were correlated with PI. These observations suggest that EEG and TCD changes reflect related physiological processes during early cocaine abstinence. C1 [Herning, Ronald I.] NIDA, Neuroimaging Res Branch, IRP, NIH,Dept Hlth & Human Serv,Biomed Res Ctr, Baltimore, MD 21224 USA. [Copersino, Marc L.; Gorelick, David A.] NIDA, Clin Pharmacol & Therapeut Branch, IRP, NIH,Dept Hlth & Human Serv,Biomed Res Ctr, Baltimore, MD 21224 USA. [Better, Warren] NIDA, Mol Neuropsychiat Branch, IRP, NIH,Dept Hlth & Human Serv,Biomed Res Ctr, Baltimore, MD 21224 USA. RP Herning, RI (reprint author), NIDA, Neuroimaging Res Branch, IRP, NIH,Dept Hlth & Human Serv,Biomed Res Ctr, Suite 200 NIDA,251 Bayview Blvd, Baltimore, MD 21224 USA. EM rHerning@intra.rida.nih.gov FU Intramural NIH HHS [ZIA DA000241-17] NR 40 TC 5 Z9 5 U1 0 U2 3 PU EEG & CLINICAL NEUROSCIENCE SOC (E C N S) PI WHEATON PA 805 W LIBERTY DR, PO BOX 725, WHEATON, IL 60187 USA SN 1550-0594 J9 CLIN EEG NEUROSCI JI Clin. EEG Neurosci. PD JAN PY 2009 VL 40 IS 1 BP 39 EP 42 PG 4 WC Clinical Neurology; Neurosciences; Neuroimaging; Psychiatry; Psychology SC Neurosciences & Neurology; Psychiatry; Psychology GA 410NV UT WOS:000263585400007 PM 19278131 ER PT J AU Pinsky, PF Schoen, RE Weissfeld, JL Church, T Yokochi, LA Doria-Rose, VP Prorok, P AF Pinsky, Paul F. Schoen, Robert E. Weissfeld, Joel L. Church, Timothy Yokochi, Lance A. Doria-Rose, V. Paul Prorok, Philip TI The Yield of Surveillance Colonoscopy by Adenoma History and Time to Examination SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY LA English DT Article ID COLORECTAL-CANCER; FLEXIBLE SIGMOIDOSCOPY; SCREENING COLONOSCOPY; RANDOMIZED-TRIAL; POLYPS; COLON; PREVENTION; CELECOXIB; INTERVAL; RISK AB Background & Aims: Surveillance colonoscopy is recommended for subjects with a history of adenomas but there is limited information on the yield of surveillance. Methods: A sample of subjects in the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial with abnormal flexible sigmoidoscopy and follow-up colonoscopy were queried about subsequent surveillance colonoscopy over a 10-year period. Medical records were obtained to verify procedure dates and histologic findings. Subjects with advanced adenomas, nonadvanced adenoma nonadenomatous polyps, and no polyps at baseline were included. Results: At the first surveillance, 10.5% had advanced adenoma and 37% had any adenoma in the advanced adenoma group (n = 1057), compared with rates of 6.8% and 32% (nonadvanced adenoma: n = 765), 4.9% and 22% (nonadenomatous polyps: n = 658), and 3.1% and 16% (no polyps: n = 127) (P < .0001, linear trend test). Mean (SD) time intervals (years) from baseline colonoscopy to first surveillance were 3.4 (2.0) for advanced adenoma, 4.3 (2.0) for nonadvanced adenoma, 4.5 (2.0) for nonadenomatous polyps, and 4.7 (2.0) for no polyps. There were no increasing (or decreasing) trends in the observed rate of advanced adenoma or any adenoma with time to the initial surveillance examination in any baseline group. Among subjects with a second surveillance examination, adenoma findings at both baseline and first surveillance influenced the rates of advanced adenoma and any adenoma at second surveillance. Conclusions: Subjects with baseline advanced adenomas are more likely to have recurrent advanced adenomas at initial surveillance. The lack of association between recurrence rates and time to surveillance suggests limitations in our understanding of the biology of adenoma development. C1 [Pinsky, Paul F.; Doria-Rose, V. Paul; Prorok, Philip] NCI, Canc Prevent Div, Bethesda, MD 20892 USA. [Doria-Rose, V. Paul] NCI, Canc Prevent Fellowship Program, Off Prevent Oncol, Bethesda, MD 20892 USA. [Schoen, Robert E.; Weissfeld, Joel L.] Univ Pittsburgh, Pittsburgh, PA USA. [Church, Timothy] Univ Minnesota, Sch Publ Hlth, Minneapolis, MN USA. [Yokochi, Lance A.] Pacific Hlth Res Inst, Honolulu, HI USA. RP Pinsky, PF (reprint author), 6130 Execut Blvd,EPN 3064, Bethesda, MD 20892 USA. EM pp4f@nih.gov OI Doria-Rose, Vincent/0000-0002-8802-5143; Church, Timothy R./0000-0003-3292-5035 FU National Cancer Institute FX Supported in part by contracts from the National Cancer Institute. NR 22 TC 44 Z9 44 U1 0 U2 4 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 1542-3565 J9 CLIN GASTROENTEROL H JI Clin. Gastroenterol. Hepatol. PD JAN PY 2009 VL 7 IS 1 BP 86 EP 92 DI 10.1016/j.cgh.2008.07.014 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 399TK UT WOS:000262822000016 PM 18829395 ER PT J AU Ashida, S Hadley, DW Vaughn, BK Kuhn, NR Jenkins, JF Koehly, LM AF Ashida, S. Hadley, D. W. Vaughn, B. K. Kuhn, N. R. Jenkins, J. F. Koehly, L. M. TI The impact of familial environment on depression scores after genetic testing for cancer susceptibility SO CLINICAL GENETICS LA English DT Article DE cancer worry; CES-D; family relationships; genetic testing; hereditary nonpolyposis colorectal cancer; Lynch syndrome; social environment ID NONPOLYPOSIS COLORECTAL-CANCER; PSYCHOLOGICAL DISTRESS; HEREDITARY BREAST; BRCA1; UPDATE; EXPERIENCE; SISTERS; SYSTEM; FUTURE; MODEL AB The associations between characteristics of family relationships and family trends in cancer worry and the psychological adjustment of recipients of genetic testing for cancer susceptibility were investigated. Data provided by 178 individuals from 24 families with Lynch syndrome who participated in a cohort study investigating psychological and behavioral outcomes of genetic testing were used. Responses from multiple family members were aggregated to construct family trends representing norms and departure from norms in cancer worry. Lower perceived family cohesion at baseline and decrease in this variable at 6 months after receipt of test results were associated with higher depression scores at 12 months. More variability in cancer worry among family members at baseline was also associated with higher depression scores at 12 months. Increase in family conflict was associated with decrease in depression scores among individuals from families with higher levels of cancer worry on average and less variability among the members. Family relationships and family trends in levels of cancer worry may play important roles in the psychological adjustment of genetic test recipients. The findings highlight the complexity of familial environment surrounding individuals that undergo genetic testing and suggest the benefits of considering these factors when providing genetic services. C1 [Ashida, S.; Hadley, D. W.; Kuhn, N. R.; Koehly, L. M.] NHGRI, Social & Behav Res Branch, NIH, Bethesda, MD 20892 USA. [Vaughn, B. K.] Univ Texas Austin, Coll Educ, Austin, TX 78712 USA. [Jenkins, J. F.] NHGRI, Off Director, NIH, Bethesda, MD 20892 USA. RP Ashida, S (reprint author), 31 Ctr Dr,31-B1B37C MSC 2073, Bethesda, MD USA. EM ashidas@mail.nih.gov FU National Human Genome Research Institute; National Cancer Institute FX This research was supported by the Intramural Research Programs of the National Human Genome Research Institute and the National Cancer Institute at the National Institutes of Health in Bethesda, Maryland. We thank our participants for the willingness to share their lives with us for without their efforts this work would not be possible. NR 39 TC 7 Z9 7 U1 0 U2 0 PU WILEY-BLACKWELL PUBLISHING, INC PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0009-9163 J9 CLIN GENET JI Clin. Genet. PD JAN PY 2009 VL 75 IS 1 BP 43 EP 49 DI 10.1111/j.1399-0004.2008.01104.x PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 389XP UT WOS:000262129200008 PM 19021640 ER PT J AU Ahmed, ZM Riazuddin, S Khan, SN Friedman, PL Riazuddin, S Friedman, TB AF Ahmed, Z. M. Riazuddin, S. Khan, S. N. Friedman, P. L. Riazuddin, S. Friedman, T. B. TI USH1H, a novel locus for type I Usher syndrome, maps to chromosome 15q22-23 SO CLINICAL GENETICS LA English DT Article DE 15q22-23; deafness; DFNB48; retinitis pigmentosa; Usher syndrome; USH1H; vestibular dysfunction ID NONSYNDROMIC HEARING-LOSS; SYNDROME TYPE 1F; TRANSCRIPTION FACTOR; INNER-EAR; RETINITIS-PIGMENTOSA; DEAFNESS LOCUS; ASHKENAZI JEWS; MUTATIONS; GENE; PCDH15 AB Usher syndrome (USH) is a hereditary disorder associated with sensorineural hearing impairment, progressive loss of vision attributable to retinitis pigmentosa (RP) and variable vestibular function. Three clinical types have been described with type I (USH1) being the most severe. To date, six USH1 loci have been reported. We ascertained two large Pakistani consanguineous families segregating profound hearing loss, vestibular dysfunction, and RP, the defining features of USH1. In these families, we excluded linkage of USH to the 11 known USH loci and subsequently performed a genome-wide linkage screen. We found a novel USH1 locus designated USH1H that mapped to chromosome 15q22-23 in a 4.92-cM interval. This locus overlaps the non-syndromic deafness locus DFNB48 raising the possibility that the two disorders may be caused by allelic mutations. C1 [Ahmed, Z. M.; Riazuddin, S.; Friedman, T. B.] Natl Inst Deafness & Other Commun Disorders, Sect Human Genet, Mol Genet Lab, NIH, Rockville, MD 20850 USA. [Khan, S. N.; Riazuddin, S.] Univ Punjab, Natl Ctr Excellence Mol Biol, Lahore, Pakistan. [Friedman, P. L.] NIH, Internal Med Consult Serv, Hatfield Clin Res Ctr, Bethesda, MD USA. RP Friedman, TB (reprint author), Natl Inst Deafness & Other Commun Disorders, Sect Human Genet, Mol Genet Lab, NIH, 5 Res Court,Rm 2A-19, Rockville, MD 20850 USA. EM friedman@nidcd.nih.gov RI Nasim Khan, Shaheen/F-2135-2015 FU Higher Education Commission, Islamabad, Pakistan; Ministry of Science and Technology, Islamabad, Pakistan; National Institute on Deafness and Other Communication Disorders; National Institutes of Health [1 ZO1 DC000039-11] FX The authors are grateful to the families who made this research possible. We thank Julie Schultz, Andrew Griffith, Anne Madeo, Karen Friderici and Dennis Drayna for suggestions regarding this manuscript. This study was supported by the Higher Education Commission, Islamabad, Pakistan; Ministry of Science and Technology, Islamabad, Pakistan and by intramural funds to T. B. F. from the National Institute on Deafness and Other Communication Disorders, National Institutes of Health (1 ZO1 DC000039-11). NR 40 TC 17 Z9 17 U1 0 U2 2 PU WILEY-BLACKWELL PUBLISHING, INC PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0009-9163 J9 CLIN GENET JI Clin. Genet. PD JAN PY 2009 VL 75 IS 1 BP 86 EP 91 DI 10.1111/j.1399-0004.2008.01038.x PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 389XP UT WOS:000262129200014 PM 18505454 ER PT J AU Ahmadzadeh, M Johnson, L Heemskerk, B Wunderlich, J Rosenberg, S AF Ahmadzadeh, Mojgan Johnson, Laura Heemskerk, Bianca Wunderlich, John Rosenberg, Steven TI Tumor Antigen-specific CD8 T Cells Infiltrating the Tumor Express High Levels of PD-1 and are Functionally Impaired SO CLINICAL IMMUNOLOGY LA English DT Meeting Abstract CT 9th Annual Meeting of the Federation-of-Clinical-Immunology-Societies CY JUN 11-14, 2009 CL San Francisco, CA SP Federat Clin Immunol Soc C1 [Ahmadzadeh, Mojgan; Johnson, Laura; Heemskerk, Bianca; Wunderlich, John; Rosenberg, Steven] NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1521-6616 J9 CLIN IMMUNOL JI Clin. Immunol. PY 2009 VL 131 BP S38 EP S38 DI 10.1016/j.clim.2009.03.108 PG 1 WC Immunology SC Immunology GA 449PK UT WOS:000266342300103 ER PT J AU Brydges, S Mueller, J McGeough, M Pena, C Misaghi, A Gandhi, C Boyle, D Firestein, G Horner, A Soroosh, P Putnam, C Watford, W O'Shea, J Kastner, D Hoffman, H AF Brydges, Susannah Mueller, James McGeough, Matthew Pena, Carla Misaghi, Amirhossein Gandhi, Chhavi Boyle, David Firestein, Gary Horner, Anthony Soroosh, Pejman Putnam, Chris Watford, Wendy O'Shea, John Kastner, Daniel Hoffman, Hal TI Animal Models of Inflammasomapathy Solely Implicate the Innate Immune System in Pathogenesis, with an Important but not Universal Role for IL-1 beta SO CLINICAL IMMUNOLOGY LA English DT Meeting Abstract CT 9th Annual Meeting of the Federation-of-Clinical-Immunology-Societies CY JUN 11-14, 2009 CL San Francisco, CA SP Federat Clin Immunol Soc C1 [Brydges, Susannah; McGeough, Matthew; Pena, Carla; Misaghi, Amirhossein; Gandhi, Chhavi; Boyle, David; Firestein, Gary; Horner, Anthony] Univ Calif San Diego, La Jolla, CA 92093 USA. [Soroosh, Pejman] La Jolla Inst Allergy & Immunol, La Jolla, CA USA. [Watford, Wendy; O'Shea, John; Kastner, Daniel] NIAMSD, Bethesda, MD 20892 USA. [Mueller, James; Putnam, Chris; Hoffman, Hal] Ludwig Inst Canc Res, La Jolla, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1521-6616 J9 CLIN IMMUNOL JI Clin. Immunol. PY 2009 VL 131 BP S13 EP S14 DI 10.1016/j.clim.2009.03.033 PG 2 WC Immunology SC Immunology GA 449PK UT WOS:000266342300030 ER PT J AU Foster, S Reuben, J Cohen, E Asthana, D Lu, M Thompson, B Paul, M Glaze, D Shahzeidi, S Colin, A Miller, T Harris, L Armstrong, D Scott, G Brouwers, P McMullen-Jackson, C Himic, L Schwarzwald, H Lipshultz, S Shearer, W AF Foster, Samuel Reuben, James Cohen, Evan Asthana, Deshratn Lu, Ming Thompson, Bruce Paul, Mary Glaze, Daniel Shahzeidi, Shahriar Colin, Andrew Miller, Tracie Harris, Lynnette Armstrong, Daniel Scott, Gwendolyn Brouwers, Pim McMullen-Jackson, Chivon Himic, Lisa Schwarzwald, Heidi Lipshultz, Steven Shearer, William TI Circadian Regulation of IL-6, IL-1 beta and IL-1RA Levels is Disrupted in HIV-infected Children SO CLINICAL IMMUNOLOGY LA English DT Meeting Abstract CT 9th Annual Meeting of the Federation-of-Clinical-Immunology-Societies CY JUN 11-14, 2009 CL San Francisco, CA SP Federat Clin Immunol Soc C1 [Reuben, James; Cohen, Evan] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA. [Foster, Samuel; Paul, Mary; Glaze, Daniel; Harris, Lynnette; McMullen-Jackson, Chivon; Schwarzwald, Heidi; Shearer, William] Baylor Coll Med, Houston, TX 77030 USA. [Asthana, Deshratn; Shahzeidi, Shahriar; Colin, Andrew; Miller, Tracie; Armstrong, Daniel; Scott, Gwendolyn; Himic, Lisa; Lipshultz, Steven] Univ Miami, Leonard M Miller Sch Med, Miami, FL USA. [Lu, Ming; Thompson, Bruce] CIin Trials & Surveys Corp, Baltimore, MD USA. [Brouwers, Pim] NIMH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1521-6616 J9 CLIN IMMUNOL JI Clin. Immunol. PY 2009 VL 131 BP S55 EP S55 DI 10.1016/j.clim.2009.03.157 PG 1 WC Immunology SC Immunology GA 449PK UT WOS:000266342300151 ER PT J AU Heimall, J Fessler, M Jain, A AF Heimall, Jennifer Fessler, Margaret Jain, Ashish TI Eosinophilic Esophagitis and Atopic Dermatitis Treated with Omalizumab in a Patient with NEMO Defect SO CLINICAL IMMUNOLOGY LA English DT Meeting Abstract CT 9th Annual Meeting of the Federation-of-Clinical-Immunology-Societies CY JUN 11-14, 2009 CL San Francisco, CA SP Federat Clin Immunol Soc C1 [Heimall, Jennifer; Fessler, Margaret; Jain, Ashish] NIAID, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1521-6616 J9 CLIN IMMUNOL JI Clin. Immunol. PY 2009 VL 131 BP S141 EP S141 DI 10.1016/j.clim.2009.03.414 PG 1 WC Immunology SC Immunology GA 449PK UT WOS:000266342300406 ER PT J AU Heimall, J Freeman, A Davis, J Hsu, A Shaw, P Holland, S AF Heimall, Jennifer Freeman, Alexandra Davis, Joie Hsu, Amy Shaw, Pamela Holland, Steven TI Genotype-phenotype Correlations in STAT3 Mutated Hyper IgE Syndrome (HIES) Patients SO CLINICAL IMMUNOLOGY LA English DT Meeting Abstract CT 9th Annual Meeting of the Federation-of-Clinical-Immunology-Societies CY JUN 11-14, 2009 CL San Francisco, CA SP Federat Clin Immunol Soc C1 [Heimall, Jennifer; Freeman, Alexandra; Davis, Joie; Hsu, Amy; Shaw, Pamela; Holland, Steven] NIAID, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1521-6616 J9 CLIN IMMUNOL JI Clin. Immunol. PY 2009 VL 131 BP S101 EP S101 DI 10.1016/j.clim.2009.03.293 PG 1 WC Immunology SC Immunology GA 449PK UT WOS:000266342300285 ER PT J AU Mannino, E Gharib, A Hsu, A Heimall, J Holland, S Freeman, A AF Mannino, Elizabeth Gharib, Ahmed Hsu, Amy Heimall, Jennifer Holland, Steven Freeman, Alexandra TI Coronary Artery Abnormalities in Hyperimmunoglobulin E Syndrome SO CLINICAL IMMUNOLOGY LA English DT Meeting Abstract CT 9th Annual Meeting of the Federation-of-Clinical-Immunology-Societies CY JUN 11-14, 2009 CL San Francisco, CA SP Federat Clin Immunol Soc C1 [Mannino, Elizabeth; Gharib, Ahmed; Hsu, Amy; Heimall, Jennifer; Holland, Steven; Freeman, Alexandra] NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1521-6616 J9 CLIN IMMUNOL JI Clin. Immunol. PY 2009 VL 131 BP S97 EP S97 DI 10.1016/j.clim.2009.03.282 PG 1 WC Immunology SC Immunology GA 449PK UT WOS:000266342300274 ER PT J AU Milner, J Hsu, A Freeman, A Heimall, J Brenchley, J Pittaluga, S Douek, D Holland, S AF Milner, Joshua Hsu, Amy Freeman, Alexandra Heimall, Jennifer Brenchley, Jason Pittaluga, Stefunia Douek, Daniel Holland, Steven TI Somatic Mosaicism for STAT3 Mutation Unveils Critical Role in Human T-cell Memory Development and B Cell Help SO CLINICAL IMMUNOLOGY LA English DT Meeting Abstract CT 9th Annual Meeting of the Federation-of-Clinical-Immunology-Societies CY JUN 11-14, 2009 CL San Francisco, CA SP Federat Clin Immunol Soc C1 [Milner, Joshua; Hsu, Amy; Freeman, Alexandra; Heimall, Jennifer; Brenchley, Jason; Douek, Daniel; Holland, Steven] NIAID, Bethesda, MD 20892 USA. [Pittaluga, Stefunia] NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1521-6616 J9 CLIN IMMUNOL JI Clin. Immunol. PY 2009 VL 131 BP S94 EP S94 DI 10.1016/j.clim.2009.03.272 PG 1 WC Immunology SC Immunology GA 449PK UT WOS:000266342300264 ER PT J AU Milner, J Lily, C Ward, J Finkelman, F Paul, W Orekov, T AF Milner, Joshua Lily, Cheng Ward, Jerrold Finkelman, Fred Paul, William Orekov, Tatyana TI Acute Exposure to IL-4 Reveals a Novel Pathway for Induction of Hemophagocytosis and Histiocytosis SO CLINICAL IMMUNOLOGY LA English DT Meeting Abstract CT 9th Annual Meeting of the Federation-of-Clinical-Immunology-Societies CY JUN 11-14, 2009 CL San Francisco, CA SP Federat Clin Immunol Soc C1 [Milner, Joshua; Lily, Cheng; Ward, Jerrold; Paul, William] NIAID, Bethesda, MD 20892 USA. [Finkelman, Fred; Orekov, Tatyana] Univ Cincinnati, Cincinnati, OH USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1521-6616 J9 CLIN IMMUNOL JI Clin. Immunol. PY 2009 VL 131 BP S33 EP S34 DI 10.1016/j.clim.2009.03.094 PG 2 WC Immunology SC Immunology GA 449PK UT WOS:000266342300089 ER PT J AU Orban, T Farkas, K Jalahej, H Kis, J Treszl, A Falk, B Reijonen, H Wolfsdorf, J Ricker, A Matthews, J Tchao, N Sayre, P Bianchine, P AF Orban, Tihamer Farkas, Klara Jalahej, Heyam Kis, Janos Treszl, Andras Falk, Ben Reijonen, Helena Wolfsdorf, Joseph Ricker, Alyne Matthews, Jeffrey Tchao, Nadia Sayre, Peter Bianchine, Peter TI Autoantigen Specific Regulatory T Cells Induced in Patients with Type 1 Diabetes Mellitus SO CLINICAL IMMUNOLOGY LA English DT Meeting Abstract CT 9th Annual Meeting of the Federation-of-Clinical-Immunology-Societies CY JUN 11-14, 2009 CL San Francisco, CA SP Federat Clin Immunol Soc C1 [Orban, Tihamer; Farkas, Klara; Jalahej, Heyam] Joslin Diabet Ctr, Boston, MA 02215 USA. [Kis, Janos] Polyclin Hosp Bros, Budapest, Hungary. [Treszl, Andras] Semmelweis Univ, H-1085 Budapest, Hungary. [Falk, Ben; Reijonen, Helena] Virginia Mason, Seattle, WA USA. [Wolfsdorf, Joseph; Ricker, Alyne] Childrens Hosp, Boston, MA 02115 USA. [Matthews, Jeffrey; Tchao, Nadia; Sayre, Peter] UCSF, San Francisco, CA USA. [Bianchine, Peter] NIAID, Bethesda, DC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1521-6616 J9 CLIN IMMUNOL JI Clin. Immunol. PY 2009 VL 131 SU S BP S83 EP S83 DI 10.1016/j.clim.2009.03.243 PG 1 WC Immunology SC Immunology GA 449PK UT WOS:000266342300236 ER PT J AU Rother, K Brown, R Wrigh, E Morales, M Compbell, C Horlon, D Orlander, P Duan, ZG Brod, S AF Rother, Kristina Brown, Rebecca Wrigh, Elizabeth Morales, Miriam Compbell, Carol Horlon, David Orlander, Philip Duan, Zhigang Brod, Staley TI Ingested IFN-alpha2A Prolongs the 'Honeymoon' Phase in New Onset Type 1 Diabetes Mellitus (T1D) in a Phase II Randomized Clinical Trial (RCT) SO CLINICAL IMMUNOLOGY LA English DT Meeting Abstract CT 9th Annual Meeting of the Federation-of-Clinical-Immunology-Societies CY JUN 11-14, 2009 CL San Francisco, CA SP Federat Clin Immunol Soc C1 [Morales, Miriam; Orlander, Philip; Brod, Staley] Univ Texas Houston, Bellaire, TX USA. [Rother, Kristina; Brown, Rebecca; Wrigh, Elizabeth; Compbell, Carol; Horlon, David; Duan, Zhigang] NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1521-6616 J9 CLIN IMMUNOL JI Clin. Immunol. PY 2009 VL 131 BP S107 EP S107 DI 10.1016/j.clim.2009.03.311 PG 1 WC Immunology SC Immunology GA 449PK UT WOS:000266342300303 ER PT J AU Snow, A Marsh, R Krummey, S Roehrs, P Zhang, KJ Filipovich, L Su, H Bleesing, J Lenordo, M AF Snow, Andrew Marsh, Rebecca Krummey, Scott Roehrs, Philip Zhang, Kejian Filipovich, Lisa Su, Helen Bleesing, Jacob Lenordo, Michael TI SAP Augments Proximal T Cell Receptor Signal Strength Necessary for Restimulation-induced Apoptosis of Activated T Cells SO CLINICAL IMMUNOLOGY LA English DT Meeting Abstract CT 9th Annual Meeting of the Federation-of-Clinical-Immunology-Societies CY JUN 11-14, 2009 CL San Francisco, CA SP Federat Clin Immunol Soc C1 [Snow, Andrew; Krummey, Scott; Su, Helen; Lenordo, Michael] NIAID, NIH, Bethesda, MD 20892 USA. [Marsh, Rebecca; Roehrs, Philip; Zhang, Kejian; Filipovich, Lisa; Bleesing, Jacob] Cincinnati Childrens Hosp, Med Ctr, Cincinnati, OH USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1521-6616 J9 CLIN IMMUNOL JI Clin. Immunol. PY 2009 VL 131 BP S160 EP S160 DI 10.1016/j.clim.2009.03.473 PG 1 WC Immunology SC Immunology GA 449PK UT WOS:000266342300466 ER PT J AU Song, YJ Meylan, F Fuss, I Davidson, T Shevach, E Siegel, R AF Song, Yun-Jeong Meylan, Francoise Fuss, Ivan Davidson, Todd Shevach, Ethan Siegel, Richard TI TL1A-DR3 Interactions in T-cell Mediated Autoimmunity; an Attractive Target for Immunotherapy SO CLINICAL IMMUNOLOGY LA English DT Meeting Abstract CT 9th Annual Meeting of the Federation-of-Clinical-Immunology-Societies CY JUN 11-14, 2009 CL San Francisco, CA SP Federat Clin Immunol Soc C1 [Song, Yun-Jeong; Meylan, Francoise; Fuss, Ivan; Davidson, Todd; Shevach, Ethan; Siegel, Richard] NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1521-6616 J9 CLIN IMMUNOL JI Clin. Immunol. PY 2009 VL 131 BP S74 EP S74 DI 10.1016/j.clim.2009.03.215 PG 1 WC Immunology SC Immunology GA 449PK UT WOS:000266342300208 ER PT J AU Tran, D Shevach, E AF Tran, Dat Shevach, Ethan TI Selective Expression of Latency Associated Peptide (LAP) and IL-1 Receptor Type I/II (CD121a/CD121b) on Activated Human FOXP3+Regulatory T Cells Allows for Their Purification from Expansion Cultures for Potential Immunotherapy SO CLINICAL IMMUNOLOGY LA English DT Meeting Abstract CT 9th Annual Meeting of the Federation-of-Clinical-Immunology-Societies CY JUN 11-14, 2009 CL San Francisco, CA SP Federat Clin Immunol Soc C1 [Tran, Dat; Shevach, Ethan] NIAID, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1521-6616 J9 CLIN IMMUNOL JI Clin. Immunol. PY 2009 VL 131 BP S81 EP S82 DI 10.1016/j.clim.2009.03.239 PG 2 WC Immunology SC Immunology GA 449PK UT WOS:000266342300232 ER PT J AU Tran, D Shevach, E AF Tran, Dat Shevach, Ethan TI GARP (LRRC32) is Essential for the Surface Expression of Latent TGF beta on Platelets and Activated FOXP3+Regulatory T Cells by Anchoring it to the Membrane SO CLINICAL IMMUNOLOGY LA English DT Meeting Abstract CT 9th Annual Meeting of the Federation-of-Clinical-Immunology-Societies CY JUN 11-14, 2009 CL San Francisco, CA SP Federat Clin Immunol Soc C1 [Tran, Dat; Shevach, Ethan] NIAID, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1521-6616 J9 CLIN IMMUNOL JI Clin. Immunol. PY 2009 VL 131 BP S40 EP S40 DI 10.1016/j.clim.2009.03.113 PG 1 WC Immunology SC Immunology GA 449PK UT WOS:000266342300108 ER PT J AU Joy, MS Gipson, DS Dike, M Powell, L Thompson, A Vento, S Eddy, A Fogo, AB Kopp, JB Cattran, D Trachtman, H AF Joy, Melanie S. Gipson, Debbie S. Dike, Mary Powell, Leslie Thompson, Amber Vento, Suzanne Eddy, Allison Fogo, Agnes B. Kopp, Jeffrey B. Cattran, Daniel Trachtman, Howard TI Phase I Trial of Rosiglitazone in FSGS: I. Report of the FONT Study Group SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article ID CHRONIC-RENAL-FAILURE; PHARMACOKINETICS; DISEASE; CYTOCHROME-P450; METABOLISM AB Background and objectives: Patients with primary focal segmental glomerulosclerosis (FSGS) who are resistant to standard therapy are at high risk for progressive chronic kidney disease. Prevention of renal fibrosis represents a promising strategy to slow or halt kidney function decline. This paper presents the results of a Phase I clinical trial of rosiglitazone, a thiazolidinedione, that exerts antifibrotic effects in animal models of FSGS. The primary goal was assessment of safety, tolerability, and pharmacokinetics (PK) of rosiglitazone. Design, setting, participants, & measurements; Eleven patients, including eight boys/men and three girls/women, with mean age 15 +/- 6 yr and estimated GFR 131 +/- 62 ml/min/1.73 m(2), received rosiglitazone, 3 mg/m(2)/d for 16 wk. PK was assessed twice, after the initial dose and after attaining steady state, in a General Clinical Research Center. Results: There were no serious adverse events or cardiovascular complications. Rosiglitazone was well tolerated by all patients, as judged by the Treatment Satisfaction Questionnaire for Medication. The PK studies indicated that the area under the curve was decreased by 40 to 50% and oral clearance of rosiglitazone was increased by 250 to 300% in patients with resistant FSGS compared with healthy controls and patients with nonproteinuric stage 2 chronic kidney disease. Conclusions: Rosiglitazone therapy was safe and well tolerated. PK assessment of potential novel therapies for resistant FSGS is necessary to define appropriate dosing regimens. There is rationale to evaluate the efficacy of rosiglitazone as all antifibrotic agent for resistant FSGS in Phase II/III clinical trials. C1 [Vento, Suzanne; Trachtman, Howard] Schneider Childrens Hosp, N Shore Long Isl Jewish Hlth Syst, Div Nephrol, New Hyde Pk, NY 11040 USA. [Joy, Melanie S.; Gipson, Debbie S.; Dike, Mary; Powell, Leslie; Thompson, Amber] Univ N Carolina, Kidney Ctr, Chapel Hill, NC USA. [Joy, Melanie S.; Gipson, Debbie S.; Dike, Mary; Powell, Leslie; Thompson, Amber] Univ N Carolina, Div Nephrol & Hypertens, Chapel Hill, NC USA. [Joy, Melanie S.] Univ N Carolina, Sch Pharm, Div Pharmacotherapy & Expt Therapeut, Chapel Hill, NC USA. [Joy, Melanie S.] Univ N Carolina, Sch Pharm, Div Mol Pharmaceut, Chapel Hill, NC USA. [Eddy, Allison] Seattle Childrens Hosp, Div Nephrol, Seattle, WA USA. [Fogo, Agnes B.] Vanderbilt Univ, Med Ctr, Dept Pathol, Nashville, TN 37232 USA. [Kopp, Jeffrey B.] NIDDKD, Kidney Dis Branch, NIH, Bethesda, MD 20892 USA. [Cattran, Daniel] Univ Hlth Network, Toronto Gen Res, Toronto, ON, Canada. RP Trachtman, H (reprint author), Schneider Childrens Hosp, N Shore Long Isl Jewish Hlth Syst, Div Nephrol, 269-01 76th Ave, New Hyde Pk, NY 11040 USA. EM trachtma@lij.edu OI Eddy, Allison/0000-0002-3560-7510; Trachtman, Howard/0000-0001-7447-9489; Kopp, Jeffrey/0000-0001-9052-186X FU National Institutes Of Health; NIDDK Intramural Research Program; [R21-DK70341] FX This work was supported by a grant from the National Institutes Of Health (NIH)-National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) (R21-DK70341) to Howard Trachtman and funds from the NIDDK Intramural Research Program to Jeffrey B. Kopp. The authors thank lose Groenboom for his technical assistance in measuring; the plasma rosiglitazone and N-desinethylrosigHtazone levels and Dr, Philip C. Sinith, Associate Professor, School of Pharmacy, University of North Carolina (UNC), for his critical comments on this manuscript. NR 23 TC 19 Z9 20 U1 0 U2 0 PU AMER SOC NEPHROLOGY PI WASHINGTON PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA SN 1555-9041 J9 CLIN J AM SOC NEPHRO JI Clin. J. Am. Soc. Nephrol. PD JAN PY 2009 VL 4 IS 1 BP 39 EP 47 DI 10.2215/CJN.02310508 PG 9 WC Urology & Nephrology SC Urology & Nephrology GA 397SA UT WOS:000262681200009 PM 19073787 ER PT J AU Koenigs, M Ukueberuwa, D Campion, P Grafman, J Wassermann, E AF Koenigs, Michael Ukueberuwa, Dede Campion, Paul Grafman, Jordan Wassermann, Eric TI Bilateral frontal transcranial direct current stimulation: Failure to replicate classic findings in healthy subjects SO CLINICAL NEUROPHYSIOLOGY LA English DT Article DE Emotion; Cognition; Frontal lobe; Direct current; Behavior; Electrical; Non-invasive; Brain stimulation ID NONINVASIVE BRAIN-STIMULATION; PREFRONTAL CORTEX; DC STIMULATION; DOUBLE-BLIND; MAGNETIC STIMULATION; MAJOR DEPRESSION; POLARIZATION; MEMORY; DAMAGE; TRIAL AB Objective: There has been no modern effort to replicate, further characterize, or quantify the dramatic effects on affect described in controlled studies from the 1960s using bilateral frontal electrodes with an extra-cephalic reference in a mixed group composed primarily of mildly depressed individuals. We performed a comprehensive, quantitative assessment of the effects of bifrontal TDCS on emotion in 21 healthy subjects. Methods: In a double-blind crossover study, we administered tests of emotional state, affect, emotional decision-making, arousal, and psychomotor functions during sham, anodal, and cathodal TDCS. Results: We found no systematic effects on any measure, despite two subjects who had pronounced mood effects in the predicted direction. There were no adverse events. Conclusions: In line with some other studies, we found no consistent effects of bifrontal TDCS on measures of emotional function of psychomotor performance. Significance: These results demonstrate the safety of bilateral anterior frontal TDCS with an extra-cephalic reference, but raise questions about its effectiveness as a modulator of mood and emotional cognition, at least in healthy subjects. Published by Elsevier Ireland Ltd. on behalf of International Federation of Clinical Neurophysiology. C1 [Koenigs, Michael; Ukueberuwa, Dede; Campion, Paul; Wassermann, Eric] Natl Inst Neurol Disorders & Stroke, Brain Stimulat Unit, NIH, Bethesda, MD 20892 USA. [Koenigs, Michael] Univ Wisconsin, Dept Psychiat, Madison, WI 53719 USA. [Grafman, Jordan] Natl Inst Neurol Disorders & Stroke, Cognit Neurosci Sect, NIH, Bethesda, MD 20892 USA. RP Wassermann, E (reprint author), Natl Inst Neurol Disorders & Stroke, Brain Stimulat Unit, NIH, 10 Ctr Dr,MSC 1440, Bethesda, MD 20892 USA. EM wassermanne@ninds.nih.gov OI Grafman, Jordan H./0000-0001-8645-4457; Koenigs, Michael/0000-0002-5799-4881; Campion, Paul/0000-0002-9569-5321 FU Intramural Research Program; NINDS; NIH FX This work was supported by the Intramural Research Program, NINDS, NIH. The authors wish to thank Ms. Devee Schoenberg for editing the manuscript. NR 32 TC 35 Z9 35 U1 1 U2 11 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 1388-2457 J9 CLIN NEUROPHYSIOL JI Clin. Neurophysiol. PD JAN PY 2009 VL 120 IS 1 BP 80 EP 84 DI 10.1016/j.clinph.2008.10.010 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 400RA UT WOS:000262885000011 PM 19027357 ER PT J AU Soldin, OP Mattison, DR AF Soldin, Offie P. Mattison, Donald R. TI Sex Differences in Pharmacokinetics and Pharmacodynamics SO CLINICAL PHARMACOKINETICS LA English DT Review ID SERUM-PROTEIN BINDING; GENDER-DIFFERENCES; MENSTRUAL-CYCLE; ORAL-CONTRACEPTIVES; OCCUPATIONAL-HEALTH; IRON-ABSORPTION; PREGNANT-WOMEN; PLASMA-LEVELS; WEIGHT-GAIN; AGE AB Significant differences that exist between the sexes affect the prevalence, incidence and severity of a broad range of diseases and conditions. Men and women also differ in their response to drug treatment. It is therefore essential to understand these reactions in order to appropriately conduct risk assessment and to design safe and effective treatments. Even from that modest perspective, how and when we use drugs can result in unwanted and unexpected outcomes. This review summarizes the sex-based differences that impact on pharmacokinetics, and includes a general comparison of clinical pharmacology as it applies to men, women and pregnant women. Sex-related or pregnancy-induced changes in drug absorption, distribution, metabolism and elimination, when significant, may guide changes in dosage regimen or therapeutic monitoring to increase its effectiveness or reduce potential toxicity. Given those parameters, and our knowledge of sex differences, we can derive essentially all factors necessary for therapeutic optimization. Since this is a rapidly evolving area, it is essential for the practitioner to review drug prescribing information and recent literature in order to fully understand the impact of these differences on clinical therapeutics. C1 [Soldin, Offie P.] Georgetown Univ, Med Ctr, Ctr Study Sex Differences, Dept Med, Washington, DC 20057 USA. [Soldin, Offie P.] Georgetown Univ, Med Ctr, Ctr Study Sex Differences, Dept Oncol & Physiol, Washington, DC 20057 USA. [Soldin, Offie P.; Mattison, Donald R.] NICHHD, OPRU, NIH, Rockville, MD USA. RP Soldin, OP (reprint author), Georgetown Univ, Med Ctr, Lombardi Comprehens Canc Ctr, LL, S-166,3800 Reservoir Rd NW, Washington, DC 20057 USA. EM os35@georgetown.edu RI Mattison, Donald/C-2015-2009; Mattison, Donald/L-4661-2013 OI Mattison, Donald/0000-0001-5623-0874 FU Flight Attendant Medical Research Institute (FAMRI; Miami, FL, USA); National Institutes of Health/National Institute of Child Health and Human Development Obstetrics-Fetal Pharmacology Research Unit (OPRU) Network (Rockville, MD, USA) [5U10HD047890-S]; Office of Research on Women's Health (Bethesda, MD, USA) FX The authors wish to thank Drs Anne Zajicek and Alexander Vinks for reading the manuscript critically, and Mr Daniel O'Mara for helping with manuscript preparation. NR 124 TC 95 Z9 97 U1 2 U2 15 PU ADIS INT LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 1311, NEW ZEALAND SN 0312-5963 J9 CLIN PHARMACOKINET JI Clin. Pharmacokinet. PY 2009 VL 48 IS 3 BP 143 EP 157 PG 15 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 445WP UT WOS:000266082500001 PM 19385708 ER PT J AU Brar, S Ramchandani, VA George, DT Venitz, J AF Brar, S. Ramchandani, V. A. George, D. T. Venitz, J. TI EFFECTS OF SMOKING ON THE beta-CARBOLINES, HARMAN AND NORHARMAN, IN A HEALTHY POPULATION AND DURING ALCOHOL DETOXIFICATION SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract CT 110th Annual Meeting of the American-Society-for-Clinical-Pharmacology-and-Therapeutics CY MAR 18-21, 2009 CL National Harbor, MD SP Amer Soc Clin Pharmacol & Therapeut C1 [Brar, S.; Venitz, J.] Virginia Commonwealth Univ, Richmond, VA USA. [Ramchandani, V. A.; George, D. T.] NIAAA, NIH, Bethesda, MD USA. NR 0 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 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JAN PY 2009 VL 85 BP S37 EP S37 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 399RH UT WOS:000262816500116 ER PT J AU Byrd, DP Lemmon, CR Soule, TA Schrieber, SJ Wahed, AS Wen, Z Smith, PC Afdhal, NH Belle, SH Navarro, VJ Reddy, KR Hoskins, JM Doo, E Liu, Q Berman, J Fried, MW Hawke, RL AF Byrd, D. P. Lemmon, C. R. Soule, T. A. Schrieber, S. J. Wahed, A. S. Wen, Z. Smith, P. C. Afdhal, N. H. Belle, S. H. Navarro, V. J. Reddy, K. R. Hoskins, J. M. Doo, E. Liu, Q. Berman, J. Fried, M. W. Hawke, R. L. TI INFLUENCE OF UGT1A1*28 POLYMORPHISM AND PLASMA CASPASE-3/7 ACTIVITY ON THE SINGLE DOSE PHARMACOKINETICS (PK) OF SILYMARIN (SM) FLAVONOLIGNANS. SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract CT 110th Annual Meeting of the American-Society-for-Clinical-Pharmacology-and-Therapeutics CY MAR 18-21, 2009 CL National Harbor, MD SP Amer Soc Clin Pharmacol & Therapeut C1 [Byrd, D. P.; Lemmon, C. R.; Soule, T. A.; Schrieber, S. J.; Wen, Z.; Smith, P. C.; Hoskins, J. M.; Fried, M. W.; Hawke, R. L.] Univ N Carolina, Chapel Hill, NC USA. [Wahed, A. S.; Belle, S. H.] Univ Pittsburgh, Pittsburgh, PA USA. [Afdhal, N. H.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. [Navarro, V. J.] Thomas Jefferson Univ, Philadelphia, PA 19107 USA. [Reddy, K. R.] Univ Penn, Philadelphia, PA 19104 USA. [Doo, E.] NIDDK, Bethesda, MD USA. [Liu, Q.; Berman, J.] Natl Ctr Complementary & Alternat Med, Bethesda, MD USA. NR 0 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 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JAN PY 2009 VL 85 BP S15 EP S15 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 399RH UT WOS:000262816500046 ER PT J AU Gao, T Chamberlain, CE Lee, S Goldstein, JA Ring, MS Hale, DA Kirk, AD Mannon, RB Hon, Y AF Gao, T. Chamberlain, C. E. Lee, S. Goldstein, J. A. Ring, M. S. Hale, D. A. Kirk, A. D. Mannon, R. B. Hon, Y. TI DIFFERING SIROLIMUS-INDUCED HYPERLIPIDEMIA AND RESPONSE TO STATIN THERAPY BETWEEN CYP3A5 EXPRESSERS AND NON-EXPRESSERS IN KIDNEY TRANSPLANTATION. SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract CT 110th Annual Meeting of the American-Society-for-Clinical-Pharmacology-and-Therapeutics CY MAR 18-21, 2009 CL National Harbor, MD SP Amer Soc Clin Pharmacol & Therapeut C1 [Gao, T.; Chamberlain, C. E.; Hon, Y.] NIH, Ctr Clin, Dept Pharm, Bethesda, MD 20892 USA. [Lee, S.; Goldstein, J. A.] NIEHS, Res Triangle Pk, NC 27709 USA. [Ring, M. S.; Hale, D. A.; Kirk, A. D.; Mannon, R. B.] NIDDK, Bethesda, MD USA. RI Kirk, Allan/B-6905-2012 NR 0 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 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JAN PY 2009 VL 85 BP S74 EP S74 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 399RH UT WOS:000262816500236 ER PT J AU Garrett, M Pithavala, YK Rini, BI Rixe, O Bukowski, RM Kim, S Amantea, MA Houk, BE AF Garrett, M. Pithavala, Y. K. Rini, B. I. Rixe, O. Bukowski, R. M. Kim, S. Amantea, M. A. Houk, B. E. TI INFLUENCE OF SELECTED DEMOGRAPHIC AND CLINICAL FACTORS ON THE PHARMACOKINETICS (PK) AND EFFICACY OF AXITINIB (AG-013736; AG) IN HEALTHY VOLUNTEERS (HVS) AND METASTATIC RENAL CELL CARCINOMA (MRCC) PATIENTS SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract CT 110th Annual Meeting of the American-Society-for-Clinical-Pharmacology-and-Therapeutics CY MAR 18-21, 2009 CL National Harbor, MD SP Amer Soc Clin Pharmacol & Therapeut C1 [Garrett, M.; Pithavala, Y. K.; Kim, S.; Amantea, M. A.; Houk, B. E.] Pfizer Inc, San Diego, CA USA. [Rini, B. I.; Bukowski, R. M.] Cleveland Clin, Taussig Canc Ctr, Cleveland, OH 44106 USA. [Rixe, O.] NCI, Bethesda, MD 20892 USA. NR 0 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 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JAN PY 2009 VL 85 BP S43 EP S43 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 399RH UT WOS:000262816500136 ER PT J AU Hamza, M Wang, X Wu, T Dionne, RA AF Hamza, M. Wang, X. Wu, T. Dionne, R. A. TI IL-6, IL-8 AND CCL2 ARE CORRELATED TO PAIN INTENSITY BUT NOT MODULATED BY KETOROLAC IN A CLINICAL MODEL OF ACUTE INFLAMMATORY PAIN SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract CT 110th Annual Meeting of the American-Society-for-Clinical-Pharmacology-and-Therapeutics CY MAR 18-21, 2009 CL National Harbor, MD SP Amer Soc Clin Pharmacol & Therapeut C1 [Hamza, M.; Wang, X.; Dionne, R. A.] NINR, NIH, Bethesda, MD 20892 USA. [Wu, T.] NIDCR, NIH, Bethesda, MD USA. RI Hamza, May/A-5053-2010 OI Hamza, May/0000-0002-7637-3060 NR 0 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 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JAN PY 2009 VL 85 SU 1 BP S42 EP S42 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 399RH UT WOS:000262816500132 ER PT J AU Hamza, M Wang, X Adam, A Carmona, GN Dionne, RA AF Hamza, M. Wang, X. Adam, A. Carmona, G. N., Sr. Dionne, R. A. TI KETOROLAC DOES NOT MODULATE NITRIC OXIDE, KININ B-1 RECEPTOR OR ITS ENDOGENOUS LIGANDS AT THE EARLY PHASE OF ACUTE INFLAMMATORY PAIN IN THE ORAL SURGERY MODEL SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract CT 110th Annual Meeting of the American-Society-for-Clinical-Pharmacology-and-Therapeutics CY MAR 18-21, 2009 CL Natl Harbor, MD SP Amer Soc Clin Pharmacol & Therapeut C1 [Hamza, M.; Wang, X.; Dionne, R. A.] NINR, NIH, Bethesda, MD 20892 USA. [Adam, A.] Univ Montreal, Fac Pharm, Montreal, PQ H3C 3J7, Canada. [Carmona, G. N., Sr.] NIDCR, NIH, Bethesda, MD USA. NR 0 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 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JAN PY 2009 VL 85 SU 1 BP S42 EP S42 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 399RH UT WOS:000262816500131 ER PT J AU Hon, Y Sun, H Lin, E Swenson, ER Machado, R Gladwin, MT AF Hon, Y. Sun, H. Lin, E. Swenson, E. R. Machado, R. Gladwin, M. T. TI NITRITE (NO2-) CONSUMPTION AND ELIMINATION AND DISTRIBUTION D) KINETICS DURING AND AFTER EXERCISE SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract CT 110th Annual Meeting of the American-Society-for-Clinical-Pharmacology-and-Therapeutics CY MAR 18-21, 2009 CL National Harbor, MD SP Amer Soc Clin Pharmacol & Therapeut C1 [Hon, Y.] NIH, Ctr Clin, Dept Pharm, Bethesda, MD 20892 USA. [Sun, H.] SunTech Res Inst, Rockville, MD USA. [Lin, E.; Machado, R.; Gladwin, M. T.] NHLBI, Bethesda, MD 20892 USA. [Swenson, E. R.] Univ Washington, Seattle, WA 98195 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JAN PY 2009 VL 85 BP S34 EP S34 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 399RH UT WOS:000262816500107 ER PT J AU Hon, Y Sun, H Dejam, A Gladwin, MT AF Hon, Y. Sun, H. Dejam, A. Gladwin, M. T. TI A PHYSIOLOGICAL PHARMACOKINETIC MODEL (PPKM) CHARACTERIZES THE IN VIVO METABOLIC AND DISPOSITION PATHWAYS OF NITRITE (NO2-), NITRATE (NO3-), METHEMOGLOBIN (METHB), AND IRON NITROSYLHEMOGLOBIN (NOHB) SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract CT 110th Annual Meeting of the American-Society-for-Clinical-Pharmacology-and-Therapeutics CY MAR 18-21, 2009 CL National Harbor, MD SP Amer Soc Clin Pharmacol & Therapeut C1 [Hon, Y.] NIH, Ctr Clin, Dept Pharm, Bethesda, MD 20892 USA. [Sun, H.] SunTech Res Inst, Rockville, MD USA. [Dejam, A.; Gladwin, M. T.] NHLBI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JAN PY 2009 VL 85 BP S35 EP S35 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 399RH UT WOS:000262816500108 ER PT J AU Jain, L Woo, S Dahut, WL Kohn, EC Kummar, S Gutierrez, M Yarchoan, R Giaccone, G Azad, NS Venitz, J Figg, WD AF Jain, L. Woo, S. Dahut, W. L. Kohn, E. C. Kummar, S. Gutierrez, M. Yarchoan, R. Giaccone, G. Azad, N. S. Venitz, J. Figg, W. D. TI POPULATION PHARMACOKINETICS OF SORAFENIB IN CANCER PATIENTS SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract CT 110th Annual Meeting of the American-Society-for-Clinical-Pharmacology-and-Therapeutics CY MAR 18-21, 2009 CL National Harbor, MD SP Amer Soc Clin Pharmacol & Therapeut C1 [Jain, L.; Woo, S.; Dahut, W. L.; Kohn, E. C.; Kummar, S.; Gutierrez, M.; Yarchoan, R.; Giaccone, G.; Azad, N. S.; Figg, W. D.] NCI, Bethesda, MD 20892 USA. [Venitz, J.] Virginia Commonwealth Univ, Richmond, VA USA. RI Figg Sr, William/M-2411-2016 NR 0 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 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JAN PY 2009 VL 85 BP S43 EP S44 PG 2 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 399RH UT WOS:000262816500137 ER PT J AU Lemmon, CCR Byrd, DP Schrieber, SJ Soule, TA Wahed, AS Wen, Z Smith, PC Afdhal, NH Belle, SH Navarro, VJ Reddy, KR Berman, J Liu, Q Doo, E Fried, MW Hawke, RL AF Lemmon, C. C. R. Byrd, D. P. Schrieber, S. J. Soule, T. A. Wahed, A. S. Wen, Z. Smith, P. C. Afdhal, N. H. Belle, S. H. Navarro, V. J. Reddy, K. R. Berman, J. Liu, Q. Doo, E. Fried, M. W. Hawke, R. L. TI SILYMARIN (SM) STEADY-STATE PHARMACOKINETICS (PK) AND INFLUENCE ON HCV VIRAL LOAD IN NON-CIRRHOTIC PATIENTS WITH CHRONIC HEPATITIS C. SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract CT 110th Annual Meeting of the American-Society-for-Clinical-Pharmacology-and-Therapeutics CY MAR 18-21, 2009 CL National Harbor, MD SP Amer Soc Clin Pharmacol & Therapeut C1 [Lemmon, C. C. R.; Byrd, D. P.; Schrieber, S. J.; Soule, T. A.; Wen, Z.; Smith, P. C.; Fried, M. W.; Hawke, R. L.] Univ N Carolina, Chapel Hill, NC USA. [Wahed, A. S.; Belle, S. H.] Univ Pittsburgh, Pittsburgh, PA USA. [Afdhal, N. H.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA. [Navarro, V. J.] Thomas Jefferson Univ, Philadelphia, PA 19107 USA. [Reddy, K. R.] Univ Penn, Philadelphia, PA 19104 USA. [Berman, J.; Liu, Q.] Natl Ctr Complementary & Alternat Med, Bethesda, MD USA. [Doo, E.] NIDDK, Bethesda, MD USA. NR 0 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 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JAN PY 2009 VL 85 BP S9 EP S10 PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 399RH UT WOS:000262816500029 ER PT J AU Ramchandani, VA Issa, J Momenan, R Hommer, DW AF Ramchandani, V. A. Issa, J. Momenan, R. Hommer, D. W. TI INFLUENCE OF AGE AND SEX ON ELIMINATION RATES AND SUBJECTIVE EFFECTS OF INTRAVENOUS ALCOHOL IN SOCIAL DRINKERS SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract CT 110th Annual Meeting of the American-Society-for-Clinical-Pharmacology-and-Therapeutics CY MAR 18-21, 2009 CL National Harbor, MD SP Amer Soc Clin Pharmacol & Therapeut C1 [Ramchandani, V. A.; Issa, J.; Momenan, R.; Hommer, D. W.] Natl Inst Alcohol Abuse & Alcoholism, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JAN PY 2009 VL 85 BP S92 EP S92 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 399RH UT WOS:000262816500292 ER PT J AU Wagner, JA Vassileva, M Ghosh, S Kochan, J Prince, MJ Schneider, B Velasquez, J Wang, M Wright, E Ennis, M AF Wagner, J. A. Vassileva, M. Ghosh, S. Kochan, J. Prince, M. J. Schneider, B. Velasquez, J. Wang, M. Wright, E. Ennis, M. TI EVALUATION OF THE UTILITY OF ADIPONECTIN AS A BIOMARKER PREDICTIVE OF GLYCEMIC EFFICACY BY POOLING EXISTING CLINICAL TRIAL DATA FROM PREVIOUSLY CONDUCTED STUDIES SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract CT 110th Annual Meeting of the American-Society-for-Clinical-Pharmacology-and-Therapeutics (ASCPT) CY MAR 18-21, 2009 CL Natl Harbor, MD SP Amer Soc Clin Pharmacol & Therapeut (ASCPT) C1 [Wagner, J. A.] Merck & Co Inc, Rahway, NJ 07065 USA. [Vassileva, M.] Fdn NIH, Bethesda, MD USA. [Ghosh, S.] GlaxoSmithKline, Res Triangle Pk, NC USA. [Kochan, J.] Hoffmann La Roche Inc, Nutley, NJ 07110 USA. [Prince, M. J.] Eli Lilly & Co, Indianapolis, IN 46285 USA. [Schneider, B.] US FDA, Rockville, MD 20857 USA. [Velasquez, J.] NIAAA, Bethesda, MD USA. [Wang, M.] Eli Lilly & Co, Indianapolis, IN 46285 USA. [Wright, E.] NIDDK, Bethesda, MD USA. [Ennis, M.] Quintiles, Austin, TX USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0009-9236 EI 1532-6535 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JAN PY 2009 VL 85 SU 1 BP S20 EP S20 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 399RH UT WOS:000262816500061 ER PT J AU Woo, S Gardner, ER Chen, X Ockers, SB Baum, CE Sissung, TM Price, DK Frye, R Peikarz, RL Bates, SE Figg, WD AF Woo, S. Gardner, E. R. Chen, X. Ockers, S. B. Baum, C. E. Sissung, T. M. Price, D. K. Frye, R. Peikarz, R. L. Bates, S. E. Figg, W. D. TI POPULATION PHARMACOKINETICS OF CYCLIC DEPSIPEPTIDE FK228 IN PATIENTS WITH CUTANEOUS T-CELL LYMPHOMA AND RELAPSED PERIPHERAL T-CELL LYMPHOMA SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Meeting Abstract CT 110th Annual Meeting of the American-Society-for-Clinical-Pharmacology-and-Therapeutics CY MAR 18-21, 2009 CL National Harbor, MD SP Amer Soc Clin Pharmacol & Therapeut C1 [Woo, S.; Gardner, E. R.; Chen, X.; Ockers, S. B.; Baum, C. E.; Sissung, T. M.; Price, D. K.; Frye, R.; Peikarz, R. L.; Bates, S. E.; Figg, W. D.] NCI, Bethesda, MD 20892 USA. RI Figg Sr, William/M-2411-2016 NR 0 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 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JAN PY 2009 VL 85 BP S66 EP S66 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 399RH UT WOS:000262816500209 ER PT B AU Gattorno, M Martini, A Goldbach-Mansky, R Aubert, P Ferguson, PJ AF Gattorno, Marco Martini, Alberto Goldbach-Mansky, Raphaela Aubert, Pamela Ferguson, Polly J. BE Stone, JH TI Monogenic Autoinflammatory Syndromes SO CLINICIAN'S PEARLS AND MYTHS IN RHEUMATOLOGY LA English DT Article; Book Chapter ID FAMILIAL MEDITERRANEAN FEVER; RECURRENT MULTIFOCAL OSTEOMYELITIS; MUCKLE-WELLS-SYNDROME; CONGENITAL DYSERYTHROPOIETIC ANEMIA; MULTISYSTEM INFLAMMATORY DISEASE; HYPER-IGD SYNDROME; INTERLEUKIN-1 RECEPTOR ANTAGONIST; PERIODIC SYNDROME TRAPS; CIAS1 MUTATIONS; PAPA SYNDROME C1 [Gattorno, Marco; Martini, Alberto] Univ Genoa, Inst G Gaslini, I-16147 Genoa, Italy. [Ferguson, Polly J.] Childrens Hosp, Dept Pediat Rheumatol, Iowa City, IA 52242 USA. [Goldbach-Mansky, Raphaela; Aubert, Pamela] Natl Inst Arthritis & Musculoskeletal Dis, NIH, Bethesda, MD 20892 USA. RP Gattorno, M (reprint author), Univ Genoa, Inst G Gaslini, I-16147 Genoa, Italy. NR 96 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES BN 978-1-84800-933-2 PY 2009 BP 33 EP 49 DI 10.1007/978-1-84800-934-9_5 PG 17 WC Rheumatology SC Rheumatology GA BMM83 UT WOS:000272857400005 ER PT B AU Targoff, IN Oddis, CV Plotz, PH Miller, FW Gourley, M AF Targoff, Ira N. Oddis, Chester V. Plotz, Paul H. Miller, Frederick W. Gourley, Mark BE Stone, JH TI Inflammatory Myopathies SO CLINICIAN'S PEARLS AND MYTHS IN RHEUMATOLOGY LA English DT Article; Book Chapter ID TRANSFER-RNA-SYNTHETASE; SIGNAL RECOGNITION PARTICLE; MYOSITIS-SPECIFIC AUTOANTIBODIES; INTERSTITIAL LUNG-DISEASE; CLINICAL CHARACTERISTICS; ANTI-JO-1 ANTIBODIES; DERMATOMYOSITIS; POLYMYOSITIS; FEATURES; CANCER C1 [Targoff, Ira N.] Oklahoma Med Res Fdn Arthritis & Immunol, Oklahoma City, OK 73104 USA. [Oddis, Chester V.] Univ Pittsburgh Med Rheumatol, Pittsburgh, PA 15261 USA. [Plotz, Paul H.] NIAMSD, Arthritis & Rheumatism Branch, Bethesda, MD 20892 USA. [Miller, Frederick W.] NIEHS, Environm Autoimmun Grp, NIH, Bethesda, MD 20892 USA. [Gourley, Mark] Natl Inst Arthritis & Musculoskeletal Dis, NIH, Bethesda, MD 20892 USA. RP Targoff, IN (reprint author), Oklahoma Med Res Fdn Arthritis & Immunol, 825 NE 13th St, Oklahoma City, OK 73104 USA. OI Miller, Frederick/0000-0003-2831-9593 NR 35 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES BN 978-1-84800-933-2 PY 2009 BP 191 EP 199 DI 10.1007/978-1-84800-934-9_18 PG 9 WC Rheumatology SC Rheumatology GA BMM83 UT WOS:000272857400018 ER PT B AU Reed, AM Pilkington, CA Feldman, BM Pachman, LM Rider, LG AF Reed, Ann M. Pilkington, Clarissa A. Feldman, Brian M. Pachman, Lauren M. Rider, Lisa G. BE Stone, JH TI Juvenile Dermatomyositis SO CLINICIAN'S PEARLS AND MYTHS IN RHEUMATOLOGY LA English DT Article; Book Chapter ID IDIOPATHIC INFLAMMATORY MYOPATHIES; CLINICAL CHARACTERISTICS; INTERNATIONAL CONSENSUS; DISEASE-ACTIVITY; MUSCLE BIOPSY; CHILDREN; AUTOANTIBODY; POLYMYOSITIS; CALCINOSIS; ASSOCIATIONS C1 [Reed, Ann M.] Mayo Clin, Rochester, MN 55905 USA. [Pilkington, Clarissa A.] UCL, Great Ormond St Rheumatol Dept, London, England. [Feldman, Brian M.] Univ Toronto SickKids, Toronto, ON M5G 1X8, Canada. [Pachman, Lauren M.] Northwestern Univ, Feinberg Sch Med, Childrens Mem Hosp, Childrens Mem Res Ctr,Div Rheumatol,Dept Pediat, Chicago, IL 60614 USA. [Rider, Lisa G.] NIEHS, Environm Autoimmun Grp, NIH, Bethesda, MD 20892 USA. RP Reed, AM (reprint author), Mayo Clin, 200 1st St SW, Rochester, MN 55905 USA. OI Rider, Lisa/0000-0002-6912-2458 NR 37 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES BN 978-1-84800-933-2 PY 2009 BP 201 EP 209 DI 10.1007/978-1-84800-934-9_19 PG 9 WC Rheumatology SC Rheumatology GA BMM83 UT WOS:000272857400019 ER PT J AU Schneeweiss, S Setoguchi, S Brookhart, MA Kaci, L Wang, PS AF Schneeweiss, Sebastian Setoguchi, Soko Brookhart, M. Alan Kaci, Liljana Wang, Philip S. TI Assessing Residual Confounding of the Association between Antipsychotic Medications and Risk of Death using Survey Data SO CNS DRUGS LA English DT Article ID ALL-CAUSE MORTALITY; BODY-MASS INDEX; UNMEASURED CONFOUNDERS; COGNITIVE IMPAIRMENT; ELDERLY-PATIENTS; HIP-FRACTURES; CLAIMS DATA; DEMENTIA; THERAPEUTICS; INFORMATION AB Background: Nonrandomised studies on the causal effects of psychotropic medications may be biased by patient characteristics that are not fully adjusted. Objectives: Studies using linked claims databases found that typical antipsychotic medications were associated with increased short-term mortality compared with atypical antipsychotics. It has been suggested that such results may be due to residual confounding by factors that cannot be measured in claims databases. Using detailed survey data we identified the direction and magnitude of such residual confounding. Design: Cross-sectional survey data. Participants: 17 776 participants aged >= 65 years from the Medicare Current Beneficiary Survey (MCBS). Measurements: To determine the association between typical antipsychotic use and potential confounding factors we assessed five factors not measured in Medicare claims data but in the MCBS, i.e. body mass index, smoking, activities of daily living (ADL) score, cognitive impairment and Rosow-Breslau physical impairment scale. We estimated adjusted associations between these factors and antipsychotic use. Combined with literature estimates of the independent effect of confounders on death, we computed the extent of residual confounding caused by a failure to adjust for these factors. Results: Comparing typical antipsychotic users with atypical antipsychotic users, we found that not adjusting for impairments in the ADL score led to an underestimation of the association with death (-13%), as did a failure to adjust for cognitive impairment (-7%). The combination of all five unmeasured confounders resulted in a net confounding of -5% (range -19% to +2%). After correction, the reported association between typical antipsychotic use and death compared with atypical antipsychotic use was slightly increased from a relative risk (RR) of 1.37 to 1.44 (95% CI 1.33, 1.56). Comparing any antipsychotic use with non-users would result in overestimations of > 50% if cognitive impairment remained unadjusted. Conclusion: Claims data studies tend to underestimate the association of typical antipsychotics with death compared with atypical antipsychotics because of residual confounding by measures of frailty. Studies comparing antipsychotic use with non-users may substantially overestimate harmful effects of antipsychotics. C1 [Schneeweiss, Sebastian; Setoguchi, Soko; Brookhart, M. Alan; Kaci, Liljana] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Pharmacoepidemiol & Pharmacoecon, Boston, MA 02120 USA. [Wang, Philip S.] NIMH, Div Serv & Intervent Res, Rockville, MD 20857 USA. RP Schneeweiss, S (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Pharmacoepidemiol & Pharmacoecon, 1620 Tremont St Suite 3030, Boston, MA 02120 USA. EM schneeweiss@post.harvard.edu RI Schneeweiss, Sebastian/C-2125-2013 FU National Institute on Aging [ROI-AG021950, ROIAG023178]; National Institute of Mental Health [ROI MH078708]; Agency for Healthcare Research and Quality [2-ROI-HS10881]; Department of Health and Human Services, Rockville, MD, USA FX No sources of funding were used to assist in the preparation of this study. Dr Schneeweiss has received support from the National Institute on Aging (ROI-AG021950, ROIAG023178), the National Institute of Mental Health (ROI MH078708) and the Agency for Healthcare Research and Quality (2-ROI-HS10881), Department of Health and Human Services, Rockville, MD, USA, and is principal investigator of the Brigham and Women's Hospital DEcIDE Research Center funded by the Agency for Healthcare Research and Quality. All other authors have no conflicts of interest that are directly relevant to the content of this study. NR 36 TC 17 Z9 17 U1 6 U2 9 PU ADIS INT LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 1311, NEW ZEALAND SN 1172-7047 EI 1179-1934 J9 CNS DRUGS JI CNS Drugs PY 2009 VL 23 IS 2 BP 171 EP 180 PG 10 WC Clinical Neurology; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 411DQ UT WOS:000263628600006 PM 19173375 ER PT J AU Vitiello, B AF Vitiello, Benedetto TI Combined Cognitive-Behavioural Therapy and Pharmacotherapy for Adolescent Depression Does it Improve Outcomes Compared with Monotherapy? SO CNS DRUGS LA English DT Article ID RANDOMIZED CONTROLLED-TRIAL; SEROTONIN REUPTAKE INHIBITORS; PLACEBO-CONTROLLED TRIAL; ROUTINE SPECIALIST CARE; MAJOR DEPRESSION; COST-EFFECTIVENESS; DOUBLE-BLIND; CHILDREN; TADS; FLUOXETINE AB Adolescent depression can be effectively treated with selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine, or with specific forms of psychotherapy, such as cognitive-behavioural therapy (CBT) and interpersonal therapy. A single course of any of these treatments, however, leaves between one-third and one-half of patients insufficiently improved and still depressed. In an effort to increase effectiveness, medication and CBT have been combined (COMB). A few controlled clinical trials have recently compared COMB with monotherapy. TADS (Treatment for Adolescents with Depression Study) randomly assigned 439 adolescents with major depressive disorder to fluoxetine, CBT, COMB or clinical management with placebo. After 12 weeks of treatment, both fluoxetine and COMB reduced depression more than CBT or placebo did, but only COMB was effective in inducing remission, achieving functional recovery and reducing suicidal ideation. After 36 weeks of treatment, there was no difference in improvement among treatments, but more suicidal events occurred in the medication only group than in the CBT only group. However, in another trial, ADAPT (Adolescent Depression and Psychotherapy Trial), involving 208 youths, no advantages of COMB over usual care with an SSRI could be detected. In a third trial, TORDIA (Treatment of Resistant Depression in Adolescence), which randomized 334 patients with an major depression unresponsive to previous SSRI treatment, COMB produced a greater response rate than medication monotherapy. These and other, smaller trials of COMB in adolescent depression are reviewed in this article. It is concluded that, while there is no univocal support for the superiority of COMB, two controlled trials indicate that COMB has a more favourable benefit/risk balance than monotherapy in adolescent depression. It remains to be determined for which patient subgroups and in which clinical settings COMB may be most advantageous. C1 NIMH, Bethesda, MD 20892 USA. RP Vitiello, B (reprint author), NIMH, Room 7147,6001 Executive Blvd, Bethesda, MD 20892 USA. EM bvitiell@mail.nih.gov FU Intramural NIH HHS [Z99 MH999999] NR 36 TC 9 Z9 10 U1 0 U2 14 PU ADIS INT LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 1311, NEW ZEALAND SN 1172-7047 J9 CNS DRUGS JI CNS Drugs PY 2009 VL 23 IS 4 BP 271 EP 280 PG 10 WC Clinical Neurology; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 444NS UT WOS:000265988300001 PM 19374457 ER PT J AU Zarate, CA Manji, HK AF Zarate, Carlos A. Manji, Husseini K. TI Protein Kinase C Inhibitors Rationale for Use and Potential in the Treatment of Bipolar Disorder SO CNS DRUGS LA English DT Review ID GENOME-WIDE ASSOCIATION; HIGH-DOSE TAMOXIFEN; BREAST-CANCER; STRIATAL SYNAPTOSOMES; DOPAMINE TRANSPORT; MOOD STABILIZERS; PLACE PREFERENCE; SODIUM VALPROATE; WORKING-MEMORY; ACUTE MANIA AB Bipolar disorder is one of the most severely debilitating of all medical illnesses. For a large number of patients, outcomes are quite poor. The illness results in tremendous suffering for patients and their families and commonly impairs functioning and workplace productivity. Risks of increased morbidity and mortality, unfortunately, are frequent occurrences as well. Until recently, little has been known about the specific molecular and cellular underpinnings of bipolar disorder. Such knowledge is crucial for the prospect of developing specific targeted therapies that are more effective and that have a more rapid onset of action than currently available treatments. Exciting recent data suggest that regulation of certain signalling pathways may be involved in the aetiology of bipolar disorder and that these pathways may be profitably targeted to treat the disorder. In particular, mania is associated with overactive protein kinase C (PKC) intracellular signalling, and recent genome-wide association studies of bipolar disorder have implicated an enzyme that reduces the activation of PKC. Importantly, the current mainstays in the treatment of mania, lithium (a monovalent cation) and valproate (a small fatty acid) indirectly inhibit PKC. In addition, recent clinical studies with the relatively selective PKC inhibitor tamoxifen add support to the relevance of the PKC target in bipolar disorder. Overall, a growing body of work both on a preclinical and clinical level indicates that PKC signalling may play an important role in the pathophysiology and treatment of bipolar disorder. The development of CNS-penetrant PKC inhibitors may have considerable benefit for this devastating illness. C1 [Zarate, Carlos A.; Manji, Husseini K.] Lab Mol Pathophysiol & Expt Therapeut, Bethesda, MD USA. [Zarate, Carlos A.; Manji, Husseini K.] NIMH, Mood & Anxiety Disorders Res Program, Bethesda, MD 20892 USA. RP Zarate, CA (reprint author), 10 Ctr Dr,Mark O Hatfield CRC,Unit 7 SE,Rm 7-3445, Bethesda, MD 20892 USA. EM zaratec@mail.nih.gov FU National Institute of Mental Heath; Stanley Medical Research Institute FX We would like to acknowledge the support of the Intramural Research Program of the National Institute of Mental Heath, the Stanley Medical Research Institute. The authors have no conflicts of interest that are directly relevant to the content of this review. Husseini K. Manji is currently employed by Johnson & Johnson Pharmaceuticals Research and Development. NR 80 TC 45 Z9 45 U1 1 U2 3 PU ADIS INT LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 1311, NEW ZEALAND SN 1172-7047 J9 CNS DRUGS JI CNS Drugs PY 2009 VL 23 IS 7 BP 569 EP 582 PG 14 WC Clinical Neurology; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 469CN UT WOS:000267873100003 PM 19552485 ER PT J AU Bhuvaneswar, CG Baldessarini, RJ Harsh, VL Alpert, JE AF Bhuvaneswar, Chaya G. Baldessarini, Ross J. Harsh, Veronica L. Alpert, Jonathan E. TI Adverse Endocrine and Metabolic Effects of Psychotropic Drugs Selective Clinical Review SO CNS DRUGS LA English DT Review ID INDUCED WEIGHT-GAIN; PLACEBO-CONTROLLED TRIAL; NEPHROGENIC DIABETES-INSIPIDUS; ANTIPSYCHOTIC-INDUCED HYPERPROLACTINEMIA; TREATMENT-RESISTANT SCHIZOPHRENIA; SEROTONIN REUPTAKE INHIBITORS; POLYCYSTIC OVARIAN SYNDROME; INDUCED SEXUAL DYSFUNCTION; BONE-MINERAL DENSITY; BIPOLAR-I DISORDER AB The article critically reviews selected, clinically significant, adverse endocrine and metabolic effects associated with psychotropic drug treatments, including hyperprolactinaemia, hyponatraemia, diabetes insipidus, hypothyroidism, hyperparathyroidism, sexual dysfunction and virilization, weight loss, weight gain and metabolic syndrome (type 2 diabetes mellitus, dyslipidaemia and hypertension). Such effects are prevalent and complex, but can be managed clinically when recognized. They encourage continued critical assessment of benefits versus risks of psychotropic drugs and underscore the importance of close coordination of psychiatric and general medical care to improve long-term health of psychiatric patients. Options for management of hyperprolactinaemia include lowering doses, switching to agents such as aripiprazole, clozapine or quetiapine, managing associated osteoporosis, carefully considering the use of dopamine receptor agonists; and ruling out stress, oral contraceptive use and hypothyroidism as contributing factors. Disorders of water homeostasis may include syndrome of inappropriate antidiuretic hormone (SIADH), managed by water restriction or slow replacement by hypertonic saline along with drug discontinuation. Safe management of diabetes insipidus, commonly associated with lithium, involves switching mood stabilizer and consideration of potassium-sparing diuretics. Clinical hypothyroidism may be a more useful marker than absolute cut-offs of hormone values, and may be associated with quetiapine, antidepressant and lithium use, and managed by thyroxine replacement. Hyper-parathyroidism requires comprehensive medical evaluation for occult tumours. Hypocalcaemia, along with multiple other psychiatric and medical causes, may result in decreased bone density and require evaluation and management. Strategies for reducing sexual dysfunction with psychotropics remain largely unsatisfactory. Finally, management strategies for obesity and metabolic syndrome are reviewed in light of the recent expert guidelines, including risk assessment and treatments, such as monoamine transport inhibitors, anticonvulsants; and cannabinoid receptor antagonists, as well as lifestyle changes. C1 [Bhuvaneswar, Chaya G.] Univ Penn, Dept Psychiat, Philadelphia, PA 19104 USA. [Baldessarini, Ross J.; Alpert, Jonathan E.] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA. [Baldessarini, Ross J.; Alpert, Jonathan E.] Massachusetts Gen Hosp, Boston, MA 02114 USA. [Baldessarini, Ross J.] McLean Hosp, Belmont, MA 02178 USA. [Harsh, Veronica L.] NIMH, Behav Endocrinol Branch, Bethesda, MD 20892 USA. RP Bhuvaneswar, CG (reprint author), Univ Penn, Hosp Univ Penn, Outpatient Clin, Dept Psychiat, 3535 Market St,2nd Floor, Philadelphia, PA 19104 USA. EM cbhospitalpsychiatry@live.com OI Alpert, Jonathan/0000-0002-4332-908X FU American Psychiatric Institute for Research and Education (APIRE); NIMH Diversity Supplement; Bruce J. Anderson Foundation; McLean Private Donors Fund FX Dr Bhuvaneswar has received training awards from: Merck, Janssen, Johnson and Johnson, Novartis, Sepracor, Cypress Bio and Infiniti Pharmaceuticals. Dr Baldessarini has recently been a consultant or investigator-initiated research collaborator with: Auritec, Biotrofix, IFA SpA, Janssen, JDS, Lilly, NeuroHealing, Novartis, Solvay and SK-BioPharmaceuticals Corporations. Dr Harsh has no relevant disclosures. Dr Alpert is a consultant or has received research support from: Aspect Medical Systems, Lilly, Forest, Organon, Pamlab, Pfizer and Pharmavite, and honoraria from Organon and Janssen Corportions. No author is a member of pharmaceutical speakers' bureaus nor do they or family members hold equity positions in biomedical or pharmaceutical corporations. NR 248 TC 27 Z9 27 U1 6 U2 20 PU ADIS INT LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 1311, NEW ZEALAND SN 1172-7047 J9 CNS DRUGS JI CNS Drugs PY 2009 VL 23 IS 12 BP 1003 EP 1021 PG 19 WC Clinical Neurology; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 538EV UT WOS:000273168000002 PM 19958039 ER PT J AU Horvath, T Madi, BC Iuppa, IM Kennedy, GE Rutherford, G Read, JS AF Horvath, Tara Madi, Banyana C. Iuppa, Irene M. Kennedy, Gail E. Rutherford, George Read, Jennifer S. TI Interventions for preventing late postnatal mother-to-child transmission of HIV SO COCHRANE DATABASE OF SYSTEMATIC REVIEWS LA English DT Review ID HUMAN-IMMUNODEFICIENCY-VIRUS; BREAST-FED CHILDREN; LEUKOCYTE PROTEASE INHIBITOR; 1ST 6 MONTHS; RANDOMIZED-TRIAL; HIV-1-INFECTED WOMEN; COTE-DIVOIRE; VERTICAL TRANSMISSION; VITAMIN SUPPLEMENTS; UNITED-STATES AB Background Worldwide, mother-to-child transmission (MTCT) of human immunodeficiency virus type 1 (HIV) represents the most common means by which children acquire HIV infection. Efficacious and effective interventions to prevent in utero and intrapartum transmission of HIV infection have been developed and implemented. However, a large proportion of MTCT of HIV occurs postnatally, through breast milk transmission. Objectives The objectives of this systematic review were to collate and assess the evidence regarding interventions to decrease late postnatal MTCT of HIV, and to determine the efficacy of such interventions in decreasing late postnatal MTCT of HIV, increasing overall survival, and increasing HIV-free survival. Search strategy Electronic searches were undertaken using PubMed, EMBASE and other databases for 1980-2008. Hand searches of reference lists of pertinent reviews and studies, as well as abstracts from relevant conferences, were also conducted. Experts in the field were contacted to locate any other studies. The search strategy was iterative. Selection criteria Randomized clinical trials assessing the efficacy of interventions to prevent MTCT of HIV through breast milk were included in the analysis. Other trials and intervention cohort studies with relevant data also were included, but only when randomization was not feasible due to the nature of the intervention (i. e., infant feeding modality). Data collection and analysis Data regarding HIV infection status and vital status of infants born to HIV-infected women, according to intervention, were extracted from the reports of the studies. Main results Six randomized clinical trials and one intervention cohort study were included in this review. Two trials addressed the issue of shortening the duration of (or eliminating) exposure to breast milk. In a trial of breastfeeding versus formula feeding, formula feeding was efficacious in preventing MTCT of HIV (the cumulative probability of HIV infection at 24 months was 36.7% in the breastfeeding arm and 20.5% in the formula arm [p = 0.001]), but the mortality and malnutrition rates during the first two years of life were similar in the two groups. In a trial of early cessation of breastfeeding, HIV-free survival was similar between those children who ceased breastfeeding around four months of age and those who continued breastfeeding. Another trial addressing vitamin supplementation found more cases of HIV infection among children of mothers in the vitamin A arm. Efficacy for other vitamin supplements was not shown. An intervention cohort study evaluated the risk of MTCT according to infant feeding modality, and found increased risks of MTCT among breastfed children who also received solids (hazard ratio = 10.87, p = 0.018) as well as higher 3-month mortality rates (hazard ratio = 2.06) among infants given non- breast milk feedings (instead of exclusive breastfeeding). Three trials evaluated antiretroviral prophylaxis to breastfeeding infants. One trial found that breastfeeding with zidovudine prophylaxis (transmission rate = 9.0%) was not as effective as formula feeding (transmission rate 5.6%) in preventing late postnatal HIV transmission (p = 0.04). Breastfeeding with zidovudine prophylaxis and formula feeding had comparable HIV-free survival rates at 18 months (p = 0.60). Two trials of extended nevirapine prophylaxis demonstrated efficacy. In the first (data combined from trials conducted in three different countries), a six-week course of nevirapine resulted in a lower risk of HIV transmission by six weeks of age (p=0.009), but not at six months of age (p = 0.016). In the second, nevirapine administration until 14 weeks of age (5.2%) or nevirapine with zidovudine until 14 weeks of age (6.4%) resulted in significantly lower risks of MTCT of HIV by 9 months of age than a control regimen of peripartum prophylaxis (10.6%) (p < 0.001). HIV-free survival was significantly better through the age of 9 months in both extended prophylaxis groups, and through the age of 15 months in the extended nevirapine group. Authors' conclusions Complete avoidance of breastfeeding is efficacious in preventing MTCT of HIV, but this intervention has significant associated morbidity (e. g., diarrheal morbidity if formula is prepared without clean water). If breastfeeding is initiated, two interventions 1). exclusive breastfeeding during the first few months of life; and 2) chronic antiretroviral prophylaxis to the infant (nevirapine alone, or nevirapine with zidovudine) are efficacious in preventing transmission. C1 [Horvath, Tara; Iuppa, Irene M.; Kennedy, Gail E.; Rutherford, George] Univ Calif San Francisco, San Francisco, CA 94143 USA. [Madi, Banyana C.] SADC Secretariat, HIV & AIDS Unit, Gaborone, Botswana. [Read, Jennifer S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Ctr Res Mothers & Children, Pediat Adolescent & Maternal AIDS Branch, NIH, Bethesda, MD USA. RP Horvath, T (reprint author), Univ Calif San Francisco, Box 1224, San Francisco, CA 94143 USA. EM thorvath@psg.ucsf.edu NR 81 TC 35 Z9 35 U1 1 U2 6 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 1469-493X J9 COCHRANE DB SYST REV JI Cochrane Database Syst Rev. PY 2009 IS 1 AR CD006734 DI 10.1002/14651858.CD006734.pub2 PG 36 WC Medicine, General & Internal SC General & Internal Medicine GA 396KZ UT WOS:000262591900080 PM 19160297 ER PT J AU Sloman, S Barbey, AK Hotaling, JM AF Sloman, Steven Barbey, Aron K. Hotaling, Jared M. TI A Causal Model Theory of the Meaning of Cause, Enable, and Prevent SO COGNITIVE SCIENCE LA English DT Article; Proceedings Paper CT 47th Annual Meeting of the Psychonomic-Society CY NOV 16-19, 2006 CL Houston, TX SP Psychon Soc DE Casual reasoning; Bayesian networks; Structural equations; Semantics of cause AB The verbs cause, enable, and prevent express beliefs about the way the world works. We offer a theory of their meaning in terms of the structure of those beliefs expressed using qualitative properties of causal models, a graphical framework for representing causal structure. We propose that these verbs refer to a causal model relevant to a discourse and that "A causes B" expresses the belief that the causal model includes a link from A to B. "A enables/allows B" entails that the model includes a link from A to B, that A represents a category of events necessary for B, and that an alternative cause of B exists. "A prevents B" entails that the model includes a link from A to B and that A reduces the likelihood of B. This theory is able to account for the results of four experiments as well as a variety of existing data on human reasoning. C1 [Sloman, Steven] Brown Univ, Providence, RI 02912 USA. [Barbey, Aron K.] NINDS, NIH, Cognit Neurosci Sect, Bethesda, MD 20892 USA. [Hotaling, Jared M.] Indiana Univ, Bloomington, IN 47405 USA. RP Sloman, S (reprint author), Brown Univ, Box 1978, Providence, RI 02912 USA. EM steven_sloman@brown.edu RI Barbey, Aron/L-7312-2015 OI Barbey, Aron/0000-0002-6092-0912 NR 27 TC 27 Z9 27 U1 1 U2 3 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0364-0213 J9 COGNITIVE SCI JI Cogn. Sci. PD JAN-FEB PY 2009 VL 33 IS 1 BP 21 EP 50 DI 10.1111/j.1551-6709.2008.01002.x PG 30 WC Psychology, Experimental SC Psychology GA 453DD UT WOS:000266589500002 PM 21585462 ER PT J AU Luo, J Huang, L Hachey, M Tiwari, R AF Luo, Jun Huang, Lan Hachey, Mark Tiwari, Ram TI Adjacency Method for Finding Connected Subsets of a Graph: An Application of Graph Theory to Spatial Statistics SO COMMUNICATIONS IN STATISTICS-SIMULATION AND COMPUTATION LA English DT Article DE Adjacency method; Cluster detection; Connected subset; Edge; Flexible shaped spatial scan statistic; Graph; Spatial scan statistic; Vertex ID RARE DISEASES; CLUSTERS; TESTS AB This article proposes the adjacency method for generating all connected subsets of a graph without generating any disconnected subset. The motivation for the method is an algorithm for finding all candidate clusters of cancer cases in a specified geographic region. Tango and Takahashi (2005) suggested the ergodic method to find all candidate clusters for flexibly shaped spatial scan statistics. The adjacency method is an improvement of the ergodic method. A slight modification of the adjacency method can also be used to determine the connectivity of a graph. A recursive algorithm for finding all connected subsets is proposed in this article. Given a graph with n vertices, the cost of storage of the algorithm is O(n(2)) and the cost of the calculation is bounded by vertical bar Omega vertical bar * O(n(2)), where Omega is the collection of all connected subsets and vertical bar Omega vertical bar is the cardinality of Omega. In some situations, vertical bar Omega vertical bar is far less than 2(n), the number of all subsets of the graph. For example, for a string with length n, vertical bar Omega vertical bar/2(n) = o((1/2 + delta)(n)), where delta > 0. C1 [Luo, Jun] Informat Management Serv Inc, Silver Spring Off, Silver Spring, MD 20904 USA. [Huang, Lan] Natl Canc Inst, Div Canc Control & Populat Sci, Rockville, MD USA. [Tiwari, Ram] FDA, CDER, Silver Spring, MD USA. RP Luo, J (reprint author), Informat Management Serv Inc, Silver Spring Off, 12501 Prosper Dr,Suite 200, Silver Spring, MD 20904 USA. EM luoj@imsweb.com FU National Cancer Institute; NIH FX Most of Ram Tiwari work was done while he was at the National Cancer Institute, NIH. The views expressed in this article do not necessarily represent those of the US Food and Drug Administration, and of the National Cancer Institute. NR 15 TC 1 Z9 1 U1 1 U2 2 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0361-0918 J9 COMMUN STAT-SIMUL C JI Commun. Stat.-Simul. Comput. PY 2009 VL 38 IS 5 BP 1136 EP 1151 DI 10.1080/03610910902807854 PG 16 WC Statistics & Probability SC Mathematics GA 423XG UT WOS:000264529500005 ER PT J AU Kim, S Das, S Chen, MH Warren, N AF Kim, Sungduk Das, Sonali Chen, Ming-Hui Warren, Nicholas TI Bayesian Structural Equations Modeling for Ordinal Response Data with Missing Responses and Missing Covariates SO COMMUNICATIONS IN STATISTICS-THEORY AND METHODS LA English DT Article DE DIC; Latent variable; Markov chain Monte Carlo; Missing at random; Ordinal response data; Random effects; VHA all employee survey data ID GENERALIZED LINEAR-MODELS; LATENT VARIABLE MODELS; GIBBS SAMPLER; REGRESSION-MODELS; CONVERGENCE; INFERENCE; BINARY AB Structural equations models (SEMs) have been extensively used to model survey data arising in the fields of sociology, psychology, health, and economics with increasing applications where self assessment questionnaires are the means to collect the data. We propose the SEM for multilevel ordinal response data from a large multilevel survey conducted by the US Veterans Health Administration (VHA). The proposed model involves a set of latent variables to capture dependence between different responses, a set of facility level random effects to capture facility heterogeneity and dependence between individuals within the same facility, and a set of covariates to account for individual heterogeneity. An effective and practically useful modeling strategy is developed to deal with missing responses and to model missing covariates in the structural equations framework. A Markov chain Monte Carlo sampling algorithm is developed for sampling from the posterior distribution. The deviance information criterion measure is used to compare several variations of the proposed model. The proposed methodology is motivated and illustrated by using the VHA All Employee Survey data. C1 [Chen, Ming-Hui] Univ Connecticut, Dept Stat, Storrs, CT 06269 USA. [Kim, Sungduk] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, NIH, Rockville, MD USA. [Das, Sonali] CSIR Built Environm, Pretoria, South Africa. [Warren, Nicholas] Univ Connecticut, Ctr Hlth, Div Publ Hlth & Populat Sci, Storrs, CT 06269 USA. RP Chen, MH (reprint author), Univ Connecticut, Dept Stat, 215 Glenbrook Rd,U-4120, Storrs, CT 06269 USA. EM mhchen@stat.uconn.edu FU Eunice Kennedy Shriver National Institute of Child Health and Human Development; National Institutes of Health [GM 70335, CA 74015]; University of Connecticut; VHA National Center for Organizational Development FX The authors wish to thank the Guest Editor and a referee for helpful comments which have led to an improvement of this article. The authors also wish to acknowledge and thank the Veterans Health Administration and the National Center for Organizational Development for access to the All Employee Survey (AES) 2001 data and their substantial efforts to insure the quality and integrity of these data. Dr. Kim's research is supported by the Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development; National Institutes of Health. Dr. Chen's research was partially supported by NIH grants #GM 70335 and #CA 74015 and a Faculty Large Research Grant from University of Connecticut. Dr. Warren's research was funded by the VHA National Center for Organizational Development. NR 36 TC 1 Z9 1 U1 0 U2 6 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0361-0926 J9 COMMUN STAT-THEOR M JI Commun. Stat.-Theory Methods PY 2009 VL 38 IS 16-17 BP 2748 EP 2768 AR PII 914063405 DI 10.1080/03610910902936299 PG 21 WC Statistics & Probability SC Mathematics GA 485TN UT WOS:000269147300012 ER PT J AU Stylianou, M AF Stylianou, Mario TI Derivation of Exact Distributions Following an Up-and-Down Design SO COMMUNICATIONS IN STATISTICS-THEORY AND METHODS LA English DT Article DE Biased coin up-and-down design; Dose finding; Exact distribution; Phase I trial; Toxicity AB Use of large sample theory in sequential designs, such as the up-and-down designs, to estimate parameters of interest may not be appropriate when the sample size is small, as is the case with many phase I clinical trials. In these situations, it may be desirable to derive the exact distribution of various statistics of interest. Having the exact distribution will enable us to calculate exact probabilities, moments or confidence intervals. We show how one can derive these exact distributions by enumerating all possible outcomes. We also derive a formula to obtain the total number of all possible treatment outcomes using the biased up-and-down design. These results will enable the experimenter to plan a phase I study with more confidence. C1 NHLBI, Off Biostat Res, Bethesda, MD 20892 USA. RP Stylianou, M (reprint author), NHLBI, Off Biostat Res, 6701 Rockledge Dr,Room 9198, Bethesda, MD 20892 USA. EM stylianm@nih.gov NR 10 TC 0 Z9 0 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0361-0926 J9 COMMUN STAT-THEOR M JI Commun. Stat.-Theory Methods PY 2009 VL 38 IS 16-17 BP 3190 EP 3197 AR PII 914064151 DI 10.1080/03610920902947709 PG 8 WC Statistics & Probability SC Mathematics GA 485TN UT WOS:000269147300041 ER PT J AU Lachenbruch, PA Miller, FW Rider, LG AF Lachenbruch, Peter A. Miller, Frederick W. Rider, Lisa G. TI On Determining the Effects of Therapy on Disease Damage in Non Randomized Studies with Multiple Treatments: A Study of Juvenile Myositis SO COMMUNICATIONS IN STATISTICS-THEORY AND METHODS LA English DT Article CT Joint Statistical Meetings of the American-Statistical-Association CY JUL 29-AUG 02, 2007 CL Salt Lake City, UT SP Amer Stat Assoc DE Multiple treatments; Myositis; Propensity scoring ID VARIABLE SELECTION AB This article discusses predicting damage in patients with juvenile myositis after treatment with various medications. These data were taken from medical records and not randomized. Investigators advocate using propensity scores for analysis of such non randomized studies in order to reduce the effect of selection of treatment. Thus far, the studies have typically been comparing drug administration versus no drug after including a propensity score to compensate for potential bias in selecting patients for use of the agent. In this study, we use propensity scoring for multiple treatments given singly or in combination. We study two methods. We use a multiple logistic regression model with continuous propensity scores and a model that develops strata based on the dichotomous treatment assignment (received drug or not). We find the multiple logistic regression models predict damage better than the dichotomous model. In many cases, the propensity score also accounts for the effect of the treatment. C1 [Lachenbruch, Peter A.] Oregon State Univ, Dept Publ Hlth, Corvallis, OR 97330 USA. [Miller, Frederick W.; Rider, Lisa G.] NIEHS, US Dept HHS, Environm Autoimmun Grp, NIH, Bethesda, MD USA. RP Lachenbruch, PA (reprint author), Oregon State Univ, Dept Publ Hlth, Corvallis, OR 97330 USA. EM peter.lachenbruch@oregonstate.edu OI Rider, Lisa/0000-0002-6912-2458; Miller, Frederick/0000-0003-2831-9593 FU Intramural NIH HHS [Z01 ES101081-06, ZIA ES101081-08] NR 9 TC 0 Z9 0 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0361-0926 J9 COMMUN STAT-THEOR M JI Commun. Stat.-Theory Methods PY 2009 VL 38 IS 18 BP 3268 EP 3281 AR PII 914971507 DI 10.1080/03610920802468681 PG 14 WC Statistics & Probability SC Mathematics GA 494KF UT WOS:000269810900002 PM 20209035 ER PT J AU Thomas, EV Phillippy, KH Brahamsha, B Haaland, DM Timlin, JA Elbourne, LDH Palenik, B Paulsen, IT AF Thomas, E. V. Phillippy, K. H. Brahamsha, B. Haaland, D. M. Timlin, J. A. Elbourne, L. D. H. Palenik, B. Paulsen, I. T. TI Statistical Analysis of Microarray Data with Replicated Spots: A Case Study with Synechococcus WH8102 SO COMPARATIVE AND FUNCTIONAL GENOMICS LA English DT Article ID GENE-EXPRESSION; SYSTEM; DESIGN AB Until recently microarray experiments often involved relatively few arrays with only a single representation of each gene on each array. A complete genome microarray with multiple spots per gene (spread out spatially across the array) was developed in order to compare the gene expression of a marine cyanobacterium and a knockout mutant strain in a defined artificial seawater medium. Statistical methods were developed for analysis in the special situation of this case study where there is gene replication within an array and where relatively few arrays are used, which can be the case with current array technology. Due in part to the replication within an array, it was possible to detect very small changes in the levels of expression between the wild type and mutant strains. One interesting biological outcome of this experiment is the indication of the extent to which the phosphorus regulatory system of this cyanobacterium affects the expression of multiple genes beyond those strictly involved in phosphorus acquisition. Copyright (C) 2009 E. V. Thomas et al. C1 [Thomas, E. V.] Sandia Natl Labs, Dept Independent Surveillance Assessment & Stat, Albuquerque, NM 87185 USA. [Phillippy, K. H.] NIH, Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA. [Brahamsha, B.; Palenik, B.] Univ Calif San Diego, Scripps Inst Oceanog, La Jolla, CA 92093 USA. [Haaland, D. M.; Timlin, J. A.] Sandia Natl Labs, Dept Biomol Anal & Imaging, Albuquerque, NM 87185 USA. [Elbourne, L. D. H.; Paulsen, I. T.] Macquarie Univ, Dept Chem & Biomol Sci, Sydney, NSW 2109, Australia. RP Thomas, EV (reprint author), Sandia Natl Labs, Dept Independent Surveillance Assessment & Stat, POB 5800, Albuquerque, NM 87185 USA. EM evthoma@sandia.gov RI Elbourne, Liam/G-6150-2011; Paulsen, Ian/K-3832-2012; OI Elbourne, Liam/0000-0002-9784-0959; Paulsen, Ian/0000-0001-9015-9418; Timlin, Jerilyn/0000-0003-2953-1721 NR 20 TC 4 Z9 4 U1 0 U2 3 PU HINDAWI PUBLISHING CORPORATION PI NEW YORK PA 410 PARK AVENUE, 15TH FLOOR, #287 PMB, NEW YORK, NY 10022 USA SN 1531-6912 J9 COMP FUNCT GENOM JI Compar. Funct. Genom. PY 2009 AR 950171 DI 10.1155/2009/950171 PG 11 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA 440TW UT WOS:000265723600001 PM 19404483 ER PT J AU Zemskova, MS Celi, FS AF Zemskova, Marina S. Celi, Francesco S. BE Preedy, VR Burrow, GN Watson, RR TI The Use of Lithium as an Adjuvant in Radioactive Iodine Treatment of Thyroid Cancer SO COMPREHENSIVE HANDBOOK OF IODINE: NUTRITIONAL, BIOCHEMICAL, PATHOLOGICAL AND THERAPEUTIC ASPECTS LA English DT Article; Book Chapter ID RECOMBINANT HUMAN THYROTROPIN; RANDOMIZED CLINICAL-TRIAL; RADIOIODINE ABLATION; REMNANT ABLATION; 30 MCI; I-131; THERAPY; CARCINOMA; THYROTOXICOSIS; PAPILLARY AB The effects of lithium on the thyroid gland have been known to clinicians for over a century and this compound has been successfully used in the treatment of hyperthyroid states. The narrow therapeutic range of lithium has, on the other hand, limited the use of this drug for the long-term treatment of thyroid disorders. The main effects of lithium salts on thyroid gland are the result of an increased uptake of iodine within the gland, ultimately reducing hormone synthesis and release. The use of short-term lithium therapy as an adjunct to radioablation of thyroid cancer by I-131 radioactive iodine (RAI) therapy has been advocated by several authors. The success of this treatment is dependent on the degree of uptake and the adequate retention of I-131 in thyroid tissue. The two most important factors influencing the uptake of radionuclide in the thyroid remnant or cancer are represented by TSH-induced sodium iodide symporter expression and dietary and/or pharmacological depletion of iodide. Conversely, methods to enhance I-131 retention in thyroid tissue are limited, and among them lithium carbonate appears to be able to reliably increase I-131 retention in thyroid tissue without excess toxicity. The use of lithium could thus represent a viable modality to increase the effectiveness of RAI, and to potentially reduce the overall dose of I-131, without affecting the success of the treatment. C1 [Zemskova, Marina S.] NICHHD, Reprod Biol & Med Branch, NIH, Bethesda, MD 20892 USA. [Celi, Francesco S.] NIDDK, Clin Endocrinol Branch, NIH, Bethesda, MD 20892 USA. RP Zemskova, MS (reprint author), NICHHD, Reprod Biol & Med Branch, NIH, Bethesda, MD 20892 USA. NR 61 TC 0 Z9 0 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 978-0-08-092086-3 PY 2009 BP 1001 EP 1006 DI 10.1016/B978-0-12-374135-6.00103-5 PG 6 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Nutrition & Dietetics SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Nutrition & Dietetics GA BCR55 UT WOS:000311104900104 ER PT B AU Zhao, YD Simon, R AF Zhao, Yingdong Simon, Richard BE Russe, AS TI DECONVOLUTION OF POSITIONAL SCANNING SYNTHETIC COMBINATORIAL LIBRARIES: MATHEMATICAL MODELS AND BIOINFORMATICS APPROACHES SO COMPUTATIONAL BIOLOGY: NEW RESEARCH LA English DT Article; Book Chapter ID T-CELL EPITOPES; PEPTIDE LIBRARIES; MULTIPLE-SCLEROSIS; LYME-DISEASE; IDENTIFICATION; LIGANDS; BINDING; PREDICTION; RECEPTOR; CLONE AB Combinatorial peptide library technology has been proven to be a powerful approach to both T-cell epitope determination and analysis of TCR specificity and degeneracy. During the past ten years, we have developed mathematical models and bioinformatics approaches for deconvolution of positional scanning synthetic combinatorial libraries (PS-SCL). PS-SCL are composed of trillions of peptides systematically arranged in mixtures with defined amino acids at each position. Starting from the mathematical model building to deconvolute the spectrum of PS-SCL, we proposed a biometrical approach using the score matrix to systematically search the protein databases for putative antigenic peptide candidates. We then evaluated of the assumption of independent contribution of the side chains of the amino acids in peptides and applied more sophisticated machine learning algorithms to improve the prediction accuracy based on synthesized peptide data. Finally, we implemented the above approach into a web based tool for searching protein database for T-cell epitopes based on experimental data from PS-SCL with the website employed a strong statistical analysis package, relational database and Java applets. Our work has provided a sound basis for PS-SCL data analysis and has been proven efficient and successful for identifying target antigens and highly active peptide mimics. C1 [Zhao, Yingdong; Simon, Richard] NCI, Biometr Res Branch, NIH, Bethesda, MD 20892 USA. RP Zhao, YD (reprint author), NCI, Biometr Res Branch, NIH, Bethesda, MD 20892 USA. EM zhaoy@mail.nih.gov; rsimon@mail.nih.gov NR 20 TC 0 Z9 0 U1 1 U2 1 PU NOVA SCIENCE PUBLISHERS, INC PI HAUPPAUGE PA 400 OSER AVE, STE 1600, HAUPPAUGE, NY 11788-3635 USA BN 978-1-60692-040-4 PY 2009 BP 375 EP 388 PG 14 WC Mathematical & Computational Biology SC Mathematical & Computational Biology GA BKU78 UT WOS:000269295600021 ER PT J AU Ying, ZG Udupa, JK Liu, JM Saha, PK AF Ying Zhuge Udupa, Jayaram K. Liu, Jiamin Saha, Punam K. TI Image background inhomogeneity correction in MRI via intensity standardization SO COMPUTERIZED MEDICAL IMAGING AND GRAPHICS LA English DT Article DE MRI; Field inhomogeneity; Standardization; Image filtering; Image segmentation ID RETROSPECTIVE CORRECTION; TISSUE CLASSIFICATION; BIAS FIELD; SCALE; SEGMENTATION; BRAIN; NONUNIFORMITY; ALGORITHMS AB An automatic, simple, and image intensity standardization-based strategy for correcting background inhomogeneity in MR images is presented in this paper. image intensities are first transformed to a standard intensity gray scale by a standardization process. Different tissue sample regions are then obtained from the standardized image by simply thresholding based on fixed intensity intervals. For each tissue region, a polynomial is fitted to the estimated discrete background intensity variation. Finally, a combined polynomial is determined and used for correcting the intensity inhomogeneity in the whole image. The above procedure is repeated on the corrected image iteratively until the size of the extracted tissue regions does not change significantly in two successive iterations. Intensity scale standardization is effected to make sure that the corrected image is not biased by the fitting strategy. The method has been tested on a number of simulated and clinical MR images. These tests and a comparison with the method of non-parametric non-uniform intensity normalization (N3) indicate that the method is effective in background intensity inhomogeneity correction and may have a slight edge over the N3method. (C) 2008 Elsevier Ltd. All rights reserved. C1 [Ying Zhuge; Udupa, Jayaram K.] Univ Penn, Dept Radiol, Med Image Proc Grp, Philadelphia, PA 19104 USA. [Liu, Jiamin] NIH, Dept Diagnost Radiol, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA. [Saha, Punam K.] Univ Iowa, Dept Elect & Comp Engn, Iowa City, IA 52242 USA. RP Udupa, JK (reprint author), Univ Penn, Dept Radiol, Med Image Proc Grp, 4th Floor,Blockley Hall,423 Guardian Dr, Philadelphia, PA 19104 USA. EM jay@mipg.upenn.edu RI Saha, Punam /F-8833-2011 FU DHHS [NS 37172] FX The research reported here is supported by a DHHS Grant NS 37172. NR 24 TC 4 Z9 4 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0895-6111 J9 COMPUT MED IMAG GRAP JI Comput. Med. Imaging Graph. PD JAN PY 2009 VL 33 IS 1 BP 7 EP 16 DI 10.1016/j.compmedimag.2008.09.004 PG 10 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 397WF UT WOS:000262692200002 ER PT B AU Gavara, N Chadwick, RS AF Gavara, N. Chadwick, R. S. BE Cooper, NP Kemp, DT TI MEASUREMENT OF ANISOTROPIC MECHANICAL PROPERTIES OF THE TECTORIAL MEMBRANE SO CONCEPTS AND CHALLENGES IN THE BIOPHYSICS OF HEARING LA English DT Proceedings Paper CT 10th International Workshop on the Mechanics of Hearing CY JUL 27-31, 2008 CL Keele Univ, Staffordshire, ENGLAND SP Oticon Fdn, Otodynam Ltd, Starkey Lab Ltd, MED EL, Polytec GmbH, Tucker Davis Technol HO Keele Univ ID STEREOCILIA AB The tectorial membrane (TM) in the cochlea is an anisotropic tissue with a key role in hearing. The TM's structural and mechanical anisotropy is provided by oriented collagen bundles about 1 micron thick. Here we report the three elastic moduli that characterize the TM, as well as the novel technique used to measure the mechanical properties of an anisotropic material. We have measured mechanical anisotropy by combining Atomic Force Microscopy (AFM) and optical tracking of microspheres. The surface Green's tensor for an incompressible anisotropic material was then used to compute the elastic moduli from imposed forces and the resulting surface deformations. Our results suggest a critical role of TM's strong anisotropy by enhancing the cochlear amplifier. C1 [Gavara, N.; Chadwick, R. S.] Natl Inst Deafness & Other Commun Disorders, Auditory Mech Sect, NIH, Bethesda, MD 20892 USA. RP Gavara, N (reprint author), Natl Inst Deafness & Other Commun Disorders, Auditory Mech Sect, NIH, 10 Ctr Dr,MSC 1417, Bethesda, MD 20892 USA. NR 12 TC 0 Z9 0 U1 0 U2 1 PU WORLD SCIENTIFIC PUBL CO PTE LTD PI SINGAPORE PA PO BOX 128 FARRER RD, SINGAPORE 9128, SINGAPORE BN 978-981-283-377-8 PY 2009 BP 276 EP 282 DI 10.1142/9789812833785_0043 PG 7 WC Biophysics SC Biophysics GA BKL64 UT WOS:000268443600043 ER PT B AU Iwasa, KH Sul, B Fang, J Sinha, GP AF Iwasa, K. H. Sul, B. Fang, J. Sinha, G. P. BE Cooper, NP Kemp, DT TI CELLULAR BASIS OF THE COCHLEAR AMPLIFIER SO CONCEPTS AND CHALLENGES IN THE BIOPHYSICS OF HEARING LA English DT Proceedings Paper CT 10th International Workshop on the Mechanics of Hearing CY JUL 27-31, 2008 CL Keele Univ, Staffordshire, ENGLAND SP Oticon Fdn, Otodynam Ltd, Starkey Lab Ltd, MED EL, Polytec GmbH, Tucker Davis Technol HO Keele Univ ID HAIR-CELLS; MICROMECHANICS; AMPLIFICATION; TRANSDUCTION; FREQUENCY; MODEL; CA2+ AB Three issue,, regarding the cellular basis for cochlear amplifier are discussed. First, regarding the mechanism of electromotility, we Present our recent; experimental data that demonstrate that conformational transitions of prestin-based membrane motor involve both membrane area and thickness. Namely the conformation that has larger membrane area is thinner. Second, we show that the effectiveness of hair bundle motility is less than that of electromotility as cochlear amplifier for the mammalian ear. Third, we examine factors that could enhance electromotility. Although we found that the cochlear microphonic can enhance the effectiveness of electromotility, it alone is insufficient to counteract viscous drag beyond 10 kHz. This result suggests additional mechanisms for enhancing the efficiency of electromotility. C1 [Iwasa, K. H.; Sul, B.; Fang, J.; Sinha, G. P.] NIDCD, Biophys Sect, NIH, Rockville, MD 20850 USA. RP Iwasa, KH (reprint author), NIDCD, Biophys Sect, NIH, Rockville, MD 20850 USA. NR 12 TC 0 Z9 0 U1 1 U2 1 PU WORLD SCIENTIFIC PUBL CO PTE LTD PI SINGAPORE PA PO BOX 128 FARRER RD, SINGAPORE 9128, SINGAPORE BN 978-981-283-377-8 PY 2009 BP 303 EP 309 DI 10.1142/9789812833785_0047 PG 7 WC Biophysics SC Biophysics GA BKL64 UT WOS:000268443600047 ER PT S AU McCormick, KA AF McCormick, Kathleen A. BE Saranto, K Brennan, PF Park, HA Tallberg, M Ensio, A TI Individualizing Cancer Care with Interoperable Information Systems SO CONNECTING HEALTH AND HUMANS SE Studies in Health Technology and Informatics LA English DT Proceedings Paper CT 10th International Congress on Nursing Informatics CY JUN 28-JUL 01, 2009 CL Helsinki, FINLAND SP Finnish Nurses Assoc DE Interoperability; standards harmonization; cancer research and care; translational cancer care; nursing impact AB There are three levels of interoperable informatics that are co-occurring in the United States to link data to provide more comprehensive care to patients. One is the National Health Information Network (NHIN) that is establishing use case scenarios and standards for interoperability for patients with multiple conditions. The second is the National Cancer Institute's project that supports the enterprise work called the Cancer Bioinformatics Grid (caBIG (R)) in linking clinical care with bioinformatics, tissue repositories, and imaging for patients with cancer. The third is in the area of translating the discoveries of biology to bedside care through the National Institutes of Health (NI H) translational research efforts to get these new biomedical and genomic discoveries in practice in multiple healthcare delivery environments. These developments are becoming global networks in the diagnosis and cure of cancer as the primary outcome. This paper describes the national efforts and fie global connection to Europe through the caBIG (R) program. The European program that is beginning to link to cancer research internationally is the National Cancer Research Institute (NCRI) in the United Kingdom. They are developing the NCRI Oncology Information Exchange (ONIX) to provide the cancer research community with the ability to share information. C1 [McCormick, Kathleen A.] SAIC Frederick Inc, NCI Frederick, Gaithersburg, MD USA. EM kathleen.a.mccormick@saic.com FU PHS HHS [HHSN261200800001E] NR 12 TC 2 Z9 2 U1 0 U2 1 PU I O S PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 0926-9630 BN 978-1-60750-024-7 J9 ST HEAL T PY 2009 VL 146 BP 383 EP 390 DI 10.3233/978-1-60750-024-7-383 PG 8 WC Health Policy & Services; Nursing SC Health Care Sciences & Services; Nursing GA BMS75 UT WOS:000273498700069 PM 19592871 ER PT S AU Tanda, G Newman, AH Katz, JL AF Tanda, Gianluigi Newman, Amy H. Katz, Jonathan L. BE Enna, SJ Williams, M TI Discovery of Drugs to Treat Cocaine Dependence: Behavioral and Neurochemical Effects of Atypical Dopamine Transport Inhibitors SO CONTEMPORARY ASPECTS OF BIOMEDICAL RESEARCH: DRUG DISCOVERY SE Advances in Pharmacology LA English DT Article; Book Chapter ID DISCRIMINATIVE STIMULUS PROPERTIES; CHLORO-BENZTROPINE ANALOGS; MOLECULAR-FIELD ANALYSIS; RHESUS-MONKEYS; IN-VIVO; NUCLEUS-ACCUMBENS; 3-ALPHA-DIPHENYLMETHOXYTROPANE ANALOGS; INTRACEREBRAL MICRODIALYSIS; POPULATION PHARMACOKINETICS; EXTRACELLULAR DOPAMINE AB Stimulant drugs acting at the dopamine transporter (DAT), like cocaine, are widely abused, yet effective medical treatments for this abuse have not been found. Analogs of benztropine (BZT) that, like cocaine, act at the DAT have effects that differ from cocaine and in some situations block the behavioral, neurochemical, and reinforcing actions of cocaine. Neurochemical studies of dopamine levels in brain and behavioral studies have demonstrated that BZT analogs have a relatively slow onset and reduced maximal effects compared to cocaine. Pharmacokinetic studies, however, indicated that the BZT analogs rapidly access the brain at concentrations above their in vitro binding affinities, while binding in vivo demonstrates apparent association rates for BZT analogs lower than that for cocaine. Additionally, the off-target effects of these compounds do not fully explain their differences from cocaine. Initial structure-activity studies indicated that BZT analogs bind to DAT differently from cocaine and these differences have been supported by site-directed mutagenesis studies of the DAT. In addition, BZT analog-mediated inhibition of uptake was more resistant to mutations producing inward conformational DAT changes than cocaine analogs. The BZT analogs have provided new insights into the relation between the molecular and behavioral actions of cocaine and the diversity of effects produced by dopamine transport inhibitors. Novel interactions of BZT analogs with the DAT suggest that these drugs may have a pharmacology that would be useful in their development as treatments for cocaine abuse. C1 [Tanda, Gianluigi; Katz, Jonathan L.] NIDA, Psychobiol Sect, Medicat Discovery Res Branch, Intramural Res Program,Dept Hlth & Human Serv,NIH, Baltimore, MD 21224 USA. [Newman, Amy H.] NIDA, Med Chem Sect, Medicat Discovery Res Branch, Intramural Res Program,Dept Hlth & Human Serv,NIH, Baltimore, MD 21224 USA. RP Tanda, G (reprint author), NIDA, Psychobiol Sect, Medicat Discovery Res Branch, Intramural Res Program,Dept Hlth & Human Serv,NIH, Baltimore, MD 21224 USA. RI Tanda, Gianluigi/B-3318-2009; OI Tanda, Gianluigi/0000-0001-9526-9878; Katz, Jonathan/0000-0002-1068-1159 FU Intramural NIH HHS NR 122 TC 30 Z9 31 U1 1 U2 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1054-3589 BN 978-0-12-378643-2 J9 ADV PHARMACOL JI Adv. Pharmacol. PY 2009 VL 57 BP 253 EP 289 DI 10.1016/S1054-3589(08)57007-4 PG 37 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA BCR76 UT WOS:000311112300008 PM 20230764 ER PT J AU Chakraborty, H Moore, J Carlo, WA Hartwell, TD Wright, LL AF Chakraborty, Hrishikesh Moore, Janet Carlo, Waldemar A. Hartwell, Tyler D. Wright, Linda L. TI A simulation based technique to estimate intracluster correlation for a binary variable SO CONTEMPORARY CLINICAL TRIALS LA English DT Article DE Intracluster correlation; ICC; Simulation; Binary variable; Cluster randomized trials ID CLUSTER-RANDOMIZED-TRIALS; INTRACLASS CORRELATION; SAMPLE-SIZE; CORRELATION-COEFFICIENT; DESIGN; RESUSCITATION; HEALTH AB Cluster randomized trials have become the design of choice for evaluating the effect of selected interventions on well-known health indicators such as neonatal mortality rate, episiotomy rate, and postpartum hemorrhage rate in a community setting. Determining the sample size of a cluster randomized trial requires a reliable estimate of cluster size and the intracluster correlation (ICC), because sample size can be substantially impacted by these parameters. During the design phase of a trial, the investigators may have estimates of the valid range of the health indicator which is the primary outcome variable. Furthermore, investigators often have an estimate of the average cluster size or range of cluster sizes that exist among the proposed samples they are planning to include in the trial. We present in this article a simulation technique to estimate the ICC value and its distribution for known binary outcome variables and a varying number of clusters and cluster sizes. We applied this technique to estimate ICC values and confidence intervals for a multi-country trial assessing the effect of neonatal resuscitation to decrease seven-day neonatal mortality, where communities within a country were clusters. This simulation technique can be used to estimate the possible ranges of the ICC values and to help to design an appropriately powered trial. (C) 2008 Elsevier Inc. All rights reserved. C1 [Chakraborty, Hrishikesh; Moore, Janet; Hartwell, Tyler D.] RTI Int, Stat & Epidemiol Div, Res Triangle Pk, NC 27709 USA. [Carlo, Waldemar A.] Univ Alabama Birmingham, Dept Pediat, Birmingham, AL USA. [Wright, Linda L.] NICHHD, NIH, Bethesda, MD 20892 USA. RP Chakraborty, H (reprint author), RTI Int, Stat & Epidemiol Div, Res Triangle Pk, NC 27709 USA. EM hchakraborty@rti.org FU National Institute of Child Health and Human Development (NICHD) [U01 HD40636, U01 HD043464-01]; Bill and Melinda Gates Foundation FX Grant support: This work was funded through grants from the National Institute of Child Health and Human Development (NICHD) U01 HD40636 and U01 HD043464-01 and the Bill and Melinda Gates Foundation. NR 28 TC 11 Z9 11 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 1551-7144 EI 1559-2030 J9 CONTEMP CLIN TRIALS JI Contemp. Clin. Trials PD JAN PY 2009 VL 30 IS 1 BP 71 EP 80 DI 10.1016/j.cct.2008.07.008 PG 10 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA 396PO UT WOS:000262603800012 PM 18723124 ER PT J AU Chalasani, NP Sanyal, AJ Kowdley, KV Robuck, PR Hoofnagle, J Kleiner, DE Unalp, A Tonascia, J AF Chalasani, Naga P. Sanyal, Arun J. Kowdley, Kris V. Robuck, Patricia R. Hoofnagle, Jay Kleiner, David E. Uenalp, Aynur Tonascia, James CA NASH CRN Res Grp TI Pioglitazone versus vitamin E versus placebo for the treatment of non-diabetic patients with non-alcoholic steatohepatitis: PIVENS trial design SO Contemporary Clinical Trials LA English DT Article DE Non-alcoholic steatohepatitis; Pioglitazone; Thiazolidinedione; Peroxisome proliferator-activated receptor-gamma (PPAR-gamma); Vitamin E; RRR-alpha-tocopherol; Randomized controlled trial ID FATTY LIVER-DISEASE; HEPATIC CYTOCHROME-P450 2E1; INSULIN-RESISTANCE; NATURAL-HISTORY; ALANINE AMINOTRANSFERASE; UNITED-STATES; ASSOCIATION; ROSIGLITAZONE; METAANALYSIS; PREVALENCE AB Background: Non-alcoholic steatohepatitis (NASH) is a common liver disease associated with obesity and diabetes. NASH is a progressive disorder that can lead to cirrhosis and liver failure. Insulin resistance and oxidative stress are thought to play important roles in its pathogenesis. There is no definitive treatment for NASH. Objectives: PIVENS is conducted to test the hypotheses that treatment with pioglitazone, a thiazolidinedione insulin sensitizer, or vitamin E, a naturally available antioxidant, will lead to improvement in hepatic histology in non-diabetic adults with biopsy proven NASH. Design: PIVENS is a randomized, multicenter, double-masked, placebo-controlled trial to evaluate whether 96 weeks of treatment with pioglitazone or vitamin E improves hepatic histology in non-diabetic adults with NASH compared to treatment with placebo. Before and post-treatment liver biopsies are read centrally in a masked fashion for an assessment of steatohepatitis and a NAFLD Activity Score (NAS) consisting of steatosis, lobular inflammation, and hepatocyte ballooning. The primary outcome measure is defined as either an improvement in NAS by 2 or more in at least two NAS features, or a post-treatment NAS of 3 or less, and improvement in hepatocyte ballooning by 1 or more, and no worsening of fibrosis. Methods: PIVENS enrollment started in January 2005 and ended in January 2007 with 247 patients randomized to receive either pioglitazone (30 mg q.d.), vitamin E (800 IU q.d.), or placebo for 96 weeks. Participants will be followed for an additional 24 weeks after stopping the treatment. The study protocol incorporates the use of several validated questionnaires and specimen banking. This protocol was approved by all participating center Institutional Review Boards (IRBs) and an independent Data and Safety Monitoring Board (DSMB) which was established for monitoring the accumulated interim data as the trial progresses to ensure patient safety and to review efficacy as well as the quality of data collection and overall study management. (ClinicalTrials.gov number, NCT00063622.) (C) 2008 Elsevier Inc. All rights reserved. C1 [Uenalp, Aynur] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD 21205 USA. [Sanyal, Arun J.] Virginia Commonwealth Univ, Richmond, VA USA. [Kowdley, Kris V.] Virginia Mason Med Ctr, Seattle, WA 98101 USA. [Robuck, Patricia R.; Hoofnagle, Jay] NIDDK, Bethesda, MD USA. [Kleiner, David E.] NCI, Bethesda, MD 20892 USA. [Chalasani, Naga P.] Indiana Univ, Sch Med, Indianapolis, IN USA. RP Unalp, A (reprint author), Johns Hopkins Univ, Bloomberg Sch Publ Hlth, 615 N Wolfe St,Room W5010, Baltimore, MD 21205 USA. EM aunalp@jhsph.edu OI Kleiner, David/0000-0003-3442-4453 FU National Institute of Diabetes and Digestive and Kidney Diseases [U01DK061718, U01DK061728, U01DK061731, U01DK061732, U01DK061734, U01DK061737, U01DK061738, U01DK061730, U01DK061713]; National Institute of Child Health and Human Development; Intramural Research Program of the National Cancer Institute; National Institutes of Health General Clinical Research Centers or Clinical and Translational Science Awards [UL1RR024989, M01RR000750, RR02413101, M01RR000827, UL1RR02501401, M01RR000065] FX Grant support: The Non-alcoholic Steatohepatitis Clinical Research Network (NASH CRN) is supported by the National Institute of Diabetes and Digestive and Kidney Diseases grants U01DK061718, U01DK061728, U01DK061731, U01DK061732, U01DK061734, U01DK061737, U01DK061738, U01DK061730, U01DK061713, and the National Institute of Child Health and Human Development. This study is supported in part by the Intramural Research Program of the National Cancer Institute. Other grant support include following National Institutes of Health General Clinical Research Centers or Clinical and Translational Science Awards: UL1RR024989, M01RR000750, RR02413101, M01RR000827, UL1RR02501401, M01RR000065. NR 49 TC 64 Z9 66 U1 0 U2 6 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 1551-7144 J9 CONTEMP CLIN TRIALS JI Contemp. Clin. Trials PD JAN PY 2009 VL 30 IS 1 BP 88 EP 96 DI 10.1016/j.cct.2008.09.003 PG 9 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA 396PO UT WOS:000262603800014 PM 18804555 ER PT J AU Yamaguchi, N Kitchener, AC Driscoll, CA Macdonald, DW AF Yamaguchi, Nobuyuki Kitchener, Andrew C. Driscoll, Carlos A. Macdonald, David W. TI Divided infraorbital foramen in the lion (Panthera leo): its implications for colonisation history, population bottlenecks, and conservation of the Asian lion (P. l. persica) SO CONTRIBUTIONS TO ZOOLOGY LA English DT Article DE cave lion; Gujarat; India; skull; spelaea; tiger ID GENETIC DIVERSITY; PHYLOGEOGRAPHY; ORIGIN AB A divided infraorbital foramen is an important morphological feature in lion taxonomy and has previously been considered to occur only in the Asian lion, Panthera leo persica. Based on an examination of 498 lion skulls from museum collections in Europe and southern Africa, we report for the first time on the prevalence of the divided infraorbital foramen in African lions, as well as its occurrence in the tiger, A tigris and the extinct Pleistocene European cave lion, P. leo spelaea. The higher frequency of this characteristic in Asian lions may have occurred after the lion colonised Asia, and can be considered an important morphological feature characterising this population. It is not clear whether recent anthropogenic population bottlenecks have influenced changes in its prevalence over the last 200 years. C1 [Yamaguchi, Nobuyuki; Driscoll, Carlos A.; Macdonald, David W.] Univ Oxford, Wildlife Conservat Res Unit, Abingdon OX13 5QL, Oxon, England. [Yamaguchi, Nobuyuki] Univ Qatar, Dept Biol & Environm Sci, Doha, Qatar. [Kitchener, Andrew C.] Natl Museums Scotland, Dept Nat Sci, Edinburgh EH1 1JF, Midlothian, Scotland. [Driscoll, Carlos A.] NCI, Lab Genom Div, Frederick, MD 21702 USA. RP Yamaguchi, N (reprint author), Univ Oxford, Wildlife Conservat Res Unit, Tubney House,Abingdon Rd, Abingdon OX13 5QL, Oxon, England. EM yamaguchi@qu.edu.qa NR 25 TC 2 Z9 2 U1 2 U2 13 PU UNIV AMSTERDAM PI AMSTERDAM PA LIBRARY FACULTY BIOLOGY, PLANTAGE MIDDENLAAN 45, AMSTERDAM, 1018 DC, NETHERLANDS SN 1383-4517 J9 CONTRIB ZOOL JI Contrib. Zool. PY 2009 VL 78 IS 2 BP 77 EP 83 PG 7 WC Zoology SC Zoology GA 504IJ UT WOS:000270609300004 ER PT J AU Reeves, SW Ellwein, LB Kim, T Constantine, R Lee, PP AF Reeves, Sherman W. Ellwein, Leon B. Kim, Terry Constantine, Roberta Lee, Paul P. TI Keratoconus in the Medicare Population SO CORNEA LA English DT Article DE keratoconus; epidemiology; elderly; Medicare; claims data ID PREVALENCE; COHORT; CARE AB Purpose: To investigate the population-based prevalence of keratoconus in US individuals aged 65 years and older. Design: Multiyear retrospective cross-sectional claims analysis. Methods: Fee-for-service claims from a 5% national sample of Medicare beneficiaries aged 65 years and older were reviewed. Claims records were queried on an annual basis for the years 1999 through 2003 for ICD-9 codes specific to keratoconus. The number of beneficiaries with keratoconus-related claims was counted for each calendar year. Results: The number of beneficiaries receiving care for keratoconus rose steadily from 15.7/100,000 beneficiaries in 1999 to 18.5/100,000 in 2003, averaging 17.5/100,000 across the 5 years of the Study. Keratoconus rates declined with increasing age but did not differ by gender. Keratoconus care was more prevalent in whites than in other races. Conclusions: Keratoconus is ail uncommon disease in the Medicare population. Longitudinal analysis of Medicare claims data may provide a useful tool for monitoring uncommon diseases, such as keratoconus, in the elderly. C1 [Reeves, Sherman W.] Minnesota Eye Consultants, Minneapolis, MN 55404 USA. [Ellwein, Leon B.] NEI, Natl Inst Hlth, Bethesda, MD 20892 USA. [Kim, Terry; Lee, Paul P.] Duke Univ, Sch Med, Dept Ophthalmol, Ctr Eye, Durham, NC USA. [Constantine, Roberta] Res Triangle Inst, RTI Int, Raleigh, NC USA. RP Reeves, SW (reprint author), Minnesota Eye Consultants, 710 E 24th St,Suite 106, Minneapolis, MN 55404 USA. EM swreeves@mneye.com OI Lee, Paul/0000-0002-3338-136X FU National Eye Institute under DHHS [223-02-0090]; Research to Prevent Blindness; Research to Pi-event Blindness, Inc., New York, NY; Alcon; Allergan; ISTA; BD Ophthalmic; Hyperbranch Medical corporations; Merck corporations FX Financial disclosures: S.W.R. has received speaking honoraria and/or consulting reimbursement from the Allergan; L.B.E.-none,- TK. has received speaking honoraria, grant support, and/or consulting reimbursement from the Alcon, Allergan, ISTA, BD Ophthalmic, and Hyperbranch Medical corporations. R. C-none. P.P.L. has received speaking honoraria, grant support, and/or consulting reimbursement from the Alcon, Allergan, Pfizer; and Merck corporations. The authors do not have any proprietary or commercial interests related to the reported research. NR 12 TC 15 Z9 15 U1 0 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0277-3740 J9 CORNEA JI Cornea PD JAN PY 2009 VL 28 IS 1 BP 40 EP 42 PG 3 WC Ophthalmology SC Ophthalmology GA 388GZ UT WOS:000262009600010 PM 19092403 ER PT J AU Wise, SP AF Wise, S. P. BE Jenkin, MRM Harris, LR TI Prefrontal cortex and the neurophysiology of visual knowledge: perception, action, attention, memory, strategies and goals SO CORTICAL MECHANISMS OF VISION LA English DT Article; Book Chapter ID WORKING-MEMORY; NEURONAL-ACTIVITY; NEURAL ACTIVITY; FRONTAL-CORTEX; ABSTRACT RULES; RHESUS-MONKEYS; UNIT-ACTIVITY; REPRESENTATION; OBJECTS; LOBE C1 NIMH, Lab Syst Neurosci, Bethesda, MD 20892 USA. RP Wise, SP (reprint author), NIMH, Lab Syst Neurosci, 49 Convent Dr,MSC 4401, Bethesda, MD 20892 USA. NR 64 TC 0 Z9 0 U1 2 U2 2 PU PRINCETON UNIV PRESS PI PRINCETON PA 41 WILLIAM ST, PRINCETON, NJ 08540 USA BN 978-0-521-88961-2 PY 2009 BP 273 EP 298 PG 26 WC Neurosciences SC Neurosciences & Neurology GA BBJ46 UT WOS:000307051200012 ER PT J AU Solomon, SB Minneci, PC Deans, KJ Feng, J Eichacker, PQ Banks, SM Danner, RL Natanson, C Solomon, MA AF Solomon, Steven B. Minneci, Peter C. Deans, Katherine J. Feng, Jing Eichacker, Peter Q. Banks, Steven M. Danner, Robert L. Natanson, Charles Solomon, Michael A. TI Effects of intra-aortic balloon counterpulsation in a model of septic shock SO CRITICAL CARE MEDICINE LA English DT Article DE sepsis; balloon pumping; Staphylococcus aureus; canine; septic shock; intra-aortic ID INTRA-AORTIC BALLOON; CANINE MODEL; CLINICAL-EXPERIENCE; HEMODYNAMIC SUPPORT; CARDIOGENIC SHOCK; ESCHERICHIA-COLI; SEVERE SEPSIS; DYSFUNCTION; COMPLICATIONS; AUGMENTATION AB Background: Fluid refractory septic shock can develop into a hypodynamic cardiovascular state in both children and adults. Despite management of these patients with empirical inotropic therapy (with or without a vasodilator), mortality remains high. Objectives: The effect of cardiovascular support using intra-aortic balloon counterpulsation was investigated in a hypodynamic, mechanically ventilated canine sepsis model in which cardiovascular and pulmonary support were titrated based on treatment protocols. Methods: Each week, three animals (n = 33, 10-12 kg) were administered intrabronchial Staphylococcus aureus challenge and then randomized to receive intra-aortic balloon counterpulsation for 68 hrs or no intra-aortic balloon counterpulsation (control). Bacterial doses were increased over the study (4-8 x 10(9) Cfu/kg) to assess the effects of intra-aortic balloon counter-pulsation during sepsis with increasing risk of death. Main Results: Compared with lower bacterial doses (4-7 x 10(9) colony-forming units/kg), control animals challenged with the highest dose (8 x 109 colony-forming units/kg) had a greater risk of death (mortality rate 86% vs. 17%), with worse lung injury ([A - a]0(2)), and renal dysfunction (creatinine).These sicker animals required higher norepinephrine infusion rates to maintain blood pressure (and higher F10(2)) and positive end-expiratory pressure levels to maintain oxygenation (p <= 0.04 for all). In animals receiving the highest bacterial dose, intra-aortic balloon counterpulsation improved survival time (23.4 +/- 10 hrs longer; p = 0.003) and lowered norepinephrine requirements (0.43 +/- 0.17 mu g/kg/min; p = 0.002) and systemic vascular resistance index (1.44 +/- 0.57 dynes/s/cm(5)/kg; p = 0.0001) compared with controls. Despite these beneficial effects, intra-aortic balloon counterpulsation was associated with an increase in blood urea nitrogen (p = 0.002) and creatinine (p = 0.12). In animals receiving lower doses of bacteria, intra-aortic balloon counterpulsation had no significant effects on survival or renal function. Conclusions. In a canine model of severe septic shock with a low cardiac index, intra-aortic balloon counterpulsation prolongs survival time and lowers vasopressor requirements. (Grit Care Med 2009; 37:7-18) C1 [Solomon, Steven B.; Minneci, Peter C.; Deans, Katherine J.; Feng, Jing; Eichacker, Peter Q.; Banks, Steven M.; Danner, Robert L.; Natanson, Charles; Solomon, Michael A.] NIH, Ctr Clin, Dept Crit Care Med, Bethesda, MD 20892 USA. [Minneci, Peter C.; Deans, Katherine J.] Childrens Hosp Philadelphia, Dept Surg, Philadelphia, PA 19104 USA. [Solomon, Michael A.] NHLBI, Cardiol Branch, NIH, Bethesda, MD 20892 USA. RP Solomon, SB (reprint author), NIH, Ctr Clin, Dept Crit Care Med, Bethesda, MD 20892 USA. EM ssolomon@cc.nih.gov FU National Institutes of Health; Datascope Corporation FX Datascope Corporation provided funding ($19,378) designated to support a 6-month lease of the ultrasound machine used for this animal study. In addition to the funds for the ultrasound, Datascope loaned the Critical Care Medicine Department three intra-aortic balloon counterpulsation devices (system 98XT) and supplied 26 sterile intra - aortic balloons. This funding represents <5% of the cost of the study. Datascope Corporation, as part of the agreement with the National Institutes of Health, did not participate in the collection or analysis of the data or the manuscript. NR 40 TC 12 Z9 13 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD JAN PY 2009 VL 37 IS 1 BP 7 EP 18 DI 10.1097/CCM.0b013e31818727bf PG 12 WC Critical Care Medicine SC General & Internal Medicine GA 391YK UT WOS:000262269900002 PM 19050641 ER PT J AU Sweeney, DA Natanson, C Eichacker, PQ AF Sweeney, Daniel A. Natanson, Charles Eichacker, Peter Q. TI Recombinant human activated protein C, package labeling, and hemorrhage risks SO CRITICAL CARE MEDICINE LA English DT Editorial Material ID SEVERE SEPSIS; SAFETY; TRIAL; ADULTS C1 [Sweeney, Daniel A.; Natanson, Charles; Eichacker, Peter Q.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA. RP Sweeney, DA (reprint author), NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA. NR 16 TC 13 Z9 13 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD JAN PY 2009 VL 37 IS 1 BP 327 EP 329 DI 10.1097/CCM.0b013e3181935102 PG 3 WC Critical Care Medicine SC General & Internal Medicine GA 391YK UT WOS:000262269900046 PM 19112285 ER PT J AU O'Grady, NP Kalil, A Barie, P Bleck, T AF O'Grady, Naomi P. Kalil, Andre Barie, Philip Bleck, Thomas TI Misguided guidelines on noninvasive thermometry The authors reply SO CRITICAL CARE MEDICINE LA English DT Letter ID TEMPORAL ARTERY C1 [O'Grady, Naomi P.] NIH, Dept Crit Care Med, Bethesda, MD 20892 USA. [Kalil, Andre] Univ Nebraska, Div Infect Dis, Omaha, NE 68182 USA. [Barie, Philip] Weill Cornell Med Coll, Div Crit Care & Trauma, New York, NY USA. [Bleck, Thomas] Northwestern Univ, Div Pulm & Crit Care, Chicago, IL 60611 USA. RP O'Grady, NP (reprint author), NIH, Dept Crit Care Med, Bethesda, MD 20892 USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD JAN PY 2009 VL 37 IS 1 BP 383 EP 384 DI 10.1097/CCM.0b013e3181932cd6 PG 2 WC Critical Care Medicine SC General & Internal Medicine GA 391YK UT WOS:000262269900089 ER PT J AU Pepe, PE Copass, MK Sopko, G AF Pepe, Paul E. Copass, Michael K. Sopko, George TI Clinical trials in the out-of-hospital setting: Rationale and strategies for successful implementation SO CRITICAL CARE MEDICINE LA English DT Article DE resuscitation; trauma; injury; research; clinical trials; outcomes data; cardiac arrest; cardiopulmonary resuscitation; CPR; sudden death; emergency medical services; EMS; survival rates; informed consent; exception to consent; ethics; community consultation; population-based research out-of-hospital; prehospital ID MEDICAL-SERVICES SYSTEM; HIGH-DOSE EPINEPHRINE; STANDARD CARDIOPULMONARY-RESUSCITATION; AMERICAN-HEART-ASSOCIATION; CARDIAC-ARREST; INFORMED-CONSENT; COMMUNITY CONSULTATION; VENTRICULAR-FIBRILLATION; EMERGENCY RESEARCH; MYOCARDIAL-INFARCTION AB Cardiopulmonary arrest and trauma are two of the major epidemics of our time. In most cases, the final outcome is altered, for better or for worse, by how interventions are provided in the prehospital setting, making that venue critical for lifesaving community research efforts. In certain venues, out-of-hospital emergency medical services personnel are highly skilled at managing resuscitations and routinely operate under strict, highly scrutinized protocols, resulting in extraordinary study compliance. Larger patient enrollment derived from population-based investigations can lead to faster study completion, less selection bias, higher-powered data, and enhanced subgroup analysis. Most importantly, the concomitant training, expert protocol development, and rigid scrutiny all lead to improved patient outcomes, regardless of study intervention. For successful implementation, emergency medical services personnel should be involved in study design, and utilize routine, automated data collection. Technologies should be provided that simplify tasks and diminish confounding variables. Considering that exception to informed consent is a critical component, prospective education and involvement of the medical community, community leaders, employee groups and the media, long before protocol implementation, is essential. Such efforts should be led by respected, academically authoritative, grassroots emergency medical services medical directors and trauma chiefs, preferably those based at the main trauma centers or public receiving facilities. (Crit Care Med 2009; 37[Suppl:S91-S101) C1 [Pepe, Paul E.] Univ Texas SW Med Ctr Dallas, Sch Publ Hlth, Dept Med, Dallas, TX 75390 USA. [Pepe, Paul E.] Univ Texas SW Med Ctr Dallas, Sch Publ Hlth, Dept Surg, Dallas, TX 75390 USA. [Pepe, Paul E.] Univ Texas SW Med Ctr Dallas, Sch Publ Hlth, Dept Pediat, Dallas, TX 75390 USA. [Pepe, Paul E.] Univ Texas SW Med Ctr Dallas, Programs Emergency Med, Dallas, TX 75390 USA. [Pepe, Paul E.] City Dallas Med Emergency Serv Publ Safety Publ H, Dallas, TX USA. [Pepe, Paul E.] Dallas Metropolitan Area BioTel Emergency Med Ser, Dallas, TX USA. [Copass, Michael K.] Univ Washington, Dept Med & Neurol, Seattle, WA 98195 USA. [Copass, Michael K.] Univ Washington, Emergency Serv, Emergency Trauma Ctr, Harborview Med Ctr, Seattle, WA 98195 USA. [Copass, Michael K.] Seattle Fire Dept Med One EMS Program, Seattle, WA USA. [Sopko, George] NHLBI, Div Cardiovasc Dis, Resuscitat Outcomes Consortium, NIH, Bethesda, MD 20892 USA. RP Pepe, PE (reprint author), Univ Texas SW Med Ctr Dallas, Sch Publ Hlth, Dept Med, Dallas, TX 75390 USA. EM paul.pepe@utsw.edu OI Sopko, George/0000-0002-5482-8992 NR 88 TC 12 Z9 12 U1 1 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD JAN PY 2009 VL 37 IS 1 BP S91 EP S101 DI 10.1097/CCM.0b013e318192154d PG 11 WC Critical Care Medicine SC General & Internal Medicine GA 391YO UT WOS:000262270300013 PM 19104231 ER PT J AU Yang, YZ AF Yang, Yingzi TI Skeletal Morphogenesis during Embryonic Development SO CRITICAL REVIEWS IN EUKARYOTIC GENE EXPRESSION LA English DT Review DE cartilage; bone; chondrocyte; osteoblast; cell signaling; transcription factor; growth plate; patterning; osteochondral progenitors ID GROWTH-FACTOR RECEPTOR-3; APICAL ECTODERMAL RIDGE; VERTEBRATE LIMB DEVELOPMENT; HORMONE-RELATED PEPTIDE; INHIBITS CHONDROCYTE PROLIFERATION; ENDOCHONDRAL BONE-DEVELOPMENT; SYNOVIAL JOINT FORMATION; NOTCH SIGNALING PATHWAY; SONIC-HEDGEHOG; ALAGILLE-SYNDROME AB A unique feature of vertebrate embryonic development is the formation of the skeletal system, which not only fulfills mechanical, supportive, and protective roles, but also regulates several important homeostatic processes systemically in adult animals. The skeletal system is a mesoderm-derived organ and its formation starts from mesenchymal condensations, in which skeletal precursor cells, also known as osteochondral progenitors, give rise to either chondrocytes to form the cartilage or osteoblasts to form the bone. This difference in the initial fate choices of osteochondral progenitors also determines whether ossification is endochondral or intramembranous. Like all other organogenetic processes, the development of skeletons, although mostly mineralized in adult lives, is controlled by tightly regulated programs of cell proliferation, differentiation, survival, and organization. In this review, we will discuss the entire embryonic developmental processes of the skeletal system. This review will particularly focus on how cell-cell signaling and transcription factors regulate multiple aspects of skeletal development. C1 NHGRI, Dev Genet Sect, Genet Dis Res Branch, Bethesda, MD 20892 USA. RP Yang, YZ (reprint author), NHGRI, Dev Genet Sect, Genet Dis Res Branch, 49 Convent Dr,MSC 4472, Bethesda, MD 20892 USA. EM yingzi@mail.nih.gov FU NHGRI FX This work is supported by the intramural research program of the NHGRI and I thank Darryl Leja and Julia Fekecs for generating the figures. NR 187 TC 28 Z9 33 U1 0 U2 11 PU BEGELL HOUSE INC PI REDDING PA 50 CROSS HIGHWAY, REDDING, CT 06896 USA SN 1045-4403 EI 2162-6502 J9 CRIT REV EUKAR GENE JI Crit. Rev. Eukaryot. Gene Expr. PY 2009 VL 19 IS 3 BP 197 EP 218 PG 22 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 500OV UT WOS:000270313600004 PM 19883365 ER PT J AU Ross, AC Russell, RM Miller, SA Munro, IC Rodricks, JV Yetley, EA Julien, E AF Ross, A. Catharine Russell, Robert M. Miller, Sanford A. Munro, Ian C. Rodricks, Joseph V. Yetley, Elizabeth A. Julien, Elizabeth TI Application of a Key Events Dose-Response Analysis to Nutrients: A Case Study with Vitamin A (Retinol) SO CRITICAL REVIEWS IN FOOD SCIENCE AND NUTRITION LA English DT Review DE dose-response; tolerable upper intake levels; vitamin A; retinol; uncertainty factors; homeostatic mechanisms ID BINDING-PROTEIN; EMBRYONIC-DEVELOPMENT; PLASMA RETINOL; BETA-CAROTENE; IN-VIVO; ACID; METABOLISM; RATS; ESTERS; DIFFERENTIATION AB The methodology used to establish tolerable upper intake levels (UL) for nutrients borrows heavily from risk assessment methods used by toxicologists. Empirical data are used to identify intake levels associated with adverse effects, and Uncertainty Factors (UF) are applied to establish ULs, which in turn inform public health decisions and standards. Use of UFs reflects lack of knowledge regarding the biological events that underlie response to the intake of a given nutrient, and also regarding the sources of variability in that response. In this paper, the Key Events Dose-Response Framework (KEDRF) is used to systematically consider the major biological steps that lead from the intake of the preformed vitamin A to excess systemic levels, and subsequently to increased risk of adverse effects. Each step is examined with regard to factors that influence whether there is progression toward the adverse effect of concern. The role of homeostatic mechanisms is discussed, along with the types of research needed to improve understanding of dose-response for vitamin A. This initial analysis illustrates the potential of the KEDRF as a useful analytical tool for integrating current knowledge regarding dose-response, generating questions that will focus future research efforts, and clarifying how improved knowledge and data could be used to reduce reliance on UFs. C1 [Julien, Elizabeth] ILSI Res Fdn, Washington, DC 20005 USA. [Ross, A. Catharine] Penn State Univ, Dept Nutr Sci, University Pk, PA 16802 USA. [Russell, Robert M.] Tufts Univ, Boston, MA 02111 USA. [Miller, Sanford A.] Univ Maryland, Cent Food Nutr & Agr Policy, College Pk, MD 20742 USA. [Rodricks, Joseph V.] ENVIRON Int Corp, Arlington, VA USA. [Yetley, Elizabeth A.] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA. RP Julien, E (reprint author), ILSI Res Fdn, 1156 15th St NW,2nd Floor, Washington, DC 20005 USA. EM bjulien@ilsi.org FU ILSI Research Foundation; Health Canada; Ajinomoto; Coca-Cola Company; Groupe Danone; Kellogg Company; Kraft Foods, Inc.; Mars, Inc.; Mead Johnson Nutritionals; Monsanto Company; Nestle; PepsiCo, Inc.; Procter Gamble Company; Syngenta Ltd.; Flavor Extract Manufacturers Association; Grocery Manufacturers Association FX Financial support for this project from the following sources is gratefully acknowledged: ILSI Research Foundation, Health Canada, Ajinomoto, Coca-Cola Company, Groupe Danone, Kellogg Company, Kraft Foods, Inc., Mars, Inc., Mead Johnson Nutritionals, Monsanto Company, Nestle, PepsiCo, Inc., The Procter & Gamble Company, Syngenta Ltd., Flavor Extract Manufacturers Association, and Grocery Manufacturers Association. Assistance from Ms. Julie Fitzpatrick with coordination of the final preparation of these papers is also gratefully acknowledged. NR 54 TC 14 Z9 14 U1 1 U2 4 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1040-8398 J9 CRIT REV FOOD SCI JI Crit. Rev. Food Sci. Nutr. PY 2009 VL 49 IS 8 BP 708 EP 717 AR PII 914016756 DI 10.1080/10408390903098749 PG 10 WC Food Science & Technology; Nutrition & Dietetics SC Food Science & Technology; Nutrition & Dietetics GA 485CX UT WOS:000269099500004 PM 19690996 ER PT J AU Ma, HT Beaven, MA AF Ma, Hong-Tao Beaven, Michael A. TI Regulation of Ca2+ Signaling with Particular Focus on Mast Cells SO CRITICAL REVIEWS IN IMMUNOLOGY LA English DT Review DE store-operated calcium entry (SOCE); calcium channels; TRPC; Orai1; mitochondria; pharmacologic probes; review ID INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; BASOPHILIC LEUKEMIA-CELLS; ACTIVATED CALCIUM CURRENT; 2-AMINOETHOXYDIPHENYL BORATE 2-APB; FC-EPSILON-RI; PROTEIN-COUPLED-RECEPTORS; PANCREATIC ACINAR-CELLS; CURRENT I-CRAC; ANAPHYLACTIC HISTAMINE-SECRETION; CYTOSOLIC PHOSPHOLIPASE A(2) AB Calcium signals mediate diverse cellular functions in immunological cells. Early studies with mast cells, then a preeminent model for studying Ca2+-dependent exocytosis, revealed several basic features of calcium signaling in non-electrically excitable cells. Subsequent studies in these and other cells further defined the basic processes such as inositol 1,4,5-trisphosphate-mediated release of Ca2+ from Ca2+ stores in the endoplasmic reticulum (ER); coupling of ER store depletion to influx of external Ca2+ through a calcium-release activated calcium (CRAC) channel now attributed to the interaction of the ER Ca2+ sensor, stromal interacting molecule-1 (STIM1), with a unique Ca2+-channel protein, Orai1/CRACM1, and subsequent uptake of excess Ca2+ into ER and mitochondria through ATP-dependent Ca2+ pumps. In addition, transient receptor potential channels and ion exchangers also contribute to the generation of calcium signals that may be global or have dynamic (e.g., waves and oscillations) and spatial resolution for specific functional readouts. This review discusses past and recent developments in this field of research, the pharmacologic agents that have assisted in these endeavors, and the mast cell as an exemplar for sorting out how calcium signals may regulate multiple outputs in a single cell. C1 [Ma, Hong-Tao; Beaven, Michael A.] NHLBI, Lab Mol Immunol, Natl Inst Hlth, Bethesda, MD 20892 USA. RP Beaven, MA (reprint author), NHLBI, Lab Mol Immunol, Natl Inst Hlth, Room 8N109 Bldg 10, Bethesda, MD 20892 USA. EM beavenm@nhlbi.nih.gov FU National Heart, Lung, and Blood Institute of the National Institutes of Health FX This work is supported by the intramural program of the National Heart, Lung, and Blood Institute of the National Institutes of Health. NR 322 TC 42 Z9 42 U1 2 U2 6 PU BEGELL HOUSE INC PI REDDING PA 50 CROSS HIGHWAY, REDDING, CT 06896 USA SN 1040-8401 J9 CRIT REV IMMUNOL JI Crit. Rev. Immunol. PY 2009 VL 29 IS 2 BP 155 EP 186 PG 32 WC Immunology SC Immunology GA 460SI UT WOS:000267207000004 PM 19496745 ER PT J AU Puri, A Loomis, K Smith, B Lee, JH Yavlovich, A Heldman, E Blumenthal, R AF Puri, Anu Loomis, Kristin Smith, Brandon Lee, Jae-Ho Yavlovich, Amichai Heldman, Eliahu Blumenthal, Robert TI Lipid-Based Nanoparticles as Pharmaceutical Drug Carriers: From Concepts to Clinic SO CRITICAL REVIEWS IN THERAPEUTIC DRUG CARRIER SYSTEMS LA English DT Review DE lipid-based nanoparticles; drug delivery; solid lipid nanoparticles; liposomes; nanostructured lipid carriers; bolaamphiphiles; cancer therapy ID PEGYLATED LIPOSOMAL DOXORUBICIN; B-CELL LYMPHOMA; STERICALLY STABILIZED LIPOSOMES; EXPERIMENTAL VISCERAL LEISHMANIASIS; PROTEIN ADSORPTION PATTERNS; ANTIBODY-MODIFIED LIPOSOMES; TARGETED GENE DELIVERY; NON-HODGKIN-LYMPHOMA; BREAST-CANCER CELLS; TUMOR-BEARING MICE AB In recent years, various nanotechnology platforms in the area of medical biology, including both diagnostics and therapy, have gained remarkable attention. Moreover, research and development of engineered multifunctional nanoparticles as pharmaceutical drug carriers have spurred exponential growth in applications to medicine in the last decade. Design principles of these nanoparticles, including nano-emulsions, dendrimers, nano-gold, liposomes, drug-carrier conjugates, antibody-drug complexes, and magnetic nanoparticles, are primarily based on unique assemblies of synthetic, natural, or biological components, including but not limited to synthetic polymers, metal ions, oils, and lipids as their building blocks. However, the potential success of these particles in the clinic relies on consideration of important parameters such as nanoparticle fabrication strategies, their physical properties, drug loading efficiencies, drug release potential, and, most importantly, minimum toxicity of the carrier itself. Among these, lipid-based nanoparticles bear the advantage of being the least toxic for in vivo applications, and significant progress has been made in the area of DNA/RNA and drug delivery using lipid-based nanoassemblies. In this review, we will primarily focus on the recent advances and updates on lipid-based nanoparticles for their projected applications in drug delivery. We begin with a review of current activities in the field of liposomes (the so-called honorary nanoparticles), and challenging issues of targeting and triggering will be discussed in detail. We will further describe nanoparticles derived from a novel class of amphipathic lipids called bolaamphiphiles with unique lipid assembly features that have been recently examined as drug/DNA delivery vehicles. Finally, an overview of an emerging novel class of particles (based on lipid components other than phospholipids), solid lipid nanoparticles and nanostructured lipid carriers will be presented. We conclude with a few examples of clinically successful formulations of currently available lipid-based nanoparticles. C1 [Puri, Anu; Loomis, Kristin; Smith, Brandon; Lee, Jae-Ho; Yavlovich, Amichai; Heldman, Eliahu; Blumenthal, Robert] NCI, CCR Nanobiol Program, NIH, Frederick, MD 21702 USA. RP Puri, A (reprint author), NCI, CCR Nanobiol Program, NIH, Bldg 469,Rm 216A,POB B,Miller Dr, Frederick, MD 21702 USA. EM apuri@helix.nih.gov FU National Institutes of Health, National Cancer Institute, Center for Cancer Research FX This research was supported by the Intramural Research Program of the National Institutes of Health, National Cancer Institute, Center for Cancer Research. We thank Dr. Kshitij Gupta for critical reading of the manuscript. NR 297 TC 168 Z9 176 U1 15 U2 178 PU BEGELL HOUSE INC PI DANBURY PA 50 NORTH ST, DANBURY, CT 06810 USA SN 0743-4863 EI 2162-660X J9 CRIT REV THER DRUG JI Crit. Rev. Ther. Drug Carr. Syst. PY 2009 VL 26 IS 6 BP 523 EP 580 PG 58 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 590AH UT WOS:000277195000001 PM 20402623 ER PT J AU Kushnarenko, SV Romadanova, NV Reed, BM AF Kushnarenko, Svetlana V. Romadanova, Natalia V. Reed, Barbara M. TI COLD ACCLIMATION IMPROVES REGROWTH OF CRYOPRESERVED APPLE SHOOT TIPS SO CRYOLETTERS LA English DT Article DE acclimation; cold hardiness; germplasm; long-term storage; LT(50); Malus domestica; Malus sieversii ID ENCAPSULATION-DEHYDRATION; PROPAGATED PLANTS; VITRIFICATION; PEAR; CULTURES; PRECULTURE; STORAGE AB Cryopreservation is important for safeguarding the genetic resources of apple germplasm in Kazakhstan, the center of origin for apples. In this study, conducted with five apple genotypes [Malus domestica Borkh. and Malus sieversii (Ledeb.) M. Roem] we determined cold hardiness and the effect of cold acclimation on shoot tip recovery following cryopreservation using two techniques. Apple shoot tips were cold acclimated (CA) for 0 to 6 weeks and cryopreserved using PVS2 vitrification and encapsulation dehydration (ED). Cold hardiness was indicated by the temperature at which 50% of the shoot tips were lethally injured (LT(50)). For non-acclimated shoots, LT(50) ranged from -6.7 degrees C to -9.3 degrees C. These LT(50) values resembled the natural cold hardiness of field grown plants and resulted in 10-12% regrowth after cryopreservation. Acclimated plantlets had LT(50) values of -12 degrees C to -15 degrees C after I to 3 weeks CA, and after 3 weeks CA, cryopreservation resulted in 65% regrowth. There were no significant differences between the two techniques for regrowth of shoot tips after,each cold acclimation period. Overall, 2 to 5 weeks CA produced high regrowth for each of the five cultivars tested. Three weeks of alternating temperature CA can be recommended as a standard protocol for Malus germplasm cryopreservation. These conditions resulted in I moderate (60%) to high (80%) recovery for all five genotypes tested with both cryopreservation methods used. C1 [Kushnarenko, Svetlana V.; Romadanova, Natalia V.] Natl Biotechnol Ctr, Inst Plant Biol & Biotechnol, Alma Ata 050040, Kazakhstan. [Reed, Barbara M.] ARS, USDA, Corvallis, OR 97333 USA. RP Kushnarenko, SV (reprint author), Natl Biotechnol Ctr, Inst Plant Biol & Biotechnol, Timiryazev Str 45, Alma Ata 050040, Kazakhstan. EM svetlana_bio@mail.ru OI Reed, Barbara/0000-0003-0079-8473 FU International Science and Technology Center [K-428] FX This project was funded by the International Science and Technology Center project K-428 "Germplasm preservation of fruit, berry cultures and grapes in Kazakhstan." NR 32 TC 20 Z9 22 U1 0 U2 6 PU CRYO LETTERS PI LONDON PA C/O ROYAL VETERINARY COLLEGE, ROYAL COLLEGE ST, LONDON NW1 0TU, ENGLAND SN 0143-2044 J9 CRYOLETTERS JI CryoLetters PD JAN-FEB PY 2009 VL 30 IS 1 BP 47 EP 54 PG 8 WC Biology; Physiology SC Life Sciences & Biomedicine - Other Topics; Physiology GA 422LU UT WOS:000264430300006 PM 19274311 ER PT J AU Montalvo, V Gery, I AF Montalvo, Vanessa Gery, Igal TI Constitutive Pro-Apoptotic Molecules are Differentially Expressed in the Fetal and Adult Mouse Eye SO CURRENT EYE RESEARCH LA English DT Article DE apoptosis; constitutive molecules; fetal vs; adult eye; intrinsic and extrinsic pathways; real-time PCR ID BCL-2 FAMILY-MEMBERS; PROGRAMMED CELL-DEATH; PHOTORECEPTOR APOPTOSIS; RETINAL DEGENERATION; IMMUNE PRIVILEGE; FAS LIGAND; PROTEINS; BAX; MORPHOGENESIS; PATHWAY AB Purpose: To compare gene expression of pro-apoptotic molecules in the fetal and adult mouse eye. Materials and Methods: Eyes were collected from groups of BALB/c mice, at embryonic ages E16 and E18 (fetal) or 6-8 weeks of age (adult). RNA extracted from pooled eyes was analyzed by real-time PCR for transcript levels of pro-apoptotic molecules involved in the intrinsic or extrinsic pathway of apoptosis. Results: Transcripts of intrinsic pathway molecules, Bad, Bak, and Bax, were relatively more highly expressed in the fetal mouse eyes, whereas extrinsic pathway molecules, Fas, FasL, and TRAIL had greater expression in the adult eyes. Conclusions: Different mechanisms of apoptosis are prominent at the fetal and mature stages of the mouse eye. C1 [Montalvo, Vanessa; Gery, Igal] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA. [Montalvo, Vanessa] Howard Univ, Coll Med, Dept Anat, Washington, DC USA. RP Gery, I (reprint author), NEI, Immunol Lab, NIH, Bldg 10,Room 10N208,10 Ctr Dr, Bethesda, MD 20892 USA. EM geryi@nei.nih.gov FU National Eye Institute, National Institutes of Health FX This work was supported by the Intramural Research Program of the National Eye Institute, National Institutes of Health. We thank Drs. Charles E. Egwuagu and Cheng-Rong Yu for their advice and support and Barbara P. Vistica for assistance. NR 27 TC 0 Z9 0 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0271-3683 J9 CURR EYE RES JI Curr. Eye Res. PY 2009 VL 34 IS 4 BP 328 EP 332 AR PII 910504646 DI 10.1080/02713680902741688 PG 5 WC Ophthalmology SC Ophthalmology GA 434RT UT WOS:000265292500011 PM 19373582 ER PT B AU Zheng, YL Amin, ND Rudrabhatla, P Kesavapany, S Pant, HC AF Zheng, Ya-Li Amin, Niranjana D. Rudrabhatla, Parvathi Kesavapany, Sashi Pant, Harish C. BE Maccioni, RB Perry, G TI Neuronal Cytoskeleton Regulation and Neurodegeneration SO CURRENT HYPOTHESES AND RESEARCH MILESTONES IN ALZHEIMER'S DISEASE LA English DT Proceedings Paper CT International Summit Meeting on Current Hypotheses on Alzheimer Disease CY NOV 22-25, 2007 CL Renaca, CHILE ID WEIGHT NEUROFILAMENT PROTEIN; DEPENDENT KINASE-5 ACTIVITY; MYELINATING SCHWANN-CELLS; TANDEM MASS-SPECTROMETRY; DOMAIN PHOSPHORYLATION; AXONAL-TRANSPORT; NF-M; CDK5; P35; PATHOLOGY AB The biology of neurodegeneration program evolved from the laboratory studying the basic biology of neuronal cytoskeletal protein phosphorylation during development and normal function in the adult. To understand the molecular basis of neurodegeneration, our major focus has been to study the regulation of compartment-specific patterns of cytoskeletal protein phosphorylation in neuronal perikarya and axons. We have demonstrated that the phosphorylation of the numerous acceptor sites on proline-directed serine and thronine (Pro-Ser/Thr) residue proteins such as tau and neurofilaments is tightly regulated. The phosphorylation of these molecules is generally confined to the axonal compartment. It was recognized that in neurodegenerative disorders such as Alzheirner's disease (AD) and amyotrophic lateral sclerosis (ALS), the pathology was characterized by an accumulation of aberrantly phosphorylated cytoskeletal proteins in cell bodies, suggesting that topographic regulation had been compromised. This led inevitably into studies of neurodegeneration in cell culture and model mice with emphasis on a specific neuronal protein kinases, for example, cyclin-dependent kinase 5 (Cdk5), that target numerous neuronal proteins including cytoskeletal proteins, which when deregulated may be responsible for the pathology seen in neurodegeneration. In cell systems, neuronal stress leads to deregulated kinases, for example, Cdk5, accompanied by abnormal cytoskeletal protein phosphorylation and cell death characteristic of neurodegeneration. In this chapter, efforts are made to answer some of the following questions. (1) How is the cytoskeletal protein phosphorylation topographically and stably regulated in their proline-directed Ser/Thr residues in neurons? (2) What factors are responsible for the regulation and deregulation of Cdk5 in neurons? C1 [Zheng, Ya-Li; Amin, Niranjana D.; Rudrabhatla, Parvathi; Kesavapany, Sashi; Pant, Harish C.] NINDS, Cytoskeletal Prot Regulat Sect, Neurochem Lab, NIH, Bethesda, MD 20892 USA. RP Pant, HC (reprint author), NINDS, Cytoskeletal Prot Regulat Sect, Neurochem Lab, NIH, Bethesda, MD 20892 USA. EM panth@ninds.nih.gov RI Perry, George/A-8611-2009 OI Perry, George/0000-0002-6547-0172 NR 46 TC 0 Z9 0 U1 0 U2 2 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES BN 978-0-387-87994-9 PY 2009 BP 63 EP + DI 10.1007/978-0-387-87995-6_6 PG 20 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA BJF06 UT WOS:000265335200006 ER PT J AU Kawai, T Malech, HL AF Kawai, Toshinao Malech, Harry L. TI WHIM syndrome: congenital immune deficiency disease SO CURRENT OPINION IN HEMATOLOGY LA English DT Article DE apoptosis; B-cell lymphopenia; G-protein coupled receptor; G-protein coupled receptor kinase 3; human papilloma virus; hypogammaglobulinemia; myelokathexis; neutropenia; stromal cell-derived factor 1; warts ID COLONY-STIMULATING FACTOR; TERMINUS-TRUNCATED CXCR4; CHEMOKINE RECEPTOR CXCR4; BETA-ARRESTIN; HIV-1 ENTRY; SEVERE NEUTROPENIA; FACTOR-I; MYELOKATHEXIS; HYPOGAMMAGLOBULINEMIA; IMMUNODEFICIENCY AB Purpose of review Warts, hypogammaglobulinemia, infections, and myelokathexis (WHIM) syndrome is characterized by susceptibility to human papilloma virus infection-induced warts and carcinomas; neutropenia, B-cell lymphopenia and hypogammaglobulinema-related infections; and bone marrow myelokathexis (myeloid hyperplasia with apoptosis). The purpose of this report is to review new findings about WHIM. Recent findings Most WHIM patients have heterozygous C-terminus deletion mutations of the intracellular carboxy terminus of the chemokine receptor CXCR4. WHIM leukocytes have enhanced responses to CXCL12, the cognate ligand of CXCR4. Enhanced activity of CXCR4 delays release of mature neutrophils from bone marrow, resulting in neutropenia and apoptosis of mature neutrophils retained in the marrow. Finding two patients with WHIM who do not have detectable mutations of CXCR4 but whose cells are hyperresponsive to CXCL12 raises the possibility that there is more than one genetic basis for WHIM. One patient had low levels of G-protein receptor kinase 3, and the functional hyperactivity response to CXCL12 was corrected by forced gene transfer-mediated overexpression of G-protein receptor kinase 3, implicating defects in function of this protein as a potential alternate genetic cause of WHIM. Summary Subjects reviewed include clinical presentation, diagnosis, and treatment of WHIM and advances in understanding the genetic basis of WHIM. C1 [Malech, Harry L.] NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA. [Kawai, Toshinao] Jikei Univ, Sch Med, Dept Pediat, Tokyo, Japan. RP Malech, HL (reprint author), NIAID, Host Def Lab, NIH, Bldg 10,Room 5-3750,10 Ctr Dr,MSC-1456, Bethesda, MD 20892 USA. EM hmalech@nih.gov OI Malech, Harry/0000-0001-5874-5775 FU Intramural NIH HHS [Z01 AI000645-16] NR 58 TC 83 Z9 85 U1 3 U2 12 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1065-6251 J9 CURR OPIN HEMATOL JI Curr. Opin. Hematol. PD JAN PY 2009 VL 16 IS 1 BP 20 EP 26 DI 10.1097/MOH.0b013e32831ac557 PG 7 WC Hematology SC Hematology GA 391EB UT WOS:000262215200005 PM 19057201 ER PT J AU Bagni, R Whitby, D AF Bagni, Rachel Whitby, Denise TI Kaposi's sarcoma-associated herpesvirus transmission and primary infection SO CURRENT OPINION IN HIV AND AIDS LA English DT Article DE HIV; Kaposi's sarcoma-associated herpesvirus; transmission AB Purpose of review Kaposi's sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8, is the causal agent of Kaposi's sarcoma, one of the commonest cancers in HIV-infected individuals. Transmission and risk factors for infection by KSHV are not fully understood. The purpose of this review is to highlight recent advances in our understanding of KSHV transmission in various settings. Recent findings KSHV and HIV are both common in southern Africa where KSHV infection occurs during childhood via saliva. HIV infection is a major risk factor for KSHV infection. In developed countries, KSHV transmission among men who have sex with men is related to sexual risk factors such as number of sexual partners and to sexual practices involving saliva. KSHV can be transmitted by transfusion of infected blood, but storage of blood products diminishes the risk. Summary Recent reports have provided much additional insight into KSHV transmission in different populations, but have also provided a number of important questions for the research and public health communities. Most critically, the role of HIV in increasing risk for KSHV infection and the possible effects on KSHV prevalence, and consequently the incidence of Kaposi's sarcoma warrants urgent further study. C1 [Bagni, Rachel; Whitby, Denise] NCI, SAIC Frederick, AIDS & Canc Virus Program, Viral Oncol Sect, Frederick, MD 21702 USA. RP Whitby, D (reprint author), NCI, SAIC Frederick, AIDS & Canc Virus Program, Viral Oncol Sect, Frederick, MD 21702 USA. EM whitbyd@ncifcrf.gov NR 39 TC 25 Z9 25 U1 1 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1746-630X J9 CURR OPIN HIV AIDS JI Curr. Opin. HIV AIDS PD JAN PY 2009 VL 4 IS 1 BP 22 EP 26 DI 10.1097/COH.0b013e32831add5a PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA V19OY UT WOS:000208082900005 PM 19339936 ER PT J AU Goyal, R Bulua, AC Nikolov, NP Schwartzberg, PL Siegel, RM AF Goyal, Ramona Bulua, Ariel C. Nikolov, Nikolay P. Schwartzberg, Pamela L. Siegel, Richard M. TI Rheumatologic and autoimmune manifestations of primary immunodeficiency disorders SO CURRENT OPINION IN RHEUMATOLOGY LA English DT Review DE autoimmunity; immune regulation; lymphopenia; primary immunodeficiency disorders; Wiskott-Aldrich syndrome ID WISKOTT-ALDRICH-SYNDROME; CHRONIC GRANULOMATOUS-DISEASE; COMMON VARIABLE IMMUNODEFICIENCY; LINKED LYMPHOPROLIFERATIVE DISEASE; SYSTEMIC LUPUS-ERYTHEMATOSUS; T-CELL HOMEOSTASIS; HYPER-IGM SYNDROME; SYNDROME PROTEIN; OMENN-SYNDROME; DEFICIENT MICE AB Purpose of review Although it may seem paradoxical, primary immunodeficiency disorders are frequently complicated by autoimmune and inflammatory conditions. These conditions pose significant diagnostic and therapeutic challenges for clinicians caring for these patients. There have been a number of new insights into how immunodeficiencies can predispose to autoimmunity, and rheumatologists should understand the basis for and manifestations of autoimmunity in primary immunodeficiency disorders to more effectively care for these patients. Recent findings A number of mechanisms have recently been found to link primary immunodeficiencies and autoimmunity, including increased homeostatic proliferation in primary immunodeficiencies associated with lymphopenia and defects in regulatory T cells in the Wiskott-Aldrich syndrome. Primary immunodeficiencies that affect the innate immune system can also lead to inappropriate inflammation through impairing negative regulatory mechanisms in innate immune cells. Summary The realization that primary immunodeficiencies can also impair negative regulation of immune responses has provided a new framework for the understanding of autoimmunity associated with these Conditions. These insights may lead to new, more targeted therapies for autoimmune complications in primary immunodeficiency patients. C1 [Bulua, Ariel C.; Siegel, Richard M.] NIDCD, Mol Physiol & Therapeut Branch, NIH, Bethesda, MD 20892 USA. [Goyal, Ramona] NIAMS, Off Clin Director, NIH, Bethesda, MD USA. [Nikolov, Nikolay P.] NIAMS, Autoimmun Branch, NIH, Bethesda, MD USA. [Schwartzberg, Pamela L.] NHGRI, Genet Dis Res Branch, Bethesda, MD USA. RP Siegel, RM (reprint author), NIDCD, Mol Physiol & Therapeut Branch, NIH, Bldg 10 Rm 13C103, Bethesda, MD 20892 USA. EM rsiegel@nih.gov RI Siegel, Richard/C-7592-2009 OI Siegel, Richard/0000-0001-5953-9893 FU Intramural NIH HHS [Z01 AR041133-07, Z99 AR999999] NR 58 TC 25 Z9 30 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1040-8711 J9 CURR OPIN RHEUMATOL JI Curr. Opin. Rheumatol. PD JAN PY 2009 VL 21 IS 1 BP 78 EP 84 DI 10.1097/BOR.0b013e32831cb939 PG 7 WC Rheumatology SC Rheumatology GA 392XT UT WOS:000262336200014 PM 19077721 ER PT J AU Kummar, S AF Kummar, Shivaani TI Multiple Myeloma Foreword SO CURRENT PROBLEMS IN CANCER LA English DT Editorial Material C1 [Kummar, Shivaani] Natl Canc Inst, Ctr Canc Res, NIH, Bethesda, MD USA. RP Kummar, S (reprint author), Natl Canc Inst, Ctr Canc Res, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0147-0272 J9 CURR PROB CANCER JI Curr. Probl. Cancer PD JAN-FEB PY 2009 VL 33 IS 1 BP 6 EP 6 PG 1 WC Oncology SC Oncology GA 421YM UT WOS:000264394200002 PM 19254625 ER PT S AU Jin, R Wang, SJ Zhou, ZH AF Jin, Rong Wang, Shijun Zhou, Zhi-Hua GP IEEE TI Learning a Distance Metric from Multi-instance Multi-label Data SO CVPR: 2009 IEEE CONFERENCE ON COMPUTER VISION AND PATTERN RECOGNITION, VOLS 1-4 SE IEEE Conference on Computer Vision and Pattern Recognition LA English DT Proceedings Paper CT IEEE-Computer-Society Conference on Computer Vision and Pattern Recognition Workshops CY JUN 20-25, 2009 CL Miami Beach, FL SP IEEE Comp Soc ID NONLINEAR DIMENSIONALITY REDUCTION; FRAMEWORK AB Multi-instance multi-label learning (MIML) refers to the learning problems where each example is represented by a bag/collection of instances and is labeled by multiple labels. An example application of MIML is visual object recognition in which each image is represented by multiple key points (i.e., instances) and is assigned to multiple object categories. In this paper, we study the problem of learning a distance metric from multi-instance multi-label data. It is significantly more challenging than the conventional setup of distance metric learning because it is difficult to associate instances in a bag with its assigned class labels. We propose an iterative algorithm for MIML distance metric learning: it first estimates the association between instances in a bag and its assigned class labels, and learns a distance metric from the estimated association by a discriminative analysis; the learned metric will be used to update the association between instances and class labels, which is further used to improve the learning of distance metric. We evaluate the proposed algorithm by the task of automated image annotation, a well known MIML problem. Our empirical study shows an encouraging result when combining the proposed algorithm with citation-kNN, a state-of-the-art algorithm for multi-instance learning. C1 [Jin, Rong] Michigan State Univ, Dept Comp Sci & Engn, E Lansing, MI 48824 USA. [Wang, Shijun] Natl Inst Hlth, Dept Radiol & Imaging Sci, Bethesda, MD 20892 USA. [Zhou, Zhi-Hua] Nanjing Univ, Natl Key Lab Novel Software Technol, Nanjing 210093, Jiangsu, Peoples R China. RP Jin, R (reprint author), Michigan State Univ, Dept Comp Sci & Engn, E Lansing, MI 48824 USA. EM rongjin@cse.msu.edu; wangshi@cc.nih.gov; zhouzh@lamda.nju.edu.cn FU NSF [IIS-0643494]; US ARO [W911NF-08-1-0403]; NSFC [60635030, 60721002]; 863 Program [2007AA01Z169]; JiangsuSF [BK2008018] FX This research was supported partially by NSF (IIS-0643494), US ARO (W911NF-08-1-0403), NSFC (60635030, 60721002), 863 Program (2007AA01Z169), JiangsuSF (BK2008018), Jiangsu 333 Program and MSRA IST Program. Any opinions, findings, and conclusions or recommendations expressed in this material are those of the authors and do not necessarily reflect the views of these funding agencies. We also would like to thank Kobus Barnard for providing data used in their ECCV2002 paper. NR 23 TC 21 Z9 23 U1 0 U2 1 PU IEEE PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 USA SN 1063-6919 BN 978-1-4244-3992-8 J9 PROC CVPR IEEE PY 2009 BP 896 EP + PG 2 WC Computer Science, Artificial Intelligence SC Computer Science GA BPK14 UT WOS:000279038000115 ER PT J AU Modi, WS Romanov, M Green, ED Ryder, O AF Modi, W. S. Romanov, M. Green, E. D. Ryder, O. TI Molecular Cytogenetics of the California Condor: Evolutionary and Conservation Implications SO CYTOGENETIC AND GENOME RESEARCH LA English DT Article DE Avian molecular cytogenetics; California condor; Z chromosome in birds ID CHICKEN GALLUS-GALLUS; BIRD KARYOTYPES; Z-CHROMOSOME; REARRANGEMENTS; SYNTENY; DIFFERENTIATION; FALCONIFORMES; GENOMICS AB Evolutionary cytogenetic comparisons involved 5 species of birds (California condor, chicken, zebra finch, collared flycatcher and black stork) belonging to divergent taxonomic orders. Seventy-four clones from a condor BAC library containing 80 genes were mapped to condor chromosomes using FISH, and 15 clones containing 16 genes were mapped to the stork Z chromosome. Maps for chicken and finch were derived from genome sequence databases, and that for flycatcher from the published literature. Gene content and gene order were highly conserved when individual condor, chicken, and zebra finch autosomes were compared, confirming that these species largely retain karyotypes close to the ancestral condition for neognathous birds. However, several differences were noted: zebra finch chromosomes 1 and 1A are homologous to condor and chicken chromosomes 1, the CHUNK1 gene appears to have transposed on condor chromosome 1, condor chromosomes 4 and 9 and zebra finch chromosomes 4 and 4A are homologous to chicken chromosome arms 4q and 4p, and novel inversions on chromosomes 4, 12 and 13 were found. Condor and stork Z chromosome gene orders are collinear and differentiated by a series of inversions/transpositions when compared to chicken, zebra finch, or flycatcher; phylogenetic analyses suggest independent rearrangement along the chicken, finch, and flycatcher lineages. Copyright (C) 2009 S. Karger AG, Basel C1 [Modi, W. S.; Romanov, M.; Ryder, O.] San Diego Zoos Inst Conservat Res, Div Genet, Escondido, CA 92027 USA. [Green, E. D.] NHGRI, Bethesda, MD 20892 USA. [Green, E. D.] NIH, Intramural Sequencing Ctr, Bethesda, MD 20892 USA. RP Modi, WS (reprint author), San Diego Zoos Inst Conservat Res, Div Genet, Escondido, CA 92027 USA. EM wmodi@sandiegozoo.org RI Romanov, Michael/O-9419-2014 OI Romanov, Michael/0000-0003-3584-4644 FU National Human Genome Research Institute; Seaver Institute FX S. Charter, J. Fronczek, D. Gallagher, and M. Houck offered technical assistance. This work was supported in part by the Intramural Research Program of the National Human Genome Research Institute and the Seaver Institute. NR 24 TC 3 Z9 3 U1 6 U2 17 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1424-8581 J9 CYTOGENET GENOME RES JI Cytogenet. Genome Res. PY 2009 VL 127 IS 1 BP 26 EP 32 DI 10.1159/000272458 PG 7 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 570LP UT WOS:000275679900006 PM 20051671 ER PT S AU Donnelly, RP Young, HA Rosenberg, AS AF Donnelly, Raymond P. Young, Howard A. Rosenberg, Amy S. BE Donnelly, RP TI An Overview of Cytokines and Cytokine Antagonists as Therapeutic Agents SO CYTOKINE THERAPIES: NOVEL APPROACHES FOR CLINICAL INDICATIONS SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on Cytokine Therapies - Novel Approaches for Clinical Indications CY MAR 26-27, 2009 CL New York Acad Sci, New York, NY SP US FDA, BioLegend, Invitrogen, PBL InterferonSource HO New York Acad Sci DE cytokines; inflammation; interferons; interleukins; receptors ID INTERFERON-GAMMA; INTERLEUKIN-10; AUTOIMMUNITY; DISEASES; COMPLEX; ALPHA AB Cytokine-based therapies have the potential to provide novel treatments for cancer, autoimmune diseases, and many types of infectious disease. However, to date, the full clinical potential of cytokines as drugs has been limited by a number of factors. To discuss these limitations and explore ways to overcome them, the FDA partnered with the New York Academy of Sciences in March 2009 to host a two-day forum to discuss more effective ways to harness the clinical potential of cytokines and cytokine antagonists as therapeutic agents. The first day was focused primarily on the use of recombinant cytokines as therapeutic agents for treatment of human diseases. The second day focused largely on the use of cytokine antagonists as therapeutic agents for treatment of human diseases. This issue of the Annals includes more than a dozen papers that summarize much of the information that was presented during this very informative two-day conference. C1 [Donnelly, Raymond P.; Rosenberg, Amy S.] US FDA, Div Therapeut Prot, Ctr Drug Evaluat & Res, Bethesda, MD 20892 USA. [Young, Howard A.] NCI, Expt Immunol Lab, Ctr Canc Res, Frederick, MD 21701 USA. RP Donnelly, RP (reprint author), US FDA, Div Therapeut Prot, Ctr Drug Evaluat & Res, Bldg 29A,Room 3B-15,29 Lincoln Dr, Bethesda, MD 20892 USA. EM Raymond.Donnelly@fda.hhs.gov; Raymond.Donnelly@fda.hhs.gov NR 30 TC 3 Z9 3 U1 0 U2 1 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXEN, ENGLAND SN 0077-8923 BN 978-1-57331-783-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2009 VL 1182 BP 1 EP 13 DI 10.1111/j.1749-6632.2009.05382.x PG 13 WC Immunology; Medicine, Research & Experimental; Multidisciplinary Sciences SC Immunology; Research & Experimental Medicine; Science & Technology - Other Topics GA BOV08 UT WOS:000277730400001 PM 20074270 ER PT S AU Sportes, C Gress, RE Mackall, CL AF Sportes, Claude Gress, Ronald E. Mackall, Crystal L. BE Donnelly, RP TI Perspective on Potential Clinical Applications of Recombinant Human Interleukin-7 SO CYTOKINE THERAPIES: NOVEL APPROACHES FOR CLINICAL INDICATIONS SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on Cytokine Therapies - Novel Approaches for Clinical Indications CY MAR 26-27, 2009 CL New York Acad Sci, New York, NY SP US FDA, BioLegend, Invitrogen, PBL InterferonSource HO New York Acad Sci DE interleukin; cytokine; T cell ID RECEPTOR-DEFICIENT MICE; SEVERE COMBINED IMMUNODEFICIENCY; T-CELL REGENERATION; B-LINEAGE CELLS; INFLUENZA VACCINATION; INTENSIVE CHEMOTHERAPY; LYMPHOCYTE DEPLETION; ANTIBODY-RESPONSE; IMMUNE-RESPONSE; ADJUVANT IL-7 AB Interleukin-7 has critical and nonredundant roles in T cell development, hematopoiesis, and postdevelopmental immune functions as a prototypic homeostatic cytokine. Based on a large body of preclinical evidence, it may have multiple therapeutic applications in immunodeficiency states, either physiologic (immuno-senescence), pathologic (HIV) or iatrogenic (postchemotherapy and posthematopoietic stem cell transplant) and may have roles in immune reconstitution or enhancement of immunotherapy. Early clinical development trials in humans show that, within a short time, rhIL-7 administration results in a marked preferential expansion of both naive and memory CD4 and CD8 T cell pools with a tendency toward enhanced CD8 expansion. As a result, lymphopenic or normal older hosts develop an expanded circulating T cell pool with a profile that resembles that seen earlier in life with increased T cell repertoire diversity. These results, along with a favorable toxicity profile, open a wide perspective of potential future clinical applications. C1 [Mackall, Crystal L.] NCI, Pediat Oncol Branch, NIH, DHHS, Bethesda, MD 20892 USA. [Sportes, Claude; Gress, Ronald E.] NCI, Expt Transplantat & Immunol Branch, NIH, DHHS, Bethesda, MD 20892 USA. RP Mackall, CL (reprint author), NCI, Pediat Oncol Branch, NIH, DHHS, 10 Ctr Dr,CRC Room 1-3750, Bethesda, MD 20892 USA. EM mack-allc@mail.nih.gov NR 60 TC 12 Z9 12 U1 0 U2 1 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXEN, ENGLAND SN 0077-8923 BN 978-1-57331-783-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2009 VL 1182 BP 28 EP 38 DI 10.1111/j.1749-6632.2009.05075.x PG 11 WC Immunology; Medicine, Research & Experimental; Multidisciplinary Sciences SC Immunology; Research & Experimental Medicine; Science & Technology - Other Topics GA BOV08 UT WOS:000277730400003 PM 20074272 ER PT S AU Miller, CHT Maher, SG Young, HA AF Miller, Catriona H. T. Maher, Stephen G. Young, Howard A. BE Donnelly, RP TI Clinical Use of Interferon-gamma SO CYTOKINE THERAPIES: NOVEL APPROACHES FOR CLINICAL INDICATIONS SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on Cytokine Therapies - Novel Approaches for Clinical Indications CY MAR 26-27, 2009 CL New York Acad Sci, New York, NY SP US FDA, BioLegend, Invitrogen, PBL InterferonSource HO New York Acad Sci DE Interferon-gamma; Actimmune; HuZaf ID IDIOPATHIC PULMONARY-FIBROSIS; CHRONIC HEPATITIS-C; SYSTEMIC-LUPUS-ERYTHEMATOSUS; LONG-TERM TREATMENT; DOUBLE-BLIND TRIAL; OVARIAN-CANCER; IFN-GAMMA; MULTICENTER TRIAL; INFANTILE OSTEOPETROSIS; RHEUMATOID-ARTHRITIS AB Interferon gamma (IFN-gamma), a pleotropic cytokine, has been shown to be important to the function of virtually all immune cells and both innate and adaptive immune responses. In 1986, early clinical trials of this cytokine began to evaluate its therapeutic potential. The initial studies focused on the tolerability and pharmacology of IFN-gamma and systematically determined its antitumor and anti-infection activities. In the 20-plus years since those first trials, IFN-gamma has been used in a wide variety of clinical indications, which are reviewed in this article. C1 [Miller, Catriona H. T.; Young, Howard A.] NCI, Ctr Canc Res, Canc & Inflammat Program, Expt Immunol Lab, Frederick, MD 21702 USA. [Maher, Stephen G.] St James Hosp, Trinity Coll Dublin, Dept Surg, Trinity Ctr Hlth Sci, Dublin 8, Ireland. RP Young, HA (reprint author), NCI, Ctr Canc Res, Canc & Inflammat Program, Expt Immunol Lab, Bldg 560 RM31-16, Frederick, MD 21702 USA. EM younghow@mail.nih.gov FU National Cancer Institute, National Institutes of Health [HHSN261200800001E] FX This project has been funded in whole or in part with federal funds from the National Cancer Institute, National Institutes of Health, under Contract No. HHSN261200800001E. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. Government. NR 72 TC 103 Z9 110 U1 1 U2 17 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXEN, ENGLAND SN 0077-8923 BN 978-1-57331-783-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2009 VL 1182 BP 69 EP 79 DI 10.1111/j.1749-6632.2009.05069.x PG 11 WC Immunology; Medicine, Research & Experimental; Multidisciplinary Sciences SC Immunology; Research & Experimental Medicine; Science & Technology - Other Topics GA BOV08 UT WOS:000277730400007 PM 20074276 ER PT S AU Goldbach-Mansky, R AF Goldbach-Mansky, Raphaela BE Donnelly, RP TI Blocking Interleukin-1 in Rheumatic Diseases Its Initial Disappointments and Recent Successes in the Treatment of Autoinflammatory Diseases SO CYTOKINE THERAPIES: NOVEL APPROACHES FOR CLINICAL INDICATIONS SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on Cytokine Therapies - Novel Approaches for Clinical Indications CY MAR 26-27, 2009 CL New York Acad Sci, New York, NY SP US FDA, BioLegend, Invitrogen, PBL InterferonSource HO New York Acad Sci DE interleukin (IL-) 1; autoinflammatory diseases; neonatal onset multisystem inflammatory disease (NOMID); chronic inflammatory neurologic, cutaneous and arthritis syndrome (CINCA); deficiency of the IL-1 receptor antagonist (DIRA); NLRP3; IL1RN; IL-1Ra; anakinra; neonatal disorder; genetic disease ID JUVENILE IDIOPATHIC ARTHRITIS; PLACEBO-CONTROLLED TRIAL; ONSET STILLS-DISEASE; RECEPTOR ANTAGONIST; DOUBLE-BLIND; PERIODIC SYNDROME; INNATE IMMUNITY; SEPSIS SYNDROME; ANAKINRA; RESISTANT AB The role of the potent proinflammatory cytokine IL-1 in disease could clinically be investigated with the development of the IL-1 blocking agent anakinra (Kineret (R)), a recombinant IL-1 receptor antagonist. It was first tested in patients with sepsis without much benefit but was later FDA approved for the treatment of patients with rheumatoid arthritis. More recently IL-1 blocking therapies are used successfully to treat a new group of immune-mediated inflammatory conditions, autoinflammatory diseases. These conditions include rare hereditary fever syndromes and pediatric and adult conditions of Still's disease. Recently the FDA approved two additional longer acting IL-1 blocking agents, for the treatment of cryopyrin-associated periodic syndromes (CAPS), an IL-1 dependent autoinflammatory syndrome. The study of autoinflammatory diseases revealed mechanisms of IL-1 mediated organ damage and provided concepts to a better understanding of the pathogenesis of more common diseases such as gout and Type 2 diabetes which show initial promising results with IL-1 blocking therapy. C1 [Goldbach-Mansky, Raphaela] NIAMSD, NIH, Bethesda, MD 20892 USA. RP Goldbach-Mansky, R (reprint author), NIAMS, NIH, Bldg 10,Rm 6D-47B,10 Ctr Dr, Bethesda, MD 20892 USA. EM goldbacr@mail.nih.gov FU Intramural NIH HHS [Z01 AR041138-05, ZIA AR041138-07, Z01 AR041138-06] NR 54 TC 51 Z9 54 U1 0 U2 4 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXEN, ENGLAND SN 0077-8923 BN 978-1-57331-783-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2009 VL 1182 BP 111 EP 123 DI 10.1111/j.1749-6632.2009.05159.x PG 13 WC Immunology; Medicine, Research & Experimental; Multidisciplinary Sciences SC Immunology; Research & Experimental Medicine; Science & Technology - Other Topics GA BOV08 UT WOS:000277730400011 PM 20074280 ER PT J AU Berg, M Lundqvist, A McCoy, P Samsel, L Fan, Y Tawab, A Childs, R AF Berg, Maria Lundqvist, Andreas McCoy, Philip, Jr. Samsel, Leigh Fan, Yong Tawab, Abdul Childs, Richard TI Clinical-grade ex vivo-expanded human natural killer cells up-regulate activating receptors and death receptor ligands and have enhanced cytolytic activity against tumor cells SO CYTOTHERAPY LA English DT Article DE Bortezomib; expansion; immunotherapy; natural killer cells ID APOPTOSIS-INDUCING LIGAND; NK-CELL; EFFECTOR FUNCTIONS; BORTEZOMIB; IMMUNOTHERAPY; CYTOTOXICITY; TRANSPLANTATION; PROLIFERATION; LYMPHOCYTES; GENERATION AB Background aims Cancer immunotherapy involving natural killer (NK) cell infusions and administration of therapeutic agents modulating the susceptibility of tumors to NK-cell lysis has been proposed recently. We provide a method for expanding highly cytotoxic clinical-grade NK cells in vitro for adoptive transfer following bortezomib treatment in patients with advanced malignancies. Methods NK cells were expanded with irradiated Epstein-Barr virus-transformed lymphoblastoid cells. Expanded cells were evaluated for their phenotype, cytotoxicity, cytokine secretion, dependence on interleukin (IL)-2 and ability to retain function after cryopreservation. Results A pure population of clinical-grade NK cells expanded 490260-fold over 21 days. Expanded NK cells had increased TRAIL, FasL and NKG2D expression and significantly higher cytotoxicity against bortezomib-treated tumors compared with resting NK cells. Expanded NK cells, co-cultured with K562 and renal cell carcinoma tumor targets, secreted significantly higher levels of soluble Fas ligand 6; fgjhd IFN-, GM-CSF, TNF-, MIP-1 and MIP-1 compared with resting NK cells. Secretion of the above cytokines and NK-cell cytolytic function were IL-2 dose dependent. Cryopreservation of expanded NK cells reduced expression of NKG2D and TRAIL and NK-cell cytotoxicity, although this effect could be reversed by exposure of NK cells to IL-2. Conclusions We describe a method for large-scale expansion of NK cells with increased expression of activating receptors and death receptor ligands resulting in superior cytotoxicity against tumor cells. This ex vivo NK-cell expansion technique is currently being utilized in a clinical trial evaluating the anti-tumor activity of adoptively infused NK cells in combination with bortezomib. C1 [Berg, Maria; Lundqvist, Andreas; Childs, Richard] Natl Inst Hlth, Hematol Branch, Natl Heart Lung & Blood Inst, Bethesda, MD 20892 USA. [Fan, Yong; Tawab, Abdul] Natl Inst Hlth, Dept Transfus Med, Cell Proc Sect, Bethesda, MD 20892 USA. RP Childs, R (reprint author), Natl Inst Hlth, Hematol Branch, Natl Heart Lung & Blood Inst, Room 3-5140,Bldg 10-CRC,10 Ctr Dr MSC 1202, Bethesda, MD 20892 USA. EM childsr@nih.gov OI Lundqvist, Andreas/0000-0002-9709-2970 FU Intramural NIH HHS [Z99 HL999999] NR 27 TC 115 Z9 124 U1 1 U2 7 PU TAYLOR & FRANCIS AS PI OSLO PA KARL JOHANS GATE 5, NO-0154 OSLO, NORWAY SN 1465-3249 J9 CYTOTHERAPY JI Cytotherapy PY 2009 VL 11 IS 3 BP 341 EP 355 AR PII 909785497 DI 10.1080/14653240902807034 PG 15 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell Biology; Hematology; Medicine, Research & Experimental SC Cell Biology; Biotechnology & Applied Microbiology; Hematology; Research & Experimental Medicine GA 438US UT WOS:000265581600011 PM 19308771 ER PT J AU Fitzhugh, CD Hsieh, MM Bolan, CD Saenz, C Tisdale, JF AF Fitzhugh, Courtney D. Hsieh, Matthew M. Bolan, Charles D. Saenz, Carla Tisdale, John F. TI Granulocyte colony-stimulating factor (G-CSF) administration in individuals with sickle cell disease: time for a moratorium? SO CYTOTHERAPY LA English DT Article DE Complications; granulocyte colony-stimulating factor (G-CSF); hematopoietic stem cell; multi-organ failure; pain crisis; sickle cell disease (SCD); mobilization ID HEMOGLOBIN SC DISEASE; HEMATOPOIETIC PROGENITOR CELLS; BONE-MARROW-TRANSPLANTATION; BLOOD STEM-CELLS; PERIPHERAL-BLOOD; INTENSIVE CHEMOTHERAPY; FEBRILE NEUTROPENIA; HYDROXYUREA THERAPY; ADVERSE OUTCOMES; MOBILIZED BLOOD AB Granulocyte colony-stimulating factor (G-CSF) is used commonly in an attempt to reduce the duration of neutropenia and hospitalization in patients undergoing chemotherapy and to obtain hematopoietic stem cells (HSC) for transplantation applications. Despite the relative safety of administration of G-CSF in most individuals, including subjects with sickle cell trait, severe and life-threatening complications have been reported when used in individuals with sickle cell disease (SCD), including those who were asymptomatic and undiagnosed prior to administration. The administration of G-CSF has now been reported in a total of 11 individuals with SCD. Seven developed severe adverse events, including vaso-occlusive episodes, acute chest syndrome, multiorgan system failure and death. Precautions, including minimizing the peak white blood cell count, dividing or reducing the G-CSF dose and red blood cell transfusions to reduce sickle hemoglobin (HbS) levels, have been employed with no consistent benefit. These reported data indicate that administration of G-CSF in individuals with SCD should be undertaken only in the absence of alternatives and after full disclosure of the risks involved. Unless further data demonstrate safety, routine usage of G-CSF in individuals with SCD should be avoided. C1 [Fitzhugh, Courtney D.; Hsieh, Matthew M.; Tisdale, John F.] NIDDK, Mol & Clin Hematol Branch, NIH, Bethesda, MD USA. [Fitzhugh, Courtney D.] NCI, POB, NIH, Bethesda, MD 20892 USA. [Bolan, Charles D.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA. [Saenz, Carla] NIH, Dept Bioeth, Ctr Clin, Bethesda, MD 20892 USA. RP Tisdale, JF (reprint author), 9000 Rockville Pike,Bldg 10,9N116, Bethesda, MD 20892 USA. EM johntis@mail.nih.gov FU National Institute of Diabetes; Digestive and Kidney Diseases; National Heart; Lung and Blood Institute; Clinical Center Department of Bioethics at the National Institutes of Health FX This work was supported by the intramural research program of the National Institute of Diabetes, Digestive and Kidney Diseases, the National Heart, Lung and Blood Institute, and the Clinical Center Department of Bioethics at the National Institutes of Health. The opinions expressed here are the authors' and do not reflect the policies and positions of the National Institutes of Health, the US Public Health Service or the US Department of Health and Human Services. NR 55 TC 21 Z9 21 U1 0 U2 0 PU TAYLOR & FRANCIS AS PI OSLO PA KARL JOHANS GATE 5, NO-0154 OSLO, NORWAY SN 1465-3249 J9 CYTOTHERAPY JI Cytotherapy PY 2009 VL 11 IS 4 BP 464 EP 471 DI 10.1080/14653240902849788 PG 8 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell Biology; Hematology; Medicine, Research & Experimental SC Cell Biology; Biotechnology & Applied Microbiology; Hematology; Research & Experimental Medicine GA 465GC UT WOS:000267569600011 PM 19513902 ER PT J AU Melenhorst, JJ AF Melenhorst, J. Joseph TI Optimizing T-cell expansion: have we reached the limit? SO CYTOTHERAPY LA English DT Editorial Material ID BONE-MARROW-TRANSPLANTATION; ANTIGEN-PRESENTING CELLS; ADOPTIVE TRANSFER; LYMPHOCYTES; RESTORATION; LEUKEMIA; IMMUNITY; THERAPY C1 NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA. RP Melenhorst, JJ (reprint author), NHLBI, Hematol Branch, NIH, Bldg 10 CRC,Rm 3-5320,10 Ctr Dr, Bethesda, MD 20892 USA. EM Jan.Melenhorst@nih.hhs.gov NR 15 TC 1 Z9 1 U1 0 U2 2 PU TAYLOR & FRANCIS AS PI OSLO PA KARL JOHANS GATE 5, NO-0154 OSLO, NORWAY SN 1465-3249 J9 CYTOTHERAPY JI Cytotherapy PY 2009 VL 11 IS 7 BP 813 EP 814 DI 10.3109/14653240903387163 PG 2 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell Biology; Hematology; Medicine, Research & Experimental SC Cell Biology; Biotechnology & Applied Microbiology; Hematology; Research & Experimental Medicine GA 523AS UT WOS:000272043100002 PM 19903094 ER PT J AU Cannon, RO AF Cannon, Richard O., III TI Bone marrow-derived cells for cardiac repair SO CYTOTHERAPY LA English DT Editorial Material ID MESENCHYMAL STEM-CELLS; ACUTE MYOCARDIAL-INFARCTION; PROGENITOR CELLS; CARDIOMYOCYTES; TRANSPLANTATION; CARDIOMYOPATHY; DIFFERENTIATE; CXCR4; MODEL; TRIAL C1 [Cannon, Richard O., III] NHLBI, Translat Med Branch, Div Intramural Res, NIH, Bethesda, MD 20892 USA. RP Cannon, RO (reprint author), Bldg 10-CRC,Room 5-3330,10 Ctr Dr, Bethesda, MD 20892 USA. EM cannonr@nih.gov NR 24 TC 0 Z9 0 U1 0 U2 0 PU TAYLOR & FRANCIS AS PI OSLO PA KARL JOHANS GATE 5, NO-0154 OSLO, NORWAY SN 1465-3249 J9 CYTOTHERAPY JI Cytotherapy PY 2009 VL 11 IS 8 BP 977 EP 979 DI 10.3019/14653240903424081 PG 3 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell Biology; Hematology; Medicine, Research & Experimental SC Cell Biology; Biotechnology & Applied Microbiology; Hematology; Research & Experimental Medicine GA 579EQ UT WOS:000276350900001 PM 19929460 ER PT J AU Blum, A Childs, RW Smith, A Patibandla, S Zalos, G Samsel, L Mccoy, JP Calandra, G Csako, G Cannon, RO AF Blum, Arnon Childs, Richard W. Smith, Aleah Patibandla, Sushmitha Zalos, Gloria Samsel, Leigh McCoy, J. Philip Calandra, Gary Csako, Gyorgy Cannon, Richard O., III TI Targeted antagonism of CXCR4 mobilizes progenitor cells under investigation for cardiovascular disease SO CYTOTHERAPY LA English DT Article DE Cardiovascular disease; CXCR4 antagonism; heart disease; inflammation; progenitor cells; vascular repair ID COLONY-STIMULATING FACTOR; CORONARY-ARTERY-DISEASE; PERIPHERAL-BLOOD STEM; G-CSF; AMD3100; ANGINA; TRANSPLANTATION; INFLAMMATION; PLASMA; DONOR AB Background aims Bone marrow (BM)-derived cells may repair cardiovascular injury but populations of interest circulate in small numbers. Cytokines such as granulocyte-colony-stimulating factor mobilize cells under investigation for this purpose, including CD133(+) but require injections over multiple days and may promote inflammation. The purpose of this study was to evaluate the effects of a novel CXCR4 inhibitor (plerixafor), previously shown to mobilize CD34(+) stem cells, on CD133(+) mobilization and markers of inflammation. Methods Healthy subjects received a single subcutaneous injection of plerixafor in escalating doses: 240 mcg/kg (n=3), 320 mcg/kg (n=5) and 400 mcg/kg (n=7). CD133(+) and CD133(+)/VEGFR-2(+) cells were measured by flow cytometry at baseline, then 4-6 h following plerixafor injection. Markers of inflammation in serum were measured at baseline, then again 10 h following injection of the 400mcg/kg dose. Results Across all doses, white blood cells increased on average three-fold from baseline values. CD133(+) cells increased on average 24-fold (from 616+/-141 cells/mL to 14 713+/-4423 cells/mL, P=0.0064) without clear evidence of a dose effect. CD133(+)/VEGFR-2(+) cells ranged from 0 to 20 cells/mL at baseline and from 0 to 124 cells/mL, following plerixafor administration, although the rarity of these cells precluded a statistical analysis of this population. C-reactive protein and serum amyloid type A were not increased after the 400 mcg/kg dose. Pro-inflammatory cytokine levels were undetectable before and after plerixafor; except for macrophage inflammatory protein-1 beta, which increased slightly but significantly after the 400mcg/kg dose of plerixafor (P=0.0156). Conclusions CD133(+) cells are mobilized into the circulation following a single injection of the CXCR4 antagonist plerixafor; without clear evidence for systemic activation of inflammation. This effect may be of importance in cell-based approaches for treating cardiovascular diseases. C1 [Blum, Arnon; Patibandla, Sushmitha; Zalos, Gloria; Cannon, Richard O., III] NHLBI, Translat Med Branch, Bethesda, MD 20892 USA. [Childs, Richard W.; Smith, Aleah] NHLBI, Hematol Branch, Bethesda, MD 20892 USA. [Samsel, Leigh; McCoy, J. Philip] NHLBI, Flow Cytometry Core Facil, Bethesda, MD 20892 USA. [Calandra, Gary] Genzyme, Cambridge, MA USA. [Csako, Gyorgy; Cannon, Richard O., III] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA. RP Cannon, RO (reprint author), NIH, Dept Lab Med, Ctr Clin, Bldg 10 CRC Room 5-3330,10 Ctr Dr, Bethesda, MD 20892 USA. EM cannonr@nih.gov FU National Heart, Lung and Blood Institute; Clinical Center, National Institutes of Health FX This research was supported by the Intramural Research Programs of the National Heart, Lung and Blood Institute and the Clinical Center, National Institutes of Health. NR 18 TC 6 Z9 7 U1 0 U2 3 PU TAYLOR & FRANCIS AS PI OSLO PA KARL JOHANS GATE 5, NO-0154 OSLO, NORWAY SN 1465-3249 J9 CYTOTHERAPY JI Cytotherapy PY 2009 VL 11 IS 8 BP 1016 EP 1019 DI 10.3109/14653240903131640 PG 4 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell Biology; Hematology; Medicine, Research & Experimental SC Cell Biology; Biotechnology & Applied Microbiology; Hematology; Research & Experimental Medicine GA 579EQ UT WOS:000276350900006 PM 19929465 ER PT J AU Dogan, RI Murray, GC Neveol, A Lu, ZY AF Dogan, Rezarta Islamaj Murray, G. Craig Neveol, Aurelie Lu, Zhiyong TI Understanding PubMed (R) user search behavior through log analysis SO DATABASE-THE JOURNAL OF BIOLOGICAL DATABASES AND CURATION LA English DT Article AB This article reports on a detailed investigation of PubMed users' needs and behavior as a step toward improving biomedical information retrieval. PubMed is providing free service to researchers with access to more than 19 million citations for biomedical articles from MEDLINE and life science journals. It is accessed by millions of users each day. Efficient search tools are crucial for biomedical researchers to keep abreast of the biomedical literature relating to their own research. This study provides insight into PubMed users' needs and their behavior. This investigation was conducted through the analysis of one month of log data, consisting of more than 23 million user sessions and more than 58 million user queries. Multiple aspects of users' interactions with PubMed are characterized in detail with evidence from these logs. Despite having many features in common with general Web searches, biomedical information searches have unique characteristics that are made evident in this study. PubMed users are more persistent in seeking information and they reformulate queries often. The three most frequent types of search are search by author name, search by gene/protein, and search by disease. Use of abbreviation in queries is very frequent. Factors such as result set size influence users' decisions. Analysis of characteristics such as these plays a critical role in identifying users' information needs and their search habits. In turn, such an analysis also provides useful insight for improving biomedical information retrieval. Database URL: http://www.ncbi.nlm.nih.gov/PubMed C1 [Dogan, Rezarta Islamaj; Murray, G. Craig; Neveol, Aurelie; Lu, Zhiyong] US Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA. RP Lu, ZY (reprint author), US Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA. EM luzh@ncbi.nlm.nih.gov OI Islamaj Dogan, Rezarta/0000-0001-5651-1860 FU NIH, National Library of Medicine FX Funding for this work and open access charge is provided by the Intramural Research Program of the NIH, National Library of Medicine. NR 78 TC 21 Z9 21 U1 3 U2 12 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1758-0463 J9 DATABASE-OXFORD JI Database PY 2009 AR bap018 DI 10.1093/database/bap018 PG 18 WC Mathematical & Computational Biology SC Mathematical & Computational Biology GA V21EQ UT WOS:000208191300018 ER PT J AU Moreland, RT Ryan, JF Pan, C Baxevanis, AD AF Moreland, R. Travis Ryan, Joseph F. Pan, Christopher Baxevanis, Andreas D. TI The Homeodomain Resource: a comprehensive collection of sequence, structure, interaction, genomic and functional information on the homeodomain protein family SO DATABASE-THE JOURNAL OF BIOLOGICAL DATABASES AND CURATION LA English DT Article AB The Homeodomain Resource is a curated collection of sequence, structure, interaction, genomic and functional information on the homeodomain family. The current version builds upon previous versions by the addition of new, complete sets of homeodomain sequences from fully sequenced genomes, the expansion of existing curated homeodomain information and the improvement of data accessibility through better search tools and more complete data integration. This release contains 1534 full-length homeodomain-containing sequences, 93 experimentally derived homeodomain structures, 101 homeodomain protein-protein interactions, 107 homeodomain DNA-binding sites and 206 homeodomain proteins implicated in human genetic disorders. Database URL: The Homeodomain Resource is freely available and can be accessed at http://research.nhgri.nih.gov/homeodomain/ C1 [Moreland, R. Travis; Ryan, Joseph F.; Pan, Christopher; Baxevanis, Andreas D.] NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA. RP Baxevanis, AD (reprint author), NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA. EM andy@nhgri.nih.gov FU National Human Genome Research Institute, National Institutes of Health FX This research was supported by the Intramural Research Program of the National Human Genome Research Institute, National Institutes of Health. NR 38 TC 5 Z9 5 U1 0 U2 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1758-0463 J9 DATABASE-OXFORD JI Database PY 2009 AR bap004 DI 10.1093/database/bap004 PG 8 WC Mathematical & Computational Biology SC Mathematical & Computational Biology GA V21EQ UT WOS:000208191300004 ER PT S AU Ramaswamy, M Cleland, SY Cruz, AC Siegel, RM AF Ramaswamy, Madhu Cleland, Sophia Y. Cruz, Anthony C. Siegel, Richard M. BE Kalthoff, H TI Many Checkpoints on the Road to Cell Death: Regulation of Fas-FasL Interactions and Fas Signaling in Peripheral Immune Responses SO DEATH RECEPTORS AND COGNATE LIGANDS IN CANCER SE Results and Problems in Cell Differentiation LA English DT Article; Book Chapter ID ACTIVATION-INDUCED CELL; NF-KAPPA-B; AUTOIMMUNE LYMPHOPROLIFERATIVE SYNDROME; TUMOR-NECROSIS-FACTOR; VERSUS-HOST-DISEASE; CD4(+) T-CELLS; SYSTEMIC-LUPUS-ERYTHEMATOSUS; LIGAND GENE-EXPRESSION; KINASE-C-THETA; LIPID RAFTS AB Interactions between the TNF-family receptor Fas (CD95) and Fas Ligand (FasL, CD178) can efficiently induce apoptosis and are critical for the maintenance of immunological self-tolerance. FasL is kept under strict control by transcriptional and posttranslational regulation. Surface FasL can be cleaved by metalloproteases, resulting in shed extracellular domains, and FasL can also traffic to secretory lysosomes. Each form of FasL has distinct biological functions. Fas is more ubiquitously expressed, but its apoptosis-inducing function is regulated by a number of mechanisms including submembrane localization, efficiency of receptor signaling complex assembly and activation, and bcl-2 family members in some circumstances. When apoptosis is not induced, Fas-FasL interactions can also trigger a number of activating and proinflammatory signals. Harnessing the apoptosis-inducing potential of Fas for therapy of cancer and autoimmune disease has been actively pursued, and despite a number of unexpected side-effects that result from manipulating Fas-FasL interactions, this remains a worthy goal. C1 [Ramaswamy, Madhu; Cleland, Sophia Y.; Cruz, Anthony C.; Siegel, Richard M.] NIAMS, Immunoregulat Unit, Autoimmun Branch, NIH, Bethesda, MD 20892 USA. RP Siegel, RM (reprint author), NIAMS, Immunoregulat Unit, Autoimmun Branch, NIH, Bethesda, MD 20892 USA. EM rsiegel@nih.gov RI Kalthoff, Holger/B-1618-2010; OI Siegel, Richard/0000-0001-5953-9893 FU Intramural NIH HHS [Z99 AR999999, Z01 AR041133-07] NR 182 TC 17 Z9 20 U1 0 U2 0 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0080-1844 BN 978-3-642-03044-4 J9 RESULTS PROBL CELL D JI Results Probl. Cell Differ. PY 2009 VL 49 BP 17 EP 47 DI 10.1007/400_2008_24 D2 10.1007/978-3-642-03045-1 PG 31 WC Oncology; Cell Biology; Developmental Biology SC Oncology; Cell Biology; Developmental Biology GA BME41 UT WOS:000272009100002 PM 19132321 ER PT S AU Fujita, K Srinivasula, SM AF Fujita, Ken-ichi Srinivasula, Srinivasa M. BE Kalthoff, H TI Ubiquitination and TNFR1 Signaling SO DEATH RECEPTORS AND COGNATE LIGANDS IN CANCER SE Results and Problems in Cell Differentiation LA English DT Article; Book Chapter ID NF-KAPPA-B; TUMOR-NECROSIS-FACTOR; SYSTEMIC-LUPUS-ERYTHEMATOSUS; ALPHA-DEPENDENT APOPTOSIS; GAMMA-DEFICIENT MICE; NEURONAL CELL-DEATH; EDITING ENZYME A20; LINEAR POLYUBIQUITYLATION; DEUBIQUITINATING ENZYME; RHEUMATOID-ARTHRITIS AB Death receptors are a subset of the tumor necrosis factor receptor (TNFR) family of proteins and share a characteristic cytoplasmic motif called the "death domain." In addition to mediating cell death, these receptors regulate cell proliferation, inflammatory responses, and tumor progression. Receptor occupancy triggers the assembly of several cytoplasmic molecules into distinct complexes, each initiating separate signaling events leading to different biological responses. Post-translational modifications involving ubiquitin, a peptide of 76 amino acids, regulate events at nearly all stages of signaling. All ubiquitin chains function as docking platforms for molecules with specific recognition motifs that either propagate the signal or target the protein for proteasomal degradation. Moreover, enzymes with ubiquitin thioesterase activity (deubiquitinating enzymes, or DUBs) reverse modifications by removing the ubiquitin chains, allowing ubiquitin editing at the molecular level. Ubiquitin protein ligases (E3s), DUBs, and signaling molecules with ubiquitin recognition motifs control TNFR1 mediated cell death and activation of NF-kappa B and JNK. Here, we discuss the current understanding of how these proteins regulate TNFR1 signaling. C1 [Fujita, Ken-ichi; Srinivasula, Srinivasa M.] NCI, Lab Immune Cell Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Srinivasula, SM (reprint author), NCI, Lab Immune Cell Biol, Ctr Canc Res, NIH, Bldg 37,Room 3016A,9000 Rockville Pike, Bethesda, MD 20892 USA. EM fujitak@mail.nih.gov; srinivsr@mail.nih.gov RI Kalthoff, Holger/B-1618-2010 FU Intramural NIH HHS NR 121 TC 2 Z9 2 U1 0 U2 1 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0080-1844 BN 978-3-642-03044-4 J9 RESULTS PROBL CELL D JI Results Probl. Cell Differ. PY 2009 VL 49 BP 87 EP 114 DI 10.1007/400_2009_18 D2 10.1007/978-3-642-03045-1 PG 28 WC Oncology; Cell Biology; Developmental Biology SC Oncology; Cell Biology; Developmental Biology GA BME41 UT WOS:000272009100005 PM 19582409 ER PT J AU Ruggiero, C Cherubini, A Lauretani, F Bandinelli, S Maggio, M Di Iorio, A Zuliani, G Dragonas, C Senin, U Ferrucci, L AF Ruggiero, Carmelinda Cherubini, Antonio Lauretani, Fulvio Bandinelli, Stefania Maggio, Marcello Di Iorio, Angelo Zuliani, Giovanni Dragonas, Charalampos Senin, Umberto Ferrucci, Luigi TI Uric Acid and Dementia in Community-Dwelling Older Persons SO DEMENTIA AND GERIATRIC COGNITIVE DISORDERS LA English DT Article DE Uric acid; Risk; Dementia; Inflammation; Aging ID CHRONIC HEART-FAILURE; COGNITIVE IMPAIRMENT; ALZHEIMERS-DISEASE; METABOLIC SYNDROME; ALL-CAUSE; SERUM; INCHIANTI; HYPERTENSION; MORTALITY; OXIDASE AB Background: The biological action of uric acid (UA) in humans is controversial. UA is considered an antioxidant compound, but preclinical evidence suggests a proinflammatory action. Epidemiological studies found that hyperuricemia is associated with conditions leading to dementia. Our aim is to investigate the relationship between UA levels and dementia in older persons. Methods: Cross-sectional study performed in 1,016 community-dwelling older persons participating in the InCHIANTI study. Participants underwent determination of circulating UA levels and neuropsychological evaluation. A multivariate logistic regression model was used to estimate the probability of participants belonging to the highest and middle UA tertile to be affected by dementia compared to those in the lowest tertile. Results: Demented persons had higher UA levels (p = 0.001) and the prevalence of persons affected by dementia increased across UA tertiles (p<0.0001). Independent of several confounders, persons belonging to the highest UA tertile had a threefold (OR = 3.32; 95% CI: 1.06-10.42) higher probability to suffer from a dementia syndrome while those in the middle UA tertile tended to have a higher probability of being demented compared to those in the lowest tertile. Conclusion: In a population-based sample, high circulating UA levels are associated with an increased likelihood to be affected by a dementia syndrome. Copyright (c) 2009 S. Karger AG, Basel C1 [Ruggiero, Carmelinda] Univ Perugia, Osped S Maria Misericordia, Dept Clin & Expt Med, Inst Gerontol & Geriatr, IT-06156 Perugia, Italy. [Lauretani, Fulvio] Tuscany Reg Hlth Agcy, Florence, Italy. [Bandinelli, Stefania] ASF Geriatr Rehabil, Florence, Italy. [Maggio, Marcello] Univ Parma, Dept Internal Med & Biomed Sci, Chieti, Italy. [Di Iorio, Angelo] Univ G dAnnunzio, Lab Clin Epidemiol, Chieti, Italy. [Zuliani, Giovanni] Univ Ferrara, Sect Internal Med Gerontol & Geriatr, I-44100 Ferrara, Italy. [Dragonas, Charalampos] Univ Erlangen Nurnberg, Inst Biomed Aging, Nurnberg, Germany. [Ferrucci, Luigi] NIA, Longitudinal Studies Sect, NIH, Baltimore, MD 21224 USA. RP Ruggiero, C (reprint author), Univ Perugia, Osped S Maria Misericordia, Dept Clin & Expt Med, Inst Gerontol & Geriatr, Blocco A Piano 4,Piazzale Menghini 1, IT-06156 Perugia, Italy. EM ruggieroc07@hotmail.it RI Lauretani, Fulvio/K-5115-2016; OI Lauretani, Fulvio/0000-0002-5287-9972; Cherubini, Antonio/0000-0003-0261-9897 FU Italian Ministry of Health [ICS110.1/RF97.71]; U.S. National Institute on Aging [263 MD 9164, 263 MD 821336, N.1-AG-1-1, N.1-AG-1-2111, N01AG-5-0002]; National Institute on Aging; National Institutes of Health, Baltimore, Maryland, USA FX The InCHIANTI study baseline (1998-2000) was supported as a 'targeted project' (ICS110.1/RF97.71) by the Italian Ministry of Health and in part by the U.S. National Institute on Aging (Contracts: 263 MD 9164 and 263 MD 821336); the InCHIANTI Follow-up 1 (2001-2003) was funded by the U. S. National Institute on Aging (Contracts: N.1-AG-1-1 and N.1-AG-1-2111); the InCHIANTI Follow-ups 2 and 3 studies (2004-2010) were financed by the U.S. National Institute on Aging (Contract: N01AG-5-0002); supported in part by the Intramural research program of the National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA. NR 43 TC 22 Z9 22 U1 1 U2 6 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1420-8008 J9 DEMENT GERIATR COGN JI Dement. Geriatr. Cogn. Disord. PY 2009 VL 27 IS 4 BP 382 EP 389 DI 10.1159/000210040 PG 8 WC Geriatrics & Gerontology; Clinical Neurology; Psychiatry SC Geriatrics & Gerontology; Neurosciences & Neurology; Psychiatry GA 428SQ UT WOS:000264870500012 PM 19339776 ER PT J AU Baldauf, C Vortmeyer, AO Koch, CA Sticherling, M AF Baldauf, Claudia Vortmeyer, Alexander O. Koch, Christian A. Sticherling, Michael TI Combination of Multiple Skin Malignancies with Multiple Endocrine Neoplasia Type 1: Coincidental or Pathogenetically Related? SO DERMATOLOGY LA English DT Editorial Material DE Multiple endocrine neoplasia; Squamous cell carcinoma; Melanoma; Papillomatosis; Carcinogenesis ID RETICULATED PAPILLOMATOSIS; MEN TYPE-1; CONFLUENT; GENE; TUMOR; MELANOMA; KNUDSON C1 [Sticherling, Michael] Univ Erlangen Nurnberg, Dept Dermatol, DE-91052 Erlangen, Germany. [Baldauf, Claudia; Sticherling, Michael] Univ Leipzig, Dept Dermatol, Leipzig, Germany. [Vortmeyer, Alexander O.] NINDS, Surg Neurol Branch, NIH, Bethesda, MD USA. [Koch, Christian A.] Univ Mississippi, Med Ctr, Div Endocrinol, Jackson, MS 39216 USA. RP Sticherling, M (reprint author), Univ Erlangen Nurnberg, Dept Dermatol, Hartmannstr 14, DE-91052 Erlangen, Germany. EM michael.sticherling@uk-erlangen.de RI Koch, Christian/A-4699-2008; OI Koch, Christian/0000-0003-3127-5739; Koch, Christian/0000-0003-0678-1242 NR 24 TC 3 Z9 3 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1018-8665 J9 DERMATOLOGY JI Dermatology PY 2009 VL 219 IS 4 BP 365 EP 367 DI 10.1159/000193058 PG 3 WC Dermatology SC Dermatology GA 526XG UT WOS:000272328700017 PM 19141988 ER PT S AU Subramanian, S Koscielniak, JW Devasahayam, N Salem, G Pursley, RH Pohida, TJ Krishna, MC AF Subramanian, Sankaran Koscielniak, Janusz W. Devasahayam, Nallathamby Salem, Ghadi Pursley, Randall H. Pohida, Thomas J. Krishna, Murali C. BE Raghavachari, R Liang, R TI A novel fast imaging modality for free radicals in vivo: continuous wave (CW) EPR imaging with direct detection and rapid field scan in the presence of rotating gradients SO DESIGN AND QUALITY FOR BIOMEDICAL TECHNOLOGIES II SE Proceedings of SPIE LA English DT Proceedings Paper CT Conference on Design and Quality for Biomedical Technologies II CY JAN 26, 2009 CL San Jose, CA SP SPIE DE CW EPR; imaging; Magnetic Resonance; rapidscan; rotating gradients ID ELECTRON-PARAMAGNETIC-RESONANCE; TUMOR REDOX STATUS; MAGNETIC-RESONANCE; NMR-SPECTROSCOPY; LOW-FREQUENCY; TOOTH ENAMEL; HYPOXIA; SPECTROMETER; OXIMETRY; OXYGEN AB The work described in this presentation relates to a novel approach to Electron Paramagnetic Resonance imaging in vivo. The method employs a continuous wave approach to spectral detection without the conventional low frequency modulation and phase sensitive detection. A combination of direct detection and rapid field scan in the simultaneous presence of rotating gradients enables imaging with high temporal resolution. Since CW detection is not limited to free radical spin probes with narrow spectral lines, unlike the time-domain case, this novel approach uniquely accomplishes ultra fast functional imaging and is applicable to common redox-sensitive spin probes without line-width restriction. C1 [Subramanian, Sankaran; Koscielniak, Janusz W.; Devasahayam, Nallathamby; Krishna, Murali C.] NCI, Radiat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Subramanian, S (reprint author), NCI, Radiat Oncol Branch, Ctr Canc Res, NIH, Bldg 10, Bethesda, MD 20892 USA. NR 60 TC 0 Z9 0 U1 0 U2 0 PU SPIE-INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98227-0010 USA SN 0277-786X BN 978-0-8194-7416-2 J9 PROC SPIE PY 2009 VL 7170 AR 717008 DI 10.1117/12.809280 PG 14 WC Engineering, Biomedical; Optics; Radiology, Nuclear Medicine & Medical Imaging SC Engineering; Optics; Radiology, Nuclear Medicine & Medical Imaging GA BSS50 UT WOS:000285710000004 ER PT J AU Nalley, KA AF Nalley, Kip A. BE OBrien, T Linton, SD TI Kinetics and Catalytic Activity of Caspases SO DESIGN OF CASPASE INHIBITORS AS POTENTIAL CLINICAL AGENTS SE CRC Enzyme Inhibitors Series LA English DT Article; Book Chapter ID INTERLEUKIN-1-BETA CONVERTING-ENZYME; INDUCED-PROXIMITY MODEL; STRUCTURAL BASIS; CRYSTAL-STRUCTURE; 3-DIMENSIONAL STRUCTURE; CELL-DEATH; CD95-MEDIATED APOPTOSIS; COMBINATORIAL APPROACH; ACTIVATION; INHIBITION C1 NCI, Lab Receptor Biol & Gene Express, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Nalley, KA (reprint author), NCI, Lab Receptor Biol & Gene Express, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. NR 76 TC 0 Z9 0 U1 0 U2 1 PU CRC PRESS-TAYLOR & FRANCIS GROUP PI BOCA RATON PA 6000 BROKEN SOUND PARKWAY NW, STE 300, BOCA RATON, FL 33487-2742 USA BN 978-1-4200-4540-6 J9 CRC ENZYM INHIB SER JI CRC Enzym. Inhib. Ser. PY 2009 BP 75 EP 92 PG 18 WC Biochemistry & Molecular Biology; Cell Biology; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Cell Biology; Pharmacology & Pharmacy GA BKX94 UT WOS:000269567500005 ER PT J AU Streveler, DJ Sherlock, SM AF Streveler, Dennis J. Sherlock, Sheila M. BE Langenbrunner, JC Cashin, C ODougherty, S TI Health Management Information Systems: Linking Purchasers and Providers SO DESIGNING AND IMPLEMENTING HEALTH CARE PROVIDER PAYMENT SYSTEMS: HOW-TO MANUALS LA English DT Article; Book Chapter C1 [Streveler, Dennis J.; Sherlock, Sheila M.] Univ Hawaii, Dept Informat & Comp Sci, Honolulu, HI 96822 USA. [Streveler, Dennis J.] Natl Lib Med, Bethesda, MD 20894 USA. [Streveler, Dennis J.] World Bank, Washington, DC USA. [Streveler, Dennis J.] Asian Dev Bank, Mandaluyong, Philippines. RP Streveler, DJ (reprint author), Univ Hawaii, Dept Informat & Comp Sci, Honolulu, HI 96822 USA. EM strev@hawaii.edu; sherlock@hawaii.edu NR 23 TC 0 Z9 0 U1 0 U2 0 PU WORLD BANK INST PI WASHINGTON PA 1818 H ST NW, WASHINGTON, DC 20433 USA BN 978-0-8213-7824-3 PY 2009 BP 263 EP 306 D2 10.1596/978-0-8213-7815-1 PG 44 WC Health Care Sciences & Services SC Health Care Sciences & Services GA BZX14 UT WOS:000303193300007 ER PT J AU Suomi, SJ AF Suomi, Stephen J. BE Tremblay, RE vanAken, MAG Koops, W TI How gene-environment interactions shape biobehavioural development Lessons from studies with rhesus monkeys SO DEVELOPMENT AND PREVENTION OF BEHAVIOUR PROBLEMS: FROM GENES TO SOCIAL POLICY LA English DT Article; Book Chapter ID 5-HYDROXYINDOLEACETIC ACID CONCENTRATIONS; CEREBROSPINAL-FLUID MONOAMINE; NONHUMAN PRIMATE MODEL; SEVERE AGGRESSION; EARLY EXPERIENCE; PLASMA-CORTISOL; BEHAVIOR; POLYMORPHISM; STRESS; MACAQUES C1 Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Comparat Ethol Lab, Poolesville, MD USA. RP Suomi, SJ (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Comparat Ethol Lab, Poolesville, MD USA. NR 61 TC 3 Z9 3 U1 0 U2 3 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH ROAD, HOVE BN3 2FA, E SUSSEX, ENGLAND BN 978-0-20386-870-6 PY 2009 BP 7 EP 23 PG 17 WC Psychology, Biological; Psychology, Developmental SC Psychology GA BUJ68 UT WOS:000289522700003 ER PT J AU Chen, R Simons-Morton, B AF Chen, Rusan Simons-Morton, Bruce TI Concurrent changes in conduct problems and depressive symptoms in early adolescents: A developmental person-centered approach SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Article ID GENDER-DIFFERENCES; YOUNG ADULTHOOD; SUBSTANCE USE; ALCOHOL-USE; TRAJECTORIES; BEHAVIOR; CHILDREN; PSYCHOPATHOLOGY; RISK; BOYS AB The co-occurrence of conduct problems (CP) and depressive symptoms (DS) is an important topic in developmental psychopathology, however, research in this area is still in its early stages. Using data from a school-based longitudinal sample of 2,453 adolescents with five waves from Grade 6 to 9, we examined the prevalence, etiology, and consequences of the co-occurrence of CP and DS. A person-centered approach, general growth mixture modeling, was applied to obtain CP and DS trajectory groups. The risk factors and consequences of the co-occurrence problem were examined using the trajectory groups. As hypothesized in a nonclinical sample, a small proportion of boys (8.8%) and girls (3.7%) reported to be high in both CP and DS over time. Among the adolescents with the highest level of CP, only 6.3% of the boys and 6.0% of the girls experienced the highest level of DS. However, among those with the highest level of DS trajectories, 42.9% of the boys and 10.2% of the girls reported the highest level of CP, indicating a gender-specific risk of the co-occurrence problem for depressed boys. Psychosocial and family factors were identified as vulnerable precursors to co-occurring CP and DS, a finding in line with the multiple domain risk model for CP and the transactional model for DS. The study also found that adolescents with the co-occurrence problem were more similar to those with "pure DS" than those with "pure CP" in academic adjustment tit the ninth grade. C1 [Chen, Rusan] Georgetown Univ, Ctr New Designs Learning & Scholarship, Washington, DC 20057 USA. [Simons-Morton, Bruce] NIH, Bethesda, MD USA. RP Chen, R (reprint author), Georgetown Univ, Ctr New Designs Learning & Scholarship, 3520 Prospect St,NW 314, Washington, DC 20057 USA. EM chenrs@georgetown.edu RI Chen, Robert/B-3899-2009; OI Chen, Robert/0000-0002-8371-8629; Simons-Morton, Bruce/0000-0003-1099-6617 FU Intramural NIH HHS [Z01 HD002110-16, Z99 HD999999]; NICHD NIH HHS [N01-HD-4-3207] NR 40 TC 20 Z9 20 U1 1 U2 5 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 0954-5794 EI 1469-2198 J9 DEV PSYCHOPATHOL JI Dev. Psychopathol. PD JAN PY 2009 VL 21 IS 1 BP 285 EP 307 DI 10.1017/S0954579409000169 PG 23 WC Psychology, Developmental SC Psychology GA 397YU UT WOS:000262699100016 PM 19144234 ER PT J AU Yang, JH Pospisil, R Mage, RG AF Yang, Jiahui Pospisil, Richard Mage, Rose G. TI Expression and localization of rabbit B-cell activating factor (BAFF) and its specific receptor BR3 in cells and tissues of the rabbit immune system SO DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY LA English DT Article DE MiniBR3; Appendix; Gut-associated lymphoid tissue; Autoimmune diseases; Vaccine development ID NECROSIS-FACTOR FAMILY; TNF FAMILY; LYMPHOCYTE STIMULATOR; LUPUS-ERYTHEMATOSUS; SURVIVAL; AUTOIMMUNITY; BAFF/BLYS; APPENDIX; APRIL; BLYS AB Rabbits are widely used for vaccine development, and investigations of human infectious and autoimmune diseases such as Systemic Lupus Erythematosus (SLE). For these applications, we cloned, sequenced and expressed rabbit B-cell Activating Factor (BAFF), and localized BAFF in cells and tissues of the rabbit immune system. The rabbit homolog of the human BAFF binding site (miniBR3 peptide) within the BAFF-specific receptor BR3 was synthesized. This 26-residue core domain binds to recombinant rabbit BAFF protein. Flow cytometric analyses using purified recombinant rabbit BAFF combined with real-time PCR findings revealed that BAFF detected on peripheral blood B-cells from normal rabbits is probably complexed to BAFF receptors rather than produced by the B-cells. BAFF was detected in developing appendix of young rabbits by immunohistochemical staining Suggesting that BAFF plays a role during the period following birth when rabbit B-cell development and pre-immune antibody repertoire diversification and selection is occurring. Published by Elsevier Ltd. C1 [Yang, Jiahui; Pospisil, Richard; Mage, Rose G.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. RP Mage, RG (reprint author), NIAID, Immunol Lab, NIH, Bldg 10,Rm 11N311,10 Ctr Dr, Bethesda, MD 20892 USA. EM rmage@niaid.nih.gov RI Pospisil, Richard/B-7467-2012 FU NIH, NIAID; Oak Ridge Associated Universities FX This research was Supported by the intramural research program of the NIH, NIAID and the Oak Ridge Associated Universities. We thank Drs. Alejandro Schaffer and Richa Agarwala, NCB1 for identification and assistance with sequence analyses of a rabbit BR3-containing BAC clone, Dr. Jan Lukszo, Peptide Synthesis and Analysis Laboratory, Research Technology Branch, NIAID for synthesis of rabbit miniBR3, Thomas Hofer and Christoph Rader for help with BAFF protein expression, Rami Zahr, Jacqueline Milton and Satyajit Ray for technical assistance, and Shirley Starnes for editorial assistance, We thank Drs. Michael Mage and Christoph Rader for helpful comments about the manuscript. NR 37 TC 4 Z9 5 U1 2 U2 5 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0145-305X J9 DEV COMP IMMUNOL JI Dev. Comp. Immunol. PY 2009 VL 33 IS 5 BP 697 EP 708 DI 10.1016/j.dci.2008.12.001 PG 12 WC Immunology; Zoology SC Immunology; Zoology GA 416JD UT WOS:000264001200007 PM 19124039 ER PT J AU Gorivodsky, M Mukhopadhyay, M Wilsch-Braeuninger, M Phillips, M Teufel, A Kim, C Malik, N Huttner, W Westphal, H AF Gorivodsky, Marat Mukhopadhyay, Mahua Wilsch-Braeuninger, Michaela Phillips, Matthew Teufel, Andreas Kim, Changmee Malik, Nasir Huttner, Wieland Westphal, Heiner TI Intraflagellar transport protein 172 is essential for primary cilia formation and plays a vital role in patterning the mammalian brain SO DEVELOPMENTAL BIOLOGY LA English DT Article DE IFT172; Slb; Cilia; Node; Nodal; MHB boundary ID PLANAR CELL POLARITY; ORGANIZER SIGNAL FGF8; MOUSE EMBRYO; ISTHMIC ORGANIZER; REPRESSOR FUNCTIONS; ROSTRAL HINDBRAIN; OTX2 EXPRESSION; NODAL SIGNALS; GENE; MIDBRAIN AB IFT172, also known as Selective Lim-domain Binding protein (SLB), is a component of the intraflagellar transport (IFT) complex. In order to evaluate the biological role of the Ift172 gene, we generated a loss-of-function mutation in the mouse. The resulting Sib mutant embryos die between E12.5 and 13.0, and exhibit severe cranio-facial malformations, failure to close the cranial neural tube, holoprosencephaly, heart edema and extensive hemorrhages. Cilia outgrowth in cells of the neuroepithelium is initiated but the axonemes are severely truncated and do not contain visible microtubules. Morphological and molecular analyses revealed a global brain-patterning defect along the dorsal-ventral (DV) and anterior-posterior (AP) axes. We demonstrate that Ift172 gene function is required for early regulation of Fgf8 at the midbrain-hindbrain boundary and maintenance of the isthmic organizer. In addition, Ift172 is required for proper function of the embryonic node, the early embryonic organizer and for formation of the head organizing center (the anterior mesendoderm, or AME). We propose a model suggesting that forebrain and mid-hindbrain growth and AP patterning depends on the early function of Ift172 at gastrulation. Our data suggest that the formation and function of the node and AME in the mouse embryo relies on an indispensable role of Ift172 in cilia morphogenesis and cilia-mediated signaling. Published by Elsevier Inc. C1 [Gorivodsky, Marat; Mukhopadhyay, Mahua; Phillips, Matthew; Kim, Changmee; Malik, Nasir; Westphal, Heiner] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Lab Mammalian Genes & Dev, Program Genom Dev, NIH, Bethesda, MD USA. [Wilsch-Braeuninger, Michaela; Huttner, Wieland] Max Planck Inst Mol Cell Biol & Genet, D-01307 Dresden, Germany. [Teufel, Andreas] Johannes Gutenberg Univ Mainz, Med Klin & Poliklin 1, D-55101 Mainz, Germany. RP Westphal, H (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Lab Mammalian Genes & Dev, Program Genom Dev, NIH, Bethesda, MD USA. EM hw@mail.nih.gov FU Eunice Kennedy Shriver National Institute of Child Health and Human Development FX We thank Drs. P. Tale, M. Shen and A. Varela-Echavaria for helpful discussion and suggestions; A. Grinberg for assistance with embryonic stem cell cultures and blastocyst microinjection, R. Wu for help with genotyping, and Dr. C. Ott for helpful suggestions and technical assistance. This work was supported by funds from the intramural research program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development. NR 64 TC 38 Z9 40 U1 0 U2 3 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0012-1606 J9 DEV BIOL JI Dev. Biol. PD JAN 1 PY 2009 VL 325 IS 1 BP 24 EP 32 DI 10.1016/j.ydbio.2008.09.019 PG 9 WC Developmental Biology SC Developmental Biology GA 394PN UT WOS:000262459600003 PM 18930042 ER PT J AU Crimmins, S Sutovsky, M Chen, PC Huffman, A Wheeler, C Swing, DA Roth, K Wilson, J Sutovsky, P Wilson, S AF Crimmins, Stephen Sutovsky, Miriam Chen, Ping-Chung Huffman, Alexis Wheeler, Crystal Swing, Deborah A. Roth, Kevin Wilson, Julie Sutovsky, Peter Wilson, Scott TI Transgenic rescue of ataxia mice reveals a male-specific sterility defect SO DEVELOPMENTAL BIOLOGY LA English DT Article DE Ubiquitin; Proteasome; Testis; Usp14; Fertility ID C-TERMINAL HYDROLASE; DEUBIQUITINATING ENZYME; 26S PROTEASOME; UBIQUITIN; USP14; GENE; CELLS; DEGRADATION; EXPRESSION; SPERMATIDS AB Homozygous ataxia (ax(J)) mice have reduced expression of ubiquitin-specific protease 14 (Usp14), resulting in severe neuromuscular defects and death by 2 months of age. Transgenic expression of Usp14 exclusively in the nervous system of ax(J) mice (ax(J)-Tg) prevents early lethality and restores motor system function to the ax(J) mice, enabling an analysis of the reproductive capabilities of Usp14-deficient mice. Although female ax(J)-Tg mice had a 75% reduction of Usp14 in the ovaries, they were able to produce normal litters. Ovary transfer experiments also demonstrated that the ovaries of ax(J) mice were capable of producing viable pups. In contrast, male ax(J) and ax(J)-Tg mice displayed a 50% reduction in testicular Usp14 levels and were infertile, indicating that Usp14 is required for development and function of the male reproductive system. Immunohistochemistry experiments showed that Usp14 is found in the redundant nuclear envelope and cytoplasmic droplet of epididymal spermatozoa. Analysis of ax(J) testes demonstrated a 50% reduction in testis weight, a 100-fold reduction in sperm number and the presence of abnormal spermatozoa in the epididymis. Histological examination of the Usp14-deficient testes revealed abnormal spermatogenesis and the presence of degenerating germ cells, indicating that Usp14 and the ubiquitin proteasome system are required for spermatid differentiation during spermiogenesis. (C) 2008 Elsevier Inc. All rights reserved. C1 [Crimmins, Stephen; Chen, Ping-Chung; Huffman, Alexis; Wheeler, Crystal; Wilson, Julie; Wilson, Scott] Univ Alabama, Dept Neurobiol, Civitan Int Res Ctr, Birmingham, AL 35294 USA. [Sutovsky, Miriam] Univ Missouri, Div Anim Sci, Columbia, MO 65211 USA. [Swing, Deborah A.; Sutovsky, Peter] NCI, Canc Res Ctr, Mouse Canc Genet Program, Frederick, MD 21702 USA. [Roth, Kevin] Univ Alabama, Dept Pathol, Birmingham, AL 35294 USA. [Sutovsky, Peter] Univ Missouri, Dept Obstet Gynecol & Womens Hlth, Columbia, MO 65211 USA. RP Wilson, S (reprint author), Univ Alabama, Dept Neurobiol, Civitan Int Res Ctr, 1825 Univ Blvd,Shelby 914, Birmingham, AL 35294 USA. EM Wilson@nrc.uab.edu OI Roth, Kevin/0000-0002-0643-995X FU Food for the 21st Century Program of the University of Missouri-Columbia; USDA CSREES [2007-01319]; NIH [NS57098, NS047533] FX We thank Kathy Craighead for clerical assistance and the staff of the histology core of the University of Missouri for tissue processing and sectioning. Funding to the laboratory of P.S. was provided by the Food for the 21st Century Program of the University of Missouri-Columbia, and by the National Research Initiative Competitive Grant No. 2007-01319 from USDA CSREES. This work was supported by NIH Neuroscience Blueprint Core Grant NS57098 to the University of Alabama at Birmingham and NIH/NINDS Grant NS047533 to S.M.W. NR 31 TC 17 Z9 17 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0012-1606 J9 DEV BIOL JI Dev. Biol. PD JAN 1 PY 2009 VL 325 IS 1 BP 33 EP 42 DI 10.1016/j.ydbio.2008.09.021 PG 10 WC Developmental Biology SC Developmental Biology GA 394PN UT WOS:000262459600004 PM 18926813 ER PT J AU Choi, SJ Roodman, GD Feng, JQ Song, IS Amin, K Hart, PS Wright, JT Haruyama, N Hart, TC AF Choi, S. J. Roodman, G. D. Feng, J. Q. Song, I. S. Amin, K. Hart, P. S. Wright, J. T. Haruyama, N. Hart, T. C. TI In vivo impact of a 4 bp deletion mutation in the DLX3 gene on bone development SO DEVELOPMENTAL BIOLOGY LA English DT Article DE Rodent; Transgenic mice; DLX3; Osteoclast; Bone mineralization; Interferon-gamma ID TRICHODENTOOSSEOUS SYNDROME; OSTEOBLAST DIFFERENTIATION; COLLAGEN-SYNTHESIS; INTERFERON-GAMMA; OSTEOCLAST DIFFERENTIATION; CATHEPSIN-K; CELLS; EXPRESSION; PROTEIN; VITRO AB Distal-less 3 (DLX3) gene mutations are etiologic for Tricho-Dento-Osseous syndrome. To investigate the in vivo impact of mutant DLX3 on bone development, we established transgenic (TG) mice expressing the c.571_574delGGGG DLX-3 gene mutation (MT-DLX3) driven by a mouse 2.3 Col1A1 promoter. Micro-computed tomographic analyses demonstrated markedly increased trabecular bone volume and bone mineral density in femora from TG mice. In ex vivo experiments, TG mice showed enhanced differentiation of bone marrow stromal cells to osteoblasts and increased expression levels of bone formation markers. However, TG mice did not show enhanced dynamic bone formation rates in in vivo fluorochrome double labeling experiments. Osteoclastic differentiation capacities of bone marrow monocytes were reduced in TG mice in the presence of osteoclastogenic factors and the numbers of TRAP(+) osteoclasts on distal metaphyseal trabecular bone surfaces were significantly decreased. TRACP 5b and CTX serum levels were significantly decreased in TG mice, while IFN-gamma levels were significantly increased. These data demonstrate that increased levels of IFN-gamma decrease osteoclast bone resorption activities, contributing to the enhanced trabecular bone volume and mineral density in these TG mice. These data suggest a novel role for this DLX3 mutation in osteoclast differentiation and bone resorption. Published by Elsevier Inc. C1 [Choi, S. J.; Song, I. S.; Amin, K.; Hart, T. C.] Natl Inst Dent & Craniofacial Res, Human Craniofacial Genet Sect, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD 20854 USA. [Roodman, G. D.] Univ Pittsburgh, Dept Med, Div Hematol Oncol, Pittsburgh, PA USA. [Feng, J. Q.] Texas A&M Hlth Sci Ctr, Baylor Coll Med, Dallas, TX USA. [Hart, P. S.] NHGRI, Off Clin Director, NIH, Bethesda, MD 20892 USA. [Wright, J. T.] Univ North, Dept Pediat Dent, Chapel Hill, NC USA. [Haruyama, N.] Tohoku Univ, Sch Grad Dent, Div Oral Dysfunct Sci, Sendai, Miyagi, Japan. RP Hart, TC (reprint author), Natl Inst Dent & Craniofacial Res, Human Craniofacial Genet Sect, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD 20854 USA. EM thart@mail.nih.gov RI Haruyama, Naoto/D-1993-2011 OI Haruyama, Naoto/0000-0001-6225-5816 FU National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD FX We thank Dr. Pamela Robey and Dr. Marian Young of the National Institute of Dental and Craniofacial Research, NIH, for their critique of this manuscript. This work was supported in part by the Intramural Program of the National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD. NR 41 TC 16 Z9 18 U1 0 U2 2 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0012-1606 J9 DEV BIOL JI Dev. Biol. PD JAN 1 PY 2009 VL 325 IS 1 BP 129 EP 137 DI 10.1016/j.ydbio.2008.10.014 PG 9 WC Developmental Biology SC Developmental Biology GA 394PN UT WOS:000262459600013 PM 18996110 ER PT J AU Warren, KR Hewitt, BG AF Warren, Kenneth R. Hewitt, Brenda G. TI FETAL ALCOHOL SPECTRUM DISORDERS: WHEN SCIENCE, MEDICINE, PUBLIC POLICY, AND LAWS COLLIDE SO DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE fetal alcohol syndrome disorder; alcohol and pregnancy; maternal drinking; alcohol and history; alcohol and public policy; alcohol and medicine; prohibition; temperance movement ID GIN LANE; PREGNANCY; ANOMALIES; DRINKING; CHILDREN; INFANTS; PARENTS; RATS AB Historically, alcohol has been used for different purposes including as a part of religious observances, as a food, at times as a medicine and its well-known use as a beverage. Until relatively recently these purposes have not changed and have at times been at odds with one another, resulting in collisions among policies and practices in science, medicine, public policy and the law. One area in which this has beer particularly true is that of fetal alcohol spectrum disorders (FASD) where the adverse consequences of consumed alcohol on children in the womb and after birth may have been observed since antiquity, but the actions taken based on such observations have been influenced as much by the socio/cultural/political context of the times in which they were made as by evidence of harm. This article provides an overview of the inherent confusion when new scientific findings confront prevailing medical practice, the history involved in this confusion with respect to FASD, including public policy and legal issues that have arisen around alcohol and pregnancy, and the research and clinical challenges still being faced. Published 2009 Wiley-Liss, Inc.(dagger) Dev Disabil Res Rev 2009,15:170-175, C1 [Warren, Kenneth R.; Hewitt, Brenda G.] NIAAA, NIH, Bethesda, MD 20892 USA. RP Hewitt, BG (reprint author), NIAAA, NIH, Room 2011,56335 Fishers Lane, Bethesda, MD 20892 USA. EM bhewitt@mail.nih.gov NR 39 TC 16 Z9 16 U1 2 U2 13 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1940-5510 J9 DEV DISABIL RES REV JI Dev. Disabil. Res. Rev. PY 2009 VL 15 IS 3 BP 170 EP 175 DI 10.1002/ddrr.71 PG 6 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 497BT UT WOS:000270030100002 PM 19731390 ER PT J AU Lenroot, RK Lee, NR Giedd, JN AF Lenroot, Rhoshel K. Lee, Nancy Raitano Giedd, Jay N. TI EFFECTS OF SEX CHROMOSOME ANEUPLOIDIES ON BRAIN DEVELOPMENT: EVIDENCE FROM NEUROIMAGING STUDIES SO DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE sex chromosome; aneuploidy; neuroimaging; brain; development ID EXTRA X-CHROMOSOME; KLINEFELTER-SYNDROME; TURNER-SYNDROME; 47,XYY KARYOTYPES; 49,XXXXY SYNDROME; GENETIC FEATURES; 48,XXYY SYNDROME; XYY SYNDROME; ABNORMALITIES; CHILDREN AB Variation in the number of sex chromosomes is a relatively common genetic condition, affecting as many as 1/400 individuals. The sex chromosome aneuploidies (SCAs) are associated with characteristic behavioral and cognitive phenotypes, although the degree to which specific individuals are affected can fall within a wide range. Understanding the effects of different dosages of sex chromosome genes on brain development may help to understand the basis for functional differences in affected individuals. It may also be informative regarding how sex chromosomes contribute to typical sexual differentiation. Studies of 47,XXY males make up the bulk of the current literature of neuroimaging studies in individuals with supernumerary sex chromosomes, with a few small studies or case reports of the other SCAs. Findings in 47,XXY males typically include decreased gray and white matter volumes, with most pronounced effects in the frontal and temporal lobes. Functional studies have shown evidence of decreased lateralization. Although the hypogonadism typically found in 47,XXY males may contribute to the decreased brain volume, the observation that 47,XXX females also show decreased brain volume in the presence of normal pubertal maturation suggests a possible direct dosage effect of X chromosome genes. Additional X chromosomes, such as in 49,XXXXY males, are associated with more markedly decreased brain volume and increased incidence of white matter hyperintensities. The limited data regarding effects of having two Y chromosomes (47,XYY) do not find significant differences in brain volume, although there are some reports of increased head size. Published 2009 Wiley-Liss, Inc(dagger) Dev Disabil Res Rev 2009;15:318-327. C1 [Lenroot, Rhoshel K.] Prince Wales Med Res Inst, Sydney, NSW, Australia. [Lenroot, Rhoshel K.] Univ New S Wales, Sch Psychiat, Sydney, NSW, Australia. [Lenroot, Rhoshel K.; Lee, Nancy Raitano; Giedd, Jay N.] NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA. RP Lenroot, RK (reprint author), Prince Wales Med Res Inst, Corner Barker & Easy St, Randwick, NSW 2031, Australia. EM r.lenroot@unsw.edu.au RI Lee, Nancy Raitano/F-2565-2011; Giedd, Jay/A-3080-2008; Giedd, Jay/B-7302-2012; Giedd, Jay/J-9644-2015; Lee, Nancy/M-7492-2016 OI Giedd, Jay/0000-0003-0827-3460; Giedd, Jay/0000-0003-2002-8978; Lee, Nancy/0000-0002-6663-0713 FU Intramural NIH HHS [Z99 MH999999] NR 89 TC 27 Z9 27 U1 1 U2 12 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1940-5510 J9 DEV DISABIL RES REV JI Dev. Disabil. Res. Rev. PY 2009 VL 15 IS 4 BP 318 EP 327 DI 10.1002/ddrr.86 PG 10 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 538TS UT WOS:000273207500007 PM 20014372 ER PT J AU Castranio, T Mishina, Y AF Castranio, Trisha Mishina, Yuji TI BMP2 Is Required for Cephalic Neural Tube Closure in the Mouse SO DEVELOPMENTAL DYNAMICS LA English DT Article DE BMP2; neural tube defects; neurulation; neural tube closure; NTD; chimera ID BONE MORPHOGENETIC PROTEINS; DEVELOPING SPINAL-CORD; TGF-BETA SUPERFAMILY; EMBRYONIC-DEVELOPMENT; SONIC-HEDGEHOG; CREST CELLS; PAX-3 GENE; STEM-CELLS; DEFECTS; EXPRESSION AB BMPs have been shown to play a role in neural tube development particularly as dorsalizing factors. To explore the possibility that BMP2 could play a role in the developing neural tube (NT) beyond the lethality of Bmp2 null embryos, we created Bmp2 chimeras from Bmp2 null ES cells and WT blastocysts. Analysis of Bmp2 chimeras reveals NT defects at day 9.5 (E9.5). We found that exclusion of Bmp2 null ES cells from the dorsal NT did not always prevent defects. For further comparison, we used a Bmp2 mutant line in a mixed background. Phenotypes observed were similar to chimeras including open NT defects, postneurulation defects, and abnormal neural ectoderm in heterozygous and homozygous null embryos demonstrating a pattern of dose-dependent signaling. Our data exposes BMP2 as a unique player in the developing NT for dorsal patterning and identity, and normal cephalic neural tube closure in a dose-dependent manner. Developmental Dynamics 238:110-122, 2009. Published 2008 Wiley-Liss, Inc.dagger C1 [Castranio, Trisha] Natl Inst Environm Hlth Sci, Mol Dev Biol Grp, Lab Reproduct & Dev Toxicol, NIH, Res Triangle Pk, NC 27709 USA. [Mishina, Yuji] Univ Michigan, Sch Dent, Ann Arbor, MI 48109 USA. RP Castranio, T (reprint author), Natl Inst Environm Hlth Sci, Mol Dev Biol Grp, Lab Reproduct & Dev Toxicol, NIH, 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA. EM castran1@niehs.nih.gov FU Intramural Research Program of the NIEHS/NIH [ES071003-10] FX Grant sponsor: Intramural Research Program of the NIEHS/NIH; Grant number: ES071003-10. NR 56 TC 15 Z9 16 U1 0 U2 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 1058-8388 J9 DEV DYNAM JI Dev. Dyn. PD JAN PY 2009 VL 238 IS 1 BP 110 EP 122 DI 10.1002/dvdy.21829 PG 13 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA 394PM UT WOS:000262459500011 PM 19097048 ER PT J AU Yi, L Domyan, ET Lewandoski, M Sun, X AF Yi, Lan Domyan, Eric T. Lewandoski, Mark Sun, Xin TI Fibroblast Growth Factor 9 Signaling Inhibits Airway Smooth Muscle Differentiation in Mouse Lung SO DEVELOPMENTAL DYNAMICS LA English DT Article DE fibroblast growth factor 9 (Fgf9); lung; airway smooth muscle cells ID MULTIPLE MESENCHYMAL LINEAGES; GENE REGULATORY NETWORK; CELL PROGENITORS; FACTOR RECEPTOR; FETAL LUNG; TRANSFORMING GROWTH-FACTOR-BETA-1; BRANCHING MORPHOGENESIS; PROXIMODISTAL AXIS; FGF; EXPRESSION AB In mammalian lungs, airway smooth muscle cells (airway SMCs) are present in the proximal lung adjacent to bronchi and bronchioles, but are absent in the distal lung adjacent to terminal sacs that expand during gas exchange. Evidence suggests that this distribution is essential for the formation of a functional respiratory tree, but the underlying genetic mechanism has not been elucidated. In this study, we test the hypothesis that fibroblast growth factor 9 (Fgf9) signaling is essential to restrict SMC differentiation to the proximal lung. We show that loss of Fgf9 or conditional inactivation of Fgf receptors (Fgfr) 1 and 2 in mouse lung mesenchyme results in ectopic SMCs. Our data support a model where FGF9 maintains a SMC progenitor population by suppressing differentiation and promoting growth. This model also represents our findings on the genetic relationship between FGF9 and sonic hedgehog (SHH) in the establishment of airway SMC pattern. Developmental Dynamics 238:123-137, 2009. (C) 2008 Wiley-Liss, Inc. C1 [Yi, Lan; Domyan, Eric T.; Sun, Xin] Univ Wisconsin, Genet Lab, Madison, WI 53706 USA. [Lewandoski, Mark] NCI, Frederick Canc Res & Dev Ctr, Canc & Dev Biol Lab, Frederick, MD USA. RP Sun, X (reprint author), Univ Wisconsin, Genet Lab, Madison, WI 53706 USA. EM xsun@wisc.edu FU Burroughs-Wellcome [1002361]; American Heart Association [06100872]; NIH [5T32GM07133] FX Grant sponsor: Burroughs-Wellcome; Grant number: 1002361; Grant sponsor: American Heart Association; Grant sponsor: 06100872; Grant sponsor: NIH: Grant number: 5T32GM07133. NR 62 TC 20 Z9 20 U1 0 U2 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 1058-8388 J9 DEV DYNAM JI Dev. Dyn. PD JAN PY 2009 VL 238 IS 1 BP 123 EP 137 DI 10.1002/dvdy.21831 PG 15 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA 394PM UT WOS:000262459500012 PM 19097117 ER PT J AU Lau, JYF Burt, M Leibenluft, E Pine, DS Rijsdijk, F Shiffrin, N Eley, TC AF Lau, Jennifer Y. F. Burt, Michael Leibenluft, Ellen Pine, Daniel S. Rijsdijk, Fruhling Shiffrin, Nina Eley, Thalia C. TI Individual Differences in Children's Facial Expression Recognition Ability: The Role of Nature and Nurture SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article ID EARLY EXPERIENCE; CHILDHOOD; EMOTION; ADOLESCENCE; INFANTS AB We examined genetic and environmental influences on recognition of facial expressions in 250 pairs of 10-year-old monozygotic (83 pairs) and dizygotic (167 pairs) twins. Angry, fearful, sad, disgusted, and happy faces varying in intensity (15%-100%), head orientation, and eye gaze were presented in random order across 160 trials. Total correct recognition responses to each facial expression comprised the dependent variables. Twin data examined genetic and environmental contributions to variables and their correlations. Results support a common psychometric factor influenced primarily by additive genetic influences across expressions with discrimination of specific expressions due largely to non-shared environmental influences. C1 [Lau, Jennifer Y. F.] Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. [Lau, Jennifer Y. F.; Rijsdijk, Fruhling; Eley, Thalia C.] Kings Coll London, Social Genet & Dev Psychiat Ctr, Inst Psychiat, London, England. [Burt, Michael] Univ Durham, Dept Psychol, Durham DH1 3LE, England. [Leibenluft, Ellen; Pine, Daniel S.; Shiffrin, Nina] NIMH, Mood & Anxiety Program, NIH, Bethesda, MD 20892 USA. RP Lau, JYF (reprint author), Univ Oxford, Dept Expt Psychol, S Parks Rd, Oxford OX1 3UD, England. EM jennifer.lau@psy.ox.ac.uk RI Eley, Thalia/D-4811-2011; Rijsdijk, Fruhling/B-4191-2011; Burt, Michael/D-6684-2013 OI Burt, Michael/0000-0001-5627-6012 FU Intramural NIH HHS [ZIA MH002780-08, ZIA MH002781-08, ZIA MH002782-08]; Medical Research Council [G120/635] NR 25 TC 11 Z9 11 U1 3 U2 7 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 8756-5641 J9 DEV NEUROPSYCHOL JI Dev. Neuropsychol. PY 2009 VL 34 IS 1 BP 37 EP 51 AR PII 907770424 DI 10.1080/87565640802564424 PG 15 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA 398FD UT WOS:000262717100002 PM 19142765 ER PT J AU Carter, CS Boone, EM Pournajafi-Nazarloo, H Bales, KL AF Carter, C. Sue Boone, Ericka M. Pournajafi-Nazarloo, Hossein Bales, Karen L. TI Consequences of Early Experiences and Exposure to Oxytocin and Vasopressin Are Sexually Dimorphic SO DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE Oxytocin; Vasopressin; Pitocin; Sex differences; Early experience; Prairie voles ID VOLES MICROTUS-OCHROGASTER; MALE PRAIRIE VOLES; ESTROGEN-RECEPTOR-ALPHA; DEVELOPMENTAL EXPOSURE; PARTNER PREFERENCES; SEX-DIFFERENCES; NERVOUS-SYSTEM; MATERNAL-CARE; EXPRESSION; BEHAVIOR AB In the socially monogamous prairie vole, we have observed that small changes in early handling, as well as early hormonal manipulations can have long-lasting and sexually dimorphic effects on behavior. These changes may be mediated in part by changes in parental interactions with their young, acting on systems that rely on oxytocin (OT) and arginine vasopressin (AVP). Knowledge of both endogenous and exogenous influences on systems that rely on OT and AVP may be helpful in understanding sexually dimorphic developmental disorders, such as autism, that are characterized by increased anxiety and deficits in social behavior. Copyright (C) 2009 S. Karger AG, Basel C1 [Carter, C. Sue; Boone, Ericka M.; Pournajafi-Nazarloo, Hossein] Univ Illinois, Dept Psychiat, Brain Body Ctr, Chicago, IL 60612 USA. [Bales, Karen L.] Univ Calif Davis, Dept Psychol, Davis, CA 95616 USA. [Boone, Ericka M.] NIDA, NIH, DHHS, Bethesda, MD 20892 USA. RP Carter, CS (reprint author), Univ Illinois, Dept Psychiat, Brain Body Ctr, Chicago, IL 60612 USA. EM scarter@psych.uic.edu FU National Institutes of Health [HD38490, MH073022, HD08702, MH018882, MH072109]; National Science Foundation [0437532]; Institute for Research on Unlimited Love FX We are grateful for support from the National Institutes of Health - HD38490 ( C. S. C.), MH073022 ( C. S. C., K. L. B.), HD08702 ( K. L. B.), MH018882 ( E. M. B.), MH072109 ( E. M. B.), National Science Foundation - 0437532 ( K. L. B.) and the Institute for Research on Unlimited Love. NR 57 TC 63 Z9 65 U1 3 U2 24 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-5866 J9 DEV NEUROSCI-BASEL JI Dev. Neurosci. PY 2009 VL 31 IS 4 BP 332 EP 341 DI 10.1159/000216544 PG 10 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 468BB UT WOS:000267787200010 PM 19546570 ER PT J AU Lieb, W Pencina, MJ Lanier, KJ Tofler, GH Levy, D Fox, CS Wang, TJ D'Agostino, RB Vasan, RS AF Lieb, Wolfgang Pencina, Michael J. Lanier, Katherine J. Tofler, Geoffrey H. Levy, Daniel Fox, Caroline S. Wang, Thomas J. D'Agostino, Ralph B., Sr. Vasan, Ramachandran S. TI Association of Parental Obesity With Concentrations of Select Systemic Biomarkers in Nonobese Offspring The Framingham Heart Study SO DIABETES LA English DT Article ID PLASMINOGEN-ACTIVATOR INHIBITOR-1; C-REACTIVE PROTEIN; INSULIN-RESISTANCE ATHEROSCLEROSIS; NATRIURETIC PEPTIDE LEVELS; METABOLIC-SYNDROME; OVERWEIGHT; FIBRINOGEN; CHILDREN; MARKERS; IMPACT AB OBJECTIVE-Parental obesity is a risk factor for offspring obesity. It is unclear whether parental obesity also confers risk for obesity-associated conditions (e.g., a proinflammatory or prothrombotic state) in the absence of offspring obesity. RESEARCH DESIGN AND METHODS-We compared concentrations of multiple biomarkers representing distinct biological pathways (C-reactive protein [CRP], aldosterone, renin, B-type natriuretic peptide, NH(2)-terminal proatrial natriuretic peptide, fibrinogen, and plasminogen activator inhibitor-1) in nonobese Framingham Offspring Study participants with no parents (n = 665), one parent (n = 488), or two parents (n 119) with obesity (BMI; >= 30 kg/m(2)). RESULTS-Nonobese offspring with both parents with obesity had higher CRP levels (median 2.16 mg/l) than offspring with one parent (1.58 mg/l) or no parents (1.35 mg/l) with obesity. After multivariable adjustment, a nonlinear relationship with parental obesity became evident: compared with those without parental obesity, CRP levels were higher in offspring with two obese parents (P = 0.04) but not in offspring with only one obese parent (P = 0.76). Renin levels were more linearly related to parental obesity status, being significantly higher in offspring with one parent (P = 0.04) or two parents (P = 0.09) with obesity (P = 0.02 for trend). The other systemic biomarkers did not vary according to parental obesity status (all P > 0.05). CONCLUSIONS-Our findings suggest that offspring with a high risk of developing obesity have an altered biomarker profile, characterized by systemic inflammation and increased neurohormonal activity, even in the absence of obesity. This is consistent with the notion that parental obesity may confer an increased susceptibility to other adiposity-associated traits. Diabetes 58: 134-137,2009 C1 [Lieb, Wolfgang; Pencina, Michael J.; Levy, Daniel; Fox, Caroline S.; Wang, Thomas J.; Vasan, Ramachandran S.] Framingham Heart Dis Epidemiol Study, Framingham, MA USA. [Pencina, Michael J.; Lanier, Katherine J.; D'Agostino, Ralph B., Sr.] Boston Univ, Sch Med, Dept Math, Boston, MA 02118 USA. [Tofler, Geoffrey H.] Royal N Shore Hosp, Sydney, NSW, Australia. [Levy, Daniel; Fox, Caroline S.] NHLBI, Ctr Populat Studies, Bethesda, MD 20892 USA. [Fox, Caroline S.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Endocrinol, Boston, MA USA. [Wang, Thomas J.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Med,Div Cardiol, Boston, MA USA. [Vasan, Ramachandran S.] Boston Univ, Sch Med, Prevent Med & Cardiol Sect, Boston, MA 02118 USA. RP Vasan, RS (reprint author), Framingham Heart Dis Epidemiol Study, Framingham, MA USA. EM vasan@bu.edu RI Lieb, Wolfgang/C-1990-2012; OI Ramachandran, Vasan/0000-0001-7357-5970 FU NHLBI NIH HHS [2K24HL04334, K24 HL004334, N01-HC-25195, N01HC25195]; NIDDK NIH HHS [1R01-DK-080739, R01 DK080739] NR 24 TC 19 Z9 21 U1 0 U2 2 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA SN 0012-1797 J9 DIABETES JI Diabetes PD JAN PY 2009 VL 58 IS 1 BP 134 EP 137 DI 10.2337/db08-0918 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 390TR UT WOS:000262187100023 PM 18931036 ER PT J AU Rovner, AJ Nansel, TR AF Rovner, Alisha J. Nansel, Tonja R. TI Are Children With Type 1 Diabetes Consuming a Healthful Diet? A Review of the Current Evidence and Strategies for Dietary Change SO DIABETES EDUCATOR LA English DT Article ID GLYCEMIC CONTROL; CYSTIC-FIBROSIS; NUTRIENT INTAKE; CALCIUM INTAKE; ADOLESCENTS; NUTRITION; INTERVENTION; ADHERENCE; MELLITUS; TRIAL AB Purpose The purpose of this study is to review the literature on usual dietary intake in children with type 1 diabetes (T1D) and to discuss approaches to promote dietary change with potential efficacy. Methods Search strategies included a MEDLINE search for English-language articles that estimated usual dietary intake in children with T1D and a screening of the reference lists from original studies. The keywords used were diet, dietary intake, nutrition, type 1 diabetes, children, adolescents, and youth. Studies were included if they were observational, contained a sample of children with T1D, and estimated usual dietary intake. Results Nine studies fulfilled the criteria (6 US, 3 European). Of the 4 studies with a control group, 3 reported that both total fat and saturated fat intake were higher in the children with T1D. Six studies examined the percent of total calories from saturated fat; mean intake ranged from 11 to 15%, exceeding ADA recommendations (< 7%). Fruit, vegetable, and fiber intakes were low among children with T1D. No prior studies have addressed dietary change in this population. The behavior-change literature suggests that nutrition education alone is unlikely to be adequate, but that incorporation of behavioral approaches offers potential efficacy in promoting healthful dietary change. Conclusions Children with T1D are not meeting dietary guidelines, and in some areas their diets are less healthful than children without diabetes. As these dietary behaviors may affect the risk of long-term complications, the incorporation of behavioral approaches promoting healthy eating into routine clinical practice is warranted. C1 [Rovner, Alisha J.; Nansel, Tonja R.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, NIH, US Dept HHS, Bethesda, MD USA. RP Rovner, AJ (reprint author), NICHD, Div Epidemiol Stat & Prevent Res, NIH, DHHS, 6100 Execut Blvd,Room 7B13R,MSC 7500, Bethesda, MD 20892 USA. EM rovneral@mail.nih.gov OI Nansel, Tonja/0000-0002-8298-7595 FU Intramural NIH HHS [Z01 HD008805-01] NR 39 TC 26 Z9 27 U1 0 U2 3 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0145-7217 J9 DIABETES EDUCATOR JI Diabetes Educ. PD JAN-FEB PY 2009 VL 35 IS 1 BP 97 EP 107 DI 10.1177/0145721708326699 PG 11 WC Endocrinology & Metabolism; Public, Environmental & Occupational Health SC Endocrinology & Metabolism; Public, Environmental & Occupational Health GA 412BV UT WOS:000263699100007 PM 19244565 ER PT J AU Kreis, AJ Wong, TY Islam, FMA Klein, R Klein, BEK Cotch, MF Jenkins, AJ Shea, S Wang, JJ AF Kreis, Andreas J. Wong, Tien Yin Islam, F. M. Amirul Klein, Ronald Klein, Barbara E. K. Cotch, Mary Frances Jenkins, Alicia J. Shea, Steven Wang, Jie Jin TI Is nuclear magnetic resonance lipoprotein subclass related to diabetic retinopathy? The multi-ethnic study of atherosclerosis (MESA) SO DIABETES & VASCULAR DISEASE RESEARCH LA English DT Article DE diabetic retinopathy; NMR-lipoprotein; retinal photography; type 2 diabetes ID ABNORMALITIES; COHORT AB Objective To examine the associations between nuclear magnetic resonance (NMR) defined lipoproteins and diabetic retinopathy (DR) in a population-based sample of adults with type 2 diabetes. Research design and methods In all, 921 persons with diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA) were included. DR was assessed from retinal photographs. Lipoproteins were measured by NMR spectroscopy. Results After controlling for age, race/ethnicity, study Centre and diabetes and vascular risk factors, no consistent patterns of associations between NMR-defined lipoprotein particle concentrations and subclass with DR were evident. Conclusion The lack of association between NMR-defined lipoproteins and DR does not support clinical use of NMR spectroscopy for management of patients with DR. C1 [Kreis, Andreas J.; Wong, Tien Yin; Islam, F. M. Amirul; Wang, Jie Jin] Univ Melbourne, Ctr Eye Res Australia, East Melbourne, Vic 3002, Australia. [Klein, Ronald; Klein, Barbara E. K.] Univ Wisconsin, Sch Med & Publ Hlth, Dept Ophthalmol & Visual Sci, Madison, WI 53726 USA. [Cotch, Mary Frances] NEI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20892 USA. [Jenkins, Alicia J.] Univ Melbourne, Dept Med, Melbourne, Vic 3065, Australia. [Shea, Steven] Columbia Univ, Sch Med, Dept Med, New York, NY 10032 USA. [Shea, Steven] Columbia Univ, Sch Med, Dept Epidemiol, New York, NY 10032 USA. [Shea, Steven] Columbia Univ, Sch Publ Hlth, Dept Med, New York, NY 10032 USA. [Shea, Steven] Columbia Univ, Sch Publ Hlth, Dept Epidemiol, New York, NY 10032 USA. RP Wang, JJ (reprint author), Univ Melbourne, Ctr Eye Res Australia, 32 Gisborne St, East Melbourne, Vic 3002, Australia. EM jiejw@unimelb.edu.au RI Wang, Jie Jin/P-1499-2014; Jenkins, Alicia/N-2482-2015; OI Wang, Jie Jin/0000-0001-9491-4898; Cotch, Mary Frances/0000-0002-2046-4350; Klein, Ronald/0000-0002-4428-6237 FU National Heart, Lung, and Blood Institute [N01-HC-95159, N01-HC-95165, N01-HC-95169]; NIH [HL69979-03]; National Eye Institute [Z01EY000403] FX This research was supported by contracts N01-HC-95159 to N01-HC-95165 and N01-HC-95169 from the National Heart, Lung, and Blood Institute. Additional support was provided by NIH grant HL69979-03 (Klein R and Wong TY) and an intramural research programme award Z01EY000403 from the National Eye Institute, National Institutes of Health. NR 10 TC 1 Z9 1 U1 0 U2 1 PU SHERBORNE GIBBS LTD PI EDGBASTON PA EDGBASTON HOUSE, 3 DUCHESS PLACE, EDGBASTON, BIRMINGHAM B16 8 NH, ENGLAND SN 1479-1641 J9 DIABETES VASC DIS RE JI Diabetes Vasc. Dis. Res. PD JAN PY 2009 VL 6 IS 1 BP 40 EP 42 DI 10.3132/dvdr.2009.008 PG 3 WC Endocrinology & Metabolism; Peripheral Vascular Disease SC Endocrinology & Metabolism; Cardiovascular System & Cardiology GA 398GY UT WOS:000262721800008 PM 19156628 ER PT J AU Dropulic, LK Lederman, HM AF Dropulic, Lesia K. Lederman, Howard M. BE Hayden, RT Carroll, KC Tang, YW Wolk, DM TI Overview of Infections in the Immunocompromised Host SO DIAGNOSTIC MICROBIOLOGY OF THE IMMUNOCOMPROMISED HOST LA English DT Article; Book Chapter ID ORGAN-TRANSPLANT RECIPIENTS; EPSTEIN-BARR-VIRUS; STEM-CELL TRANSPLANTATION; CHRONIC LYMPHOCYTIC-LEUKEMIA; TUMOR-NECROSIS-FACTOR; BONE-MARROW-TRANSPLANTATION; SYSTEMIC-LUPUS-ERYTHEMATOSUS; RENAL-ALLOGRAFT RECIPIENTS; INVASIVE FUNGAL-INFECTIONS; LOW-DOSE METHOTREXATE C1 [Dropulic, Lesia K.] NIH, Lab Clin Infect Dis, Bethesda, MD 20892 USA. [Lederman, Howard M.] Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21287 USA. [Lederman, Howard M.] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21287 USA. [Lederman, Howard M.] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21287 USA. RP Dropulic, LK (reprint author), NIH, Lab Clin Infect Dis, Bldg 10, Bethesda, MD 20892 USA. NR 311 TC 2 Z9 2 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N STREET NW, WASHINGTON, DC 20036-2904 USA BN 978-1-55581-545-5 PY 2009 BP 3 EP 43 PG 41 WC Infectious Diseases; Medical Laboratory Technology; Microbiology SC Infectious Diseases; Medical Laboratory Technology; Microbiology GA BOY49 UT WOS:000278062500003 ER PT J AU Basser, PJ Ozarslan, E AF Basser, Peter J. Oezarslan, Evren BE JohansenBerg, H Behrens, TEJ TI Introduction to Diffusion MR SO DIFFUSION MRI: FROM QUANTITATIVE MEASUREMENT TO IN VIVO NEUROANATOMY LA English DT Editorial Material; Book Chapter DE Diffusion; magnetic resonance; MRI; DWI; propagator; anisotropy; diffusion tensor; q-space; apparent diffusion coefficient ID ANISOTROPIC WATER DIFFUSION; SELF-DIFFUSION; WEIGHTED MRI; NERVOUS-SYSTEM; FIELD GRADIENT; SPIN ECHOES; COEFFICIENT; TISSUE; TENSOR; MUSCLE AB Developments in the last century have led to a better understanding of diffusion, the perpetual mixing of molecules caused by thermal motion. In this chapter, the basic principles governing the diffusion phenomenon and its measurement using magnetic resonance (MR) are reviewed. The concepts of the apparent diffusion coefficient and of the diffusion propagator as well as their MR measurements are introduced from basic principles. Finally, the influence of neural tissue microstructure on the diffusion-weighted MR signal is briefly discussed. C1 [Basser, Peter J.; Oezarslan, Evren] NIH, Sect Tissue Biophys & Biomimet, Bethesda, MD 20892 USA. RP Basser, PJ (reprint author), NIH, Sect Tissue Biophys & Biomimet, 13 South Dr,Bldg 13,Room 3W16, Bethesda, MD 20892 USA. RI Ozarslan, Evren/B-4858-2013 OI Ozarslan, Evren/0000-0003-0859-1311 NR 38 TC 3 Z9 3 U1 1 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 978-0-08-087851-5 PY 2009 BP 3 EP 10 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA BCP49 UT WOS:000310964900003 ER PT J AU Bente, D Gren, J Strong, JE Feldmann, H AF Bente, Dennis Gren, Jason Strong, James E. Feldmann, Heinz TI Disease modeling for Ebola and Marburg viruses SO DISEASE MODELS & MECHANISMS LA English DT Article ID HEMORRHAGIC-FEVER; GUINEA-PIGS; EXPERIMENTAL-INFECTION; FILOVIRUS INFECTIONS; NONHUMAN-PRIMATES; RHESUS-MONKEYS; ZAIRE VIRUS; MOUSE MODEL; PATHOGENESIS; MICE AB The filoviruses Ebola and Marburg are zoonotic agents that are classified as both biosafety level 4 and category A list pathogens. These viruses are pathogenic in humans and cause isolated infections or epidemics of viral hemorrhagic fever, mainly in Central Africa. Their natural reservoir has not been definitely identified, but certain species of African bat have been associated with Ebola and Marburg infections. Currently, there are no licensed options available for either treatment or prophylaxis. Different animal models have been developed for filoviruses including mouse, guinea pig and nonhuman primates. The 'gold standard' animal models for pathogenesis, treatment and vaccine studies are rhesus and cynomolgus macaques. This article provides a brief overview of the clinical picture and the pathology/pathogenesis of human filovirus infections. The current animal model options are discussed and compared with regard to their value in different applications. In general, the small animal models, in particular the mouse, are the most feasible for high biocontainment facilities and they offer the most options for research owing to the greater availability of immunologic and genetic tools. However, their mimicry of the human diseases as well as their predictive value for therapeutic efficacy in primates is limited, thereby making them, at best, valuable initial screening tools for pathophysiology, treatment and vaccine studies. C1 [Strong, James E.; Feldmann, Heinz] Univ Manitoba, Dept Med Microbiol, Winnipeg, MB R2H 2A6, Canada. [Strong, James E.] Univ Manitoba, Dept Pediat & Child Hlth, Winnipeg, MB R2H 2A6, Canada. [Feldmann, Heinz] NIAID, Virol Lab, Div Intramural Res, NIH, Hamilton, MT 59840 USA. [Bente, Dennis; Gren, Jason; Strong, James E.] Publ Hlth Agcy Canada, Natl Microbiol Lab, Lab Zoonot Dis & Special Pathogens, Special Pathogens Program, Winnipeg, MB R3E 3R2, Canada. RP Feldmann, H (reprint author), Univ Manitoba, Dept Med Microbiol, Winnipeg, MB R2H 2A6, Canada. EM feldmannh@niaid.nih.gov RI Yurii, Eduard/R-9472-2016 OI Yurii, Eduard/0000-0001-9987-4629 NR 59 TC 82 Z9 87 U1 2 U2 52 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL, CAMBS, ENGLAND SN 1754-8403 J9 DIS MODEL MECH JI Dis. Model. Mech. PD JAN-FEB PY 2009 VL 2 IS 1-2 BP 12 EP 17 DI 10.1242/dmm.000471 PG 6 WC Cell Biology; Pathology SC Cell Biology; Pathology GA 474AL UT WOS:000268254500006 PM 19132113 ER PT J AU Kato, GJ Gladwin, MT AF Kato, Gregory J. Gladwin, Mark T. BE Steinberg, MH Forget, BG Higgs, DR Weatherall, DJ TI Mechanisms and Clinical Complications of Hemolysis in Sickle Cell Disease and Thalassemia SO DISORDERS OF HEMOGLOBIN: GENETICS, PATHOPHYSIOLOGY, AND CLINICAL MANAGEMENT, 2ND EDITION LA English DT Article; Book Chapter ID RED-BLOOD-CELLS; NITRIC-OXIDE BIOAVAILABILITY; CROSS-LINKED HEMOGLOBIN; MEMBRANE PHOSPHOLIPID ASYMMETRY; PRIAPISM FOLLOWING SPLENECTOMY; ERYTHROCYTE PHOSPHATIDYLSERINE EXPOSURE; PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA; PRIMARY PULMONARY-HYPERTENSION; RECOMBINANT HUMAN HEMOGLOBIN; TRAUMATIC HEMORRHAGIC-SHOCK C1 [Kato, Gregory J.] NIH, Sickle Cell Vasc Dis Unit, Vasc Therapeut Sect, Vasc Med Branch, Bethesda, MD 20892 USA. [Gladwin, Mark T.] Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA. [Gladwin, Mark T.] Univ Pittsburgh, Hemostasis & Vasc Biol Res Inst, Pittsburgh, PA USA. RP Kato, GJ (reprint author), NIH, Sickle Cell Vasc Dis Unit, Vasc Therapeut Sect, Vasc Med Branch, Bldg 10, Bethesda, MD 20892 USA. RI Kato, Gregory/I-7615-2014 OI Kato, Gregory/0000-0003-4465-3217 NR 283 TC 5 Z9 5 U1 0 U2 2 PU CAMBRIDGE UNIV PRESS PI CAMBRIDGE PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND BN 978-0-521-87519-6 PY 2009 BP 201 EP 224 D2 10.1017/CBO9780511596582 PG 24 WC Hematology SC Hematology GA BDM69 UT WOS:000313875700016 ER PT B AU Cheng, WH Ahn, B Bohr, VA AF Cheng, Wen-Hsing Ahn, Byungchan Bohr, Vilhelm A. BE Khanna, KK Shiloh, Y TI Linking Human RecQ Helicases to DNA Damage Response and Aging SO DNA DAMAGE RESPONSE: IMPLICATIONS ON CANCER FORMATION AND TREATMENT LA English DT Article; Book Chapter DE Aging; RecQ; Helicase; DNA damage response ID DOUBLE-STRAND BREAKS; WERNER-SYNDROME PROTEIN; ROTHMUND-THOMSON-SYNDROME; BLOOMS-SYNDROME HELICASE; ATR-DEPENDENT PHOSPHORYLATION; REPLICATION FORK PROGRESSION; MAINTAINS GENOMIC STABILITY; EARLY EMBRYONIC LETHALITY; S-PHASE ARREST; SYNDROME GENE AB Maintenance of genome integrity is crucial for the survival of an organism, Increasing evidence suggests that defective DNA damage response promotes genome instability and accelerates age-related degeneration. The RecQ family of DNA helicases plays important roles in DNA replication and the DNA damage response. There are five human RecQ helicases, amongst which mutations in BLM, WRN, and RECQ4 have been linked to human diseases displaying symptoms of accelerated aging to various degrees. Recent studies have provided new insights into the mechanisms that control early stages of the DNA damage response, and shed light on common roles of the RecQ helicases in DNA replication and the DNA damage response. Here, we review the evidence for defective DNA damage response being a feature linking mutations in RecQ helicases to premature aging diseases. Data are accumulating to suggest that RecQ helicases impart signaling and repair functions in the response to DNA damage. C1 [Cheng, Wen-Hsing] Univ Maryland, Dept Nutr & Food Sci, College Pk, MD 20742 USA. [Ahn, Byungchan] Univ Ulsan, Dept Life Sci, Ulsan 680749, South Korea. [Bohr, Vilhelm A.] NIA, Lab Mol Gerontol, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA. RP Cheng, WH (reprint author), Univ Maryland, Dept Nutr & Food Sci, College Pk, MD 20742 USA. EM whcheng@umd.edu; bbccahn@mail.ulsan.ac.kr; vbohr@nih.gov NR 115 TC 0 Z9 0 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES BN 978-90-481-2560-9 PY 2009 BP 331 EP 347 DI 10.1007/978-90-481-2561-6_15 D2 10.1007/978-90-481-2561-6 PG 17 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA BNA54 UT WOS:000274026400015 ER PT S AU Clark, DJ Leblanc, B AF Clark, David J. Leblanc, Benoit BE Moss, T LeBlanc, B TI Analysis of DNA Supercoiling Induced by DNA-Protein Interactions SO DNA-PROTEIN INTERACTIONS: PRINCIPLES AND PROTOCOLS, THIRD EDITION SE Methods in Molecular Biology LA English DT Article; Book Chapter DE DNA-protein interaction; Supercoiling; Topology; Chloroquine AB Certain DNA-interacting proteins induce a pronounced bending in the double helix and cause topological stresses that a-re compensated by the formation of supercoils in DNA. Such supercoils, when forming on a circular plasmid, give rise to a series of topoisomers that run at different speeds during electrophoresis. The number of supercoils introduced in the plasmid can provide information on the protein; it can for example help determine the number of nucleosomes that are assembled on the plasmid or indicate whether the DNA-bending activity of a transcription factor is important enough to cause a topological stress. Because a DNA-protein activity can lead to either an overwinding or an underwinding of the helix, supercoiling can occur in either direction. Determining whether a plasmid contains positively or negatively supercoiled DNA is possible, thanks to an agarose get containing an intercalating agent known to positively supercoil DNA, such as chloroquine. The speed of migration of the topoisomers varies in a characteristic way in the presence and absence of the agent. Topoisomer standards can furthermore be generated to allow the easy evaluation of the number of supercoils induced in a plasmid by a DNA-protein interaction. C1 [Clark, David J.] NICHHD, NIH, Bethesda, MD 20892 USA. [Leblanc, Benoit] Univ Sherbrooke, Fac Sci, Dept Biol, Sherbrooke, PQ J1K 2R1, Canada. RP Clark, DJ (reprint author), NICHHD, NIH, Bethesda, MD 20892 USA. NR 8 TC 11 Z9 11 U1 1 U2 3 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA SN 1064-3745 BN 978-1-60327-014-4 J9 METHODS MOL BIOL JI Methods Mol. Biol. PY 2009 VL 543 BP 523 EP 535 DI 10.1007/978-1-60327-015-1_30 D2 10.1007/978-1-60327-015-1 PG 13 WC Biochemical Research Methods SC Biochemistry & Molecular Biology GA BKK40 UT WOS:000268378400030 PM 19378184 ER PT S AU Zwieb, C Adhya, S AF Zwieb, Christian Adhya, Sankar BE Moss, T LeBlanc, B TI Plasmid Vectors for the Analysis of Protein-Induced DNA Bending SO DNA-PROTEIN INTERACTIONS: PRINCIPLES AND PROTOCOLS, THIRD EDITION SE Methods in Molecular Biology LA English DT Article; Book Chapter DE DNA bending; Protein-DNA complexes; Replication; Recombination; Transcription ID REGULATORY PROTEINS; COMPLEXES AB Bending is not only required to accommodate DNA within the cell but also is a mechanism used by proteins to initiate DNA replication, transcription, and recombination. Determining the angles by which regulatory DNA segments deviate from linearity upon binding of proteins is a necessary step toward a better understanding of a large number of essential biological functions. The pBend plasmids contain duplicate sets of restriction sites and, when combined with "gel shift" experiments, allow the straightforward determination of the bending angle in a DNA molecule. The steps for successfully carrying Out a binding/bending experiment are described. They include the cloning of the protein-binding site into the chosen pBend vector, the isolation of a series of DNA fragments with identical in length but variable placing of the protein-binding site, and the gel electrophoretic analysis of the free and protein-bound fragments. C1 [Zwieb, Christian] Univ Texas Hlth Sci Ctr Tyler, Dept Mol Biol, Tyler, TX USA. [Adhya, Sankar] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. RP Zwieb, C (reprint author), Univ Texas Hlth Sci Ctr Tyler, Dept Mol Biol, Tyler, TX USA. NR 8 TC 5 Z9 5 U1 0 U2 4 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA SN 1064-3745 BN 978-1-60327-014-4 J9 METHODS MOL BIOL JI Methods Mol. Biol. PY 2009 VL 543 BP 547 EP 562 DI 10.1007/978-1-60327-015-1_32 D2 10.1007/978-1-60327-015-1 PG 16 WC Biochemical Research Methods SC Biochemistry & Molecular Biology GA BKK40 UT WOS:000268378400032 PM 19378186 ER PT J AU Khan, SG Oh, KS Emmert, S Imoto, K Tamura, D DiGiovanna, JJ Shahlavi, T Armstrong, N Baker, CC Neuburg, M Zalewski, C Brewer, C Wiggs, E Schiffmann, R Kraemer, KH AF Khan, Sikandar G. Oh, Kyu-Seon Emmert, Steffen Imoto, Kyoko Tamura, Deborah DiGiovanna, John J. Shahlavi, Tala Armstrong, Najealicka Baker, Carl C. Neuburg, Marcy Zalewski, Chris Brewer, Carmen Wiggs, Edythe Schiffmann, Raphael Kraemer, Kenneth H. TI XPC initiation codon mutation in xeroderma pigmentosum patients with and without neurological symptoms SO DNA REPAIR LA English DT Article DE DNA repair; Molecular genetics; Sensorineural hearing loss; Skin cancer; Xeroderma pigmentosum ID DNA-REPAIR GENE; CYCLOBUTANE PYRIMIDINE DIMERS; MESSENGER-RNA LEVELS; GROUP-C; COCKAYNE-SYNDROME; TRICHOTHIODYSTROPHY FIBROBLASTS; ULTRAVIOLET-RADIATION; IN-VIVO; CELL; DAMAGE AB Two unrelated xeroderma pigmentosum (XP) patients, with and without neurological abnormalities, respectively, had identical defects in the XPC DNA nucleotide excision repair (NER) gene. Patient XP21BE, a 27-year-old woman, had developmental delay and early onset of sensorineural hearing loss. In contrast, patient XP329BE, a 13-year-old boy, had a normal neurological examination. Both patients had marked lentiginous hyperpigmentation and multiple skin cancers at an early age. Their cultured fibroblasts showed similar hypersensitivity to killing by UV and reduced repair of DNA photoproducts. Cells from both patients had a homozygous c.2T>G mutation in the XPC gene which changed the ATG initiation codon to arginine (AGG). Both had low levels of XPC message and no detectable XPC protein on Western blotting. There was no functional XPC activity in both as revealed by the failure of localization of XPC and other NER proteins at the sites of UV-induced DNA damage in a sensitive in vivo immunofluorescence assay. XPC cDNA containing the initiation codon mutation was functionally inactive in a post-UV host cell reactivation (HCR) assay. Microsatellite markers flanking the XPC gene showed only a small region of identity (similar to 30 kBP), indicating that the patients were not closely related. Thus, the initiation codon mutation resulted in DNA repair deficiency in cells from both patients and greatly increased cancer susceptibility. The neurological abnormalities in patient XP21BE may be related to close consanguinity and simultaneous inheritance of other recessive genes or other gene modifying effects rather than the influence of XPC gene itself. Published by Elsevier B.V. C1 [Kraemer, Kenneth H.] NCI, Basic Res Lab, CCR, DNA Repair Sect,NIH, Bethesda, MD 20892 USA. [Baker, Carl C.] NCI, Lab Clin Oncol, NIH, Bethesda, MD 20892 USA. [DiGiovanna, John J.] Brown Univ, Dept Dermatol, Div Dermatopharmacol, Warren Alpert Med Sch, Providence, RI 02912 USA. [Neuburg, Marcy] Med Coll Wisconsin, Dept Dermatol, Milwaukee, WI 53226 USA. [Zalewski, Chris; Brewer, Carmen] Natl Inst Deafness & Other Commun Disorders, Otolaryngol Branch, NIH, Bethesda, MD USA. [Wiggs, Edythe; Schiffmann, Raphael] NINDS, Dev & Metab Neurol Branch, NIH, Bethesda, MD 20892 USA. RP Kraemer, KH (reprint author), NCI, Basic Res Lab, CCR, DNA Repair Sect,NIH, Bldg 37,Room 4002,MSC 4258, Bethesda, MD 20892 USA. EM kraemerk@nih.gov FU NIH; National Cancer Institute; Center for Cancer Research; Deutsche Forschungsgemeinschaft [EM 63/1-1] FX This research was supported by the Intramural Research Program of the NIH, National Cancer Institute, Center for Cancer Research. We are grateful to the patients and their families for their cooperation in this research. S.E. was supported in part by a grant from the Deutsche Forschungsgemeinschaft DFG (EM 63/1-1). NR 47 TC 24 Z9 25 U1 2 U2 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1568-7864 J9 DNA REPAIR JI DNA Repair PD JAN 1 PY 2009 VL 8 IS 1 BP 114 EP 125 DI 10.1016/j.dnarep.2008.09.007 PG 12 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA 388YX UT WOS:000262057500012 PM 18955168 ER PT S AU Hallett, M AF Hallett, Mark BE Murphy, N Ellis, GFR OConnor, T TI Physiology of Volition SO DOWNWARD CAUSATION AND THE NEUROBIOLOGY OF FREE WILL SE Understanding Complex Systems Springer Complexity LA English DT Article; Book Chapter DE free will; volition; agency; corollary discharge; frontal lobe; parietal lobe; premotor cortex; motor cortex ID POSITRON-EMISSION-TOMOGRAPHY; EXTERNALLY TRIGGERED MOVEMENTS; VOLUNTARY ACTION; CONSCIOUS-WILL; CORTICAL POTENTIALS; PREFRONTAL CORTEX; AWARENESS; BRAIN; INTENTION; ATTENTION AB The idea of free will is a conscious awareness of the brain concerning the nature of the movement that it produces. There is no evidence for it to be a driving force in movement generation. This review considers the physiology of movement generation and how the concepts of willing and agency might arise. Both the anatomical substrates and the timing of events are considered. Movement initiation and volition are not necessarily linked, and one line of evidence comes from consideration of patients with disorders of volition. Movement is generated subconsciously, and the conscious sense of willing the movement comes later, but the exact time of this event is difficult to assess because of the potentially illusory nature of introspection. The evidence suggests that movement is initiated in frontal lobe, particularly the mesial areas, and the sense of volition arises as the result of a corollary discharge from premotor and motor areas likely involving the parietal lobe. Agency probably involves a similar region in the parietal lobe and requires both the sense of volition and movement feedback. C1 NINDS, Human Motor Control Sect, NIH, Bethesda, MD 20892 USA. RP Hallett, M (reprint author), NINDS, Human Motor Control Sect, NIH, Bldg 10,Room 7D37,10 Ctr Dr MSC 1428, Bethesda, MD 20892 USA. EM hallettm@ninds.nih.gov NR 61 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 1860-0832 BN 978-3-642-03204-2 J9 UNDERST COMPLEX SYST PY 2009 BP 127 EP 143 DI 10.1007/978-3-642-03205-9_7 D2 10.1007/978-3-642-03205-9 PG 17 WC Neurosciences SC Neurosciences & Neurology GA BLT08 UT WOS:000270968300007 ER PT J AU Madras, BK Compton, WA Avula, D Stegbauer, T Stein, JB Clark, HW AF Madras, Bertha K. Compton, Wilson A. Avula, Deepa Stegbauer, Tom Stein, Jack B. Clark, H. Westley TI Screening, brief interventions, referral to treatment (SBIRT) for illicit drug and alcohol use at multiple healthcare sites: Comparison at intake and 6 months later SO DRUG AND ALCOHOL DEPENDENCE LA English DT Article DE Services; Treatment; Prescription drug abuse; Preventive medicine; Marijuana; Cocaine; Heroin; Methamphetamine; CPT (R) codes; Primary health care; Trauma centers ID NATIONAL EPIDEMIOLOGIC SURVEY; BRIEF MOTIVATIONAL INTERVENTION; RANDOMIZED CONTROLLED TRIAL; BRIEF PHYSICIAN ADVICE; UNITED-STATES; TRAUMA CENTER; PRESCRIPTION DRUGS; METHAMPHETAMINE USE; CLINICAL-TRIALS; SUBSTANCE USE AB Objectives: Alcohol screening and brief interventions in medical settings can significantly reduce alcohol use. Corresponding data for illicit drug use is sparse. A Federally funded screening, brief interventions. referral to treatment (SBIRT) service program, the largest of its kind to date, was initiated by the Substance Abuse and Mental Health Services Administration (SAMHSA) in a wide variety of medical settings. We compared illicit drug use at intake and 6 months after drug screening and interventions were administered. Design: SBIRT services were implemented in a range of medical settings across six states. A diverse patient population (Alaska Natives, American Indians, African-Americans. Caucasians, Hispanics), was screened and offered score-based progressive levels of intervention (brief intervention, brief treatment, referral to specialty treatment). In this secondary analysis of the SBIRT service program, drug use data was compared at intake and at a 6-month follow-up, in a sample of a randomly selected population (10%) that screened positive at baseline. Results: Of 459,599 patients screened, 22.7% screened positive for a spectrum of use (risky/problematic, abuse/addiction). The majority were recommended for a brief intervention (15.9%), with a smaller percentage recommended for brief treatment (3.2%) or referral to specialty treatment (3.7%). Among those reporting baseline illicit drug use, rates of drug use at 6-month follow-up (4 of 6 sites), were 67.7% lower (p < 0.001) and heavy alcohol use was 38.6% lower (p < 0.001), with comparable findings across sites, gender, race/ethnic, age subgroups. Among persons recommended for brief treatment or referral to specialty treatment, self-reported improvements in general health (p < 0.001), mental health (p < 0.001), employment (p < 0.001), housing status (p < 0.001), and criminal behavior (P < 0.001) were found. Conclusions: SBIRT was feasible to implement and the self-reported patient status at 6 months indicated significant improvements over baseline, for illicit drug use and heavy alcohol use, with functional domains improved, across a range of health care settings and a range of patients. Published by Elsevier Ireland Ltd. C1 [Madras, Bertha K.] Harvard Univ, Sch Med, NEPRC, Southborough, MA 01772 USA. [Compton, Wilson A.] NIDA, Div Epidemiol Serv & Prevent Res, NIH, Dept Hlth & Human Serv,Neurosci Ctr, Bethesda, MD 20892 USA. [Avula, Deepa; Stegbauer, Tom; Stein, Jack B.; Clark, H. Westley] Subst Abuse & Mental Hlth Serv Adm, Dept Hlth & Human Serv, Rockville, MD 20857 USA. RP Madras, BK (reprint author), Harvard Univ, Sch Med, NEPRC, 1 Pine Hill Dr, Southborough, MA 01772 USA. EM bertha_madras@hms.harvard.edu FU NIDA NIH HHS [K05 DA015305, K05 DA015305-05] NR 82 TC 273 Z9 275 U1 9 U2 74 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0376-8716 EI 1879-0046 J9 DRUG ALCOHOL DEPEN JI Drug Alcohol Depend. PD JAN 1 PY 2009 VL 99 IS 1-3 BP 280 EP 295 DI 10.1016/j.drugalcdep.2008.08.003 PG 16 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA 397ZH UT WOS:000262700500031 PM 18929451 ER PT J AU Vahabzadeh, M Lin, JL Mezghanni, M Epstein, DH Preston, KL AF Vahabzadeh, Massoud Lin, Jia-Ling Mezghanni, Mustapha Epstein, David H. Preston, Kenzie L. TI Automation in an addiction treatment research clinic: Computerised contingency management, ecological momentary assessment and a protocol workflow system SO DRUG AND ALCOHOL REVIEW LA English DT Article DE clinical decision support system; contingency management; ecological momentary assessment; protocol workflow; substance abuse treatment ID PROVIDER ORDER ENTRY; IMPLEMENTATION; INTEGRATION; INFORMATION; CHALLENGES; EXPERIENCE; ABSTINENCE; COCAINE AB Introduction and Aims. A challenge in treatment research is the necessity of adhering to protocol and regulatory strictures while maintaining flexibility to meet patients' treatment needs and to accommodate variations among protocols. Another challenge is the acquisition of large amounts of data in an occasionally hectic environment, along with the provision of seamless methods for exporting, mining and querying the data. Design and Methods. We have automated several major functions of our outpatient treatment research clinic for studies in drug abuse and dependence. Here we describe three such specialised applications: the Automated Contingency Management (ACM) system for the delivery of behavioural interventions, the transactional electronic diary (TED) system for the management of behavioural assessments and the Protocol Workflow System (PWS) for computerised workflow automation and guidance of each participant's daily clinic activities. These modules are integrated into our larger information system to enable data sharing in real time among authorised staff. Results. ACM and the TED have each permitted us to conduct research that was not previously possible. In addition, the time to data analysis at the end of each study is substantially shorter. With the implementation of the PWS, we have been able to manage a research clinic with an 80 patient capacity, having an annual average of 18 000 patient visits and 7300 urine collections with a research staff of five. Finally, automated data management has considerably enhanced our ability to monitor and summarise participant safety data for research oversight. Discussion and Conclusions. When developed in consultation with end users, automation in treatment research clinics can enable more efficient operations, better communication among staff and expansions in research methods. [Vahabzadeh M, Lin J-L, Mezghanni M, Epstein DH, Preston KL. Automation in an addiction treatment research clinic: Computerised contingency management, ecological momentary assessment and a protocol workflow system. Drug Alcohol Rev 2009; 28: 3-11] C1 [Vahabzadeh, Massoud; Lin, Jia-Ling] NIDA, Biomed Informat Sect, Adm Management Branch, IRP,NIH,DHHS, Baltimore, MD 21224 USA. [Mezghanni, Mustapha] Johns Hopkins Bayview Med Ctr, Baltimore, MD USA. [Epstein, David H.; Preston, Kenzie L.] NIDA, Treatment Sect, Clin Pharmacol & Therapeut Branch, IRP,NIH,DHHS, Baltimore, MD 21224 USA. RP Vahabzadeh, M (reprint author), NIDA, Biomed Informat Sect, Adm Management Branch, IRP,NIH,DHHS, 251 Bayview Blvd,Suite 200,Room 02A242, Baltimore, MD 21224 USA. EM massoudv@nih.gov RI Preston, Kenzie/J-5830-2013 OI Preston, Kenzie/0000-0003-0603-2479 FU Intramural NIH HHS [Z01 DA000175-13, Z01 DA000499-01, Z01 DA000500-01, Z99 DA999999] NR 26 TC 6 Z9 6 U1 1 U2 6 PU WILEY-BLACKWELL PUBLISHING, INC PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0959-5236 J9 DRUG ALCOHOL REV JI Drug Alcohol Rev. PD JAN PY 2009 VL 28 IS 1 BP 3 EP 11 DI 10.1111/j.1465-3362.2008.00007.x PG 9 WC Substance Abuse SC Substance Abuse GA 412WH UT WOS:000263754400002 PM 19320669 ER PT J AU Auttachoat, W Germolec, DR Collins, BJ Luebke, RW White, KL Guo, TL AF Auttachoat, Wimolnut Germolec, Dori R. Collins, Bradley J. Luebke, Robert W. White, Kimber L., Jr. Guo, Tai L. TI Immunotoxicological profile of chloroform in female B6C3F1 mice when administered in drinking water SO DRUG AND CHEMICAL TOXICOLOGY LA English DT Article DE Chloroform; Immunotoxicity; Disinfection by-products ID MALE OSBORNE-MENDEL; MALE F344 RATS; CELL-PROLIFERATION; CORN-OIL; LISTERIA-MONOCYTOGENES; ORGANIC-COMPOUNDS; IMMUNE-RESPONSE; NASAL PASSAGES; AD-LIBITUM; LIVER AB Chloroform can be formed as a disinfection by-product during water chlorination, one of the primary modalities for purifying municipal water supplies for human consumption. The aim of this study was to characterize the immunotoxic effects of chloroform in female B6C3F1 mice when exposure occurred via the drinking water. Consistent with human exposure, female B6C3F1 mice were exposed to chloroform-containing drinking water at 2.5, 10, 25, 100, and 250 ppm for 28 days. The examined endpoints included the effects of chloroform on body and organ weights, water consumption, hematology, innate immunity, humoral immunity, and cell-mediated immunity. The functions of natural killer, B-, and T-cells were not altered by chloroform in drinking water at the concentrations tested, except that an increase in splenocyte basal proliferation was observed at chloroform levels of 100 and 250 ppm. Following chloroform administration, there was a decreased number of circulating neutrophils in the blood in all treatment groups, but neutrophil function in lung homogenates, as evaluated using an assay for myeloperoxidase activity following lipopolysaccharide and N-Formyl-Met-Leu-Phe stimulation, was not compromised. Further, the results of host resistance to Listeria monocytogenes infection also suggested that neutrophil function was normal. At the highest treatment level of chloroform (250 ppm), erythrocyte number and hemoglobin levels were significantly decreased. Some significant changes were also observed for body weights, water consumption, and organ weights; however, most of these effects were only observed at the highest treatment level of chloroform (250 ppm). Taken together, the results demonstrate that while chloroform administered via the drinking water affects body weight and selected hematological parameters at high dose levels, overall immune responses, as measured in several tests for immune function, are not compromised. C1 [Auttachoat, Wimolnut; White, Kimber L., Jr.; Guo, Tai L.] Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, Richmond, VA 23298 USA. [Germolec, Dori R.; Collins, Bradley J.] NIEHS, Res Triangle Pk, NC 27709 USA. [Luebke, Robert W.] US EPA, Immunotoxicol Branch, Expt Toxicol Div, NHEERL, Res Triangle Pk, NC 27711 USA. RP Guo, TL (reprint author), Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, POB 980613, Richmond, VA 23298 USA. EM tlguo@vcu.edu FU EPA [DW75937992]; NIEHS [ES55094] FX This work was supported, in part, by EPA Interagency Agreement DW75937992 and the Division of Intramural Research at the NIEHS through Contract ES55094. The authors would like to thank D.L. Musgrove and R.D. Brown for their technical help, and M.J. Smith for proofreading. NR 47 TC 8 Z9 8 U1 0 U2 1 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0148-0545 J9 DRUG CHEM TOXICOL JI Drug Chem. Toxicol. PD JAN PY 2009 VL 32 IS 1 BP 77 EP 87 DI 10.1080/01480540802433880 PG 11 WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy; Toxicology SC Chemistry; Pharmacology & Pharmacy; Toxicology GA 453DM UT WOS:000266590400011 PM 19514942 ER PT J AU Lorenzi, PL Weinstein, JN AF Lorenzi, Philip L. Weinstein, John N. TI ASPARAGINE SYNTHETASE: A NEW POTENTIAL BIOMARKER IN OVARIAN CANCER SO DRUG NEWS & PERSPECTIVES LA English DT Article ID GENE-EXPRESSION; PREDICTIVE BIOMARKER; GLUTAMINE DEPLETION; DRUG SCREEN; CELL-LINES; PROTEIN; DNA; PHOSPHORYLATION; CHEMOTHERAPY; DEPRIVATION AB L-Asparaginase (L-ASP) is an enzyme drug that has been an asset to leukemia treatment regimens for four decades. Variability in its clinical efficacy, however, has prompted the search for biomarkers capable of distinguishing responders from non-responders. In that regard, the NCI-60 cell line panel has served as a biomarker discovery platform and has led to the identification of a correlation between L-ASP efficacy and asparagine synthetase (ASNS) expression in cultured cells. The presence of that correlation in the ovarian subpanel of the NCI-60 has made a case for repositioning L-ASP to ovarian cancer. This review presents an overview of the biomarker development process, summarizes the efforts that have been invested thus far in developing ASNS as a biomarker for ovarian cancer treatment, highlights the role of RNAi and the limitations of the NCI-60 in that process, and addresses important considerations for next steps in the development of ASNS as a predictive biomarker. C1 [Lorenzi, Philip L.] NCI, Genom & Bioinformat Grp, Mol Pharmacol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA. [Weinstein, John N.] Univ Texas MD Anderson Canc Ctr, Dept Bioinformat & Computat Biol, Houston, TX 77030 USA. RP Lorenzi, PL (reprint author), NCI, Genom & Bioinformat Grp, Mol Pharmacol Lab, Ctr Canc Res,NIH, 37 Convent Dr, Bethesda, MD 20892 USA. EM lorenzip@mail.nih.gov FU NIGMS; NIH; National Cancer Institute, Center for Cancer Research FX We are grateful to our NIH collaborators Natasha Caplen, Elise Kohn, Michael Birrer, Bill Reinhold, Sudhir Varma, Jenny Llamas, Scott Martin, Paul Goldsmith, Michele Gunsior, Yves Pommier, Mark Raffeld, Laurent Ozbun, Amy Hutchinson and Stephen Chanock for their roles in making possible the work cited here and for valuable discussions. We also thank Daniel Von Hoff (TGen), Ivan Horak (Enzon Pharmaceuticals) and Aby Buchbinder (Enzon Pharmaceuticals) for valuable discussions. PLL is supported by a Pharmacology Research Associate Fellowship from NIGMS, NIH and by the Intramural Research Program of the NIH, National Cancer Institute, Center for Cancer Research. The authors declare ownership interest in an NIH patent based on previously published work. NR 37 TC 13 Z9 15 U1 1 U2 3 PU PROUS SCIENCE, SA PI BARCELONA PA PO BOX 540, PROVENZA 388, 08025 BARCELONA, SPAIN SN 0214-0934 J9 DRUG NEWS PERSPECT JI Drug News Perspect. PD JAN-FEB PY 2009 VL 22 IS 1 BP 61 EP 64 DI 10.1358/dnp.2009.22.1.1303820 PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 414EX UT WOS:000263847800007 PM 19209300 ER PT B AU Gergely, S To, KKW Polgar, O Robey, RW Bates, SE AF Gergely Szakacs To, Kenneth Kin Wah Polgar, Orsolya Robey, Robert W. Bates, Susan E. BE Mehta, K Siddik, ZH TI Multidrug Resistance Mediated by MDR-ABC Transporters SO DRUG RESISTANCE IN CANCER CELLS LA English DT Article; Book Chapter DE ABC transporter; P-glycoprotein; ABCG2; Drug resistance; Drug transporters ID ACUTE MYELOID-LEUKEMIA; SOUTHWEST-ONCOLOGY-GROUP; EXPRESSING P-GLYCOPROTEIN; BREAST-CANCER CELLS; BCRP MESSENGER-RNA; DRUG EFFLUX PUMP; PHASE-III; PROMOTER REGION; GENE-EXPRESSION; PROTEIN MRP1 AB Cancer cells are constantly being selected for survival and proliferation. During this process, tumor cells often co-opt basic physiological mechanisms to protect themselves from toxic chemotherapy. Of these mechanisms, the one that is most commonly encountered in laboratory studies is the increased cellular efflux of a broad class of cytotoxic drugs that is mediated by a family of energy-dependent transporters, known as ATP-binding cassette (ABC) proteins. Although 48 human ABC transporters have been described, only a handful are likely to be involved in drug resistance. These include P-glycoprotein (Pgp), the multidrug resistance associated protein (MRP), and the breast cancer resistance protein (BCRP), also termed ABCG2. In this chapter, we will provide an overview of the general structural and mechanistic features of the human ABC transporters thought to be involved in multidrug resistance in cancer cells. These transporters call no longer be understood only as candidate drug targets for overcoming multidrug resistance. Rather, these transporters are involved in multiple normal tissues in protection from drugs and xenobiotics. These include the blood brain barrier, oral bioavailability of drugs and xenobiotics through expression of transporters in the GI tract, drug disposition, and fetal protection through expression at the maternal-fetal barrier. We describe emerging information related to their potential role in drug and xenobiotic resistance and argue that studies of this drug resistance mechanism Should continue ill the laboratory and in the clinic. C1 [To, Kenneth Kin Wah; Polgar, Orsolya; Robey, Robert W.; Bates, Susan E.] NCI, NIH, Bethesda, MD 20892 USA. [Bates, Susan E.] Med Oncol Branch, Bethesda, MD 20892 USA. [Gergely Szakacs] Hungarian Acad Sci, Inst Enzymol, H-1113 Budapest, Hungary. RP Bates, SE (reprint author), Med Oncol Branch, Bldg 10 Rm 12N226,9000 Rockville Pike, Bethesda, MD 20892 USA. EM sebates@helix.nih.gov RI To, Kenneth /M-4500-2013 OI To, Kenneth /0000-0003-2755-0283 NR 109 TC 0 Z9 0 U1 4 U2 7 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES BN 978-0-387-89444-7 PY 2009 BP 1 EP 20 DI 10.1007/978-0-387-89445-4_1 D2 10.1007/978-0-387-89445-4 PG 20 WC Oncology; Cell Biology; Pharmacology & Pharmacy SC Oncology; Cell Biology; Pharmacology & Pharmacy GA BKK61 UT WOS:000268390000001 ER PT J AU Fontana, RJ Watkins, PB Bonkovsky, HL Chalasani, N Davern, T Serrano, J Rochon, J AF Fontana, Robert J. Watkins, Paul B. Bonkovsky, Herbert L. Chalasani, Naga Davern, Timothy Serrano, Jose Rochon, James CA DILIN Study Grp TI Drug-Induced Liver Injury Network (DILIN) Prospective Study Rationale, Design and Conduct SO DRUG SAFETY LA English DT Article ID UNITED-STATES; CAUSALITY ASSESSMENT; RHEUMATOID-ARTHRITIS; HEPATITIS-B; HEPATOTOXICITY; DISEASE; SURVEILLANCE; ASSOCIATION; FAILURE; RELIABILITY AB Background: Drug-induced liver injury (DILI) is an uncommon adverse drug reaction of increasing importance to the medical community, pharmaceutical industry, regulatory agencies and the general public. Objectives: The Drug-Induced Liver Injury Network (DILIN) was established to advance understanding and research into DILI by initiating a prospective registry of patients with bona fide DILI for future studies of host clinical, genetic, environmental and immunological risk factors. The DILIN was also charged with developing standardized nomenclature, terminology and causality assessment instruments. Methods: Five clinical sites, a data coordinating centre and senior scientists from the National Institute of Diabetes and Digestive and Kidney Diseases initiated the DILIN prospective study in September 2004. Eligible patients are required to meet minimal laboratory or histological criteria within 6 months of DILI onset and have other competing causes of liver injury excluded. Patients in the general community setting with pre-existing HIV, hepatitis B virus or hepatitis C virus infections and/or abnormal baseline liver biochemistries are eligible for enrolment. In addition, subjects with liver injury due to herbal products are eligible to participate. Control patients without DILI are also to be recruited in the future. Results: All referred subjects undergo an extensive review of available laboratory, pathology and imaging studies. Subjects who meet pre-defined eligibility criteria at the 6-month study visit are followed for 2 years to better define the natural history of chronic DILI. Causality assessment is determined by a panel of three hepatologists who independently assign a causality score ranging from 1 (definite) to 5 (unlikely) as well as a severity score ranging from 1 (mild) to 5 (fatal). During the first 3 years, 367 subjects were enrolled into the DILIN prospective study. Conclusion: DILIN is a multicentre research network charged with improving our understanding of the aetiologies, risk factors and outcomes of DILI in the US. The network is meeting the targeted enrolment of ten patients per month and is developing a repository of clinical data and biological samples for future studies of DILI pathogenesis and outcome. C1 [Fontana, Robert J.] Univ Michigan, Sch Med, Dept Internal Med, Ann Arbor, MI USA. [Watkins, Paul B.] Univ N Carolina, Dept Internal Med, Chapel Hill, NC USA. [Bonkovsky, Herbert L.] Ctr Liver & Digest Dis, Dept Internal Med, Charlotte, NC USA. [Bonkovsky, Herbert L.] Carolinas Med Ctr, Dept Med, Charlotte, NC 28203 USA. [Bonkovsky, Herbert L.] Carolinas Med Ctr, Cannon Res Ctr, Charlotte, NC 28203 USA. [Bonkovsky, Herbert L.] Univ Connecticut, Ctr Hlth, Dept Med, Farmington, CT USA. [Bonkovsky, Herbert L.] Univ N Carolina, Dept Med, Chapel Hill, NC USA. [Chalasani, Naga] Indiana Univ, Dept Internal Med, Indianapolis, IN 46204 USA. [Davern, Timothy] Univ Calif San Francisco, Dept Internal Med, San Francisco, CA 94143 USA. [Serrano, Jose] NIDDK, Liver Dis Res Branch, NIH, Bethesda, MD USA. [Rochon, James] Duke Clin Res Inst, Durham, NC USA. RP Fontana, RJ (reprint author), 3912 Taubman Ctr, Ann Arbor, MI 48109 USA. EM rfontana@med.umich.edu FU NIDDK NIH HHS [1U01DK065193, 1U01DK065176, 1U01DK065184, 1U01DK065201, 1U01DK065211, 1U01DK065238, U01 DK065176, U01 DK065184, U01 DK065193, U01 DK065201, U01 DK065211, U01 DK065238] NR 47 TC 141 Z9 147 U1 1 U2 8 PU ADIS INT LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 1311, NEW ZEALAND SN 0114-5916 J9 DRUG SAFETY JI Drug Saf. PY 2009 VL 32 IS 1 BP 55 EP 68 PG 14 WC Public, Environmental & Occupational Health; Pharmacology & Pharmacy; Toxicology SC Public, Environmental & Occupational Health; Pharmacology & Pharmacy; Toxicology GA 406VF UT WOS:000263322300005 PM 19132805 ER PT J AU Tosh, DK Jacobson, KA Jeong, LS AF Tosh, D. K. Jacobson, K. A. Jeong, L. S. TI NUCLEOSIDE-BASED ADENOSINE A(3) RECEPTOR ANTAGONISTS AS DRUG CANDIDATES SO DRUGS OF THE FUTURE LA English DT Review ID SELECTIVE ANTAGONISTS; HIGHLY POTENT; STRUCTURAL DETERMINANTS; A3 RECEPTORS; DERIVATIVES; LIGANDS; ACTIVATION; EFFICACY; AGONISTS; D-4'-THIOADENOSINE AB Purine nucleoside derivatives that are selective ligands for the A(3) adenosine receptor (AR) hove been structurally modified such that their ability to activate the receptor is lost while retaining high binding affinity This loss of efficacy in otherwise selectively binding nucleosides has been shown to result in antagonism of the effects of known agonists in functional assays Modification of the ribose moiety has been the most effective strategy to accomplish this aim Steric constraints have been introduced, as well as replacement of the various hydrogen bond-donating groups, to achieve a reduction in efficacy High selectivity has recently been achieved for such nucleoside-based A(3) AR antagonists Thus, it is now possible to compare nucleoside-based A(3) antagonists with well-characterized heterocyclic nonpurine antagonists as clinical candidates for the treatment of glaucoma, asthma and inflammation C1 [Tosh, D. K.; Jeong, L. S.] Ewha Womans Univ, Coll Pharm, Med Chem Lab, Seoul 120750, South Korea. [Tosh, D. K.; Jacobson, K. A.] NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA. RP Tosh, DK (reprint author), Ewha Womans Univ, Coll Pharm, Med Chem Lab, Seoul 120750, South Korea. RI Jacobson, Kenneth/A-1530-2009 OI Jacobson, Kenneth/0000-0001-8104-1493 FU Seoul R&BD program Korea [10541]; National Institutes of Health; Can-Fite Biopharma FX This work was supported by a grant from the Seoul R&BD program (10541) Korea and partial support from the NIDDK Intramural Research Program of the National Institutes of Health and Can-Fite Biopharma NR 33 TC 5 Z9 5 U1 0 U2 4 PU PROUS SCIENCE, SA-THOMSON REUTERS PI BARCELONA PA PO BOX 540, PROVENZA 388, 08025 BARCELONA, SPAIN SN 0377-8282 J9 DRUG FUTURE JI Drug Future PD JAN PY 2009 VL 34 IS 1 BP 43 EP 52 DI 10.1358/dof.2009.34.11286494 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 561MP UT WOS:000274981900006 ER PT B AU White, MJ AF White, Michael J. BE Collinson, M Adazu, K White, M Findley, S TI Migration and Demographic Surveillance: An Overview of Opportunities and Challenges SO DYNAMICS OF MIGRATION, HEALTH AND LIVELIHOODS: INDEPTH NETWORK PERSPECTIVES LA English DT Editorial Material; Book Chapter ID LABOR MIGRATION; UNITED-STATES; FERTILITY; REMITTANCES; MIGRANTS; RETURN; GHANA C1 [White, Michael J.] INDEPTH Network, Migrat & Urbanizat Working Grp, Sci Advisory Comm, Accra, Ghana. [White, Michael J.] Brown Univ, Providence, RI 02912 USA. [White, Michael J.] Brown, Providence, RI USA. [White, Michael J.] Princeton Univ, Princeton, NJ 08544 USA. [White, Michael J.] Urban Inst, Washington, DC 20037 USA. [White, Michael J.] Woodrow Wilson Int Ctr Scholars, Washington, DC USA. [White, Michael J.] Populat Assoc Amer, Washington, DC USA. [White, Michael J.] NICHD Populat Studies Comm, Bethesda, MD USA. [White, Michael J.] Assoc Populat Ctr, Berkeley, CA USA. RP White, MJ (reprint author), Populat Studies & Training Ctr, Providence, RI USA. NR 23 TC 2 Z9 2 U1 0 U2 0 PU ASHGATE PUBLISHING LTD PI ALDERSHOT PA GOWER HOUSE, CROFT ROAD, ALDERSHOT GU11 3HR, ENGLAND BN 978-0-7546-9726-8; 978-0-7546-7875-5 PY 2009 BP 3 EP 18 PG 16 WC Demography; Public, Environmental & Occupational Health SC Demography; Public, Environmental & Occupational Health GA BA3HG UT WOS:000334254900003 ER PT J AU Griffin, JA AF Griffin, James A. TI Professional Development and Preschool Intervention Research: I Would Rather Have a Talking Frog INTRODUCTION SO EARLY EDUCATION AND DEVELOPMENT LA English DT Editorial Material C1 Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, US Dept HHS, Bethesda, MD 20892 USA. RP Griffin, JA (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, US Dept HHS, Bethesda, MD 20892 USA. NR 9 TC 1 Z9 1 U1 0 U2 1 PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 1040-9289 J9 EARLY EDUC DEV JI Early Educ. Dev. PY 2009 VL 20 IS 3 BP 373 EP 376 DI 10.1080/10409280902967367 PG 4 WC Education & Educational Research; Psychology, Educational; Psychology, Developmental SC Education & Educational Research; Psychology GA 453PO UT WOS:000266623600001 ER PT B AU Newbold, R Heindel, JJ AF Newbold, Retha Heindel, Jerrold J. BE Newnham, JP Ross, MG TI Developmental Origins of Health and Disease: The Importance of Environmental Exposures SO EARLY LIFE ORIGINS OF HUMAN HEALTH AND DISEASE LA English DT Article; Book Chapter ID BISPHENOL-A; DIETHYLSTILBESTROL DES; PERINATAL EXPOSURE; MAMMARY-GLAND; IN-UTERO; OBESITY; ADENOCARCINOMA; ADIPOCYTES; HYPOTHESIS; ESTROGENS C1 [Heindel, Jerrold J.] NIEHS, Div Extramural Res & Training, Res Triangle Pk, NC 27709 USA. [Newbold, Retha] NIEHS, Dev Endocrinol & Endocrine Disruptor Sect, Mol Toxicol Lab, Div Intramural Res, Res Triangle Pk, NC 27709 USA. RP Heindel, JJ (reprint author), NIEHS, Div Extramural Res & Training, Mail Drop EC-23, Res Triangle Pk, NC 27709 USA. EM heindelj@niehs.nih.gov NR 37 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND BN 978-3-8055-9139-3 PY 2009 BP 42 EP 51 DI 10.1159/000221152 PG 10 WC Genetics & Heredity; Public, Environmental & Occupational Health; Pediatrics SC Genetics & Heredity; Public, Environmental & Occupational Health; Pediatrics GA BKY99 UT WOS:000269656800005 ER PT B AU Troisi, R Silva, ID Newbold, R AF Troisi, Rebecca Silva, Isabel dos Santos Newbold, Retha BE Newnham, JP Ross, MG TI Prenatal Risk Factors for Breast Cancer and Clues to the Underlying Biological Mechanisms from Animal and Human Studies SO EARLY LIFE ORIGINS OF HUMAN HEALTH AND DISEASE LA English DT Article; Book Chapter ID MAMMARY-GLAND; REPRODUCTIVE-TRACT; NEONATAL EXPOSURE; RECEPTOR LEVELS; IN-UTERO; DIETHYLSTILBESTROL; TUMORIGENESIS; HYPOTHESIS; GROWTH; ALTERS C1 [Troisi, Rebecca] NCI, Div Canc Epidemiol & Genet, NIH, US Dept HHS, Bethesda, MD 20892 USA. [Troisi, Rebecca] Dartmouth Coll, Hitchcock Med Ctr, Dartmouth Med Sch, Dept Community & Family Med, Hanover, NH 03756 USA. [Newbold, Retha] NIEHS, Dev Endocrinol & Endocrine Disruptor Sect, Mol Toxicol Lab, NIH,Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. [Silva, Isabel dos Santos] London Sch Hyg & Trop Med, Dept Epidemiol & Populat Hlth, London WC1, England. RP Troisi, R (reprint author), Dartmouth Hitchcock Med Ctr, Room 854,7297 Rubin Bldg,1 Med Ctr Dr, Lebanon, NH 03756 USA. EM troisir@mail.nih.gov NR 24 TC 1 Z9 1 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND BN 978-3-8055-9139-3 PY 2009 BP 184 EP 192 DI 10.1159/000221164 PG 9 WC Genetics & Heredity; Public, Environmental & Occupational Health; Pediatrics SC Genetics & Heredity; Public, Environmental & Occupational Health; Pediatrics GA BKY99 UT WOS:000269656800017 ER PT J AU Bermudez-Millan, A Hromi-Fiedler, A Damio, G Segura-Perez, S Perez-Escamilla, R AF Bermudez-Millan, Angela Hromi-Fiedler, Amber Damio, Grace Segura-Perez, Sofia Perez-Escamilla, Rafael TI Egg Contribution Towards the Diet of Pregnant Latinas SO ECOLOGY OF FOOD AND NUTRITION LA English DT Article DE egg; food intake; nutrients; Latinas; pregnancy; WIC program ID LOW-INCOME WOMEN; PHYSICAL-ACTIVITY; MEXICAN-AMERICAN; POSTPARTUM; KNOWLEDGE; HEALTH; FOODS; US AB Proper nutrition during gestation is important to prevent adverse pregnancy outcomes. Eggs contain many important nutrients necessary for fetal development and human survival. Three focus groups were conducted with Latina women living in Connecticut to identify cultural beliefs toward egg consumption during pregnancy, traditional egg dishes, and methods of preparation. A cross-sectional study was then carried out with a sample of predominately Puerto Rican pregnant Latinas (N = 241) to identify the frequency of consumption of eggs and egg-containing dishes as well as methods of preparation using a tailored food frequency questionnaire modified for this population. Paired sample t-tests were used to examine if there were differences in weekly mean egg intake patterns between the year prior to the pregnancy and during pregnancy based on a Food Frequency Questionnaire. Women were categorized into eggs consumers and non-consumers if they consumed or did not consume eggs during the previous day based on 24-hour recall data. Independent-sample t-test and chi-square cross-tabulation analyses were conducted to examine the association between egg consumption and nutrient intake categories. Results showed that eggs and egg-containing traditional dishes are consumed by Latinas before and during pregnancy. Egg consumers had higher intakes of protein, fat, vitamin K, vitamin E, selenium, beta carotene, lutein and zeaxanthin, cholesterol, total polyunsaturated fatty acids, and docosahexaenoic acid. Eggs contribute significantly to the diet of pregnant Latinas. C1 [Bermudez-Millan, Angela; Damio, Grace; Segura-Perez, Sofia] Hispan Hlth Council, Ctr Community Nutr, Connecticut NIH Export Ctr Excellence Eliminating, Hartford, CT 06106 USA. [Hromi-Fiedler, Amber; Perez-Escamilla, Rafael] Univ Connecticut, Dept Nutr Sci, Connecticut NIH Export Ctr Excellence Eliminating, Storrs, CT USA. RP Bermudez-Millan, A (reprint author), Hispan Hlth Council, Ctr Community Nutr, Connecticut NIH Export Ctr Excellence Eliminating, 175 Main St, Hartford, CT 06106 USA. EM angelabmillan@yahoo.com FU NIMHD NIH HHS [P20 MD001765-05, P20MD001765, P20 MD001765] NR 31 TC 1 Z9 1 U1 0 U2 4 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0367-0244 J9 ECOL FOOD NUTR JI Ecol. Food Nutr. PY 2009 VL 48 IS 5 BP 383 EP 403 DI 10.1080/03670240903170517 PG 21 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 548CY UT WOS:000273938400003 PM 21883065 ER PT J AU Deng, Y Golinelli-Cohen, MP Smirnova, E Jackson, CL AF Deng, Yi Golinelli-Cohen, Marie-Pierre Smirnova, Elena Jackson, Catherine L. TI A COPI coat subunit interacts directly with an early-Golgi localized Arf exchange factor SO EMBO REPORTS LA English DT Article DE guanine nucleotide exchange factor (GEF); COPI; ADP-ribosylation factor (Arf); small G protein; Golgi ID BREFELDIN-A; DISTINCT FUNCTIONS; APPENDAGE DOMAIN; PROTEIN COMPLEX; NUCLEOTIDE; GBF1; TRANSPORT; RECRUITMENT; MECHANISM; MEMBRANES AB Arf (ADP-ribosylation factor) family small G proteins are crucial regulators of intracellular transport. The active GTP-bound form of Arf interacts with a set of proteins-effectors-which mediate the downstream signalling events of Arf activation. A well-studied class of Arf1 effectors comprises the coat complexes, such as the cis-Golgi-localized COPI (coat protein complex I) coat, and trans-Golgi network-endosomal clathrin coats. At least five different coats require Arf1-GTP to localize to organelle membranes. How a single Arf protein recruits different coat complexes to distinct membrane sites raises the question of how specificity is achieved. Here, we propose a molecular mechanism of this specificity for the COPI coat by showing a direct and specific interaction between a COPI subunit and a cis-Golgi localized subfamily of Arf guanine nucleotide exchange factors (GEFs) that takes place independently of Arf1 activation. In this way, a specific output on Arf1 activation can be programmed before the exchange reaction by the GEF itself. C1 [Deng, Yi; Smirnova, Elena; Jackson, Catherine L.] NICHHD, Cell Biol & Metab Program, NIH, Bethesda, MD 20892 USA. [Golinelli-Cohen, Marie-Pierre; Jackson, Catherine L.] CNRS, Lab Enzymol & Biochim Struct, Gif Sur Yvette, France. RP Jackson, CL (reprint author), NICHHD, Cell Biol & Metab Program, NIH, 18 Lib Dr, Bethesda, MD 20892 USA. EM catherine.jackson@lebs.cnrs-gif.fr RI Jackson, Catherine/A-3421-2013; Golinelli, Marie-Pierre/K-4287-2013 OI Jackson, Catherine/0000-0002-0843-145X; Golinelli, Marie-Pierre/0000-0002-6738-8631 FU Intramural NIH HHS NR 21 TC 29 Z9 32 U1 0 U2 4 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1469-221X J9 EMBO REP JI EMBO Rep. PD JAN PY 2009 VL 10 IS 1 BP 58 EP 64 DI 10.1038/embor.2008.221 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 387ER UT WOS:000261935000013 PM 19039328 ER PT J AU Esona, MD Geyer, A Banyai, K Page, N Aminu, M Armah, GE Hull, J Steele, DA Glass, RI Gentsch, JR AF Esona, Mathew D. Geyer, Annelise Banyai, Krisztian Page, Nicola Aminu, Maryam Armah, George E. Hull, Jennifer Steele, Duncan A. Glass, Roger I. Gentsch, Jon R. TI Novel Human Rotavirus Genotype G5P[7] from Child with Diarrhea, Cameroon SO EMERGING INFECTIOUS DISEASES LA English DT Article ID STRAINS; REASSORTMENT; DIVERSITY AB We report characterization of a genotype G5P[7] human rotavirus (HRV) from a child in Cameroon who had diarrhea. Sequencing of all 11 gene segments showed similarities to >= 5 genes each from porcine and human rotaviruses. This G5P[7] strain exemplifies the importance of heterologous animal rotaviruses in generating HRV genetic diversity through reassortment. C1 [Esona, Mathew D.; Hull, Jennifer; Gentsch, Jon R.] Ctr Dis Control & Prevent, Atlanta, GA 30333 USA. [Geyer, Annelise] Univ Limpopo, Pretoria, South Africa. [Banyai, Krisztian] Assoc Publ Hlth Labs, Washington, DC USA. [Page, Nicola] Natl Inst Communicable Dis, Johannesburg, South Africa. [Aminu, Maryam] Ahmadu Bello Univ, Zaria, Nigeria. [Armah, George E.] Noguchi Mem Res Inst, Accra, Ghana. [Steele, Duncan A.] Program Appropriate Technol Hlth, Seattle, WA USA. [Glass, Roger I.] NIH, Bethesda, MD 20892 USA. RP Esona, MD (reprint author), Ctr Dis Control & Prevent, 1600 Clifton Rd NE,Mailstop G04, Atlanta, GA 30333 USA. EM mdi4@cdc.gov OI Page, Nicola/0000-0001-5845-4417; Banyai, Krisztian/0000-0002-6270-1772 FU Gastroenteritis and Respiratory Viruses Laboratory Branch at CDC FX Dr Esona is an associate research fellow in the Gastroenteritis and Respiratory Viruses Laboratory Branch at CDC. His primary research interest is the molecular epidemiology of enteric viruses. NR 14 TC 45 Z9 46 U1 0 U2 4 PU CENTERS DISEASE CONTROL PI ATLANTA PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA SN 1080-6040 J9 EMERG INFECT DIS JI Emerg. Infect. Dis PD JAN PY 2009 VL 15 IS 1 BP 83 EP 86 DI 10.3201/eid1501.080899 PG 4 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 393AG UT WOS:000262342700019 PM 19116059 ER PT J AU Torborg, CL McBain, CJ AF Torborg, C. L. McBain, C. J. BE Schwartzkroin, PA TI Properties of Interneurons and their Relation to Epilepsy SO ENCYCLOPEDIA OF BASIC EPILEPSY RESEARCH, VOLS 1-3 LA English DT Article; Book Chapter ID GATED K+ CHANNELS; FAST-SPIKING; KV3 CHANNELS; EXPRESSION; SUBPOPULATIONS; NEURONS C1 [Torborg, C. L.; McBain, C. J.] NICHD, LCSN, NIH, Bethesda, MD USA. RP Torborg, CL (reprint author), NICHD, LCSN, NIH, Bethesda, MD USA. NR 12 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA BN 978-0-12-373961-2 PY 2009 BP 625 EP 630 PG 6 WC Medicine, Research & Experimental; Clinical Neurology SC Research & Experimental Medicine; Neurosciences & Neurology GA BFJ85 UT WOS:000320162800107 ER PT J AU Bough, KJ Dingledine, R AF Bough, K. J. Dingledine, R. BE Schwartzkroin, PA TI Anticonvulsant Mechanisms of a Ketogenic Diet SO ENCYCLOPEDIA OF BASIC EPILEPSY RESEARCH, VOLS 1-3 LA English DT Article; Book Chapter C1 [Bough, K. J.] NIH, Bethesda, MD 20892 USA. [Dingledine, R.] Emory Univ, Atlanta, GA 30322 USA. RP Bough, KJ (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA. NR 14 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA BN 978-0-12-373961-2 PY 2009 BP 681 EP 687 PG 7 WC Medicine, Research & Experimental; Clinical Neurology SC Research & Experimental Medicine; Neurosciences & Neurology GA BFJ85 UT WOS:000320162800116 ER PT J AU Theodore, WH AF Theodore, W. H. BE Schwartzkroin, PA TI PET Neurotransmitter Receptor Imaging in Epilepsy SO ENCYCLOPEDIA OF BASIC EPILEPSY RESEARCH, VOLS 1-3 LA English DT Article; Book Chapter ID TEMPORAL-LOBE EPILEPSY; POSITRON-EMISSION-TOMOGRAPHY; NORMAL MRI; BINDING; CHILDREN C1 NINDS, NIH, Bethesda, MD 20892 USA. RP Theodore, WH (reprint author), NINDS, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA. NR 16 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA BN 978-0-12-373961-2 PY 2009 BP 1563 EP 1567 PG 5 WC Medicine, Research & Experimental; Clinical Neurology SC Research & Experimental Medicine; Neurosciences & Neurology GA BFJ85 UT WOS:000320162800263 ER PT J AU Lane, WS Cochran, EK Jackson, JA Scism-Bacon, JL Corey, IB Hirsch, IB Skyler, JS AF Lane, Wendy S. Cochran, Elaine K. Jackson, Jeffrey A. Scism-Bacon, Jamie L. Corey, Ilene B. Hirsch, Irl B. Skyler, Jay S. TI HIGH-DOSE INSULIN THERAPY: IS IT TIME FOR U-500 INSULIN? SO ENDOCRINE PRACTICE LA English DT Review ID TYPE-2 DIABETES-MELLITUS; REGULAR INSULIN; CARDIOVASCULAR EVENTS; CLINICAL-COURSE; RESISTANCE; METAANALYSIS; ABSORPTION; DISEASE; OBESITY; RISK AB Objective: To provide an overview of U-500 regular insulin action, review published clinical studies with U-500 regular insulin, and offer guidance to practicing endocrinologists for identifying patients for whom U-500 regular insulin may be appropriate. Methods: This review has been produced through a synthesis of relevant published literature compiled via a literature search (MEDLINE search of the English-language literature published between January 1969, and July 2008, related to U-500, insulin resistance, concentrated insulin, high-dose insulin, insulin pharmacokinetics, and diabetes management) and the authors' collective clinical experience. Results: The obesity epidemic is contributing to all increase in the prevalence of type 2 diabetes, as well as to increasing insulin requirements in insulin-treated patients. Many of these patients exhibit severe insulin resistance, manifested by daily insulin requirements of 200 units or greater or more than 2 units/kg. Delivering an appropriate insulin volume to these patients can be difficult and inconvenient and may be best accomplished with U-500 regular insulin by multiple daily injections or with continuous subcutaneous insulin infusion, rather than with standard U-100 insulin. Implementation of U-500 regular insulin in patients previously oil other insulin formulations is described with a treatment algorithm covering dosage requirements ranging from 150 to more than 600 units per day oil the basis of the authors' experience. Conclusion: Regimen conversion of appropriately selected patients from high-dose, U-100 insulin to U-500 regular insulin therapy oil the basis of the recommendations presented in this article may potentially result in improved glycemic control and lower cost. (Endocr Pract. 2009;15:71-79) C1 [Lane, Wendy S.] Mt Diabet & Endocrine Ctr, Asheville, NC 28803 USA. [Cochran, Elaine K.] NIDDKD, NIH, Bethesda, MD 20892 USA. [Jackson, Jeffrey A.; Scism-Bacon, Jamie L.; Corey, Ilene B.] Eli Lilly & Co, US Med Div, Indianapolis, IN 46285 USA. [Hirsch, Irl B.] Univ Washington, Med Ctr, Seattle, WA 98195 USA. [Skyler, Jay S.] Univ Miami, Miller Sch Med, Miami, FL 33136 USA. RP Lane, WS (reprint author), Mt Diabet & Endocrine Ctr, 1998 Hendersonville Rd, Asheville, NC 28803 USA. EM mountaindiabetes@msn.com RI Skyler, Jay/F-4211-2016 NR 48 TC 61 Z9 61 U1 0 U2 2 PU AMER ASSOC CLINICAL ENDOCRINOLOGISTS PI JACKSONVILLE PA 245 RIVERSIDE AVENUE, STE 200, JACKSONVILLE, FL 32202 USA SN 1530-891X EI 1934-2403 J9 ENDOCR PRACT JI Endocr. Pract. PD JAN-FEB PY 2009 VL 15 IS 1 BP 71 EP 79 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 437NO UT WOS:000265494400016 PM 19211405 ER PT J AU Sakamoto, A Weinstein, LS Plagge, A Eckhaus, M Kelsey, G AF Sakamoto, Akio Weinstein, Lee S. Plagge, Antonius Eckhaus, Michael Kelsey, Gavin TI GNAS Haploinsufficiency Leads to Subcutaneous Tumor Formation With Collagen and Elastin Deposition and Calcification SO ENDOCRINE RESEARCH LA English DT Article DE GNAS; Tumor Formation; Elastin; Calcification ID SMOOTH-MUSCLE-CELLS; GS-ALPHA GENE; MATRIX METALLOPROTEINASES; GROWTH-FACTOR; TISSUE; PROLIFERATION; ELASTOLYSIS; FIBROBLASTS; DEGRADATION; ACTIVATION AB Introduction. The heterotrimeric G protein -subunit Gs links receptors to stimulation of cAMP/protein kinase A signaling, which inhibits skin fibroblast proliferation and collagen synthesis. We now describe the development of fibrous tumors in mice with heterozygous disruption of the Gnas gene, which encodes Gs and other gene products. Methods and Results. Disruption of Gnas exon 2 on either the maternal or paternal allele (GnasE2-/+) results in fibromas or angiofibromas on the ears, paws and tail beginning at 4 months of age. The tumors were composed of fibroblastic cell proliferation with collagen and elastin deposition and calcification, and seemed to be associated with mechanical skin damage. The presence of calcification was associated with greater amounts of matrix metalloproteinase-2, suggesting an association between calcium deposition and extracellular matrix degradation. Osteoblast-specific markers were absent, consistent with the calcification not being secondary to ossification. Molecular studies showed that the tumors were not associated with deletion of the wild-type allele, making it unlikely that these tumors resulted from homozygous loss of Gs. Conclusions. These findings provide in vivo evidence that Gs pathways inhibit fibroblast and endothelial proliferation and matrix deposition. C1 [Sakamoto, Akio; Weinstein, Lee S.] NIDDK, Metab Dis Branch, NIH, Bethesda, MD USA. [Plagge, Antonius; Eckhaus, Michael; Kelsey, Gavin] Babraham Inst, Lab Dev Genet & Imprinting, Cambridge, England. RP Sakamoto, A (reprint author), Kyushu Univ, Grad Sch Med Sci, Dept Orthopaed Surg, Higashi Ku, 3-1-1 Maidashi, Fukuoka 8128582, Japan. EM akio@med.kyushu-u.ac.jp OI Kelsey, Gavin/0000-0002-9762-5634 FU Intramural Research Program; National Institute of Diabetes and Digestive and Kidney Diseases; National Institutes of Health FX This work was supported by the Intramural Research Program of the National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health. NR 18 TC 5 Z9 6 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0743-5800 J9 ENDOCR RES JI Endocr. Res. PY 2009 VL 34 IS 1-2 BP 1 EP 9 AR PII 910863607 DI 10.1080/07435800902841280 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 462QO UT WOS:000267370900001 PM 19557586 ER PT J AU Torres, SM Walker, DM McCash, CL Carter, MM Ming, J Cordova, EM Pons, RM Cook, DL Seilkop, SK Copeland, WC Walker, VE AF Torres, Salina M. Walker, Dale M. McCash, Consuelo L. Carter, Meghan M. Ming, Jessica Cordova, Edmund M. Pons, Rachel M. Cook, Dennis L., Jr. Seilkop, Steven K. Copeland, William C. Walker, Vernon E. TI Mutational Analysis of the Mitochondrial tRNA Genes and Flanking Regions in Umbilical Cord Tissue from Uninfected Infants Receiving AZT-Based Therapies for Prophylaxis of HIV-1 SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Review DE antiretrovirals; AZT; DGGE; mitochondrial DNA mutation; nucleoside analogs; 3TC; tRNA genes; transplacental exposure ID REVERSE-TRANSCRIPTASE INHIBITORS; GRADIENT GEL-ELECTROPHORESIS; TO-CHILD TRANSMISSION; ACTIVE ANTIRETROVIRAL THERAPY; HUMAN LYMPHOBLASTOID-CELLS; BLOOD MONONUCLEAR-CELLS; IN-VITRO EXPOSURE; PERINATAL EXPOSURE; NUCLEOSIDE ANALOGS; INFECTED PATIENTS AB A sensitive vertical denaturing gradient gel electrophoresis (DGGE) method, using 13 unipolar psoralen-clamped PCR primer pairs, was developed for detecting sequence variants in the 22 tRNA genes and flanking regions (together spanning similar to 21%) of the human mitochondrial genome. A study was conducted to determine (i) if mitochondrial DNA (mtDNA) polymorphisms and/or mutations were detectable in healthy newborns and (ii) if preparturn 3'-azido-2',3'-dideoxythymidine (AZT) based HIV-1 prophylaxis was associated with significant increases in mtDNA mutations and changes in the degree of heteroplasmy of sequence variants in uninfected infants born to HIV-1-infected mothers. DGGE analysis of umbilical cord tissue (where vascular endothelium and smooth muscle cells are the major source of mtDNA) showed that mtDNA sequence variants were significantly elevated by threefold in AZT-treated infants compared with unexposed controls (P < 0.001), with 24 changes observed in 19/52 (37%) treated newborns (averaging 0.46 changes/subject) versus only eight changes found in 7155 (13%) unexposed newborns (averaging 0.15 changes/subject). Six distinct sequence variants occurring in unexposed controls were predominately synonymous and homoplasmic, representing previously reported polymorphisms. Uninfected infants exposed to a combination of AZT and 2',3'-dideoxy-3'-thiacytidine and "maternal HIV-1" had a significant shift in the spectrum of mutations (P = 0.04) driven by increases in non-synonymous heteroplasmic sequence variants at polymorphic sites (10 distinct variants) and novel sites (four distinct variants). While the weight of evidence suggests that prepartum AZT-based prophylaxis produces mtDNA mutations, additional research is needed to determine the degree to which fetal responses to maternal HIV-1 infection, in the absence of antiretroviral treatment, contribute to prenatal mtDNA mutagenesis. Environ. Mal. Mutagen. 50:10-26, 2009. (C) 2008 Wiley-Liss, Inc. C1 [Walker, Dale M.; Walker, Vernon E.] BioMosaics Inc, Burlington, VT 05405 USA. [Torres, Salina M.; Walker, Dale M.; McCash, Consuelo L.; Carter, Meghan M.; Ming, Jessica; Cordova, Edmund M.; Pons, Rachel M.; Cook, Dennis L., Jr.; Walker, Vernon E.] Lovelace Resp Res Inst, Albuquerque, NM USA. [Seilkop, Steven K.] SKS Consulting Serv, Silver City, NC USA. [Copeland, William C.] NIEHS, Mol Genet Lab, NIH, Res Triangle Pk, NC 27709 USA. RP Walker, VE (reprint author), BioMosaics Inc, 655 Spear St,Bldg C, Burlington, VT 05405 USA. EM v.walker@biomosaics.com FU National Institute of Environmental Health Sciences [R01 HD033648, R01 HL072727, 1 F31 HL0S1928]; The National Institute of Child Health and Human Development; National Cancer Institute; Office of AIDS Research; The National Heart, Lung, and Blood Institute FX The National Institute of Child Health and Human Development, the National Cancer Institute, the Office of AIDS Research, The National Heart, Lung, and Blood Institute. NR 105 TC 9 Z9 9 U1 0 U2 4 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PD JAN PY 2009 VL 50 IS 1 BP 10 EP 26 DI 10.1002/em.20433 PG 17 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 396AO UT WOS:000262564800004 PM 19031409 ER PT J AU Shiao, YH AF Shiao, Yih-Horng TI Genetic Signature for Human Risk Assessment: Lessons From Trichloroethylene SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Review DE trichloroethylene; carcinogenesis; VHL; Ras; hypomethylation; kidney; liver ID HIPPEL-LINDAU-DISEASE; INDUCED LIVER-TUMORS; LI-FRAUMENI-SYNDROME; DICHLOROACETIC ACID; SOMATIC MUTATIONS; HUMAN GENOME; HUMAN CANCER; CONDITIONAL INACTIVATION; VASCULAR TUMORS; B6C3F1 MICE AB Trichloroethylene (TCE), an organic solvent commonly used for metal degreasing and as a chemical additive, is a significant environmental contaminant that poses health concerns in humans. The US Environmental Protection Agency (EPA) is currently revising the 2001 TCE human risk assessment draft. The next draft is expected to be ready in 2008. TCE metabolites are detectable in humans and carry varying potencies for induction of cancers in animals. Genomic mechanisms have been explored in animals and humans to link TCE to carcinogenesis. DNA analysis provides an opportunity for detection of unique genetic alterations representing a signature of ICE exposure. These alterations can arise from genotoxic and nongenotoxic pathways at multiple points throughout tumorigenesis. Although fixation of alterations may require several stages of selection and modification, the spectra can be specific to ICE. Only a fraction of these alterations eventually lead to tumor formation and some contribute to tumor progression. Genetic events in two major TCE target organs are reviewed, including the VHL gene in kidney, and the Ras gene and genome-wide hypomethylation in liver. Attempts to identify a genetic signature of ICE exposure are challenged by inconsistent findings, lack of evidence of promutagenic lesions, biological relevance of specific genomic changes, and likelihood of coexposures. For human risk assessment, genome-wide screening is useful and is possible with the development of new DNA-sequencing technologies. Genetic screening for preneoplastic and tumor tissues from high-risk population is proposed to exclude the noise of passenger mutations and genetic polymorphisms. Environ. Mal. Mutagen. 50:68-77, 2009. Published 2008 Wiley-Liss, Inc. C1 NCI, NIH, Comparat Carcinogenesis Lab, Ft Detrick, MD 21702 USA. RP Shiao, YH (reprint author), NCI, NIH, Comparat Carcinogenesis Lab, Bldg 538,Room 205A,w 7th St, Ft Detrick, MD 21702 USA. EM shiao@mail.ncifcrf.gov FU Intramural NIH HHS [Z99 CA999999] NR 70 TC 10 Z9 10 U1 0 U2 4 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PD JAN PY 2009 VL 50 IS 1 BP 68 EP 77 DI 10.1002/em.20432 PG 10 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 396AO UT WOS:000262564800009 PM 19031419 ER PT J AU Gottipolu, RR Wallenborn, JG Karoly, ED Schladweiler, MC Ledbetter, AD Krantz, T Linak, WP Nyska, A Johnson, JA Thomas, R Richards, JE Jaskot, RH Kodavanti, UP AF Gottipolu, Reddy R. Wallenborn, J. Grace Karoly, Edward D. Schladweiler, Mette C. Ledbetter, Allen D. Krantz, Todd Linak, William P. Nyska, Abraham Johnson, Jo Anne Thomas, Ronald Richards, Judy E. Jaskot, Richard H. Kodavanti, Urmila P. TI One-Month Diesel Exhaust Inhalation Produces Hypertensive Gene Expression Pattern in Healthy Rats SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE air pollution; cardiac gene expression profile; diesel exhaust; hypertension; mitochondria; particulate matter ID PARTICULATE MATTER PM; OXIDATIVE STRESS; APOE(-/-) MICE; BLOOD-PRESSURE; AIR-POLLUTION; WISTAR-KYOTO; PARTICLES; PULMONARY; RESPONSES; EXPOSURE AB BACKGROUND: Exposure to diesel exhaust (DE) is linked to vasoconstriction, endothelial dysfunction, and myocardial ischemia in compromised individuals. OBJECTIVE: We hypothesized that DE inhalation would cause greater inflammation, hematologic alterations, and cardiac molecular impairment in spontaneously hypertensive (SH) rats than in healthy Wistar Kyoto (WKY) rats. METHODS AND RESULTS: Male rats (12-14 weeks of age) were exposed to air or DE from a 30-kW Deutz engine at 500 or 2,000 mu g/m(3), 4 hr/day, 5 days/week for 4 weeks. Neutrophilic influx was noted in the lung lavage fluid of both strains, but injury markers were minimally changed. Particle-laden macrophages were apparent histologically in DE-exposed rats. Lower baseline cardiac antioxidant enzyme activities were present in SH than in WKY rats; however, no DE effects were noted. Cardiac mitochondrial aconitase activity decreased after DE exposure in both strains. Electron microscopy indicated abnormalities in cardiac mitochondria of control SH but no DE effects. Gene expression profiling demonstrated alterations in 377 genes by DE in WKY but none in SH rats. The direction of DE-induced changes in WKY mimicked expression pattern of control SH rats without DE. Most genes affected by DE were down-regulated in WKY. The same genes were down-regulated in SH without DE producing a hypertensive-like expression pattern. The down-regulated genes included those that regulate compensatory response, matrix metabolism, mitochondrial function, and oxidative stress response. No up-regulation of inflammatory genes was noted. CONCLUSIONS: We provide the evidence that DE inhalation produces a hypertensive-like cardiac gene expression pattern associated with mitochondrial oxidative stress in healthy rats. C1 [Gottipolu, Reddy R.; Schladweiler, Mette C.; Ledbetter, Allen D.; Krantz, Todd; Thomas, Ronald; Richards, Judy E.; Jaskot, Richard H.; Kodavanti, Urmila P.] US EPA, ETD, NHEERL, Off Res & Dev, Res Triangle Pk, NC 27709 USA. [Wallenborn, J. Grace] Univ N Carolina, Sch Publ Hlth, Chapel Hill, NC USA. [Karoly, Edward D.] US EPA, Off Res & Dev, Natl Hlth & Environm Effects Res Lab, Human Studies Div, Res Triangle Pk, NC 27709 USA. [Linak, William P.] US EPA, Off Res & Dev, Natl Risk Management Res Lab, Air Pollut Prevent & Control Div, Res Triangle Pk, NC 27709 USA. [Nyska, Abraham] Tel Aviv Univ, IL-69978 Tel Aviv, Israel. [Johnson, Jo Anne] NIEHS, Lab Expt Pathol, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. RP Kodavanti, UP (reprint author), US EPA, ETD, NHEERL, Off Res & Dev, B143-01,109 TW Alexander Dr, Res Triangle Pk, NC 27709 USA. EM kodavanti.urmila@epa.gov NR 46 TC 29 Z9 29 U1 0 U2 3 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 2009 VL 117 IS 1 BP 38 EP 46 DI 10.1289/ehp.11647 PG 9 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 394WN UT WOS:000262483900027 PM 19165385 ER PT J AU Bronstein, J Carvey, P Chen, H Cory-Slechta, D DiMonte, D Duda, J English, P Goldman, S Grate, S Hansen, J Hoppin, J Jewell, S Kamel, F Koroshetz, W Langston, JW Logroscino, G Nelson, L Ravina, B Rocca, W Ross, GW Schettler, T Schwarzschild, M Scott, B Seegal, R Singleton, A Steenland, K Tanner, CM Van Den Eeden, S Weisskopf, M AF Bronstein, Jeff Carvey, Paul Chen, Honglei Cory-Slechta, Deborah DiMonte, Donato Duda, John English, Paul Goldman, Samuel Grate, Stephen Hansen, Johnni Hoppin, Jane Jewell, Sarah Kamel, Freya Koroshetz, Walter Langston, James W. Logroscino, Giancarlo Nelson, Lorene Ravina, Bernard Rocca, Walter Ross, George W. Schettler, Ted Schwarzschild, Michael Scott, Bill Seegal, Richard Singleton, Andrew Steenland, Kyle Tanner, Caroline M. Van Den Eeden, Stephen Weisskopf, Marc TI Meeting Report: Consensus Statement-Parkinson's Disease and the Environment: Collaborative on Health and the Environment and Parkinson's Action Network (CHE PAN) Conference 26-28 June 2007 SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE cholesterol; coffee; dairy products; diet; dopamine; fatty acids; metals; nonsteroidal anti-inflammatory drugs; Parkinson's disease; pesticides; polychlorinated biphenyls; smoking; statins; urate ID BODY-MASS INDEX; ALPHA-SYNUCLEIN; RISK-FACTORS; LEWY BODIES; PESTICIDE EXPOSURE; SUBSTANTIA-NIGRA; VITAMIN-C; COFFEE; MEN; METAANALYSIS AB BACKGROUND: Parkinson's disease (PD) is the second most common neurodegenerative disorder. People with PD, their families, scientists, health care providers, and the general public are increasingly interested in identifying environmental contributors to PD risk. METHODS: In June 2007, a multidisciplinary group of experts gathered in Sunnyvale, California, USA, to assess what is known about the contribution of environmental factors to PD. RESULTS: We describe the conclusions around which they came to consensus with respect to environmental contributors to PD risk. We conclude with a brief summary of research needs. CONCLUSIONS: PD is a complex disorder, and multiple different pathogenic pathways and mechanisms can ultimately lead to PD. Within the individual there are many determinants of PD risk, and within populations, the causes of PD are heterogeneous. Although rare recognized genetic mutations are sufficient to cause PD, these account for < 10% of PD in the U.S. population, and incomplete penetrance suggests that environmental factors may be involved. Indeed, interplay among environmental factors and genetic makeup likely influences the risk of developing PD. There is a need for further understanding of how risk factors interact, and studying PD is likely to increase understanding of other neurodegenerative disorders. C1 [DiMonte, Donato; Goldman, Samuel; Jewell, Sarah; Langston, James W.; Tanner, Caroline M.] Parkinsons Inst, Sunnyvale, CA 94085 USA. [DiMonte, Donato; Goldman, Samuel; Jewell, Sarah; Langston, James W.; Tanner, Caroline M.] Ctr Clin, Sunnyvale, CA USA. [Bronstein, Jeff] Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA. [Carvey, Paul] Rush Univ, Med Ctr, Chicago, IL 60612 USA. [Chen, Honglei; Hoppin, Jane; Kamel, Freya] NIEHS, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. [Cory-Slechta, Deborah] Univ Rochester, Sch Med & Dent, Rochester, NY USA. [Duda, John] Parkinsons Dis Res Educ & Clin Ctr, Philadelphia, PA USA. [English, Paul] Calif Dept Hlth Serv, Oakland, CA USA. [Grate, Stephen] USA, Med Res & Mat Command, Ft Detrick, MD USA. [Hansen, Johnni] Danish Canc Soc, Inst Canc Epidemiol, Copenhagen, Denmark. [Koroshetz, Walter] NINDS, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. [Logroscino, Giancarlo] Univ Bari, Bari, Italy. [Nelson, Lorene] Stanford Univ, Sch Med, Stanford, CA 94305 USA. [Ravina, Bernard] Univ Rochester, Sch Med, Rochester, NY USA. [Rocca, Walter] Mayo Clin, Rochester, MN USA. [Ross, George W.] Pacific Hlth Res Inst, Honolulu, HI USA. [Schettler, Ted] Sci & Environm Hlth Network, Ames, IA USA. [Schwarzschild, Michael] Massachusetts Gen Hosp, Boston, MA 02114 USA. [Scott, Bill] Univ Miami, Miller Sch Med, Miami, FL 33136 USA. [Seegal, Richard] New York State Dept Hlth, Albany, NY USA. [Singleton, Andrew] NIH, Bethesda, MD 20892 USA. [Steenland, Kyle] Rollins Sch Publ Hlth, Atlanta, GA USA. [Van Den Eeden, Stephen] Kaiser Permanente, Oakland, CA USA. [Weisskopf, Marc] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. RP Tanner, CM (reprint author), Parkinsons Inst, 675 Almanor Ave, Sunnyvale, CA 94085 USA. EM ctanner@thepi.org RI Singleton, Andrew/C-3010-2009; Nelson, Lorene/D-1305-2011; LOGROSCINO, GIANCARLO/K-5148-2016; OI LOGROSCINO, GIANCARLO/0000-0003-0423-3242; Jewell, Sarah/0000-0002-9877-2599; Kamel, Freya/0000-0001-5052-6615; Chen, Honglei/0000-0003-3446-7779 NR 79 TC 32 Z9 33 U1 0 U2 2 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 2009 VL 117 IS 1 BP 117 EP 121 DI 10.1289/ehp.11702 PG 5 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 394WN UT WOS:000262483900039 PM 19165397 ER PT J AU Scheidt, P Dellarco, M Dearry, A AF Scheidt, Peter Dellarco, Michael Dearry, Allen TI A Major Milestone for the National Children's Study SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Editorial Material C1 [Scheidt, Peter; Dellarco, Michael] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Natl Childrens Study, NIH, US Dept HHS, Bethesda, MD 20892 USA. [Dearry, Allen] NIEHS, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA. RP Scheidt, P (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Natl Childrens Study, NIH, US Dept HHS, Bethesda, MD 20892 USA. EM dearry@niehs.nih.gov NR 0 TC 6 Z9 6 U1 0 U2 0 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 2009 VL 117 IS 1 BP A13 EP A13 DI 10.1289/ehp.12416 PG 1 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 394WN UT WOS:000262483900002 PM 19165365 ER PT J AU Bloom, MS Buck-Louis, GM Schisterman, EF Kostyniak, PJ Vena, JE AF Bloom, Michael S. Buck-Louis, Germaine M. Schisterman, Enrique F. Kostyniak, Paul J. Vena, John E. TI Changes in maternal serum chlorinated pesticide concentrations across critical windows of human reproduction and development SO ENVIRONMENTAL RESEARCH LA English DT Article DE Critical windows; Organochlorine pesticides; Persistent organic pollutants; Pregnancy; Pregnancy loss ID ORGANOCHLORINE COMPOUNDS; PREGNANCY; WOMEN; HEALTH; MILK; DETERMINANTS; CONTAMINANTS; ADJUSTMENT; PLASMA; COHORT AB Investigators often employ a single cross-sectional measure of in utero exposure when evaluating associations between organochlorine (OCs) pesticides/metabolites and adverse reproductive outcomes. Few data are available on the stability of exposures to OCs over critical windows of human reproduction and development inclusive of the periconception window. Our objective was to measures changes in OC concentrations prior to conception and throughout pregnancy or after 12 unsuccessful months attempting pregnancy. Seventy-nine women planning pregnancy were prospectively enrolled and followed for up to 12 menstrual cycles. Blood specimens were obtained for toxicologic analysis of seven OCs from participating women at baseline (preconception, n = 79), at the first prenatal visit following a positive pregnancy test leading to a live birth (it = 54) or after pregnancy loss (n = 10), at approximately 6 weeks post-partum (n = 53), and after 12 unsuccessful cycles (n = 9). Overall and daily rate of change in OCs concentration (ng/g serum) were estimated adjusting for serum lipids and baseline concentration. Significant (P < 0.05) decreases in the overall and daily rate of change in OCs concentrations (ng/mLserum) were observed from baseline to pregnancy for HCB (-0.032, -0.001, respectively) and trans-nonachlor (-0.050, -0.002, respectively) while oxychlordane demonstrated an increase during this critical window (0.029, 0.001, respectively). Significant decreases in aldrin (-0.002, -1.47 x 10(-4), respectively), HCB (-0.069, -0.003, respectively), and trans-nonachlor (-0.045, -0.002, respectively), and an overall increase for oxychlordane (0.015) were seen for women with pregnancy losses. Significant decreases also were observed among infertile women for aldrin (-0.003, -3.52 x 10(-6). respectively), DDE (-0.210, -4.29 x 10(-4), respectively), and HCB (-0.096, -2.03 x 10(-4), respectively), along with an increase for trans-nonachlor (0.034, 7.59 x 10(-5), respectively). These data, though limited by sample size and the possibility of laboratory measurement error, suggest that OC concentrations may change over critical windows. This underscores the importance of timing biospecimen collection to critical windows for development in the assessment of reproductive and/or developmental effects. (C) 2008 Elsevier Inc. Ail rights reserved. C1 [Bloom, Michael S.] SUNY Albany, Sch Publ Hlth, Dept Environm Hlth Sci, Rensselaer, NY 12144 USA. [Buck-Louis, Germaine M.; Schisterman, Enrique F.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, NIH, Kennedy Space Ctr, FL USA. [Kostyniak, Paul J.] SUNY Buffalo, Dept Biotech & Clin Lab Sci, Sch Med & Biomed Sci, Buffalo, NY 14260 USA. [Vena, John E.] Univ S Carolina, Arnold Sch Publ Hlth, Dept Epidemiol & Biostat, Columbia, SC 29208 USA. RP Bloom, MS (reprint author), SUNY Albany, Sch Publ Hlth, Dept Environm Hlth Sci, 1 Univ Pl,Rm 153, Rensselaer, NY 12144 USA. EM mbloom@uamail.albany.edu OI Schisterman, Enrique/0000-0003-3757-641X; Bloom, Michael/0000-0002-0028-5494; Buck Louis, Germaine/0000-0002-1774-4490 FU Great Lakes Protection Fund [RM791-3021]; Agency for Toxic Substances and Disease Registry [H751 ATH 298338]; Eunice Kennedy Shriver National Institute of Child Health and Human Development FX This research was supported in part with funding from the Great Lakes Protection Fund (RM791-3021), the Agency for Toxic Substances and Disease Registry (H751 ATH 298338), and the Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development. NR 41 TC 14 Z9 14 U1 0 U2 5 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0013-9351 J9 ENVIRON RES JI Environ. Res. PD JAN PY 2009 VL 109 IS 1 BP 93 EP 100 DI 10.1016/j.envres.2008.08.013 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health GA 394QK UT WOS:000262462100013 PM 18973878 ER PT J AU Zhu, JL Obel, C Basso, O Bech, BH Henriksen, TB Olsen, J AF Zhu, Jin Liang Obel, Carsten Basso, Olga Bech, Bodil Hammer Henriksen, Tine Brink Olsen, Jorn TI Handedness and Time to Pregnancy SO EPIDEMIOLOGY LA English DT Article ID LANGUAGE LATERALIZATION; ATYPICAL HANDEDNESS; SEXUAL ORIENTATION; MIXED-HANDEDNESS; HAND PREFERENCE; HAIR-WHORL; WOMEN; ASYMMETRY; BEHAVIOR; MEN AB Background: Nonright-handedness, particularly mixed-handedness, has been associated with a number of medical conditions. We examined whether handedness was associated with fecundity, measured by time to pregnancy. Methods: We used data on parental handedness and time to pregnancy from 2 regional birth cohorts in Denmark: the Aalborg-Odense Birth Cohort (1984-1987) and the Aarhus Birth Cohort (1990-1992) (n = 5808 and 3426, respectively). We applied discrete-time survival analysis to assess fecundity in relation to handedness. Results: In both cohorts, we saw a slightly lower fecundity in individuals who reported being mixed-handed. Conclusions: Our data showed a modest association between mixed-handedness and subfecundity, which suggests that these traits may share a common etiology, perhaps tracing back to the prenatal period. C1 [Zhu, Jin Liang; Obel, Carsten; Bech, Bodil Hammer; Olsen, Jorn] Univ Aarhus, Danish Epidemiol Sci Ctr, Dept Epidemiol, Inst Publ Hlth, DK-8000 Aarhus C, Denmark. [Obel, Carsten; Henriksen, Tine Brink] Aarhus Univ Hosp, Perinatal Epidemiol Res Unit, Dept Obstet & Gynaecol, DK-8000 Aarhus, Denmark. [Basso, Olga] Natl Inst Environm Hlth Sci, Epidemiol Branch, Dept Hlth & Human Serv, NIH, Res Triangle Pk, NC USA. [Olsen, Jorn] Univ Calif Los Angeles, Sch Publ Hlth, Dept Epidemiol, Los Angeles, CA 90024 USA. RP Zhu, JL (reprint author), Univ Aarhus, Danish Epidemiol Sci Ctr, Dept Epidemiol, Inst Publ Hlth, Vennelyst Blvd 6, DK-8000 Aarhus C, Denmark. EM zjl@soci.au.dk RI Basso, Olga/E-5384-2010; Olsen, Jorn/F-8801-2015; Bech, Bodil Hammer/B-9646-2016 OI Basso, Olga/0000-0001-9298-4921; Olsen, Jorn/0000-0001-7462-5140; FU Danish Medical Research Council [271-05-0115]; Intramural Research Program of the National Institutes of Health; National Institute of Environmental Health Sciences FX Supported by a grant from the Danish Medical Research Council (No. 271-05-0115) and, in part, by the Intramural Research Program of the National Institutes of Health, National Institute of Environmental Health Sciences. NR 35 TC 3 Z9 3 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD JAN PY 2009 VL 20 IS 1 BP 52 EP 55 DI 10.1097/EDE.0b013e31818b47d1 PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 387DB UT WOS:000261930800010 PM 19057386 ER PT J AU Cooney, MA Louis, GMB Sundaram, R McGuiness, BM Lynch, CD AF Cooney, Maureen A. Louis, Germaine M. Buck Sundaram, Rajeshwari McGuiness, Bridget M. Lynch, Courtney D. TI Validity of Self-Reported Time to Pregnancy SO EPIDEMIOLOGY LA English DT Article ID LONG-TERM RECALL; TO-PREGNANCY; FECUNDABILITY; QUESTIONNAIRE; COUPLES; SUBFERTILITY AB Background: The reliability of retrospective time to pregnancy (TTP) has been established, but its validity has been assessed in only I study, which had a short follow-up. Methods: Ninety-nine women enrolled a decade earlier in a prospective TTP study were queried by means of mailed questionnaires about the duration of time they had required to become pregnant. Their responses were compared with their earlier data from daily diaries (gold standard). Results: One-third of women could not recall their earlier TTP either in menstrual cycles or calendar months. Only 17%-19% of women recalled their TTP exactly. Agreement increased to 41%-51%, 65%-72%, and 72%-77% when defined as +/- 1, +/- 2, and +/- 3 months, respectively. Women with longer observed TTPs or previous pregnancies were more likely to under-report their TTP. Conclusions: The findings raise questions about the commonly assumed validity of self-reported TTP. Recalled TTP may introduce error when estimating fecundability or classifying couples' fecundity status. C1 [Louis, Germaine M. Buck] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, Epidemiol Branch, Rockville, MD 20852 USA. [McGuiness, Bridget M.] SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA. RP Louis, GMB (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, Epidemiol Branch, 6100 Execut Boulvard,Rm 7B03, Rockville, MD 20852 USA. EM louisg@mail.nih.gov OI Sundaram, Rajeshwari/0000-0002-6918-5002; Buck Louis, Germaine/0000-0002-1774-4490 FU Great Lakes Protection Fund [R-M791-3021]; Agency for Toxic Substances and Disease Registry [H751 ATH 298338]; Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development FX Supported by the Great Lakes Protection Fund (R-M791-3021), the Agency for Toxic Substances and Disease Registry (H751 ATH 298338), and the Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development. NR 21 TC 52 Z9 52 U1 1 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD JAN PY 2009 VL 20 IS 1 BP 56 EP 59 DI 10.1097/EDE.0b013e31818ef47e PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 387DB UT WOS:000261930800011 PM 19057382 ER PT J AU Chen, A Feresu, SA Fernandez, C Rogan, WJ AF Chen, Aimin Feresu, Shingairai A. Fernandez, Cristina Rogan, Walter J. TI Maternal Obesity and the Risk of Infant Death in the United States SO EPIDEMIOLOGY LA English DT Article ID GESTATIONAL WEIGHT-GAIN; NATIONAL-BIRTH-COHORT; BODY-MASS INDEX; PREGNANCY OUTCOMES; PREPREGNANCY WEIGHT; VITAL-STATISTICS; PRETERM BIRTH; OVERWEIGHT; PREVALENCE; STILLBIRTH AB Background: Maternal obesity (defined as prepregnancy body mass index [BMI] >= 30 kg/m(2)) is associated with increased risk of neonatal death. Its association with infant death, postneonatal death, and cause-specific infant death is less well-characterized. Methods: We studied the association between maternal obesity and the risk of infant death by using 1988 US National Maternal and Infant Health Survey data. A case-control analysis of 4265 infant deaths and 7293 controls was conducted using SUDAAN software. Self-reported prepregnancy BMI and weight gain were used in the primary analysis, whereas weight variables in medical records were used in a subset of 4308 women. Results: Compared with normal weight women (prepregnancy BMI 18.5-24.9 kg/m(2)) who gained 0.30 to 0.44 kg/wk during pregnancy, obese women had increased risk of neonatal death and overall infant death. For obese women who had weight gain during pregnancy of <0.15, 0.15 to 0.29, 0.30 to 0.44, and >= 0.45 kg/wk, the adjusted odds ratios of infant death were 1.75 (95% confidence interval = 1.28-2.39), 1.42 (1.07-1.89), 1.59 (1.00-2.51), and 2.87 (1.98-4.16), respectively. Nonobese women with very low weight gain during pregnancy also had a higher risk of infant death. The subset with weight information from medical records had similar results for recorded prepregnancy BMI and weight gain. Maternal obesity was associated with neonatal death from pregnancy complications or disorders relating to short gestation and unspecified low birth weight. Conclusions: Maternal obesity is associated with increased overall risk of infant death, mainly neonatal death. C1 [Chen, Aimin] Creighton Univ, Sch Med, Dept Prevent Med & Publ Hlth, Omaha, NE 68178 USA. [Feresu, Shingairai A.] Univ Nebraska Med Ctr, Coll Publ Hlth, Dept Epidemiol, Omaha, NE USA. [Fernandez, Cristina] Creighton Univ, Sch Med, Dept Pediat, Omaha, NE 68178 USA. [Rogan, Walter J.] Natl Inst Environm Hlth Sci, Epidemiol Branch, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC USA. RP Chen, A (reprint author), Creighton Univ, Sch Med, Dept Prevent Med & Publ Hlth, 2500 Calif Plaza, Omaha, NE 68178 USA. EM aiminchen@creighton.edu RI Rogan, Walter/I-6034-2012 OI Rogan, Walter/0000-0002-9302-0160 FU Intramural Research Program of the National Institutes of Health; National Institute of Environmental Health Sciences FX W. J. R. was supported by the Intramural Research Program of the National Institutes of Health, National Institute of Environmental Health Sciences. NR 41 TC 61 Z9 68 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD JAN PY 2009 VL 20 IS 1 BP 74 EP 81 DI 10.1097/EDE.0b013e3181878645 PG 8 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 387DB UT WOS:000261930800014 PM 18813025 ER PT J AU Zibell, G Unkruer, B Pekcec, A Bauer, B Hartz, A Miller, D Potschka, H AF Zibell, G. Unkrueer, B. Pekcec, A. Bauer, B. Hartz, A. Miller, D. Potschka, H. TI CELECOXIB PREVENTS SEIZURE-INDUCED UPREGULATION OF ENDOTHELIAL P-GLYCOPROTEIN IN THE BLOOD-BRAIN BARRIER SO EPILEPSIA LA English DT Meeting Abstract CT 8th European Congress on Epileptology CY SEP 21-25, 2008 CL Berlin, GERMANY SP Int League Epilepsy, German & Israeli Chapters C1 [Zibell, G.; Unkrueer, B.; Pekcec, A.; Potschka, H.] Univ Munich, Inst Pharmacol Toxicol & Pharm, Munich, Germany. [Bauer, B.; Hartz, A.] Univ Minnesota, Minneapolis, MN 55455 USA. [Miller, D.] NIEHS, Lab Pharmacol & Chem, NIH, Bethesda, MD 20892 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 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2009 VL 50 BP 89 EP 89 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 428WG UT WOS:000264881600303 ER PT S AU Dhungana, S Williams, JG Fessler, MB Tomer, KB AF Dhungana, Suraj Williams, Jason G. Fessler, Michael B. Tomer, Kenneth B. BE Reineke, U Schutkowski, M TI Epitope Mapping by Proteolysis of Antigen-Antibody Complexes SO EPITOPE MAPPING PROTOCOLS, SECOND EDITION SE Methods in Molecular Biology LA English DT Article; Book Chapter DE Antibody; Antigen; Epitope mapping; Linear epitope; Epitope excision and extraction; Limited proteolysis; Epitope foot-printing; Mass spectrometry; MALDI-MS; ESI-MS ID IONIZATION MASS-SPECTROMETRY; MONOCLONAL-ANTIBODY; ELECTROSPRAY-IONIZATION; CHEMICAL-MODIFICATION; LIMITED PROTEOLYSIS; PEPTIDE ANTIGENS; IMMUNE-RESPONSE; IDENTIFICATION; IMMUNOASSAYS; DETERMINANTS AB The ability to accurately characterize an epitope on an antigen is essential to understand the pathogenesis of an infectious material, and for the design and development of drugs and vaccines. Emergence of a new contagious microbial or viral variant necessitates the need for robust identification and characterization of the antigenic determinant. Recent advances have made mass spectrometry (MS) a robust and sensitive analytical tool with high mass accuracy. The use of MS to characterize peptides and proteins has gained popularity in the research arena involving protein-protein interactions. Combining the modern mass spectrometric principles of protein-protein interaction studies with the classical use of limited proteolysis, a linear epitope on a peptide or a protein antigen can be accurately mapped in a short time, compared with other traditional techniques available for epitope mapping. Additionally, complete MS analyses can be achieved with very little sample consumption. Here we discuss the overall approach to characterize the detailed interaction between a linear antigen (either a peptide or a protein antigen) and its corresponding monoclonal antibody by using MS. The steps involved in epitope excision, epitope extraction, and indirect immunosorption are Outlined thoroughly. Conditions required for MS analysis using either matrix assisted laser desorption ionization (MALDI) or electrospray ionization (ESI) sources are Summarized, with special emphasis on the experimental protocols. C1 [Dhungana, Suraj; Fessler, Michael B.] NIEHS, Lab Resp Biol, NIH, DHHS, Res Triangle Pk, NC 27709 USA. [Williams, Jason G.; Tomer, Kenneth B.] NIEHS, Struct Biol Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA. RP Dhungana, S (reprint author), NIEHS, Lab Resp Biol, NIH, DHHS, POB 12233, Res Triangle Pk, NC 27709 USA. FU Intramural NIH HHS NR 35 TC 10 Z9 11 U1 1 U2 6 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA SN 1064-3745 BN 978-1-934115-17-6 J9 METHODS MOL BIOL JI Methods Mol. Biol. PY 2009 VL 524 BP 87 EP + DI 10.1007/978-1-59745-450-6_7 D2 10.1007/978-1-59745-450-6 PG 17 WC Biochemical Research Methods SC Biochemistry & Molecular Biology GA BKJ95 UT WOS:000268335800007 PM 19377939 ER PT S AU Dhungana, S Fessler, MB Tomer, KB AF Dhungana, Suraj Fessler, Michael B. Tomer, Kenneth B. BE Reineke, U Schutkowski, M TI Epitope Mapping by Differential Chemical Modification of Antigens SO EPITOPE MAPPING PROTOCOLS, SECOND EDITION SE Methods in Molecular Biology LA English DT Article; Book Chapter DE Antibody; Antigen; Epitope mapping; Chemical modification; Conformational and discontinuous epitope; Mass spectrometry; MALDI-MS; LC/ESI-MS; H/D exchange; Acetylation ID EXCHANGE-MASS-SPECTROMETRY; AMIDE HYDROGEN-EXCHANGE; MONOCLONAL-ANTIBODY; SURFACE-TOPOLOGY; MOLECULAR CHARACTERIZATION; DISCONTINUOUS EPITOPE; ARGININE RESIDUES; PROTEIN ANTIGEN; DETERMINANTS; COMPLEXES AB Matrix-assisted laser desorption ionization or electrospray ionization mass spectrometry combined with differential chemical modification have proven to be versatile tools for epitope mapping as well as for studying diverse protein-protein and protein-ligand interactions. Characterization of a discontinuous or a conformational epitope on an antigen demands the ability to map the three-dimensional protein surface along with the interface of two interacting proteins. Classical methods of differentially derivatizing amino acid residues have been Successfully merged with highly sensitive and highly accurate mass spectrometric techniques to rapidly profile the three-dimensional protein surface and determine the surface accessibility of specific amino acid residues. Here we discuss the use of mass spectrometry to characterize discontinuous or conformational epitopes by studying antigen-antibody interactions. The steps involved in epitope mapping approaches using differential chemical modification and H/D exchange on the antigen are discussed in detail, with particular emphasis oil the experimental protocols. C1 [Dhungana, Suraj; Fessler, Michael B.] NIEHS, Lab Resp Biol, NIH, DHHS, Res Triangle Pk, NC 27709 USA. [Tomer, Kenneth B.] NIEHS, Struct Biol Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA. RP Dhungana, S (reprint author), NIEHS, Lab Resp Biol, NIH, DHHS, POB 12233, Res Triangle Pk, NC 27709 USA. FU Intramural NIH HHS NR 35 TC 3 Z9 5 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA SN 1064-3745 BN 978-1-934115-17-6 J9 METHODS MOL BIOL JI Methods Mol. Biol. PY 2009 VL 524 BP 119 EP + DI 10.1007/978-1-59745-450-6_9 D2 10.1007/978-1-59745-450-6 PG 18 WC Biochemical Research Methods SC Biochemistry & Molecular Biology GA BKJ95 UT WOS:000268335800009 PM 19377941 ER PT J AU Bhardwaj, N O'Neill, D Waldmann, T AF Bhardwaj, Nina O'Neill, David Waldmann, Thomas BE Zabriskie, JB TI Immune Regulation SO ESSENTIAL CLINICAL IMMUNOLOGY LA English DT Article; Book Chapter ID DENDRITIC CELLS; INTERLEUKIN-15; BIOLOGY; CANCER C1 [Bhardwaj, Nina] New York Canc Inst, Tumor Vaccine Ctr, New York, NY 10016 USA. [O'Neill, David] NYU, Sch Med, NYUCI Vaccine & Cell Therapy Core Facil, New York, NY USA. [Waldmann, Thomas] NCI, Cytokine Immunol & Immunotherapy Sect, Metab Branch Chief Ctr Canc Res, NIH, Washington, DC USA. RP Bhardwaj, N (reprint author), New York Canc Inst, Tumor Vaccine Ctr, New York, NY 10016 USA. NR 13 TC 0 Z9 0 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI CAMBRIDGE PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND BN 978-0-521-51681-5 PY 2009 BP 33 EP 44 DI 10.1017/CBO9780511575266.003 D2 10.1017/CBO9780511575266 PG 12 WC Immunology SC Immunology GA BDP03 UT WOS:000314283200003 ER PT J AU Robey, PG Bianco, P AF Robey, Pamela Gehron Bianco, Paolo BE Lanza, R Gearhart, J Hogan, B Melton, D Pedersen, R Thomas, ED Thomson, J Wilmut, I TI Postnatal Stem Cells in Tissue Engineering SO ESSENTIALS OF STEM CELL BIOLOGY, 2ND EDITION LA English DT Article; Book Chapter ID REPAIR; SCAFFOLDS; STATE AB The last decade has witnessed the emergence of stem cell-based tissue engineering as a means to restore normal structure and function to tissues lost due to trauma or disease. Successful translation to clinical application will rely on: (1) further characterization of the biological properties of post-natal stem cells (what they can and cannot do); (2) optimization of their isolation and ex vivo expansion; (3) formulation of appropriate scaffolds and carriers that may also include growth factors; (4) development of more advanced bioreactors to create tissues with appropriate biomechanical properties; and (5) determination of mechanisms by which to mobilize and activate endogenous stem cells. This review will highlight these aspects of stem cell-based tissue engineering, along with examples of current approaches and applications. C1 [Robey, Pamela Gehron] NIDCD, Craniofacial & Skeletal Dis Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD USA. [Bianco, Paolo] Univ Rome, Dipartimento Med Sperimentale, Rome, Italy. [Bianco, Paolo] Parco Sci Biomed San Raffaele, Rome, Italy. RP Robey, PG (reprint author), NIDCD, Craniofacial & Skeletal Dis Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD USA. NR 10 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 978-0-08-088497-4 PY 2009 BP 583 EP 590 DI 10.1016/B978-0-12-374729-7.00064-0 PG 8 WC Cell & Tissue Engineering; Cell Biology SC Cell Biology GA BCR48 UT WOS:000311099200069 ER PT B AU Nalawadi, S Shufelt, C Johnson, BD Shaw, L Braunstein, GA Pepine, CJ Azziz, R Stanczyk, F Berga, S Bittner, V Sopko, G Merz, CNB AF Nalawadi, Smruti Shufelt, Chrisandra Johnson, B. Delia Shaw, Leslee Braunstein, Glenn A. Pepine, Carl J. Azziz, Ricardo Stanczyk, Frank Berga, Sarah Bittner, Vera Sopko, George Merz, C. Noel Bairey BE Bartos, JR TI The Role of Estrogens in Cardiovascular Disease: An Update from the NHLBI-Sponsored WISE Study SO ESTROGENS: PRODUCTION, FUNCTIONS AND APPLICATIONS SE Endocrinology Research and Clinical Developments LA English DT Article; Book Chapter DE Women; Estrogens; Hormones; Cardiovascular Disease ID CORONARY-HEART-DISEASE; ISCHEMIA SYNDROME EVALUATION; BODY-MASS INDEX; HORMONE REPLACEMENT THERAPY; POLYCYSTIC-OVARY-SYNDROME; SUSPECTED MYOCARDIAL-ISCHEMIA; FUTURE-RESEARCH DIRECTIONS; BLOOD-INSTITUTE WORKSHOP; ENDOGENOUS SEX-HORMONES; BREAST-CANCER RISK AB Introduction. Cardiovascular disease (CVD) is the leading killer of women (aged over 18 years) in United States, with an annual mortality rate of over 450,000, and a majority of deaths attributable to heart disease. One in 30 female deaths is due to breast cancer in contrast to one in six deaths from heart disease. Declining ovarian estrogen levels during perimenopause and menopause have been implicated in the development of CVD. The Women's Ischemic Syndrome Evaluation (WISE) is a National Heart, Lung and Blood Institute (NHLBI)-sponsored, multi-center study designed to optimize the symptom evaluation, and diagnostic testing for ischemic heart disease. A specific aim within WISE is to study the influence of reproductive hormones on pathophysiology, symptoms and diagnostic test response of myocardial ischemia. In this chapter we discuss new data on the role of estrogen in CVD obtained from the WISE study. A synopsis and discussion of new reproductive hormone data from ten WISE publications are organized into four categories: A) Pre- and perimenopause; B) Postmenopause; Q Hormone Therapy; D) Phytoestrogens as Selective Estrogen-Receptor Modulators (SERMs). The chapter begins with a description of the WISE method of determining menopausal status. New data is presented on the topics of hypothalamic hypoestrogenemia (HHE) and coronary artery disease (CAD), including women with diabetes mellitus (DM), polycystic ovary syndrome (PCOS) and CAD, estrogen levels and statin lipid lowering medication, estrogen levels and obesity patterns, past oral contraceptive (OC) use and CAD, estrogen hormone therapy on psychological factors among women of different ethnic backgrounds, and dietary phytoestrogen-rich products relations to blood lipoproteins and coronary microvascular function. Conclusions. New research from the WISE study suggests that estrogen plays a role in CVD in women. Specific findings include: 1) the use of a simple WISE hormone algorithm can improve the accuracy of menopausal status classification for research purposes; 2) disruption of ovulatory cycling characterized by HHE appears to be associated with angiographic CAD; 3) the presence of DM and HHE predicts a greater burden for angiographic CAD; 4) in postmenopausal women with past OC use is associated with less angiographic CAD; 5) clinical features of PCOS are associated with more angiographic evidence of CAD and worsening CVD event-free survival; 6) blood estrogen levels vary according to central vs. general obesity; 7) there are ethnic differences observed between HT use and psychological health; 8) higher blood levels of the phytoestrogen, daidzein, are associated with beneficial lipoprotein levels in women with low blood estrogen; 9) higher blood level of the phytoestrogen, genistein, are associated with impaired non-endothelial-dependent and endothelial-dependent coronary microvascular function; 10) use of statins, and resultant lower cholesterol levels, are not associated with lower levels of reproductive hormones. New data from WISE study suggests that estrogen plays a role in CVD in women. Ongoing research is directed at further understanding. C1 [Nalawadi, Smruti; Shufelt, Chrisandra; Braunstein, Glenn A.; Azziz, Ricardo; Merz, C. Noel Bairey] Univ Pittsburgh, Inst Heart, Womens Heart Ctr, Pittsburgh, PA USA. [Nalawadi, Smruti; Shufelt, Chrisandra; Braunstein, Glenn A.; Azziz, Ricardo; Merz, C. Noel Bairey] Univ Pittsburgh, Dept Med, Div Endocrinol, Pittsburgh, PA USA. [Nalawadi, Smruti; Shufelt, Chrisandra; Braunstein, Glenn A.; Azziz, Ricardo; Merz, C. Noel Bairey] Univ Pittsburgh, Cedars Sinai Med Ctr, Cedars Sinai Res Inst, Dept Obstet & Gynecol, Pittsburgh, PA USA. [Johnson, B. Delia] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA. [Shaw, Leslee; Berga, Sarah] Emory Univ, Sch Med, Dept Gynecol & Obstet, Emory Program Cardiovasc Outcomes Res & Epidemiol, Atlanta, GA USA. [Pepine, Carl J.] Univ Florida, Dept Med, Div Cardiol, Gainesville, FL USA. [Stanczyk, Frank] Univ So Calif, Los Angeles, CA USA. [Bittner, Vera] Univ Alabama Birmingham, Dept Med, Div Cardiol, Birmingham, AL 35294 USA. [Sopko, George] NHLBI, Div Heart & Vasc Dis, NIH, Bethesda, MD 20892 USA. RP Merz, CNB (reprint author), 444 S San Vicente Blvd,Suite 600, Los Angeles, CA 90048 USA. EM merz@cshs.org NR 125 TC 0 Z9 0 U1 0 U2 0 PU NOVA SCIENCE PUBLISHERS, INC PI HAUPPAUGE PA 400 OSER AVE, STE 1600, HAUPPAUGE, NY 11788-3635 USA BN 978-1-60741-086-7 J9 ENDOCR RES CLIN DEV PY 2009 BP 55 EP 94 PG 40 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA BKX47 UT WOS:000269529000002 ER PT J AU Panigrahi, SK Jhingan, GD Som, I Bhattacharya, A Petri, WA Bhattacharya, S AF Panigrahi, Sunil K. Jhingan, Gagan Deep Som, Indrani Bhattacharya, Alok Petri, William A., Jr. Bhattacharya, Sudha TI Promoter Analysis of Palindromic Transcription Units in the Ribosomal DNA Circle of Entamoeba histolytica SO EUKARYOTIC CELL LA English DT Article ID RNA-POLYMERASE-I; START SITE; SEQUENCE ORGANIZATION; REGION UPSTREAM; GENE; EXPRESSION; NUCLEOLUS AB rRNA genes of Entamoeba histolytica are organized as palindromic ribosomal DNA (rDNA) units (I and II) in a 24.5-kb circle. Although the two rDNAs are identical in sequence, their upstream spacers are completely different. Since the intergenic sequences (IGS) of all rDNA copies in other organisms are conserved and contain transcription regulatory sequences, the lack of sequence conservation in the IGS prompted the question of whether both rDNAs are indeed transcriptionally active. We mapped the transcriptional start points (tsp's) and promoters of the two rDNAs. A 51-bp sequence immediately upstream of the tsp's was highly conserved in both units. In addition, both units had an A+T-rich stretch upstream of the 51-bp core. Analysis of reporter gene transcription showed promoter activity to reside in the regions from positions -86 to +123 (rDNA I) and positions -101 to +140 (rDNA II). The promoter-containing fragments from both units could bind and compete with each other for protein(s) from nuclear extracts. Protein binding was especially dependent on the A+T-rich region upstream of the 51-bp core (positions -53 to -68). The requirement of > 80 bp downstream of the tsp was striking. Although this sequence was not conserved in the two units, it could potentially fold into very long stem-loops. Both rDNAs transcribed with comparable efficiency, as measured by nuclear runon. Thus, both rDNAs share very similar organization of promoter sequences, and in exponential culture both rDNAs are transcribed. It remains to be seen whether the different IGS affect the regulation of the two units under adverse conditions. C1 [Panigrahi, Sunil K.; Jhingan, Gagan Deep] Jawaharlal Nehru Univ, Sch Environm Sci, New Delhi 110067, India. [Som, Indrani] NIDDK, LCDB, NIH, Bethesda, MD 20892 USA. [Bhattacharya, Alok] Jawaharlal Nehru Univ, Sch Life Sci, New Delhi 110 067, India. [Petri, William A., Jr.] Univ Virginia, Div Infect Dis & Int Hlth, Charlottesville, VA 22908 USA. RP Bhattacharya, S (reprint author), Jawaharlal Nehru Univ, Sch Environm Sci, New Mehrauli Rd, New Delhi 110067, India. EM sb@mail.jnu.ac.in FU NIH [TW 5655-03]; CSIR (India) FX This research was supported by a FIRCA grant (TW 5655-03) from the NIH. S. K. P. and G.D.J. acknowledge a senior fellowship from the CSIR (India). NR 23 TC 1 Z9 2 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 1535-9778 J9 EUKARYOT CELL JI Eukaryot. Cell PD JAN PY 2009 VL 8 IS 1 BP 69 EP 76 DI 10.1128/EC.00254-08 PG 8 WC Microbiology; Mycology SC Microbiology; Mycology GA 390XM UT WOS:000262197000006 PM 18978203 ER PT J AU Eisenhauer, EA Therasse, P Bogaerts, J Schwartz, LH Sargent, D Ford, R Dancey, J Arbuck, S Gwyther, S Mooney, M Rubinstein, L Shankar, L Dodd, L Kaplan, R Lacombe, D Verweij, J AF Eisenhauer, E. A. Therasse, P. Bogaerts, J. Schwartz, L. H. Sargent, D. Ford, R. Dancey, J. Arbuck, S. Gwyther, S. Mooney, M. Rubinstein, L. Shankar, L. Dodd, L. Kaplan, R. Lacombe, D. Verweij, J. TI New response evaluation criteria in solid tumours: Revised RECIST guideline (version 1.1) SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE Response criteria; Solid tumours; Guidelines ID CLINICAL-TRIALS; PHASE-II; PROSTATE-CANCER; OVARIAN-CANCER; WORKING GROUP; RECOMMENDATIONS; CHEMOTHERAPY; SURVIVAL; RE AB Background: Assessment of the change in tumour burden is an important feature of the clinical evaluation of cancer therapeutics: both tumour shrinkage (objective response) and disease progression are useful endpoints in clinical trials. Since RECIST was published in 2000, many investigators, cooperative groups, industry and government authorities have adopted these criteria in the assessment of treatment outcomes. However, a number of questions and issues have arisen which have led to the development of a revised RECIST guideline (version 1.1). Evidence for changes, summarised in separate papers in this special issue, has come from assessment of a large data warehouse (>6500 patients), simulation studies and literature reviews. Highlights of revised RECIST 1.1: Major changes include: Number of lesions to be assessed: based on evidence from numerous trial databases merged into a data warehouse for analysis purposes, the number of lesions required to assess tumour burden for response determination has been reduced from a maximum of 10 to a maximum of five total (and from five to two per organ, maximum). Assessment of pathological lymph nodes is now incorporated: nodes with a short axis of >= 15 mm are considered measurable and assessable as target lesions. The short axis measurement should be included in the sum of lesions in calculation of tumour response. Nodes that shrink to <10 mm short axis are considered normal. Confirmation of response is required for trials with response primary endpoint but is no longer required in randomised studies since the control arm serves as appropriate means of interpretation of data. Disease progression is clarified in several aspects: in addition to the previous definition of progression in target disease of 20% increase in sum, a 5 mm absolute increase is now required as well to guard against over calling PD when the total sum is very small. Furthermore, there is guidance offered on what constitutes 'unequivocal progression' of non-measurable/non-target disease, a source of confusion in the original RECIST guideline. Finally, a section on detection of new lesions, including the interpretation of FDG-PET scan assessment is included. Imaging guidance: the revised RECIST includes a new imaging appendix with updated recommendations on the optimal anatomical assessment of lesions. Future work: A key question considered by the RECIST Working Group in developing RECIST 1.1 was whether it was appropriate to move from anatomic unidimensional assessment of tumour burden to either volumetric anatomical assessment or to functional assessment with PET or MRI. It was concluded that, at present, there is not sufficient standardisation or evidence to abandon anatomical assessment of tumour burden. The only exception to this is in the use of FDG-PET imaging as an adjunct to determination of progression. As is detailed in the final paper in this special issue, the use of these promising newer approaches requires appropriate clinical validation studies. (C) 2008 Elsevier Ltd. All rights reserved. C1 [Eisenhauer, E. A.] Queens Univ, Natl Canc Inst Canada, Clin Trials Grp, Kingston, ON, Canada. [Therasse, P.] GlaxoSmithKline Biol, Rixensart, Belgium. [Bogaerts, J.; Lacombe, D.] European Org Res Treatment Canc, Ctr Data, Brussels, Belgium. [Schwartz, L. H.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. [Sargent, D.] Mayo Clin, Rochester, MN USA. [Ford, R.] RadPharm, Princeton, NJ USA. [Dancey, J.; Mooney, M.; Rubinstein, L.; Shankar, L.; Dodd, L.] NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA. [Arbuck, S.] Schering Plough Corp, Kenilworth, NJ 07033 USA. [Gwyther, S.] E Surrey Hosp, Surrey, England. [Kaplan, R.] Natl Canc Res Network, Leeds, W Yorkshire, England. [Verweij, J.] Erasmus Univ, Med Ctr, Rotterdam, Netherlands. RP Eisenhauer, EA (reprint author), Queens Univ, Natl Canc Inst Canada, Clin Trials Grp, 10 Stuart St, Kingston, ON, Canada. EM eeisenhauer@ctg.queensu.ca OI Sargent, Daniel/0000-0002-2684-4741 NR 26 TC 5518 Z9 5859 U1 76 U2 332 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD JAN PY 2009 VL 45 IS 2 BP 228 EP 247 DI 10.1016/j.ejca.2008.10.026 PG 20 WC Oncology SC Oncology GA 401NT UT WOS:000262948300002 PM 19097774 ER PT J AU Bogaerts, J Ford, R Sargent, D Schwartz, LH Rubinstein, L Lacombe, D Eisenhauer, E Verweij, J Therasse, P AF Bogaerts, Jan Ford, Robert Sargent, Dan Schwartz, Lawrence H. Rubinstein, Larry Lacombe, Denis Eisenhauer, Elizabeth Verweij, Jaap Therasse, Patrick CA RECIST Working Party TI Individual patient data analysis to assess modifications to the RECIST criteria SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE Tumour measurements; RECIST; Response; Progression ID METASTATIC-BREAST-CANCER; CELL LUNG-CANCER; PHASE-III TRIAL; 1ST-LINE CHEMOTHERAPY; EUROPEAN-ORGANIZATION; INTRAOBSERVER VARIABILITY; COLORECTAL-CANCER; SOLID TUMORS; DOXORUBICIN; PACLITAXEL AB Background: After the initial RECIST 1.0 were published in 2000, the criteria were widely implemented in the scientific oncology community. Since then, the RECIST working group has identified several issues to examine further. Two key issues that required careful, data-based assessment were the maximum number of lesions that should be assessed at each evaluation and the added value of requiring confirmation of response. Methods: To address these questions, data were obtained from 16 clinical trials in metastatic cancer, with patients enrolled between 1993 and 2005. A total of 6512 patients were included in the primary analysis dataset, accounting for over 18,000 potential target lesions. Nine percent of the included patients (n = 585) had six or more reported target lesions. The response and progression outcomes in the database were calculated using an adjusted RECIST methodology with a maximum of 5 (or 3) target lesions with/without confirmation and this was compared to the original RECIST version 1.0 which required up to 10 target lesions plus confirmation of response. Results: Assessment of 5 lesions per patient led to a difference in best overall response assignment for an estimated 209 (3.2%) patients as compared to RECIST version 1.0. However, these changes did not affect the overall response rate. Progression-free survival was only minimally affected by measuring fewer lesions. In contrast, removing the requirement for response confirmation led to a significant increase in the numbers of patients classified as responders, resulting in a relative increase of approximately 19% in response rate. An algorithm using a maximum of three target lesions shows high concordance with the 10 lesions requirement in terms of response and TTP assignment. Concern that appropriate assessment of disease within an organ requires two lesions to be followed per organ suggests the approach of following two target lesions per organ, up to a maximum of five target lesions overall. Both strategies seem reasonable based on the data warehouse. The requirement of response confirmation in trials where this is a primary end-point is recommended to be maintained as its removal would substantially increase reported response rates. (C) 2008 Elsevier Ltd. All rights reserved. C1 [Bogaerts, Jan; Lacombe, Denis] EORTC Headquarters, B-1200 Brussels, Belgium. [Ford, Robert] RadPharm, Princeton, NJ USA. [Sargent, Dan] Mayo Clin, Rochester, MN USA. [Schwartz, Lawrence H.] MSKCC, New York, NY USA. [Rubinstein, Larry] NCI, Bethesda, MD 20892 USA. [Eisenhauer, Elizabeth] Natl Canc Inst Canada, Clin Trials Grp, Kingston, ON, Canada. [Verweij, Jaap] Erasmus Univ, Med Ctr, Rotterdam, Netherlands. [Therasse, Patrick] GlaxoSmithKline Biol, Rixensart, Belgium. RP Bogaerts, J (reprint author), EORTC Headquarters, Ave Mounierlaan 83-11, B-1200 Brussels, Belgium. EM jan.bogaerts@eortc.be OI Sargent, Daniel/0000-0002-2684-4741 FU National Cancer Institute (Bethesda, Maryland, USA) [2U10 CA11488-35, 5U10 CA11488-38]; Fonds Cancer/FOCA (Belgium) FX This publication was supported by grant numbers 2U10 CA11488-35 and 5U10 CA11488-38 from the National Cancer Institute (Bethesda, Maryland, USA). Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NCI. This research project was supported by Fonds Cancer/FOCA (Belgium).; The authors wish to thank the following organisations for making the data available for this analysis:; Amgen; AstraZeneca; Breast Cancer International Research Group (BCIRG); Bristol-Myers Squibb; European Organisation for Research and Treatment of Cancer (EORTC) Breast Cancer Group and Gastrointestinal Group; Erasmus University Medical Centre, Rotterdam, The Netherlands; Genentech; Pfizer; RadPharm; Roche; Sanofi Aventis NR 28 TC 85 Z9 87 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0959-8049 EI 1879-0852 J9 EUR J CANCER JI Eur. J. Cancer PD JAN PY 2009 VL 45 IS 2 SI SI BP 248 EP 260 DI 10.1016/j.ejca.2008.10.027 PG 13 WC Oncology SC Oncology GA 401NT UT WOS:000262948300003 PM 19095437 ER PT J AU Schwartz, LH Bogaerts, J Ford, R Shankar, L Therasse, P Gwyther, S Eisenhauer, EA AF Schwartz, L. H. Bogaerts, J. Ford, R. Shankar, L. Therasse, P. Gwyther, S. Eisenhauer, E. A. TI Evaluation of lymph nodes with RECIST 1.1 SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE Response criteria; Solid tumours; Guidelines; Lymph node ID COMPUTED-TOMOGRAPHY; LUNG-CANCER; HELICAL CT; CERVICAL-CARCINOMA; CRITERIA; LYMPHADENOPATHY; METASTASES; SIZE; NECK AB Lymph nodes are common sites of metastatic disease in many solid tumours. Unlike most metastases, lymph nodes are normal anatomic structures and as such, normal lymph nodes will have a measurable size. Additionally, the imaging literature recommends that lymph nodes be measured in the short axis, since the short axis measurement is a more reproducible measurement and predictive of malignancy. Therefore, the RECIST committee recommends that lymph nodes be measured in their short axis and proposes measurement values and rules for categorising lymph nodes as normal or pathologic; either target or non-target lesions. Data for the RECIST warehouse are presented to demonstrate the potential change in response assessment following these rules. These standardised lymph node guidelines are designed to be easy to implement, focus target lesion measurements on lesions that are likely to be metastatic and prevent false progressions due to minimal change in size. (C) 2008 Elsevier Ltd. All rights reserved. C1 [Schwartz, L. H.] Mem Sloan Kettering Canc Ctr, Dept Radiol, New York, NY 10021 USA. [Bogaerts, J.] European Org Res Treatment Canc, Ctr Data, Brussels, Belgium. [Ford, R.] RadPharm, Princeton, NJ USA. [Shankar, L.] NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA. [Therasse, P.] GlaxoSmithKline Biol, Rixensart, Belgium. [Gwyther, S.] E Surrey Hosp, Surrey, England. [Eisenhauer, E. A.] Natl Canc Inst Canada, Clin Trials Grp, Kingston, ON, Canada. RP Schwartz, LH (reprint author), Mem Sloan Kettering Canc Ctr, Dept Radiol, 1275 York Ave,C-276D, New York, NY 10021 USA. EM SchwartL@mskcc.org NR 30 TC 98 Z9 101 U1 0 U2 2 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD JAN PY 2009 VL 45 IS 2 BP 261 EP 267 DI 10.1016/j.ejca.2008.10.028 PG 7 WC Oncology SC Oncology GA 401NT UT WOS:000262948300004 PM 19091550 ER PT J AU Ford, R Schwartz, L Dancey, J Dodd, LE Eisenhauer, EA Gwyther, S Rubinstein, L Sargent, D Shankar, L Therasse, P Verweij, J AF Ford, R. Schwartz, L. Dancey, J. Dodd, L. E. Eisenhauer, E. A. Gwyther, S. Rubinstein, L. Sargent, D. Shankar, L. Therasse, P. Verweij, J. TI Lessons learned from independent central renew SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE Independent central review; Central review; Imaging core laboratory; Radiology review; Central independent review ID PHASE-III TRIAL; COLORECTAL-CANCER; FLUOROURACIL; LEUCOVORIN; IRINOTECAN AB Independent central review (ICR) is advocated by regulatory authorities as a means of independent verification of clinical trial end-points dependent on medical imaging, when the data from the trials may be submitted for licensing applications [Food and Drug Administration. United States food and drug administration guidance for industry: clinical trial endpoints for the approval of cancer drugs and biologics. Rockville, MD: US Department of Health and Human Services; 2007; Committee for Medicinal Products for Human Use. European Medicines Agency Committee for Medicinal Products for Human Use (CHMP) guideline on the evaluation of anticancer medicinal products in man. London, UK: European Medicines Agency; 2006; United States Food and Drug Administration Center for Drug Evaluation and Research. Approval package for application number NDA 21-492 (oxaliplatin). Rockville, MD: US Department of Health and Human Services; 2002; United States Food and Drug Administration Center for Drug Evaluation and Research. Approval package for application number NDA 21-923 (sorafenib tosylate). Rockville, MD: US Department of Health and Human Services; 2005; United States Food and Drug Administration Center for Drug Evaluation and Research. Approval package for application number NDA 22-065 (ixabepilone). Rockville, MD: US Department of Health and Human Services; 2007; United States Food and Drug Administration Center for Drug Evaluation and Research. Approval package for application number NDA 22-059 (lapatinib ditosylate). Rockville, MD: US Department of Health and Human Services; 2007; United States Food and Drug Administration Center for Biologics Evaluation and Research. Approval package for BLA numbers 970260 and BLA Number 97-0244 (rituximab). Rockville, MD: US Department of Health and Human Services; 1997; United States Food and Drug Administration. FDA clinical review of BLA 98-0369 (Herceptin trastuzumab (rhuMAb HER2)). FDA Center for Biologics Evaluation and Research; 1998; United States Food and Drug Administration. FDA Briefing Document Oncology Drugs Advisory Committee meeting NDA 21801 (satraplatin). Rockville, MD: US Department of Health and Human Services; 2007; Thomas ES, Gomez HL, Li RK, et al. Ixabepilone plus capecitabine for metastatic breast cancer progressing after anthracycline and taxane treatment. JCO 2007(November):5210-7]. In addition, clinical trial sponsors have used ICR in Phase I-II studies to assist in critical pathway decisions including in-licensing of compounds [Cannistra SA, Matulonis UA, Penson RT, et al. Phase II study of bevacizumab in patients with platinum-resistant ovarian cancer or peritoneal serous cancer. JCO 2007(November):5180-6; Perez EA, Lerzo G, Pivot X, et al. Efficacy and safety of ixabepilone (BMS-247550) in a phase II study of patients with advanced breast cancer resistant to an anthracycline, a taxane, and capecitabine.)CO 2007(August):3407-14; Vermorken JB, Trigo J, Hitt R, et al. Open-label, uncontrolled, multicenter phase II study to evaluate the efficacy and toxicity of cetuximab as a single agent in patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck who failed to respond to platinum-based therapy. JCO 2007(June):2171-7; Ghassan KA, Schwartz L, Ricci S, et al. Phase II study of sorafenib in patients with advanced hepatocellular carcinoma. JCO 2006(September):4293-300; Boue F, Gabarre J, GaBarre J, et al. Phase II trial of CHOP plus rituximab in patients with HIV-associated non-Hodgkin's lymphoma. JCO 2006(September):4123-8; Chen HX, Mooney M, Boron M, et al. Phase II multicenter trial of bevacizumab plus fluorouracil and leucovorin in patients with advanced refractory colorectal cancer: an NCI Treatment Referral Center Trial TRC-0301. JCO 2006(July):3354-60; Ratain MJ, Eisen T, Stadler VIM, et al. Phase II placebo-controlled randomized discontinuation trial of sorafenib in patients with metastatic renal cell carcinoma. JCO 2006(June):2502-12; Jaffer AA, Lee FC, Singh DA, et al. Multicenter phase II trial of S-1 plus cisplatin in patients with untreated advanced gastric or gastroesophageal junction adenocarcinoma. JCO 2006(February):663-7; Bouche O, Raoul JL, Bonnetain F, et al. Randomized multicenter phase II trial of a biweekly regimen of fluorouracil and leucovorin (LV5FU2), LVSFU2 plus cisplatin, or LV5FU2 plus irinotecan in patients with previously untreated metastatic gastric cancer: a Federation Francophone de Cancerologie Digestive Group Study-FFCD 9803. JCO 2004(November):4319-28]. This article will focus on the definition and purpose of ICR and the issues and lessons learned in the ICR setting primarily in Phase II and III oncology studies. This will include a discussion on discordance between local and central interpretations, consequences of ICR, reader discordance during the ICR, operational considerations and the need for specific imaging requirements as part of the study protocol. (C) 2008 Elsevier Ltd. All rights reserved. C1 [Ford, R.] RadPharm, Princeton, NJ 08540 USA. [Schwartz, L.] Mem Sloan Kettering Canc Ctr, New York, NY USA. [Dodd, L. E.; Rubinstein, L.; Shankar, L.] NCI, Bethesda, MD 20892 USA. [Dancey, J.; Eisenhauer, E. A.] Natl Canc Inst Canada, Clin Trials Grp, Kingston, ON, Canada. [Gwyther, S.] E Surrey Hosp, Surrey, England. [Therasse, P.] GlaxoSmithKline Biol, Rixensart, Belgium. [Verweij, J.] Erasmus Univ, Med Ctr, Rotterdam, Netherlands. [Sargent, D.] Mayo Clin, Rochester, MN USA. RP Ford, R (reprint author), RadPharm, 100 Overlook Ctr, Princeton, NJ 08540 USA. EM ford@radpharm.com NR 28 TC 46 Z9 48 U1 0 U2 7 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD JAN PY 2009 VL 45 IS 2 BP 268 EP 274 DI 10.1016/j.ejca.2008.10.031 PG 7 WC Oncology SC Oncology GA 401NT UT WOS:000262948300005 PM 19101138 ER PT J AU Dancey, JE Dodd, LE Ford, R Kaplan, R Mooney, M Rubinstein, L Schwartz, LH Shankar, L Therasse, P AF Dancey, J. E. Dodd, L. E. Ford, R. Kaplan, R. Mooney, M. Rubinstein, L. Schwartz, L. H. Shankar, L. Therasse, P. TI Recommendations for the assessment of progression in randomised cancer treatment trials SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE Progression; Solid tumours; Randomised clinical trials ID PHASE-II TRIALS; FREE SURVIVAL; SURROGATE; DESIGN AB Progression-free survival (PFS) is an increasingly important end-point in cancer drug development. However, several concerns exist regarding the use of PFS as a basis to compare treatments. Unlike survival, the exact time of progression is unknown, so progression times might be over-estimated (or under-estimated) and, consequently, bias may be introduced when comparing treatments. In addition, the assessment of progression is subject to measurement variability which may introduce error or bias. Ideally trials with PFS as the primary end-point should be randomised and, when feasible, double-blinded. All patients eligible for study should be evaluable for the primary end-point and thus, in general, have measurable disease at baseline. Appropriate definitions should be provided in the protocol and data collected on the case-report forms, if patients with only non-measurable disease are eligible and/or clinical, or symptomatic progression are to be considered progression events for analysis. Protocol defined assessments of disease burden should be obtained at intervals that are symmetrical between arms. Independent review of imaging may be of value in randomised phase II trials and phase III trials as an auditing tool to detect possible bias. (C) 2008 Elsevier Ltd. All rights reserved. C1 [Dancey, J. E.] Queens Univ, Natl Canc Inst Canada, Clin Trials Grp, Kingston, ON, Canada. [Dodd, L. E.; Mooney, M.; Rubinstein, L.; Shankar, L.] NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA. [Ford, R.] RadPharm, Princeton, NJ USA. [Kaplan, R.] Natl Canc Res Network, Leeds, W Yorkshire, England. [Schwartz, L. H.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. [Therasse, P.] GlaxoSmithKline Biol, Rixensart, Belgium. RP Dancey, JE (reprint author), Queens Univ, Natl Canc Inst Canada, Clin Trials Grp, 10 Stuart St, Kingston, ON, Canada. EM jdancey@ctg.queensu.ca NR 13 TC 57 Z9 59 U1 0 U2 4 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD JAN PY 2009 VL 45 IS 2 BP 281 EP 289 DI 10.1016/j.ejca.2008.10.042 PG 9 WC Oncology SC Oncology GA 401NT UT WOS:000262948300007 PM 19097775 ER PT J AU Sargent, DJ Rubinstein, L Schwartz, L Dancey, JE Gatsonis, C Dodd, LE Shankar, LK AF Sargent, D. J. Rubinstein, L. Schwartz, L. Dancey, J. E. Gatsonis, C. Dodd, L. E. Shankar, L. K. TI Validation of novel imaging methodologies for use as cancer clinical trial end-points SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE Surrogate endpoint; Phase II clinical trial; Meta-analysis; Imaging endpoint; RECIST ID ADVANCED COLORECTAL-CANCER; POSITRON-EMISSION-TOMOGRAPHY; PROGRESSION-FREE SURVIVAL; ONCOLOGIC DRUG DEVELOPMENT; METASTATIC BREAST-CANCER; INDIVIDUAL PATIENT DATA; 18 RANDOMIZED-TRIALS; PHASE-II; TUMOR RESPONSE; COLON-CANCER AB The success or failure of a clinical trial, of any phase, depends critically on the choice of an appropriate primary end-point. In the setting of phases II and III cancer clinical trials, imaging end-points have historically, and continue presently to play a major role in determining therapeutic efficacy. The primary goal of this paper is to discuss the validation of imaging-based markers as end-points for phase II clinical trials of cancer therapy. Specifically, we outline the issues that must be considered, and the criteria that would need to be satisfied, for an imaging end-point to supplement or potentially replace RECIST-defined tumour status as a phase II clinical trial end-point. The key criteria proposed to judge the utility of a new end-point primarily relate to its ability to accurately and reproducibly predict the eventual phase III end-point for treatment effect, which is usually assessed by a difference between two arms on progression free or overall survival, both at the patient and more importantly at the trial level. As will be demonstrated, the level of evidence required to formally and fully validate a new imaging marker as an appropriate end-point for phase II trials is substantial. In many cases, this level of evidence will only become available by conducting a series of coordinated prospectively designed multicentre clinical trials culminating in a formal meta-analysis. We also include a discussion of situations where flexibility may be required, relative to the ideal rigorous evaluation, to accommodate inevitable real-world feasibility constraints. (C) 2008 Elsevier Ltd. All rights reserved. C1 [Sargent, D. J.] Mayo Clin, Rochester, MN 55905 USA. [Rubinstein, L.; Dodd, L. E.; Shankar, L. K.] NCI, Bethesda, MD 20892 USA. [Schwartz, L.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. [Dancey, J. E.] Natl Canc Inst Canada, Clin Trials Grp, Kingston, ON, Canada. [Gatsonis, C.] Brown Univ, Providence, RI 02912 USA. RP Sargent, DJ (reprint author), Mayo Clin, 200 1st St SW, Rochester, MN 55905 USA. EM Sargent.daniel@mayo.edu OI Sargent, Daniel/0000-0002-2684-4741 FU NCI NIH HHS [U10 CA025224-30, U01 CA079778-11, U10 CA025224, U01 CA079778] NR 44 TC 67 Z9 68 U1 1 U2 8 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD JAN PY 2009 VL 45 IS 2 BP 290 EP 299 DI 10.1016/j.ejca.2008.10.030 PG 10 WC Oncology SC Oncology GA 401NT UT WOS:000262948300008 PM 19091547 ER PT J AU Tamers, SL Agurs-Collins, T Dodd, KW Nebeling, L AF Tamers, S. L. Agurs-Collins, T. Dodd, K. W. Nebeling, L. TI US and France adult fruit and vegetable consumption patterns: an international comparison SO EUROPEAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE fruits; vegetables; United States; France; Mediterranean and Western diet; obesity ID UNITED-STATES; FRENCH PARADOX; HEALTH; FOOD; TRENDS; LEVEL; DIET AB Background/Objectives: To observe fruit and vegetable consumption as it relates to body mass index (BMI) and other variables, by analyzing the health surveys of two countries-the United States and France-with traditionally distinct diets, and identifying factors that may explain the differences. Subjects/Methods: Two nationally representative surveys that assess food intake via 24-h diet recalls. Respondents include 2126 women and 1911 men from the US National Health and Nutrition Examination Survey, and 1572 women and 1141 men from the French Nutrition Barometer Survey. Standard linear regression models and t-tests of both simple and predictive marginal means were run employing the software package SUDAAN. Results: Americans appear to consume fruits and vegetables less often than their French counterparts (1.04 vs 1.33 times per day fruits; 1.98 vs 2.29 times per day vegetables). American men consume fruits and vegetables least often (0.98 times per day fruits; 1.88 times per day vegetables) than do American women or French men (1.10 vs 1.25 times per day fruits; 2.07 vs 2.18 times per day vegetables). French women consume fruits and vegetables most often (1.41 times per day fruits; 2.41 times per day vegetables). The French have lower mean BMI than Americans (23.34 vs 28.22 women; 25.20 vs 28.02 men). Regression analyses showed that age, BMI and educational attainment are strongly associated with frequency of consumption. Conclusions: These results support our hypothesis that the French tend to eat fruits and vegetables more often than Americans. This study proves to be an important first step in determining some of the influential factors that may affect various populations' consumption of fruits and vegetables. C1 [Tamers, S. L.] NCI, Hlth Promot Res Branch, Behav Res Program, Div Canc Control & Populat Sci,NIH, Rockville, MD 20852 USA. [Dodd, K. W.] NCI, Canc Prevent Div, NIH, Bethesda, MD 20892 USA. RP Tamers, SL (reprint author), NCI, Hlth Promot Res Branch, Behav Res Program, Div Canc Control & Populat Sci,NIH, 6130 Execut Blvd,EPN Room 4087B, Rockville, MD 20852 USA. EM tamerss@mail.nih.gov NR 31 TC 27 Z9 29 U1 0 U2 6 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0954-3007 J9 EUR J CLIN NUTR JI Eur. J. Clin. Nutr. PD JAN PY 2009 VL 63 IS 1 BP 11 EP 17 DI 10.1038/ejcn.2008.2 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 392HL UT WOS:000262293700002 PM 18270525 ER PT J AU Semba, RD Ricks, MO Ferrucci, L Xue, QL Guralnik, JM Fried, LP AF Semba, R. D. Ricks, M. O. Ferrucci, L. Xue, Q-L Guralnik, J. M. Fried, L. P. TI Low serum selenium is associated with anemia among older adults in the United States SO EUROPEAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE aging; anemia; inflammation; hemoglobin; selenium ID OXIDATIVE DAMAGE; HEMOGLOBIN CONCENTRATION; RAT ERYTHROCYTES; DIETARY SELENIUM; HEME OXYGENASE-1; IRON-DEFICIENCY; MORTALITY; WOMEN; INFLAMMATION; POPULATION AB Objective: We hypothesized that low serum selenium was associated with anemia in humans. Subjects: A total of 2092 adults aged 65 and older, in the third National Nutrition Examination Survey, Phase 2 (1991-1994) (NHANES III). Methods: Examination of the relationship between serum selenium and hematological indices in NHANES III. Results: Anemia, defined by World Health Organization criteria, was present in 12.9%. Mean serum selenium among non-anemic and anemic adults was 1.60 and 1.51 mu mol l(-1) (P = 0.0003). The prevalence of anemia among adults in the lowest to highest quartiles of serum selenium was 18.3, 9.5, 9.7 and 6.9%, respectively (P = 0.0005). The proportion of adults in the lowest quartile of selenium among those who were non-anemic or who had anemia due to nutritional causes, chronic inflammation, renal disease or unexplained anemia was 9.9, 27.5, 17.5, 24.0 and 15.4%, respectively. An increase in log(e) selenium was associated with a reduced risk of anemia (odds ratio per one standard deviation increase 0.75, 95% confidence interval 0.58-0.97, P = 0.03), adjusting for age, race, education, body mass index and chronic diseases. Conclusion: Low serum selenium is independently associated with anemia among older men and women in the United States. C1 [Semba, R. D.; Ricks, M. O.; Xue, Q-L; Fried, L. P.] Johns Hopkins Med Inst, Baltimore, MD 21205 USA. [Ferrucci, L.] NIA, Longitudinal Studies Sect, Clin Res Branch, Baltimore, MD 21224 USA. [Guralnik, J. M.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA. RP Semba, RD (reprint author), Johns Hopkins Univ, 550 N Broadway,Suite 700, Baltimore, MD 21205 USA. EM rdsemba@jhmi.edu FU National Institute on Aging; National Institutes of Health [R01 AG027012, R01 AG029148]; Intramural Research Branch FX This study was sponsored by National Institute on Aging, National Institutes of Health (R01 AG027012, R01 AG029148 and y). NR 50 TC 16 Z9 17 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0954-3007 J9 EUR J CLIN NUTR JI Eur. J. Clin. Nutr. PD JAN PY 2009 VL 63 IS 1 BP 93 EP 99 DI 10.1038/sj.ejcn.1602889 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 392HL UT WOS:000262293700012 PM 17805227 ER PT J AU Berger, VW AF Berger, Vance W. TI Right conclusion, wrong method SO EUROPEAN JOURNAL OF CONTRACEPTION AND REPRODUCTIVE HEALTH CARE LA English DT Letter ID TERMINATION; PREGNANCY; ABORTION; TRIAL; WOMEN C1 NCI, Bethesda, MD 20892 USA. RP Berger, VW (reprint author), NCI, Bethesda, MD 20892 USA. EM vb78c@nih.gov FU Intramural NIH HHS [Z99 CA999999] NR 7 TC 0 Z9 0 U1 0 U2 0 PU PARTHENON PUBLISHING GROUP PI LANCASTER PA RICHMOND HOUSE, WHITE CROSS, SOUTH ROAD, LANCASTER LA1 4XQ, ENGLAND SN 1362-5187 J9 EUR J CONTRACEP REPR JI Eur. J. Contracept. Reprod. Health Care PY 2009 VL 14 IS 4 BP 317 EP 318 AR PII 910950314 DI 10.1080/13625180902943297 PG 2 WC Public, Environmental & Occupational Health; Obstetrics & Gynecology SC Public, Environmental & Occupational Health; Obstetrics & Gynecology GA 474JR UT WOS:000268280100010 PM 19418374 ER PT J AU Beaven, MA AF Beaven, Michael A. TI Our perception of the mast cell from Paul Ehrlich to now SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Review DE Adaptive immunity; Autoimmune diseases; Innate immunity; Mast cell; Paul Ehrlich ID FC-EPSILON-RI; AFFINITY IGE RECEPTOR; TOLL-LIKE RECEPTOR-2; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; CATHELICIDIN ANTIMICROBIAL PEPTIDE; SLOW-REACTING SUBSTANCE; MEDIATOR RELEASE; CHEMICAL FACTORS; INNATE IMMUNITY; GROWTH-FACTOR AB just over a century ago Paul Ehrlich received the Nobel Prize for his studies of immunity. This review describes one of his legacies, the histochemical description of the mast cell, and the research that has ensued since then. After a long period of largely descriptive studies, which revealed little about the biological role of the mast cell, the field was galvanized in the 1950s by the recognition that the mast cell was the main repository of histamine and a key participant in anaphylactic reactions. Although the mast cell was long-viewed in these terms, recent research has now shown that the mast cell also plays a key role in innate and adaptive immune responses, autoimmune disease, and possibly tissue homeostasis by virtue of its expression of a diverse array of receptors and biologically active products. in addition, the responsiveness of mast cells to immunological and pathological stimulants is highly modulated by the tissue cytokine environment and by synergistic, or inhibitory, interactions among the various mast cell receptor systems. This once enigmatic cell of Paul Ehrlich has proved to be both adaptable and multifunctional. C1 NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA. RP Beaven, MA (reprint author), NHLBI, Lab Mol Immunol, NIH, Room 8N109 Bldg 10, Bethesda, MD 20892 USA. EM beavenm@nhlbi.nih.gov FU National institutes of Health FX Geoffrey B. West who, being my external examiner in 1959, sparked my interest in the mast cell; James C. Metcalfe and John P. Moore for directing my attention toward calcium and the phosphoinositides; Henry Metzger who enlightened me on various aspects of FcE:Rl aggregation, Alasdair M. Gilfillan and many colleagues for invigorating discussions and, not least, the intramural program of National Heart, Lung, and Blood Institute at the National Institutes of Health for supporting my research over the past 40 years. NR 193 TC 84 Z9 85 U1 0 U2 7 PU WILEY-V C H VERLAG GMBH PI WEINHEIM PA PO BOX 10 11 61, D-69451 WEINHEIM, GERMANY SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD JAN PY 2009 VL 39 IS 1 BP 11 EP 25 DI 10.1002/eji.200838899 PG 15 WC Immunology SC Immunology GA 400SW UT WOS:000262889900001 PM 19130582 ER PT J AU DiPaolo, RJ Shevach, EM AF DiPaolo, Richard J. Shevach, Ethan M. TI CD4(+) T-cell development in a mouse expressing a transgenic TCR derived from a Treg SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE Repertoire development; TCR; Thymus; Tolerance; Anergy ID THYMIC EPITHELIAL-CELLS; NEGATIVE SELECTION; SELF-ANTIGEN; REPERTOIRE; DIVERSITY; PEPTIDES; RECEPTOR; ORIGIN AB CD4(+)Foxp3(+) Treg maintain peripheral tolerance and influence immune responses to foreign antigens. The thymus is an important source of Treg, but controversy exists as to whether T cells are selected into the Treg lineage based on signals received through TCR specific for self-peptides. To examine the specificity of TCR expressed by Treg and its effect on CD4(+) T-cell development, we generated Treg-TCR transgenic mice. Deletion of > 90% of CD4(+) T cells in RAG-sufficient mice, and nearly 100% deletion in RAG(-/-) mice expressing this TCR indicate that the TCR is specific for an unknown, naturally expressed peptide in the thymus. Deletion occurs late in development, suggesting this peptide is presented by APC in the thymic medulla. These studies are the first to describe the effects of expressing a Treg-TCR on CD4(+) T-cell development. The implications of our data for models of Treg selection are discussed. C1 [DiPaolo, Richard J.] St Louis Univ, Sch Med, Dept Mol Microbiol & Immunol, St Louis, MO 63104 USA. [Shevach, Ethan M.] NIAID, Cellular Immunol Sect, Immunol Lab, NIH, Bethesda, MD USA. RP DiPaolo, RJ (reprint author), St Louis Univ, Sch Med, Dept Mol Microbiol & Immunol, St Louis, MO 63104 USA. EM rdipaolo@slu.edu FU NIH FX This work was supported by intramural NIH funds. We thank Dr. Ronald Schwartz for helpful discussions, Lionell Feigenbaum for generating the TCR transgenic mice, and Kanaan Natarajan, Karen Bijwaard, Mark Ebel, Sherri Koehm, Joy Eslick and Sarah Tanksley for technical assistance. We also thank Maureen Dentin for help with statistics, and Dr. Carbone for providing the OTII-TCR-Vf35 transgenic construct. NR 20 TC 26 Z9 26 U1 0 U2 1 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD JAN PY 2009 VL 39 IS 1 BP 234 EP 240 DI 10.1002/eji.200838772 PG 7 WC Immunology SC Immunology GA 400SW UT WOS:000262889900021 PM 19065648 ER PT J AU Pati, HN Das, U Das, S Bandy, B De Clercq, E Balzarini, J Kawase, M Sakagami, H Quail, JW Stables, JP Dimmock, JR AF Pati, Hari N. Das, Umashankar Das, Swagatika Bandy, Brian De Clercq, Erik Balzarini, Jan Kawase, Masami Sakagami, Hiroshi Quail, J. Wilson Stables, James P. Dimmock, Jonathan R. TI The cytotoxic properties and preferential toxicity to tumour cells displayed by some 2,4-bis(benzylidene)-8-methyl-8-azabicyclo[3.2.1]octan-3-ones and 3,5-bis(benzylidene)-1-methyl-4-piperidones SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article DE Tropinones; 4-Piperidones; Cytotoxicity; Molecular modeling; X-ray crystallography; Mitochondria ID MITOCHONDRIAL PERMEABILITY TRANSITION; RAT-LIVER MITOCHONDRIA; CANCER-THERAPY; MANNICH-BASES; DRUG DESIGN; RESPIRATION; MECHANISM; APOPTOSIS; KETONES; PORE AB This study demonstrated that replacement of the axial protons on the C2 and C6 atoms of various 1-methyl-3,5-bis(benzylidene)-4-piperidones 3 by a dimethylene bridge leading to series 2 lowered cytotoxic potencies. Four compounds 2a and 3a-c emerged as lead molecules based on their toxicity towards different neoplasms and their selective toxicity for malignant rather than normal cells. Some possible reasons for the disparity between the IC(50) values in the two series of compounds are presented based on molecular modeling, log P values and respiration in rat liver mitochondria. (C) 2008 Elsevier Masson SAS. All rights reserved. C1 [Pati, Hari N.; Das, Umashankar; Das, Swagatika; Bandy, Brian; Dimmock, Jonathan R.] Univ Saskatchewan, Coll Pharm & Nutr, Saskatoon, SK S7N 5C9, Canada. [De Clercq, Erik; Balzarini, Jan] Katholieke Univ Leuven, Rega Inst Med Res, B-3000 Louvain, Belgium. [Kawase, Masami] Matsuyama Univ, Fac Pharmaceut Sci, Matsuyama, Ehime 7908578, Japan. [Sakagami, Hiroshi] Meikai Univ, Div Pharmacol, Dept Diagnost & Therapeut Sci, Sch Dent, Saitama 3500283, Japan. [Quail, J. Wilson] Univ Saskatchewan, Saskatoon Struct Sci Ctr, Saskatoon, SK S7N 5C9, Canada. [Stables, James P.] Natl Inst Neurol Disorders & Stroke, Rockville, MD 20852 USA. RP Dimmock, JR (reprint author), Univ Saskatchewan, Coll Pharm & Nutr, 110 Sci Pl, Saskatoon, SK S7N 5C9, Canada. EM jr.dimmock@usask.ca FU Canadian Institutes of Health Research; Flemish Fonds voor Wetenschappelijk Onderzoek (FWO); Ministry of Education, Science, Sports and Culture of Japan [19592156]; Canadian Foundation; Government of Saskatchewan FX The authors thank the following agencies and individuals who enabled this study to be undertaken. The Canadian Institutes of Health Research provided operating grants to J.R. Dimmock and B. Bandy. The Molt 4/C8, CEM and L1210 assays were undertaken by Mrs. Lizette van Berckelaer and funded by the Flemish Fonds voor Wetenschappelijk Onderzoek (FWO). A Grant-in-Aid was provided by the Ministry of Education, Science, Sports and Culture of Japan to H. Sakagami (No. 19592156). The Canadian Foundation for Innovation and the Government of Saskatchewan provided funding for the X-ray crystallography laboratory. The National Institute of Neurological Disorders and Stroke undertook the rodent toxicity studies while Ms. B. McCullough typed various drafts of the manuscript. NR 43 TC 35 Z9 38 U1 1 U2 5 PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0223-5234 J9 EUR J MED CHEM JI Eur. J. Med. Chem. PD JAN PY 2009 VL 44 IS 1 BP 54 EP 62 DI 10.1016/j.ejmech.2008.03.015 PG 9 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA 397WT UT WOS:000262693700007 PM 18468733 ER PT J AU Lim, JO Jin, MK Ryu, H Kang, DW Lee, J Pearce, LV Tran, R Toth, A Blumberg, PM AF Lim, Ju-Ok Jin, Mi-Kyoung Ryu, HyungChul Kang, Dong Wook Lee, Jeewoo Pearce, Larry V. Tran, Richard Toth, Attila Blumberg, Peter M. TI Conformationally constrained analogues of N '-(4-tert-butylbenzyl)-N(4-methylsulfonylaminobenzyl)thiourea as TRPV1 antagonists SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article DE TRPV1 antagonists; Analgesic; Conformationally constrained analogues ID HIGH-AFFINITY ANTAGONISTS; VANILLOID RECEPTOR; CAPSAICIN RECEPTORS; CHANNEL; POTENT; PAIN; REGION AB A series of bicyclic analogues having indan and tetrahydronaphthalene templates in the A-region were designed as conformationally constrained analogues of our previously reported potent TRPV1 antagonists (1, 3). The activities for rat TRPV1 of the conformationally restricted analogues were moderately or markedly diminished, particularly in the case of the tetrahydronaphthalene analogues. The analysis indicated that steric constraints at the benzylic position in the bicyclic analogues may be an important factor for their unfavorable interaction with the receptor. (C) 2008 Elsevier Masson SAS. All rights reserved. C1 [Lim, Ju-Ok; Jin, Mi-Kyoung; Ryu, HyungChul; Kang, Dong Wook; Lee, Jeewoo] Seoul Natl Univ, Coll Pharm, Pharmaceut Sci Res Inst, Med Chem Lab, Seoul 151742, South Korea. [Pearce, Larry V.; Tran, Richard; Toth, Attila; Blumberg, Peter M.] NCI, Lab Canc Biol & Genet, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Lee, J (reprint author), Seoul Natl Univ, Coll Pharm, Pharmaceut Sci Res Inst, Med Chem Lab, Seoul 151742, South Korea. EM jeewoo@snu.ac.kr RI Toth, Attila/F-4859-2010 OI Toth, Attila/0000-0001-6503-3653 FU MOST/KOSEF [R11-2007-107-02001-0]; NIH; National Cancer Institute; Center for Cancer Research FX This work was supported by the ERC program of MOST/KOSEF (R11-2007-107-02001-0) and in part by the intramural research program of the NIH, National Cancer Institute, Center for Cancer Research. NR 19 TC 2 Z9 2 U1 0 U2 2 PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0223-5234 J9 EUR J MED CHEM JI Eur. J. Med. Chem. PD JAN PY 2009 VL 44 IS 1 BP 322 EP 331 DI 10.1016/j.ejmech.2008.02.026 PG 10 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA 397WT UT WOS:000262693700035 PM 18406014 ER PT J AU Adermark, L Talani, G Lovinger, DM AF Adermark, Louise Talani, Giuseppe Lovinger, David M. TI Endocannabinoid-dependent plasticity at GABAergic and glutamatergic synapses in the striatum is regulated by synaptic activity SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Article DE anandamide; basal ganglia; LTD; L-type calcium channel; synaptic plasticity ID LONG-TERM DEPRESSION; MEDIUM SPINY NEURONS; CEREBELLAR PURKINJE-CELLS; CANNABINOID RECEPTOR; CA2+ CHANNELS; MEMBRANE-TRANSPORT; PROTEIN-SYNTHESIS; BASAL GANGLIA; CB1 RECEPTOR; RAT-BRAIN AB Long-term depression (LTD) at striatal synapses is mediated by postsynaptic endocannabinoid (eCB) release and presynaptic cannabinoid 1 receptor (CB(1)R) activation. Previous studies have indicated that eCB mobilization at excitatory synapses might be regulated by afferent activation. To further address the role of neuronal activity in synaptic plasticity we examined changes in synaptic strength induced by the L-type calcium channel activator 2,5-dimethyl-4-[2-(phenylmethyl)benzoyl]-1H-pyrrole-3-carboxylic acid methyl ester (FPL 64176, FPL) at glutamatergic and gamma-aminobutyric acid (GABA)ergic synapses in the striatum. We found that the basic mechanisms for FPL-mediated eCB signaling are the same at glutamatergic and GABAergic synapses. FPL-induced LTD (FPL-LTD) was blocked in slices treated with the CB(1)R antagonist AM251 (2 mu m), but established depression was not reversed by AM251. FPL-LTD was temperature dependent, blocked by protein translation inhibitors and prevented by intracellular loading of the anandamide transporter inhibitor VDM11 (10 mu m) at both glutamatergic and GABAergic synapses. FPL-LTD at glutamatergic synapses required paired-pulse afferent stimulation, while FPL-LTD at GABAergic synapses could be induced even in the absence of explicit afferent activation. By evaluating tetrodotoxin-insensitive spontaneous inhibitory postsynaptic currents we found that neuronal firing is vital for eCB release and LTD induction at GABAergic synapses, but not for short-term depression induced by CB(1)R agonist. The data presented here suggest that the level of neuronal firing regulates eCB signaling by modulating release from the postsynaptic cell, as well as interacting with presynaptic mechanisms to induce LTD at both glutamatergic and GABAergic synapses in the striatum. C1 [Adermark, Louise; Talani, Giuseppe; Lovinger, David M.] NIAAA, Sect Synapt Pharmacol, Lab Integrat Neurosci, NIH, Bethesda, MD 20892 USA. RP Lovinger, DM (reprint author), NIAAA, Sect Synapt Pharmacol, Lab Integrat Neurosci, NIH, Bethesda, MD 20892 USA. EM lovindav@mail.nih.gov RI Adermark, Louise/D-2297-2014 OI Adermark, Louise/0000-0002-7165-9908 FU Division of Intramural Clinical and Basic Research; NIAAA; NIH; Swedish Research Council; Swedish Society for Medical Research [2006-2425, 2006-4988, 2006-6385]; Ake Wiberg Foundation [113300049]; Swedish Society of Medicine [2008-21390] FX This work was supported by the Division of Intramural Clinical and Basic Research, NIAAA, NIH, The Swedish Research Council, the Swedish Society for Medical Research (2006-2425; 2006-4988; 2006-6385), Ake Wiberg Foundation (113300049) and The Swedish Society of Medicine (2008-21390). NR 39 TC 64 Z9 64 U1 1 U2 7 PU WILEY-BLACKWELL PUBLISHING, INC PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PD JAN PY 2009 VL 29 IS 1 BP 32 EP 41 DI 10.1111/j.1460-9568.2008.06551.x PG 10 WC Neurosciences SC Neurosciences & Neurology GA 387OO UT WOS:000261961700004 PM 19120438 ER PT J AU Wang, HL Morales, M AF Wang, Hui-Ling Morales, Marisela TI Pedunculopontine and laterodorsal tegmental nuclei contain distinct populations of cholinergic, glutamatergic and GABAergic neurons in the rat SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Article DE dopamine; LDTg; PPTg; reward; substantia nigra; ventral tegmental area ID INORGANIC-PHOSPHATE TRANSPORTER; MIDBRAIN DOPAMINERGIC-NEURONS; VESICULAR GLUTAMATE; SUBSTANTIA-NIGRA; MESOPONTINE TEGMENTUM; ACETYLTRANSFERASE IMMUNOHISTOCHEMISTRY; IMMUNOCYTOCHEMICAL LOCALIZATION; PONTOMESENCEPHALIC TEGMENTUM; NONCHOLINERGIC NEURONS; SUBTHALAMIC NUCLEUS AB The pedunculopontine tegmental nucleus (PPTg) and laterodorsal tegmental nucleus (LDTg) provide cholinergic afferents to several brain areas. This cholinergic complex has been suggested to play a role in sleep, waking, motor function, learning and reward. To have a better understanding of the neurochemical organization of the PPTg/LDTg we characterized the phenotype of PPTg/LDTg neurons by determining in these cells the expression of transcripts encoding choline acetyltransferase (ChAT), glutamic acid decarboxylase (GAD) or the vesicular glutamate transporters (vGluT1, vGluT2 and vGluT3). Within the PPTg/LDTg complex we found neurons expressing ChAT, vGluT2 or GAD transcripts, these neuronal phenotypes were intermingled, but not homogeneously distributed within the PPTg or LDTg. Previous studies suggested the presence of either glutamate or gamma-aminobutyric acid (GABA) immunolabeling in a large number of PPTg/LDTg cholinergic neurons, leading to the widespread notion that PPTg/LDTg cholinergic neurons co-release acetylcholine together with either glutamate or GABA. To assess the glutamatergic or GABAergic nature of the PPTg/LDTg cholinergic neurons, we combined in situ hybridization (to detect vGluT2 or GAD transcripts) and immunohistochemistry (to detect ChAT), and found that over 95% of all PPTg/LDTg cholinergic neurons lack transcripts encoding either vGluT2 mRNA or GAD mRNA. As the vast majority of PPTg/LDTg cholinergic neurons lack transcripts encoding essential proteins for the vesicular transport of glutamate or for the synthesis of GABA, co-release of acetylcholine with either glutamate or GABA is unlikely to be a major factor in the interactions between acetylcholine, glutamate and GABA at the postsynaptic site. C1 [Wang, Hui-Ling; Morales, Marisela] Natl Inst Drug Abuse, Intramural Res Program, Biomed Res Ctr, Baltimore, MD 21224 USA. RP Morales, M (reprint author), Natl Inst Drug Abuse, Intramural Res Program, Biomed Res Ctr, 251 Bayview Blvd, Baltimore, MD 21224 USA. EM mmorales@intra.nida.nih.gov FU Intramural Research Program of the National Institute on Drug Abuse FX This work was supported by the Intramural Research Program of the National Institute on Drug Abuse. NR 70 TC 185 Z9 186 U1 0 U2 9 PU WILEY-BLACKWELL PUBLISHING, INC PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PD JAN PY 2009 VL 29 IS 2 BP 340 EP 358 DI 10.1111/j.1460-9568.2008.06576.x PG 19 WC Neurosciences SC Neurosciences & Neurology GA 395HQ UT WOS:000262515600012 PM 19200238 ER PT J AU McNeill, A Birchall, D Straub, V Goldfarb, L Reilich, P Walter, MC Schramm, N Lochmuller, H Chinnery, PF AF McNeill, Alisdair Birchall, Daniel Straub, Volker Goldfarb, Lev Reilich, Peter Walter, Maggie C. Schramm, Nicolai Lochmueller, Hanns Chinnery, Patrick F. TI Lower Limb Radiology of Distal Myopathy due to the S60F Myotilin Mutation SO EUROPEAN NEUROLOGY LA English DT Article DE Distal myopathies; Lower limb radiology; Myotilinopathy; S60F myotilin mutation; Titin myopathy; TTID mutation; Welander distal myopathy ID MUSCULAR-DYSTROPHY; GENE; INVOLVEMENT; PHENOTYPE; MRI AB Distal myopathies are a clinically and genetically heterogenous group of disorders in which the distal limb musculature is selectively or disproportionately affected. Precisely defining specific categories is a challenge because of overlapping clinical phenotypes, making it difficult to decide which of the many known causative genes to screen in individual cases. In this study we define the distinguishing magnetic resonance imaging findings in myotilin myopathy by studying 8 genealogically unrelated cases due to the same point mutation in TTID. Proximally, the vastii, biceps femoris and semimembranosus were involved with sparing of gracilis and sartorius. Distally, soleus, gastrocnemius, tibialis anterior, extensor hallicus and extensor digitorum were involved. This pattern contrasts with other distal myopathies and provides further support for the role of imaging in the clinical investigation of muscle disease. Copyright (C) 2009 S. Karger AG, Basel C1 [Chinnery, Patrick F.] Univ Newcastle Tyne, Mitochondrial Res Grp, Sch Med, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England. [McNeill, Alisdair] Birmingham Womens Hosp, Clin Genet Unit, Birmingham, W Midlands, England. [Birchall, Daniel] Newcastle Gen Hosp, Reg Neurosci Ctr, Newcastle Upon Tyne NE4 6BE, Tyne & Wear, England. [Straub, Volker; Chinnery, Patrick F.] Int Ctr Life, Inst Human Genet, MRC Neuromuscular Ctr, Newcastle Upon Tyne, Tyne & Wear, England. [Goldfarb, Lev] Natl Inst Neurol Disorders & Stroke, Bethesda, MD USA. [Reilich, Peter; Walter, Maggie C.] Friedrich Baur Inst, Dept Neurol, Munich, Germany. [Schramm, Nicolai] Univ Munich, Munich, Germany. RP Chinnery, PF (reprint author), Univ Newcastle Tyne, Mitochondrial Res Grp, Sch Med, Framlington Pl, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England. EM p.f.chinnery@ncl.ac.uk RI mcneill, alisdair/B-1267-2012; OI Lochmuller, Hanns/0000-0003-2324-8001 FU Wellcome Trust; German Ministry of Education and Research [01GM0601] FX P. F. C. is a Wellcome Trust Senior Fellow in Clinical Science. MD-NET and TREAT-NMD (V. S., M. W., H. L.); MRC Centre for Neuromuscular Disease (P. F. C., V. S., H. K.). V. S., H. L. and M. C. W. are members of the German Muscular Dystrophy Network (MDNET 01GM0601) funded by the German Ministry of Education and Research (BMBF, Bonn, Germany); www.md-net.org.MDNET is a partner of TREAT-NMD (EC, 6th FP, proposal #036825; www.treat-nmd.eu). A. M. is an NIHR Academic Clinical Fellow. NR 24 TC 5 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0014-3022 J9 EUR NEUROL JI Eur. Neurol. PY 2009 VL 62 IS 3 BP 161 EP 166 DI 10.1159/000227266 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 472CV UT WOS:000268107700007 PM 19590214 ER PT J AU Dunnick, JK Nyska, A AF Dunnick, June K. Nyska, Abraham TI Characterization of liver toxicity in F344/N rats and B6C3F1 mice after exposure to a flame retardant containing lower molecular weight polybrominated diphenyl ethers SO EXPERIMENTAL AND TOXICOLOGIC PATHOLOGY LA English DT Article DE Flame retardant; Polybrominated diphenyl ethers; Liver toxicity ID IN-VITRO; GENE-EXPRESSION; RISK-ASSESSMENT; INDUCTION; CARCINOGENICITY; DISPOSITION; PBDES; ENVIRONMENT; METABOLISM; RODENTS AB Lower molecular weight polybrominated diphenyl ethers (PBDEs), components of flame retardants, are found in the environment and in human and animal tissues. Toxicity studies were conducted in F344/N rats and B6C3F1 mice by administering a flame retardant containing these lower molecular weight PBDEs (BDE-47, BDE-99, BDE-100, and BDE153) by oral gavage 5 days/week for 13 weeks at doses of 0.01, 5.50, 100 or 500 mg/kg/day. Liver was the primary target organ in rats and mice. Treatment-related increases in liver weights, liver cytochrome P450 (1A1, 1A2, 2B) and UDPGT (rats only) levels. and liver lesions were seen in both, rats and mice. Hepatocyte hypertrophy and vacuolization increased ill incidence and severity with treatment, and occurred at levels of 50 mg/kg and above ill rats. and at 100 mg/kg and above in mice. Liver Cyp 1A1, 1A2, and 2B levels were increased at exposure levels of 50 mg/kg and above ill rats and mice. In addition, treatment-related thyroid lesions Occurred particularly in rats. The most sensitive parameter for PBDE toxicity was the increase in liver weights which occurred at 5 mg/kg above in rats and 50mg/kg and above in mice. These results suggest that liver may be a target organ for carcinogenesis processes after long-term administration of PBDEs. A chronic PBDE study is currently being conducted by the National Toxicology Program. Published by Elsevier GmbH. C1 [Dunnick, June K.; Nyska, Abraham] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC 27709 USA. RP Dunnick, JK (reprint author), Natl Inst Environm Hlth Sci, POB 12233, Res Triangle Pk, NC 27709 USA. EM dunnickj@niehs.nih.gov FU NIEHS Intramural Program; NIH [N01-ES-45516, N01-ES-05456, N01-ES-55551] FX We thank Dr. Michael Sanders, NIEHS, and Dr. Bhanu Singh, NIEHS, for their review of this manuscript. This work was supported by the NIEHS Intramural Program. Animals were exposed to PBDEs at an NTP contract laboratory, and determinations of polybrominated diphenyl ether tissue levels were performed at another NTP Laboratory (NIH contracts N01-ES-45516, N01-ES-05456, and N01-ES-55551). NR 51 TC 18 Z9 19 U1 3 U2 9 PU ELSEVIER GMBH, URBAN & FISCHER VERLAG PI JENA PA OFFICE JENA, P O BOX 100537, 07705 JENA, GERMANY SN 0940-2993 EI 1618-1433 J9 EXP TOXICOL PATHOL JI Exp. Toxicol. Pathol. PD JAN PY 2009 VL 61 IS 1 BP 1 EP 12 DI 10.1016/j.etp.2008.06.008 PG 12 WC Pathology; Toxicology SC Pathology; Toxicology GA 405WJ UT WOS:000263254600001 PM 18774282 ER PT J AU Port, NL Wurtz, RH AF Port, Nicholas L. Wurtz, Robert H. TI Target selection and saccade generation in monkey superior colliculus SO EXPERIMENTAL BRAIN RESEARCH LA English DT Article; Proceedings Paper CT Conference on the Physiology of Mind CY NOV 15-16, 2007 CL Univ Pavia, Pavia, ITALY HO Univ Pavia DE Target selection; Superior colliculus; Saccades; Priming ID FRONTAL EYE FIELD; VISUAL-SEARCH TASK; PERCEPTUAL DECISION; DISCRIMINATION TASK; PARIETAL CORTEX; NEURONS; MACAQUE; RESPONSES; AREA; MOVEMENTS AB The superior colliculus (SC) of the monkey has been shown to be involved in not only initiation of saccades but in the selection of the target to which the saccade can be directed. The present experiments examine whether SC neuronal activity related to target selection is also related to saccade generation. In an asynchronous target task, the monkey was required to make a saccade to the first of two spots of light to appear. Using choice probability analysis over multiple trials, we determined the earliest time at which neurons in the SC intermediate layers indicated target selection. We then determined how closely the neuronal selection was correlated to saccade onset by using our asynchronous reaction time task, which allowed the monkey to make a saccade to the target as soon as the selection had been made. We found that the selection became evident at widely differing times for different neurons. Some neurons indicated target selection just before the saccade (close to the pre-saccadic burst of activity), others did so at the time of the visual response, and some showed an increase in their activity even before the target appeared. A fraction of this pre-stimulus bias resulted from a priming effect of the previous trial; a saccade to the target in the movement field on the previous trial produced both a higher level of neuronal activity and a higher probability for a saccade to that target on the current trial. We found that most of the neurons (76%) showed a correlation between selection time and reaction time. Furthermore, within this 76% of neurons, many indicated a selection very early during the visual response. There was no evidence of a sequence from target selection first and saccade selection later, but rather that target selection and saccade initiation are intertwined and are probably inseparable. C1 [Port, Nicholas L.] Indiana Univ, Sch Optometry, Bloomington, IN 47401 USA. [Port, Nicholas L.; Wurtz, Robert H.] NEI, Sensorimotor Res Lab, NIH, Bethesda, MD 20892 USA. RP Port, NL (reprint author), Indiana Univ, Sch Optometry, 800 E Atwater Ave, Bloomington, IN 47401 USA. EM nport@indiana.edu FU Intramural NIH HHS [ZIA EY000109-29] NR 50 TC 12 Z9 13 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0014-4819 J9 EXP BRAIN RES JI Exp. Brain Res. PD JAN PY 2009 VL 192 IS 3 BP 465 EP 477 DI 10.1007/s00221-008-1609-0 PG 13 WC Neurosciences SC Neurosciences & Neurology GA 384RY UT WOS:000261763100017 PM 19030853 ER PT J AU Rossi, AF Pessoa, L Desimone, R Ungerleider, LG AF Rossi, Andrew F. Pessoa, Luiz Desimone, Robert Ungerleider, Leslie G. TI The prefrontal cortex and the executive control of attention SO EXPERIMENTAL BRAIN RESEARCH LA English DT Article; Proceedings Paper CT Conference on the Physiology of Mind CY NOV 15-16, 2007 CL Univ Pavia, Pavia, ITALY HO Univ Pavia ID RIGHT FRONTAL-CORTEX; EVENT-RELATED FMRI; NEURAL MECHANISMS; VISUAL-ATTENTION; TOP-DOWN; COGNITIVE CONTROL; WORKING-MEMORY; NEURONAL-ACTIVITY; DEFICITS; LESIONS AB We review two studies aimed at understanding the role of prefrontal cortex (PFC) in the control of attention. The first study examined which attentional functions are critically dependent on PFC by removing PFC unilaterally and transecting the forebrain commissures in two macaques. The monkeys fixated a central cue and discriminated the orientation of a colored target grating presented among colored distracter gratings in either the hemifield affected by the PFC lesion or the normal control hemifield. When the cue was held constant for many trials, task performance in the affected hemifield was nearly normal. However, performance was severely impaired when the cue was switched frequently across trials. The monkeys were unimpaired in a pop-out task with changing targets that did not require top-down attentional control. Thus, the PFC lesion resulted in selective impairment in the monkeys' ability to switch top-down control. In the second study, we used fMRI to investigate the neural correlates of top-down control in humans performing tasks identical to those used in the monkey experiments. Several fronto-parietal and posterior visual areas showed enhanced activation when attention was switched, which was greater on color cueing (top-down) trials relative to pop-out trials. Taken together, our findings indicate that both frontal and parietal cortices are involved in generating top-down control signals for attentive switching, which may then be fed back to visual processing areas. The PFC in particular plays a critical role in the ability to switch attentional control on the basis of changing task demands. C1 [Ungerleider, Leslie G.] NIMH, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA. [Rossi, Andrew F.] NIMH, Div Neurosci & Basic Behav Sci, NIH, Bethesda, MD 20892 USA. [Pessoa, Luiz] Indiana Univ, Dept Psychol & Brain Sci, Bloomington, IN 47405 USA. [Desimone, Robert] MIT, McGovern Inst Brain Res, Cambridge, MA 02139 USA. RP Ungerleider, LG (reprint author), NIMH, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA. EM rossia@mail.nih.gov; lpessoa@indiana.edu; desimone@mit.edu; ungerlel@mail.nih.gov FU Intramural NIH HHS [Z01 MH002035-27]; NIMH NIH HHS [R01 MH071589, R01 MH071589-05] NR 60 TC 98 Z9 101 U1 2 U2 19 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0014-4819 J9 EXP BRAIN RES JI Exp. Brain Res. PD JAN PY 2009 VL 192 IS 3 BP 489 EP 497 DI 10.1007/s00221-008-1642-z PG 9 WC Neurosciences SC Neurosciences & Neurology GA 384RY UT WOS:000261763100019 PM 19030851 ER PT J AU Emmert, S Ueda, T Zumsteg, U Weber, P Khan, SG Oh, KS Boyle, J Laspe, P Zachmann, K Boeckmann, L Kuschal, C Bircher, A Kraemer, KH AF Emmert, Steffen Ueda, Takahiro Zumsteg, Urs Weber, Peter Khan, Sikandar G. Oh, Kyu-Seon Boyle, Jennifer Laspe, Petra Zachmann, Karolin Boeckmann, Lars Kuschal, Christiane Bircher, Andreas Kraemer, Kenneth H. TI Strict sun protection results in minimal skin changes in a patient with xeroderma pigmentosum and a novel c.2009delG mutation in XPD (ERCC2) SO EXPERIMENTAL DERMATOLOGY LA English DT Article DE cancer prevention; DNA repair; sun protection; xeroderma pigmentosum; XPD ID COCKAYNE-SYNDROME; DNA-REPAIR; GENE; TRICHOTHIODYSTROPHY; GENOTYPE; FEATURES; CANCER AB We examined the clinical, molecular and genetic features of a 16-year-old boy (XP2GO) with xeroderma pigmentosum (XP) and progressive neurological symptoms. The parents are not consanguineous. Increased sun sensitivity led to the diagnosis of XP at 2 years of age and a strict UV protection scheme was implemented. Besides recurrent conjunctivitis and bilateral pterygium, only mild freckling was present on his lips. He shows absent deep tendon reflexes, progressive sensorineural deafness and progressive mental retardation. MRI shows diffuse frontal cerebral atrophy and dilated ventricles. Symptoms of trichothiodystrophy (brittle hair with a tiger-tail banding pattern on polarized microscopy) or Cockayne syndrome (cachectic dwarfism, cataracts, pigmentary retinopathy and spasticity) were absent. XP2GO fibroblasts showed reduced post-UV cell survival (D(37) = 3.8 J/m(2)), reduced nucleotide excision repair, reduced expression of XPD mRNA and an undetectable level of XPD protein. Mutational analysis of the XPD gene in XP2GO revealed two different mutations: a common p.Arg683Trp amino acid change (c.2047C > T) known to be associated with XP and a novel frameshift mutation c.2009delG (p.Gly670Alafs*39). The latter mutation potentially behaves as a null allele. While not preventing neurological degeneration, early diagnosis and rigorous sun protection can result in minimal skin disease without cancer in XP patients. C1 [Emmert, Steffen; Laspe, Petra; Zachmann, Karolin; Boeckmann, Lars; Kuschal, Christiane] Univ Gottingen, Dept Dermatol, D-37075 Gottingen, Germany. [Ueda, Takahiro; Khan, Sikandar G.; Oh, Kyu-Seon; Boyle, Jennifer; Kraemer, Kenneth H.] NCI, Basic Res Lab, Ctr Canc Res, NIH, Bethesda, MD USA. [Zumsteg, Urs; Weber, Peter] Univ Childrens Hosp, Basel, Switzerland. [Bircher, Andreas] Univ Basel Hosp, Dept Dermatol, CH-4031 Basel, Switzerland. RP Emmert, S (reprint author), Univ Gottingen, Dept Dermatol, Von Siebold Str 3, D-37075 Gottingen, Germany. EM semmert@gwdg.de OI Kuschal, Christiane/0000-0001-6113-3585 FU Intramural Research Program of the NIH; Center for Cancer Research of the National Cancer Institute; Deutsche Forschungsgemeinschaft [EM 63/3-1, GRK 1034] FX This research was supported in part by the Intramural Research Program of the NIH and the Center for Cancer Research of the National Cancer Institute. S. E., L. B. and C. K. were supported by grants from the Deutsche Forschungsgemeinschaft (EM 63/3-1 and GRK 1034). NR 15 TC 17 Z9 17 U1 0 U2 1 PU WILEY-BLACKWELL PUBLISHING, INC PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0906-6705 J9 EXP DERMATOL JI Exp. Dermatol. PD JAN PY 2009 VL 18 IS 1 BP 64 EP 68 DI 10.1111/j.1600-0625.2008.00763.x PG 5 WC Dermatology SC Dermatology GA 382RE UT WOS:000261622300009 PM 18637129 ER PT J AU Popp, O Fahrer, J Bohr, VA Burkle, A AF Popp, O. Fahrer, J. Bohr, V. A. Buerkle, A. TI Interaction of poly(ADP-ribose) with the Werner protein and its involvement in the aging process SO EXPERIMENTAL GERONTOLOGY LA English DT Meeting Abstract CT 9th International Symposium on the Neurobiology and Neuroendocrinology of Aging CY JUL 20-25, 2008 CL Bregenz, AUSTRIA C1 [Popp, O.; Fahrer, J.; Buerkle, A.] Univ Konstanz, Chair Mol Toxicol, Constance, Germany. [Bohr, V. A.] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PD JAN-FEB PY 2009 VL 44 IS 1-2 MA 18 BP 131 EP 131 DI 10.1016/j.exger.2008.08.032 PG 1 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA 396XA UT WOS:000262623800041 ER PT J AU Stang, SL Lopez-Campistrous, A Song, X Dower, NA Blumberg, PM Wender, PA Stone, JC AF Stang, Stacey L. Lopez-Campistrous, Ana Song, Xiaohua Dower, Nancy A. Blumberg, Peter M. Wender, Paul A. Stone, James C. TI A proapoptotic signaling pathway involving RasGRP, Erk, and Bim in B cells SO EXPERIMENTAL HEMATOLOGY LA English DT Article ID BCL-2 FAMILY-MEMBERS; PROTEIN-KINASE-C; NEGATIVE SELECTION; BH3-ONLY PROTEINS; T-CELL; PHOSPHORYLATION; APOPTOSIS; ANTIGEN; ACTIVATION; DEATH AB Objective. Bryostatin-1 and related diacylglycerol (DAG) analogues activate RasGRPs in lymphocytes, thereby activating Ras and mimicking some aspects of immune receptor signaling. To define the role of RasGRPs in lymphocyte apoptosis and to identify potential therapeutic uses for DAG analogues in lymphocyte disorders, we characterized the response of lymphoma-derived cell lines to DAG analogues. Materials and Methods. Human lymphoma-derived B cell lines and mouse primary B cells were treated with bryostatin-1 or its synthetic analogue "pico." Ras signaling partners and Bcl-2 family members were studied with biochemical assays. Cellular responses were monitored using growth and apoptosis assays. Results. Stimulation of B cells with DAG analogues results in activation of protein kinase C/RasGRP-Ras-Raf-Mek-Erk signaling and phosphorylation of the proapoptotic BH3-only protein Bim. In vitro, Bim is phosphorylated by Erk on sites previously associated with increased apoptotic activity. In Toledo B cells derived from a non-Hodgkin's lymphoma (B-NHL), DAG analogue stimulation leads to extensive apoptosis. Apoptosis can be suppressed by either downregulation of Bim or overexpression of Bcl-2. It is associated with the formation of Bak - Bax complexes and increased mitochondrial membrane permeability. Toledo B-NHL cell apoptosis shows a striking dependence on sustained signaling. Conclusion. In B cells, Erk activation leads directly to phosphorylation of Bim on sites associated with activation of Bim. In Toledo B-NHL cells, the dependence of apoptosis on sustained signaling suggests that Bcl-2 family members could interpret signal duration, an important determinant of B cell receptor - mediated negative selection. Certain cases of B-NHL might respond to DAG analogue treatment by the mechanism outlined here. (C) 2009 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc. C1 [Stang, Stacey L.; Lopez-Campistrous, Ana; Song, Xiaohua; Stone, James C.] Univ Alberta, Dept Biochem, Edmonton, AB T6G 2H7, Canada. [Blumberg, Peter M.] NIH, Lab Canc Biol & Genet, Bethesda, MD 20892 USA. [Wender, Paul A.] Stanford Univ, Dept Chem & Syst Biol, Stanford, CA 94305 USA. RP Stone, JC (reprint author), Univ Alberta, Dept Biochem, Edmonton, AB T6G 2H7, Canada. EM jim.stone@ualberta.ca FU Canadian Institutes of Health Research; Alberta Cancer Board; Alberta Heritage Foundation of Medical Research; National Institutes of Health [CA31845]; National Cancer Center; Center For Cancer Research FX This work was supported by grants from Canadian Institutes of Health Research, the Alberta Cancer Board and the Alberta Heritage Foundation of Medical Research (J.C.S.), the Intramural Research Program of the National Institutes of Health, National Cancer Center, Center For Cancer Research and a grant from the National Institutes of Health (CA31845). We thank H.M. Hu for the siRNA vectors and C. Bleakley for the Bcl-2 expression vector. We thank Michele Barry, Raymond Lai, Hanne Ostergaard, Ing Swie Goping, Troy Baldwin and Eileen White for useful suggestions. NR 39 TC 23 Z9 24 U1 1 U2 4 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD JAN PY 2009 VL 37 IS 1 BP 122 EP 134 DI 10.1016/j.exphem.2008.09.008 PG 13 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA 391EL UT WOS:000262216400014 PM 19100522 ER PT J AU Singh, V Singh, K Amdekar, S Singh, DD Tripathi, P Sharma, GL Yadav, H AF Singh, Vinod Singh, Kiran Amdekar, Sarika Singh, Desh Deepak Tripathi, Parul Sharma, Ganda L. Yadav, Hariom TI Innate and specific gut-associated immunity and microbial interference SO FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY LA English DT Review DE anti-inflammatory; cytokines; gut-associated immunity; microbial interference; probiotics; replacement therapy ID INTESTINAL EPITHELIAL-CELLS; LACTIC-ACID BACTERIA; SECRETORY IGA; GASTROINTESTINAL-TRACT; LACTOBACILLUS-CASEI; COMMENSAL BACTERIA; ATOPIC DISEASE; CROHNS-DISEASE; IN-VIVO; PROBIOTICS AB Certain bacterial species isolated from the gastrointestinal microbial communities release low-molecular-weight peptides into milk products using bacteria-derived proteases that degrade milk casein, and thereby generate peptides, triggering immune responses. The intestinal microbial communities contributes to the processing of food antigens in the gut. The present study was designed to investigate the immunomodulatory effects of microbial interference to determine whether casein degraded by probiotic bacteria-derived enzymes could modulate the cytokine production and peripheral blood mononuclear cells in atopic infants with cow or other synthetic milk allergy. Without hydrolyzation, casein reduced the production of interleukin-4, which indicates that probiotics modify the structure of potentially harmful antigens and thereby alter the mode of their immunogenicity. Intraluminal bacterial antigens have been reported to elicit specific responses in the gut-associated lymphoid tissue (GALT) through the binding capacity of intraluminal bacterial antigens to epithelial cells, which allows antigen entry via enterocytes and aids in evading the tolerance function in Peyer's patches. Such tonic immune responses in the GALT may allow control of the metabolic activity and balance of the gut microbial communities. C1 [Singh, Vinod; Singh, Kiran; Amdekar, Sarika] Barkatullah Univ, Dept Microbiol, Bhopal 462026, MP, India. [Singh, Desh Deepak] Bundelkhand Univ, Inst Biomed Sci, Jhansi, Uttar Pradesh, India. [Tripathi, Parul] Int Ctr Genet Engn & Biotechnol, Basic Immunol Lab, New Delhi, India. [Sharma, Ganda L.] Inst Genom & Integrat Biol, Dept Biochem, New Delhi, India. [Yadav, Hariom] NIDDK, NIH, Bethesda, MD USA. RP Singh, V (reprint author), Barkatullah Univ, Dept Microbiol, Bhopal 462026, MP, India. EM vsingh3@rediffmail.com RI Ganju, Shahji/F-3409-2012; OI Yadav, Hariom/0000-0003-4504-1597 NR 46 TC 18 Z9 19 U1 1 U2 11 PU WILEY-BLACKWELL PUBLISHING, INC PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0928-8244 J9 FEMS IMMUNOL MED MIC JI FEMS Immunol. Med. Microbiol. PD JAN PY 2009 VL 55 IS 1 BP 6 EP 12 DI 10.1111/j.1574-695X.2008.00497.x PG 7 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 392DL UT WOS:000262283000002 PM 19077031 ER PT J AU de Lorenzo, V Galperin, M AF de Lorenzo, Victor Galperin, Michael TI Microbial systems biology: bottom up and top down SO FEMS MICROBIOLOGY REVIEWS LA English DT Editorial Material C1 [de Lorenzo, Victor] CSIC, Ctr Nacl Biotecnol, Madrid 28049, Spain. [Galperin, Michael] Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. RP de Lorenzo, V (reprint author), CSIC, Ctr Nacl Biotecnol, Campus Cantoblanco, Madrid 28049, Spain. EM vdlorenzo@cnb.csic.es; galperin@ncbi.nlm.nih.gov RI Galperin, Michael/B-5859-2013; OI Galperin, Michael/0000-0002-2265-5572; de Lorenzo, Victor/0000-0002-6041-2731 NR 0 TC 2 Z9 2 U1 0 U2 3 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0168-6445 J9 FEMS MICROBIOL REV JI Fems Microbiol. Rev. PD JAN PY 2009 VL 33 IS 1 BP 1 EP 2 DI 10.1111/j.1574-6976.2008.00147.x PG 2 WC Microbiology SC Microbiology GA 382QX UT WOS:000261621600001 PM 19054117 ER PT J AU Armstrong, AY Alvero, RJ Dunlow, S Nace, MC Baker, V Stewart, EA AF Armstrong, Alicia Y. Alvero, Ruben J. Dunlow, Susan Nace, Mary Catherine Baker, Valerie Stewart, Elizabeth A. TI Balancing the professional and personal SO FERTILITY AND STERILITY LA English DT Editorial Material DE Professional; spouse; parent ID MEDICAL MARRIAGES; SATISFACTION; LIFE; GYNECOLOGISTS; PHYSICIANS; CAREER AB Objective: To review the common roles that physicians pursue away from work and identify related challenges and potential solutions, so that individuals can develop a personalized plan for success in each of the areas. Design: Literature review. Setting: University-based and university-affiliated medical centers. Patient(s): No subjects were involved in this literature review. Intervention(s): Literature searches in Entrez PubMed and the following Websites: http://www.apgo.org, http://www.psychiatrictimes.com, as well as other data sources. Main Outcome Measure(s): Results of physician surveys and summaries of strategies for achieving work-personal life balance. Result(s): According to surveys of physicians in various specialties, a majority of physicians have high levels of job, marital, and parental satisfaction. However, professional and personal challenges faced by physicians include struggle with time management, lack of mentorship, and difficulty maintaining intimate relationships. Multiple potentially effective strategies have been described in the literature, including exerting control over hours worked, taking a long view of life that acknowledges the need for changing priorities over time, developing communication skills, seeking counseling services if needed that focus on physician relationships, and simplifying home life whenever possible. Conclusion(s): Although there are unique challenges in being a physician, partner, and parent, many of the professional challenges faced by physicians are common to many adults in the United States. Self-assessment may help individuals to clarify priorities and develop strategies that can lead to improved personal satisfaction. (Fertil Steril (R) 2009;91:18-21. (c) 2009 by American Society for Reproductive Medicine.) C1 [Armstrong, Alicia Y.] NICHHD, Reprod Biol & Med Branch, NIH, Bethesda, MD 20892 USA. [Alvero, Ruben J.] Univ Colorado, Hlth Sci Ctr, Aurora, CO USA. [Armstrong, Alicia Y.; Alvero, Ruben J.; Dunlow, Susan; Nace, Mary Catherine] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA. [Baker, Valerie] Stanford Univ, Stanford, CA 94305 USA. [Armstrong, Alicia Y.; Dunlow, Susan; Nace, Mary Catherine] Walter Reed Army Med Ctr, Washington, DC 20307 USA. [Stewart, Elizabeth A.] Mayo Clin & Mayo Sch Med, Rochester, MN USA. RP Armstrong, AY (reprint author), NICHHD, Reprod Biol & Med Branch, NIH, CRC 1 E Room 1-E-3140,10 Ctr Dr, Bethesda, MD 20892 USA. EM armstroa@mail.nih.gov FU Intramural NIH HHS NR 12 TC 3 Z9 3 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0015-0282 J9 FERTIL STERIL JI Fertil. Steril. PD JAN PY 2009 VL 91 IS 1 BP 18 EP 21 DI 10.1016/j.fertnstert.2007.10.064 PG 4 WC Obstetrics & Gynecology; Reproductive Biology SC Obstetrics & Gynecology; Reproductive Biology GA 393TU UT WOS:000262396700002 PM 18191125 ER PT J AU Greene, R Stratton, P Cleary, SD Ballweg, ML Sinaii, N AF Greene, Rebecca Stratton, Pamela Cleary, Sean D. Ballweg, Mary Lou Sinaii, Ninet TI Diagnostic experience among 4,334 women reporting surgically diagnosed endometriosis SO FERTILITY AND STERILITY LA English DT Article DE Endometriosis; diagnosis; physician specialty; adolescence; pelvic pain; symptoms; health care ID CHRONIC PELVIC PAIN; PRIMARY-CARE; DELAY; SYMPTOMS; UK AB Objective: To determine whether first physician seen and symptoms beginning in adolescence have an impact on the diagnostic experience of endometriosis. Design: Cross-sectional study of self-reported survey data. Setting: Academic research. Patient(s): Four thousand three hundred thirty-four Endometriosis Association Survey respondents reporting surgical diagnosis of endometriosis. Intervention(s): None. Main Outcome Measure(s): Specialty of first physician seen, timing of onset of symptoms, time to seeking medical care and to diagnosis, number of physicians seen, and satisfaction with care. Result(s): Almost all respondents reported pelvic pain. Fifty percent first saw a gynecologist and 45% saw a generalist for symptoms related to endometriosis. Two thirds reported symptoms beginning during adolescence; they waited longer to seek medical care than adults did. Those seeing a generalist first took longest to get diagnosed: those seeing a gynecologist first saw fewer physicians. Sometime before diagnosis, 63% were told nothing was wrong with them. Conclusion(s): Women and girls who reported seeing a gynecologist first for symptoms related to endometriosis were more likely to have a shorter time to diagnosis, to see fewer physicians, and to report a better experience overall with their physicians. The majority reported symptoms beginning during adolescence, also reporting a longer time and worse experience while obtaining a diagnosis. (Fertil Steril (R) 2009;91:32-9. (c) 2009 by American Society for Reproductive Medicine.) C1 [Sinaii, Ninet] NIH, Biostat & Clin Epidemiol Serv, Ctr Clin, Bethesda, MD 20892 USA. [Greene, Rebecca; Stratton, Pamela; Sinaii, Ninet] NICHHD, Reprod Biol & Med Branch, NIH, Bethesda, MD 20892 USA. [Cleary, Sean D.] George Washington Univ, Dept Epidemiol & Biostat, Sch Publ Hlth & Hlth Serv, Washington, DC USA. [Ballweg, Mary Lou] Endometriosis Assoc Int Headquarters, Milwaukee, WI USA. RP Sinaii, N (reprint author), NIH, Biostat & Clin Epidemiol Serv, Ctr Clin, 10 Ctr Dr,Bldg 10,Room 2N-228, Bethesda, MD 20892 USA. EM sinaiin@mail.nih.gov FU Endometriosis Association FX The authors thank the Endometriosis Association for supporting the study and use of its 1998 survey data and the National Institute of Child Health and Human Development Clinical Trials Database Team for creating the database. NR 19 TC 48 Z9 48 U1 0 U2 4 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0015-0282 EI 1556-5653 J9 FERTIL STERIL JI Fertil. Steril. PD JAN PY 2009 VL 91 IS 1 BP 32 EP 39 DI 10.1016/j.fertnstert.2007.11.020 PG 8 WC Obstetrics & Gynecology; Reproductive Biology SC Obstetrics & Gynecology; Reproductive Biology GA 393TU UT WOS:000262396700005 PM 18367178 ER PT J AU Stegmann, BL Funk, MJ Sinaii, N Hartmann, KE Segars, J Nieman, LK Stratton, P AF Stegmann, Barbara L. Funk, Michele Jonsson Sinaii, Ninet Hartmann, Katherine E. Segars, James Nieman, Lynnette K. Stratton, Pamela TI A logistic model for the prediction of endometriosis SO FERTILITY AND STERILITY LA English DT Article; Proceedings Paper CT 53rd Annual Meeting of the Society-for-Gynecologic-Investigation CY MAR 22-25, 2006 CL Toronto, CANADA SP Soc Gynecol Invest DE Endometriosis; prediction; logistic regression modeling ID PELVIC ENDOMETRIOSIS; MILD ENDOMETRIOSIS; VISUAL FINDINGS; DIAGNOSIS; LAPAROSCOPY; ACCURACY AB Objective: To develop a model that uses individual and lesion characteristics to help surgeons choose lesions that have a high probability of containing histologically confirmed endometriosis. Design: Secondary analysis of prospectively collected information. Setting: Government research hospital in the United States. Patient(s): Healthy women 18-45 years of age, with chronic pelvic pain and possible endometriosis, who were enrolled in a clinical trial. Intervention(S): All participants underwent laparoscopy, and information was collected on all visible lesions.. Lesion data were randomly allocated to a training and test data set. ! Main Outcome Measure(S): Predictive logistic regression, with the outcome of interest being histologic diagnosis of endometriosis. Result(s): After validation, the model was applied to the complete data set, with a sensitivity of 88.4% and specificity of 24.6%. The positive predictive value was 69.2%, and the negative predictive value was 53.3%, equating to correct classification of a lesion or 66.5%. Mixed color; larger width; and location in the ovarian fossa, colon, or appendix were most strongly associated with the presence of endometriosis. Conclusion(s): This model identified characteristics that indicate high and low probabilities of biopsy-proven endometriosis. It is useful as a guide in choosing appropriate lesions for biopsy, but the improvement using the model is not great enough to replace histologic confirmation of endometriosis. (Fertil Steril (R) 2009;91:51-5. (c) 2009 by American Society for Reproductive Medicine.) C1 [Stratton, Pamela] NICHHD, Reprod Biol & Med Branch, NIH, CRC, Bethesda, MD 20892 USA. [Sinaii, Ninet] NIH, Ctr Clin, Biostat & Clin Epidemiol Serv, Bethesda, MD 20892 USA. [Funk, Michele Jonsson] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA. [Funk, Michele Jonsson] Univ N Carolina, Ctr Womens Hlth Res, Chapel Hill, NC USA. [Hartmann, Katherine E.] Vanderbilt Univ, Med Ctr, Dept Obstet & Gynecol, Nashville, TN 37232 USA. RP Stratton, P (reprint author), NICHHD, Reprod Biol & Med Branch, NIH, CRC, Bldg 10,Room 1-3140,MSC 1109,10 Ctr Dr, Bethesda, MD 20892 USA. EM strattop@mail.nih.gov RI Jonsson Funk, Michele/F-6885-2011 OI Jonsson Funk, Michele/0000-0002-3756-7540 FU Intramural NIH HHS [ZIA HD000637-16, Z01 HD008728-07]; NICHD NIH HHS [T32 HD040672, T32 HD40672] NR 23 TC 8 Z9 8 U1 1 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0015-0282 J9 FERTIL STERIL JI Fertil. Steril. PD JAN PY 2009 VL 91 IS 1 BP 51 EP 55 DI 10.1016/j.fertnstert.2007.11.038 PG 5 WC Obstetrics & Gynecology; Reproductive Biology SC Obstetrics & Gynecology; Reproductive Biology GA 393TU UT WOS:000262396700008 PM 18462722 ER PT J AU Levens, ED Whitcomb, BW Kort, JD Materia-Hoover, D Larsen, FW AF Levens, Eric D. Whitcomb, Brian W. Kort, Jonathan D. Materia-Hoover, Donna Larsen, Frederick W. TI Microdose follicular flare: a viable alternative for normal-responding patients undergoing in vitro fertilization? SO FERTILITY AND STERILITY LA English DT Article DE Leuprolide acetate; microdose follicular flare; GnRH agonist; assisted reproductive technology ID INVITRO FERTILIZATION; OVARIAN RESPONSIVENESS; ORAL-CONTRACEPTIVES; POOR RESPONDERS; HORMONE AGONIST; SUPPRESSION; INDUCTION; OVULATION; PROTOCOL; CYCLES AB Objective: To compare cycle outcomes among normal-responding patients <= 30 years old receiving microdose follicular flare (MDF) and long-luteal agonist (LL). Design: Retrospective cohort study. Setting: Military-based assisted reproductive technology (ART) center. Patient(s): First autologous ART cycles among 499 women G 30 years old from January 1999 to December 2005. Intervention(s): After oral contraceptive pill (OCP) administration before cycle start, patients were nonrandomly assigned to either LL or MDF for LH surge suppression. Patients in the LL group received 1 mg/day leuprolide acetate (LA) on cycle day 21, which was reduced to 0.25 mg/day 10-14 days later. Patients in the MDF group received LA (40 kg twice a day) beginning 3 days after discontinuing OCPs. Both groups received a combination of hMG and recombinant FSH. Main Outcome Measure(s): Primary outcomes were implantation, clinical pregnancy, and live-birth rates; in-cycle variables included peak E(2), oocytes retrieved, oocyte maturity, and fertilization rate. Result(s): Multivariable models controlling for confounding by treatment indication found no significant differences between groups in implantation (MDF, 36%; LL, 38%), clinical pregnancy (MDF, 53%; LL, 56%), and live-birth rates (MDF, 47%; LL, 50%). No differences were observed in peak E,, oocytes retrieved, oocyte maturity, fertilization rate, or embryos transferred. Conclusion(s): MDF use among normal-responding ART patients produced no differences in cycle outcome when compared with LL. Therefore, MDF may be a viable alternative for normal-responding patients. (Fertil Steril (R) 2009;91:110-4. (c) 2009 by American Society for Reproductive Medicine.) C1 [Levens, Eric D.] NICHHD, Reprod Biol & Med Branch, Bethesda, MD 20892 USA. [Levens, Eric D.; Larsen, Frederick W.] Walter Reed Army Med Ctr, ART Program, Washington, DC 20307 USA. [Levens, Eric D.; Larsen, Frederick W.] Natl Naval Med Ctr, Walter Reed Army Med Ctr, NIH, Washington, DC USA. [Levens, Eric D.; Larsen, Frederick W.] Uniformed Serv Univ Hlth Sci, Washington, DC USA. [Whitcomb, Brian W.] NICHHD, Epidemiol Branch, NIH, Bethesda, MD 20892 USA. [Materia-Hoover, Donna] ART Inst Washington Inc, Washington, DC USA. RP Levens, ED (reprint author), NICHHD, Reprod Biol & Med Branch, Bldg 10,CRC,Room E1-3140,10 Ctr Dr, Bethesda, MD 20892 USA. EM levense@mail.nih.gov FU Reproductive Biology and Medicine Branch and the Epidemiology Branch; National Institute of Child Health and Human Development; National Institutes of Health; Bethesda, Maryland FX This research was supported in part by the Reproductive Biology and Medicine Branch and the Epidemiology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland. NR 16 TC 9 Z9 9 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0015-0282 J9 FERTIL STERIL JI Fertil. Steril. PD JAN PY 2009 VL 91 IS 1 BP 110 EP 114 DI 10.1016/j.fertnstert.2007.11.018 PG 5 WC Obstetrics & Gynecology; Reproductive Biology SC Obstetrics & Gynecology; Reproductive Biology GA 393TU UT WOS:000262396700017 PM 18249365 ER PT S AU Collins, JR Topol, IA Nemukhin, AV Savitsky, AP AF Collins, Jack R. Topol, Igor A. Nemukhin, Alexander V. Savitsky, Alexander P. BE Savitsky, AP Wang, Y TI Computational modeling structure and spectra of biological chromophores SO FLUORESCENCE IN VIVO IMAGING BASED ON GENETICALLY ENGINEERED PROBES: FROM LIVING CELLS TO WHOLE BODY IMAGING IV SE Proceedings of SPIE-The International Society for Optical Engineering LA English DT Proceedings Paper CT Conference on Fluorescence In Vivo Imaging Based on Genetically Engineered Probes - From Living Cells to Whole Body Imaging IV CY JAN 25-26, 2009 CL San Jose, CA SP SPIE DE biological chromophores; GFP; mTFP1; quantum modeling ID GREEN FLUORESCENT PROTEIN; GAS-PHASE; ASFP595 AB Modern computational approaches based on quantum mechanical methods to characterize structures and optical spectra of biological chromophores in the gas phase, in solutions and proteins are discussed. Primary attention is paid to the chromophores from the family of the green fluorescent protein (GFP) widely used as a biomarker in living cells. Beyond GFP, photophysical properties of the monomeric teal fluorescent protein (mTFPI) and the kindling fluorescent protein asFP595 are simulated. We apply modern quantum chemical approaches for high level calculations of the structures of the chromophore binding pockets and to estimate spectral bands corresponding to the S(0)-S(1) optical transitions. A special attention is paid to evaluate effects of point mutations in the vicinity of the chromophore group. Theoretical data provide important information on the chromophore properties aiming to interpret the results of experimental studies of fluorescent proteins. C1 [Collins, Jack R.; Topol, Igor A.] SAIC Frederick Inc, Adv Biomed Comp Ctr, Adv Technol Program, NCI Frederick, Frederick, MD 21702 USA. RP Collins, JR (reprint author), SAIC Frederick Inc, Adv Biomed Comp Ctr, Adv Technol Program, NCI Frederick, Frederick, MD 21702 USA. EM anemukhin@yahoo.com RI Savitsky, Alexander/O-9799-2015; Nemukhin, Alexander/P-9662-2015 NR 19 TC 0 Z9 0 U1 1 U2 7 PU SPIE-INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98227-0010 USA SN 0277-786X BN 978-0-8194-7437-7 J9 P SOC PHOTO-OPT INS PY 2009 VL 7191 AR 719102 DI 10.1117/12.807913 PG 5 WC Engineering, Biomedical; Optics; Radiology, Nuclear Medicine & Medical Imaging SC Engineering; Optics; Radiology, Nuclear Medicine & Medical Imaging GA BSS49 UT WOS:000285709500001 ER PT S AU Barchi, JJ AF Barchi, Joseph J., Jr. BE Gakh, AA Kirk, KL TI Structural Studies of Biologically Interesting Fluorinated Nucleosides SO FLUORINATED HETEROCYCLES SE ACS Symposium Series LA English DT Proceedings Paper CT Symposium on Fluorinated Heterocycles CY SEP 10-14, 2006 CL San Francisco, CA ID HUMAN-IMMUNODEFICIENCY-VIRUS; ANTI-HIV ACTIVITY; GENERALIZED KARPLUS EQUATION; NMR COUPLING-CONSTANTS; SUGAR RING CONFORMATION; SUBSTITUENT ELECTRONEGATIVITIES; HYDROXYL-GROUPS; DEOXY-4'-THIOPYRIMIDINE NUCLEOSIDES; MAGNETIC-RESONANCE; DAST FLUORINATION AB The use of fluorine as a surrogate for hydrogen and/or a hydroxyl group in synthetic nucleoside analogues has proved to be invaluable in the discovery of exciting new drug agents with novel biochemical properties. Being the most electronegative atom of all nonmetals, fluorine exerts distinct effects on nearly all structural elements in nucleosides and these effects are highly dependent on both the region and the stereochemistry of the fluorine substitution. Despite the dramatic influence that fluorine incorporation often has on the conformational and pharmacological properties of nucleoside analogues, there is a relatively small community of research groups that study the structural effects of fluorine substitution in detail. This review will concentrate on the current research on these effects, paying particular attention to fluorine substitution in the furanose portion of both nucleoside and nucleotide analogues. C1 NCI, Med Chem Lab, Ctr Canc Res, Frederick, MD 21702 USA. RP Barchi, JJ (reprint author), NCI, Med Chem Lab, Ctr Canc Res, Frederick, MD 21702 USA. RI Barchi Jr., Joseph/N-3784-2014 NR 85 TC 0 Z9 0 U1 1 U2 6 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 SIXTEENTH ST NW, WASHINGTON, DC 20036 USA SN 0097-6156 BN 978-0-8412-6953-8 J9 ACS SYM SER JI ACS Symp. Ser. PY 2009 VL 1003 BP 237 EP 262 PG 26 WC Chemistry, Organic SC Chemistry GA BUE60 UT WOS:000289050300011 ER PT J AU Shvartsman, SY Coppey, M Berezhkovskii, AM AF Shvartsman, Stanislav Y. Coppey, Mathieu Berezhkovskii, Alexander M. TI MAPK signaling in equations and embryos SO FLY LA English DT Review DE morphogen gradient; enzymatic cascade; signal transduction ID GROUCHO-MEDIATED REPRESSION; DROSOPHILA EMBRYOGENESIS; SPATIOTEMPORAL REGULATION; TRANSDUCTION PATHWAYS; MORPHOGEN GRADIENT; KINASE CASCADE; PROTEIN; TORSO; NUCLEAR; ULTRASENSITIVITY AB The Extracellularly Regulated Kinase/Mitogen Activated Protein Kinase (ERK/MAPK) signaling pathway is a critical regulator of cellular processes in adult and developing tissues. Depending on the cellular context, MAPK cascade can act as a rheostat, a switch, or an oscillator. The highly conserved structure of the cascade does not imply a rigid function, as was suggested by the early mathematical models of MAPK signaling, and can instead produce a wide range of input-output maps. Given a large number of pathway components and modes of regulation, it is essential to establish experimental systems that will allow both manipulating the MAPK cascade and monitoring its dynamics. The terminal patterning system in the Drosophila embryo appears to be ideally suited for this purpose. Our recent experiments characterized dynamics of the MAPK phosphorylation gradient in the terminal system and proposed that it is regulated by a cascade of diffusion-trapping modules. Here we discuss a biophysical model that can describe the observed dynamics and guide future experiments for exploring the relative importance of multiple layers of MAPK cascade regulation. C1 [Shvartsman, Stanislav Y.; Coppey, Mathieu] Princeton Univ, Lewis Sigler Inst Integrat Genom, Princeton, NJ 08544 USA. [Shvartsman, Stanislav Y.; Coppey, Mathieu] Princeton Univ, Dept Chem Engn, Princeton, NJ 08544 USA. [Berezhkovskii, Alexander M.] NIH, Math & Stat Comp Lab, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA. RP Shvartsman, SY (reprint author), Princeton Univ, Lewis Sigler Inst Integrat Genom, Princeton, NJ 08544 USA. EM stas@princeton.edu FU Intramural Research Program of the NIH [P50 GM071508, R01 RM078079, HHSN266200500021C, N01-AI-50021]; Center for Information Technology FX We thank Alistair Boettiger, Qiao Liang and Yannis Kevrekidis for numerous helpful discussions. This work was supported by the Intramural Research Program of the NIH, Center for Information Technology (Alexander M. Berezhkovskii), by the P50 GM071508 and R01 RM078079 grants from the NIH (Stanislav Y. Shvartsman), and by the NIH Contract No. HHSN266200500021C, ADB No. N01-AI-50021 (Stanislav Y. Shvartsman and Mathieu Coppey). NR 40 TC 8 Z9 9 U1 0 U2 6 PU LANDES BIOSCIENCE PI AUSTIN PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA SN 1933-6934 EI 1933-6942 J9 FLY JI Fly PD JAN-MAR PY 2009 VL 3 IS 1 BP 62 EP 67 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 402QQ UT WOS:000263028600008 PM 19182542 ER PT S AU Garavan, H Murphy, K AF Garavan, Hugh Murphy, Kevin BE Filippi, M TI Experimental Design SO FMRI TECHNIQUES AND PROTOCOLS SE Neuromethods LA English DT Article; Book Chapter DE Task design; Sample size; Scan durations; Analysis; Regression; Efficiency; Frequency ID EVENT-RELATED FMRI; SPATIAL EXTENT; METHODOLOGICAL ISSUES; ACTIVATION; POWER; CONTRAST; NUMBER; CORTEX; MEMORY AB This chapter addresses issues particular to the optimal design of fMRI experiments. It describes procedures for isolating the psychological process of interest and gives an overview of block, event-related, and participant-response dependent designs. An additional focus is placed on data analysis with emphasis on optimizing and isolating the neuroimaging signal in activated brain regions. Finally, the chapter addresses a number of practical matters including optimal sample sizes and trial durations that confront all researchers when designing their experiments. C1 [Garavan, Hugh] Trinity Coll Dublin, Sch Psychol, Dublin 2, Ireland. [Garavan, Hugh] Trinity Coll Dublin, Inst Neurosci, Dublin 2, Ireland. [Murphy, Kevin] NIMH, Sect Funct Imaging Methods, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA. RP Garavan, H (reprint author), Trinity Coll Dublin, Sch Psychol, Dublin 2, Ireland. NR 36 TC 1 Z9 1 U1 0 U2 2 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA SN 0893-2336 BN 978-1-60327-918-5 J9 NEUROMETHODS JI Neuromethods PY 2009 VL 41 BP 133 EP 149 DI 10.1007/978-1-60327-919-2_5 D2 10.1007/978-1-60327-919-2 PG 17 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA BLA05 UT WOS:000269720800005 ER PT J AU Goldfarb, LG Viadimirtsev, VA Platonov, FA Lee, HS McLean, CA Masters, CL AF Goldfarb, Lev G. Viadimirtsev, Vsevolod A. Platonov, Fyodor A. Lee, Hee-Suk McLean, Catriona A. Masters, Colin L. TI Viliuisk encephalomyelitis in Eastern Siberia - analysis of 390 cases SO FOLIA NEUROPATHOLOGICA LA English DT Article DE Viliuisk encephalomyelitis; Yakut (Sakha) Republic; Eastern Siberia; Viliui River; inflammatory brain syndrome ID VILJUISK ENCEPHALOMYELITIS; ETIOLOGY; ENVIRONMENT; HEREDITY; VIRUS AB Viliuisk encephalomyelitis (VE) is a unique disease occurring in the Yakut (Sakha) population of Eastern Siberia VE is always fatal, with some patients dying during the acute encephalitic phase of illness, those surviving the acute phase develop progressive dementia, rigidity and spastic quadriparesis as port of a more prolonged pan-encephalitic syndrome. The disease is characterized neuropathologically by multiple widespread micronecrotic foci with marked inflammatory reactions and subsequent gliosis throughout the cerebral cortex, basal ganglia, cerebellum and brain stem. The acute febrile onset with cerebrospinal fluid pleocytosis and increased protein and neuropathology showing inflammatory reactions suggest that VE is an infectious disease, but the causative agent has not been identified. Initially detected in a small mixed Yakut-Evenk population of the mid-Viliui region, the disease subsequently spread south to densely populated areas around the capital city of Yakutsk The occurrence of secondary VE cases in households and the introduction of the disease by migrants into new populations indicate that the disease is horizontally transmitted in a setting of a long intra-household contact. Although there has been a recent decline in the number of cases, increasing travel may result in further spread of this fatal disease to susceptible individuals in other regions of the world. C1 [Goldfarb, Lev G.; Lee, Hee-Suk] NINDS, NIH, Bethesda, MD 20892 USA. [Viadimirtsev, Vsevolod A.; Platonov, Fyodor A.] Inst Hlth, Yakutsk, Russia. [McLean, Catriona A.] Alfred Hosp, Dept Pathol Anat, Melbourne, Vic, Australia. [Masters, Colin L.] Mental Hlth Res Inst Victoria, Parkville, Vic, Australia. RP Goldfarb, LG (reprint author), NINDS, NIH, Room 4S06,5625 Fishers Lane,MSC 9404, Bethesda, MD 20892 USA. EM GoldfarbL@ninds.nih.gov FU Intramural Research Program of the National Institute of Neurological Disorders and Stroke, National Institutes of Health FX The authors are grateful to the patients and members of their families for participation in the study. This research was supported in part by the Intramural Research Program of the National Institute of Neurological Disorders and Stroke, National Institutes of Health. NR 35 TC 1 Z9 1 U1 0 U2 3 PU VIA MEDICA PI GDANSK PA UL SWIETOKRZYSKA 73, 80-180 GDANSK, POLAND SN 1641-4640 J9 FOLIA NEUROPATHOL JI Folia Neuropathol. PY 2009 VL 47 IS 2 BP 171 EP 181 PG 11 WC Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA 489EC UT WOS:000269401800009 PM 19618339 ER PT J AU Ferrari, PF Paukner, A Ionica, C Suomi, SJ AF Ferrari, P. F. Paukner, A. Ionica, C. Suomi, S. J. TI Early Emotional Communication between Rhesus Macaque Mothers and Infants SO FOLIA PRIMATOLOGICA LA English DT Meeting Abstract DE Facial expressions; Social exchange; Intersubjectivity C1 [Ferrari, P. F.] Univ Parma, Dipartimento Biol Evolut & Funz, I-43100 Parma, Italy. [Paukner, A.; Ionica, C.; Suomi, S. J.] Eunice Kennedy Shriver NICHD, Comparat Ethol Lab, NIH, Bethesda, MD USA. EM ferrari@biol.unipr.it RI Ionica, Consuel/A-5186-2009 NR 0 TC 0 Z9 0 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0015-5713 J9 FOLIA PRIMATOL JI Folia Primatol. PY 2009 VL 80 IS 6 BP 368 EP 368 PG 1 WC Zoology SC Zoology GA 547WF UT WOS:000273919700011 ER PT J AU Otto, M AF Otto, Michael BE Jaykus, LA Wang, HH Schlesinger, LS TI Staphylococcus aureus: THE "SUPERBUG" SO FOOD-BORNE MICROBES: SHAPING THE HOST ECOSYSTEM LA English DT Article; Book Chapter ID PANTON-VALENTINE LEUKOCIDIN; CATIONIC ANTIMICROBIAL PEPTIDES; COMMUNITY-ASSOCIATED MRSA; GRAM-POSITIVE BACTERIA; TOXIC-SHOCK-SYNDROME; BIOFILM FORMATION; SURFACE-PROTEINS; GENE-EXPRESSION; IMMUNE EVASION; SENSING SYSTEM C1 NIAID, Lab Human Bacterial Pathogenesis, NIH, Hamilton, MT 59840 USA. RP Otto, M (reprint author), NIAID, Lab Human Bacterial Pathogenesis, NIH, Hamilton, MT 59840 USA. NR 98 TC 0 Z9 0 U1 1 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N STREET NW, WASHINGTON, DC 20036-2904 USA PY 2009 BP 297 EP 309 PG 13 WC Gastroenterology & Hepatology; Microbiology SC Gastroenterology & Hepatology; Microbiology GA BOY54 UT WOS:000278065800017 ER PT S AU Brown, P AF Brown, P. BE Blackburn, CW McClure, PJ TI Transmissible spongiform encephalopathy (prion disease) SO FOODBORNE PATHOGENS: HAZARDS, RISK ANALYSIS AND CONTROL, SECOND EDITION SE Woodhead Publishing in Food Science Technology and Nutrition LA English DT Article; Book Chapter DE transmissible spongiform encephalopathy; prion disease; Creutzfeldt-Jakob disease; variant Creutzefeldt-Jakob disease; bovine spongiform encephalopathy; scrapie; pathogen decontamination; food safety ID CREUTZFELDT-JAKOB-DISEASE; CHRONIC WASTING DISEASE; VARIANT CJD VCJD; RENDERING PROCEDURES; SCRAPIE AGENT; MULE DEER; PROTEIN; INACTIVATION; BSE; IDENTIFICATION AB A variant form of Creutzfeldt-Jakob disease (vCJD) resulted from human exposure to beef products contaminated with bovine spongiform encephalopathy (BSE). In this chapter, the chronology of both disease outbreaks is recounted, with special attention to pathogenesis, difficulty of decontamination, past and present risk from BSE and other animal prion diseases and, despite the waning number of new cases of both BSE and vCJD, the need for continuing surveillance and protective measures. C1 [Brown, P.] NIH, Bethesda, MD USA. RP Brown, P (reprint author), 7815 Exeter Rd, Bethesda, MD 20814 USA. EM paulwbrown@comcast.net NR 48 TC 0 Z9 0 U1 0 U2 2 PU WOODHEAD PUBL LTD PI CAMBRIDGE PA ABINGTON HALL ABINGTON, CAMBRIDGE CB1 6AH, CAMBS, ENGLAND SN 2042-8049 BN 978-1-84569-362-6 J9 WOODHEAD PUBL FOOD S JI Woodhead Publ. Food Sci. Technol. Nutr. PY 2009 IS 176 BP 1119 EP 1139 DI 10.1533/9781845696337.3.1119 D2 10.1533/9781845696337 PG 21 WC Food Science & Technology SC Food Science & Technology GA BOD62 UT WOS:000276316900030 ER PT J AU Bhattacharjee, S Deterding, LJ Jiang, JJ Chatterjee, S Ehrenshaft, M Lardinois, O Ramirez, DC Tomer, KB Mason, RP AF Bhattacharjee, Suchandra Deterding, Leesa J. Jiang JinJie Chatterjee, Saurabh Ehrenshaft, Marilyn Lardinois, Olivier Ramirez, Dario C. Tomer, Kenneth B. Mason, Ronald P. TI Site-specific Radical Formation in DNA Induced by Fenton chemistry using ESR, Immuno-Spin Trapping, HPLC, MS and MS/MS SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Bhattacharjee, Suchandra; Deterding, Leesa J.; Jiang JinJie; Chatterjee, Saurabh; Ehrenshaft, Marilyn; Lardinois, Olivier; Tomer, Kenneth B.; Mason, Ronald P.] NIEHS, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S186 EP S186 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500535 ER PT J AU Chang, AHK Jeong, J Levine, RL AF Chang, Allen Hung-Kang Jeong, Jinsook Levine, Rodney L. TI A Non-proteasomal Catabolic Pathway for Oxidized Protein-IRP2 as a Model System SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Chang, Allen Hung-Kang; Jeong, Jinsook; Levine, Rodney L.] NHLBI NIH, Bethesda, MD 20892 USA. RI Levine, Rodney/D-9885-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S72 EP S72 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500202 ER PT J AU Chatterjee, S Lardinois, O Tucker, J Deterding, L Bonini, MG Mason, RP AF Chatterjee, Saurabh Lardinois, Olivier Tucker, Jeff Deterding, Leesa Bonini, Marcelo G. Mason, Ronald P. TI Protein Radicals Induce Follicullar Dendritic Cell Depletion and Inhibit B Cell Differentiation in Acute Systemic Inflammatory Disease SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Chatterjee, Saurabh; Lardinois, Olivier; Tucker, Jeff; Deterding, Leesa; Bonini, Marcelo G.; Mason, Ronald P.] NIEHS, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S41 EP S42 PG 2 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500110 ER PT J AU Chatterjee, S Lardinois, O Bonini, MG Deterding, L Bhattacharjee, S Stadler, K Corbett, J Tomer, KB Kadiiska, M Mason, RP AF Chatterjee, Saurabh Lardinois, Olivier Bonini, Marcelo G. Deterding, Leesa Bhattacharjee, Suchandra Stadler, Krisztian Corbett, Jean Tomer, Kenneth B. Kadiiska, Maria Mason, Ronald P. TI Site-specific CPB1 Tyrosine Nitration and Patho-Physiological Implications Following its Physical Association with NOS-3 in Experimental Sepsis SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Chatterjee, Saurabh; Lardinois, Olivier; Bonini, Marcelo G.; Deterding, Leesa; Bhattacharjee, Suchandra; Stadler, Krisztian; Corbett, Jean; Tomer, Kenneth B.; Kadiiska, Maria; Mason, Ronald P.] NIEHS, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S29 EP S29 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500072 ER PT J AU Cherukuri, MK AF Cherukuri, Murali Krishna TI REDOX MAGNETIC RESONANCE IMAGING: MONITORING TUMOR REDOX STATUS AND MOLECULAR/BIOCHEMICAL PROFILING WITH MRI SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Cherukuri, Murali Krishna] NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S11 EP S11 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500022 ER PT J AU Davis, C AF Davis, Cindy TI PROS AND CONS OF ANTIOXIDANT NUTRIENTS IN HUMAN CANCER PREVENTION SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Davis, Cindy] NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S7 EP S7 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500014 ER PT J AU Dorjgochoo, T Gao, YT Chow, WH Shu, XO Yang, G Cai, QY Rothman, N Cai, H Franke, AA Milne, GL Zheng, W Dai, Q AF Dorjgochoo, Tsogzolmaa Gao, Yu-Tang Chow, Wong-Ho Shu, Xiao-ou Yang, Gong Cai, Qiuyin Rothman, Nathaniel Cai, Hui Franke, Adrian A. Milne, Ginger L. Zheng, Wei Dai, Qi TI New Insights into the Utility of F-2-Isoprostanes as Biomarkers of Oxidative Stress: Determinants of Urinary Isoprostanes and its Metabolite in the Shanghai Women's Health Study SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Dorjgochoo, Tsogzolmaa; Shu, Xiao-ou; Yang, Gong; Cai, Qiuyin; Cai, Hui; Milne, Ginger L.; Zheng, Wei; Dai, Qi] Vanderbilt Univ, Nashville, TN 37235 USA. [Gao, Yu-Tang] Shanghai Canc Inst, Shanghai, Peoples R China. [Chow, Wong-Ho; Rothman, Nathaniel] NCI, Bethesda, MD 20892 USA. [Franke, Adrian A.] Univ Hawaii, Honolulu, HI 96822 USA. RI Milne, Ginger/D-7648-2014 OI Milne, Ginger/0000-0003-3890-151X NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 SU 1 BP S161 EP S161 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500465 ER PT J AU Ehrenshaft, M Bonini, MG Feng, L Chignell, CF Mason, RP AF Ehrenshaft, Marilyn Bonini, Marcelo G. Feng, Li Chignell, Colin F. Mason, Ronad P. TI Localization of Oxidized, N-formylkynurenine-containing Proteins in Mitochondria and Golgi of Keratinocytes SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Ehrenshaft, Marilyn; Bonini, Marcelo G.; Feng, Li; Chignell, Colin F.; Mason, Ronad P.] NIEHS NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S74 EP S74 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500208 ER PT J AU Ganini, D Kadiiska, M Mason, RP Bechara, EJH AF Ganini, Douglas Kadiiska, Maria Mason, Ronald P. Bechara, Etelvino J. H. TI Mechanism of Myoglobin/H2O2-catalyzed Oxidation of Acetoacetate and 3-methyl acetoacetate SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Ganini, Douglas] Univ Sao Paulo, Sao Paulo, Brazil. [Kadiiska, Maria; Mason, Ronald P.] NIEHS, Res Triangle Pk, NC 27709 USA. [Bechara, Etelvino J. H.] Univ Fed Sao Paulo, Diadema, Brazil. RI Bechara, Etelvino/M-6251-2013 OI Bechara, Etelvino/0000-0001-9526-2529 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 SU 1 BP S187 EP S187 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500540 ER PT J AU Isenberg, JS Bauer, E Qin, Y Miller, TW Bandle, RW Csanyi, G Pagano, PJ Bauer, PM Schnermann, J Roberts, DD AF Isenberg, Jeff S. Bauer, Eileen Qin, Yan Miller, Thomas W. Bandle, Russell W. Csanyi, Gabor Pagano, Patrick J. Bauer, Phillip M. Schnermann, Jurgen Roberts, David D. TI Thrombospondin-1, via CD47, Blocks Endothelial-Dependent Arterial Relaxation by Limiting Endothelial Nitric Oxide Synthase Activation SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Isenberg, Jeff S.; Bauer, Eileen; Csanyi, Gabor; Pagano, Patrick J.; Bauer, Phillip M.] Univ Pittsburgh, Pittsburgh, PA 15260 USA. [Qin, Yan; Miller, Thomas W.; Bandle, Russell W.; Schnermann, Jurgen; Roberts, David D.] NIH, Bethesda, MD 20892 USA. RI Roberts, David/A-9699-2008 OI Roberts, David/0000-0002-2481-2981 NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S31 EP S31 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500080 ER PT J AU Kim, J Minkler, P Anderson, V Hoppel, C AF Kim, Junhwan Minkler, Paul Anderson, Vernon Hoppel, Charles TI Distinctive Oxidized Cardiolipin Species Generated by Singlet Oxygen and Free Radical SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Kim, Junhwan; Minkler, Paul; Hoppel, Charles] Case Western Reserve Univ, Cleveland, OH 44106 USA. [Anderson, Vernon] NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S125 EP S125 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500352 ER PT J AU Lardinois, OM Tomer, KB Mason, RP Deterding, LJ AF Lardinois, Olivier M. Tomer, Kenneth B. Mason, Ronald P. Deterding, Leesa J. TI Detection and Characterization of Low Abundance Protein-based Radicals by Combined Use of Spin-trapping and Tandem Mass Spectrometry: Data Dependent versus MSe Scanning Approaches SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Lardinois, Olivier M.; Tomer, Kenneth B.; Mason, Ronald P.; Deterding, Leesa J.] NIEHS, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 SU 1 BP S182 EP S182 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500527 ER PT J AU Levine, M Espey, MG Chen, Q Sun, AY Cherukuri, MK Drisko, J AF Levine, Mark Espey, Michael Graham Chen, Qi Sun, Andrew Yang Cherukuri, Murali Krishna Drisko, Jeanne TI VITAMIN C AS A CANCER THERAPEUTIC AGENT: A MATTER OF CONCENTRATION AND H2O2 PRODUCTION SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Levine, Mark; Espey, Michael Graham; Sun, Andrew Yang; Cherukuri, Murali Krishna] NIH, Bethesda, MD 20892 USA. [Chen, Qi; Drisko, Jeanne] Univ Kansas, Lawrence, KS 66045 USA. RI Chen, Qi/D-8278-2015 OI Chen, Qi/0000-0002-7173-8411 NR 0 TC 0 Z9 0 U1 0 U2 4 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 SU 1 BP S8 EP S8 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500016 ER PT J AU Liu, ZG AF Liu, Zhenggang TI ROLES OF LIPID RAFTS AND REDOX IN REGULATING TNF SIGNALING AND CELL DEATH SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Liu, Zhenggang] NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S2 EP S2 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500005 ER PT J AU Nagababu, E Rifkind, JM AF Nagababu, Enika Rifkind, Joseph M. TI A Rapid Reaction of Nitric Oxide with Hemin-GSH Complex: a Mechanism for S-nitrosothiols Formation SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Nagababu, Enika; Rifkind, Joseph M.] NIA, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S33 EP S33 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500087 ER PT J AU Park, JW Piszczek, G Rhee, SG Chock, PB AF Park, Ji Won Piszczek, Grzegorz Rhee, Sue Goo Chock, P. Boon TI Glutathionylation of Peroxiredoxin I Regulates its Functional Change from Molecular Chaperone to Peroxidase SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Park, Ji Won; Piszczek, Grzegorz; Chock, P. Boon] NHLBI, NIH, Bethesda, MD 20892 USA. [Park, Ji Won; Rhee, Sue Goo] Ewha Womans Univ, Seoul, South Korea. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S79 EP S79 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500226 ER PT J AU Pearce, LL Stitt-Fisher, M Peterson, J Ungerman, R Wilen, D AF Pearce, Linda L. Stitt-Fisher, Molly Peterson, Jim Ungerman, Rachel Wilen, Dan TI Manganese Superoxide Dismutase does not Protect Bovine Pulmonary Artery Endothelial Cells against Ionizing Radiation at Systemic Oxygen Levels SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Pearce, Linda L.; Peterson, Jim; Ungerman, Rachel; Wilen, Dan] Univ Pittsburgh, Pittsburgh, PA 15260 USA. [Stitt-Fisher, Molly] NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S129 EP S129 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500364 ER PT J AU Piknova, B Kocharyan, A Silva, AC Schechter, AN AF Piknova, Barbora Kocharyan, Ara Silva, Afonso C. Schechter, Alan N. TI Exogenously Administered NO and Nitrite Recovers the Attenuation of Cerebral Blood Flow Response to Somatosensory Stimulation after nNOS Inhibition in the Rat SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Piknova, Barbora; Schechter, Alan N.] NIDDK, NIH, Bethesda, MD 20892 USA. [Kocharyan, Ara; Silva, Afonso C.] NINDS, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S113 EP S113 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500317 ER PT J AU Rajesh, M Mukhopadhyay, P Batkai, S Patel, V Hasko, G Pacher, P AF Rajesh, Mohanraj Mukhopadhyay, Partha Batkai, Sandor Patel, Vivek Hasko, Gyorgy Pacher, Pal TI Role of Xanthine Oxidase in the Development of Diabetic Cardiomyopathy SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Rajesh, Mohanraj; Mukhopadhyay, Partha; Batkai, Sandor; Patel, Vivek; Pacher, Pal] NIH, Bethesda, MD 20892 USA. [Hasko, Gyorgy] Univ Med & Dent New Jersey, New Jersey Med Sch, Newark, NJ 07103 USA. RI Batkai, Sandor/G-3889-2010; Batkai, Sandor/H-7983-2014 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S148 EP S148 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500426 ER PT J AU Rajesh, M Mukhopadhyay, P Batkai, S Patel, V Hasko, G Pacher, P AF Rajesh, Mohanraj Mukhopadhyay, Partha Batkai, Sandor Patel, Vivek Hasko, Gyorgy Pacher, Pal TI Cannabidiol Attenuates Myocardial Dysfunction, Fibrosis, Inflammation, Cell Death and Interrelated Signaling Pathways Associated With Diabetic Cardiomyopathy SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Rajesh, Mohanraj; Mukhopadhyay, Partha; Batkai, Sandor; Patel, Vivek; Pacher, Pal] NIH, Bethesda, MD 20892 USA. [Hasko, Gyorgy] Univ Med & Dent New Jersey, New Jersey Med Sch, Newark, NJ 07103 USA. RI Batkai, Sandor/G-3889-2010; Batkai, Sandor/H-7983-2014 NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S148 EP S148 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500427 ER PT J AU Ranguelova, K Chatterjee, S Ehrenshaft, M Ramirez, DC Kadiiska, MB Mason, RP AF Ranguelova, Kalina Chatterjee, Saurabh Ehrenshaft, Marilyn Ramirez, Dario C. Kadiiska, Maria B. Mason, Ronald P. TI Free Radical Formation by Eosinophil Peroxidase: Possible Allergic Reactions to (Bi)sulfite SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Ranguelova, Kalina; Chatterjee, Saurabh; Ehrenshaft, Marilyn; Kadiiska, Maria B.; Mason, Ronald P.] NIEHS NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S191 EP S192 PG 2 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500555 ER PT J AU Salgado, MT Rifkind, JM AF Salgado, Maria T. Rifkind, Joseph M. TI Membrane Facilitated Release of NO from Nitrite Reacted Deoxyhemoglobin SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Salgado, Maria T.; Rifkind, Joseph M.] NIA, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S35 EP S35 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500093 ER PT J AU Scarbrough, PM Mattson, DMK Aykin-Burns, N McCormick, ML Gius, D Spitz, DR AF Scarbrough, Peter M. Mattson, David M. K. Aykin-Burns, Nukhet McCormick, Michael L. Gius, David Spitz, Douglas R. TI Inhibitors of Glucose and Hydroperoxide Metabolism Enhance 17-allylamino-17-demethoxygeldanamycin Toxicity in Human Breast Cancer Cells SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Scarbrough, Peter M.; Aykin-Burns, Nukhet; McCormick, Michael L.; Spitz, Douglas R.] Univ Iowa, Iowa City, IA 52242 USA. [Mattson, David M. K.] Roswell Pk Canc Inst, Buffalo, NY USA. [Gius, David] NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S174 EP S174 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500507 ER PT J AU Siraki, AG Jiang, JJ Mason, RP AF Siraki, Arno G. Jiang, JinJie Mason, Ronald P. TI Investigating the Mechanisms of Aromatic Amine-Induced Protein Free Radical Formation by QSARS: Implications for Drug-Induced Agranulocytosis SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Siraki, Arno G.] Univ Alberta, Edmonton, AB T6G 2M7, Canada. [Jiang, JinJie; Mason, Ronald P.] NIEHS, NIH, Res Triangle Pk, NC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S131 EP S131 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500372 ER PT J AU Wood, KC Liu, VB Noguchi, A Wang, XD Raghavachari, N Kato, GJ Gladwin, MT AF Wood, Katherine Christine Liu, Virginia B. Noguchi, Audrey Wang, Xunde Raghavachari, Nalini Kato, Gregory J. Gladwin, Mark T. TI Endothelial and Blood eNOS: Shared Roles in Nitrite Homeostasis and Blood Pressure Regulation SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Wood, Katherine Christine; Liu, Virginia B.; Wang, Xunde; Raghavachari, Nalini; Kato, Gregory J.] NIH, Pulm & Vasc Med Branch, Bethesda, MD 20892 USA. [Noguchi, Audrey] NIH, NHLBI Murine Phenotyping Core, Bethesda, MD 20892 USA. [Raghavachari, Nalini; Kato, Gregory J.] NIH, Dept Crit Care Med, Bethesda, MD 20892 USA. [Gladwin, Mark T.] Univ Pittsburgh, Med Ctr, Pittsburgh, PA 15260 USA. [Gladwin, Mark T.] Univ Pittsburgh, Vasc Med Inst, Pittsburgh, PA 15260 USA. RI Kato, Gregory/I-7615-2014 OI Kato, Gregory/0000-0003-4465-3217 NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S37 EP S38 PG 2 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500102 ER PT J AU You, Z Cao, XH Harr, PJ Levine, RL AF You, Zheng Cao, Xiaohang Harr, P. John Levine, Rodney L. TI Characterization of a Covalent Polysulfide Bridge in the Cu, Zn-superoxide Dismutase Homodimer SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [You, Zheng; Levine, Rodney L.] NHLBI, NIH, Bethesda, MD USA. [Cao, Xiaohang; Harr, P. John] Univ Texas Hlth Sci, San Antonio, TX 78229 USA. RI Levine, Rodney/D-9885-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S194 EP S194 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500564 ER PT J AU Zhai, Z Gomez-Mejiba, SE Faris, RA Lutz, A Deterding, LJ Tomer, K Mason, RP Ramirez, DC AF Zhai, Zili Gomez-Mejiba, Sandra E. Faris, Rebecca A. Lutz, Azure Deterding, Leesa J. Tomer, Kenneth Mason, Ronald P. Ramirez, Dario C. TI Protein-Centered Radicals in Lipopolysaccharide-Triggered Redox Signaling in Macrophages SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Zhai, Zili; Gomez-Mejiba, Sandra E.; Faris, Rebecca A.; Lutz, Azure; Ramirez, Dario C.] Oklahoma Med Res Fdn, Oklahoma City, OK USA. [Deterding, Leesa J.; Tomer, Kenneth; Mason, Ronald P.] NIEHS, Res Triangle Pk, NC USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S83 EP S83 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500237 ER PT J AU Zhao, H Kim, G Liu, CY Levine, R AF Zhao, Hang Kim, Geumsoo Liu, Chengyu Levine, Rodney TI Differential Subcellular Overexpression of Methionine Sulfoxide Reductase A in Mouse Embryonic Fibroblast does not Enhance Its Resistance against Oxidative Stress SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 16th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 18-22, 2009 CL San Francisco, CA SP Soc Free Rad Biol & Med C1 [Zhao, Hang; Kim, Geumsoo; Levine, Rodney] NHLBI, NIH, Bethesda, MD 20892 USA. [Liu, Chengyu] NHLBI, Anim Core Facil, Bethesda, MD 20892 USA. RI Zhao, Hang/A-2558-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 2009 VL 47 BP S157 EP S157 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 522HM UT WOS:000271988500456 ER PT J AU Dasuri, K Nguyen, A Zhang, L Fernandez-Kim, OS Bruce-Keller, AJ Blalock, BA De Cabo, R Keller, JN AF Dasuri, Kalavathi Nguyen, Anhthao Zhang, Le Fernandez-Kim, Ok Sun Bruce-Keller, Annadora J. Blalock, Bradford A. De Cabo, Rafael Keller, Jeffrey N. TI Comparison of rat liver and brain proteasomes for oxidative stress-induced inactivation: Influence of ageing and dietary restriction SO FREE RADICAL RESEARCH LA English DT Article DE 4-hydroxynonenal; ageing; brain; liver; oxidative stress; proteasome ID HEPATIC STELLATE CELLS; CROSS-LINKED PROTEIN; 26S PROTEASOME; 20S PROTEASOME; MITOCHONDRIAL-FUNCTION; ALZHEIMERS-DISEASE; SKELETAL-MUSCLE; DEGRADATION; INHIBITION; UBIQUITIN AB The present study examined brain and liver derived proteasome complexes to elucidate if there is a differential susceptibility in proteasome complexes from these tissues to undergo inactivation following exposure to oxidative stressors. It then examined the influence of ageing and dietary restriction (DR) on the observed proteasome inactivation. Studies used a filtration based methodology that allows for enrichment of proteasome complexes with less tissue than is required for traditional chromatography procedures. The results indicate that the brain has much lower levels of overall proteasome activity and exhibits increased sensitivity to hydrogen peroxide mediated inactivation as compared to proteasome complexes derived from the liver. Interestingly, the brain proteasome complexes did not appear to have increased susceptibility to 4-hydroxynonenal (HNE)-induced inactivation. Surprisingly, ageing and DR induced minimal effects on oxidative stress mediated proteasome inhibition. These results indicate that the brain not only has lower levels of proteasome activity compared to the liver, but is also more susceptible to inactivation following exposure to some (but certainly not all) oxidative stressors. This data also suggest that ageing and DR may not significantly modulate the resistance of the proteasome to inactivation in some experimental settings. C1 [Dasuri, Kalavathi; Nguyen, Anhthao; Zhang, Le; Fernandez-Kim, Ok Sun; Bruce-Keller, Annadora J.; Blalock, Bradford A.; Keller, Jeffrey N.] Louisiana State Univ Syst, Pennington Biomed Res Ctr, Baton Rouge, LA 70808 USA. [De Cabo, Rafael] NIA, Lab Expt Gerontol, NIH, Baltimore, MD 21224 USA. RP Keller, JN (reprint author), Louisiana State Univ Syst, Pennington Biomed Res Ctr, 6400 Perkins Rd, Baton Rouge, LA 70808 USA. EM jeffrey.keller@pbrc.edu RI de Cabo, Rafael/E-7996-2010; DASURI, KALAVATHI/E-7381-2012; de Cabo, Rafael/J-5230-2016; OI de Cabo, Rafael/0000-0002-3354-2442; , rafael/0000-0003-2830-5693 FU National Institute of Aging [AG0257701, AG029885]; NIA FX This work was supported by grants from the National Institute of Aging (AG0257701, AG029885) and supported in part by the intramural program of the NIA. NR 70 TC 15 Z9 15 U1 0 U2 1 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1071-5762 J9 FREE RADICAL RES JI Free Radic. Res. PY 2009 VL 43 IS 1 BP 28 EP 36 AR PII 906226821 DI 10.1080/10715760802534812 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 423PZ UT WOS:000264509500005 PM 19048434 ER PT J AU Broedbaek, K Weimann, A Semba, RD Ferrucci, L Poulsen, HE AF Broedbaek, K. Weimann, A. Semba, R. D. Ferrucci, L. Poulsen, H. E. TI The association between gender and oxidative DNA and RNA damage: The role of iron status SO FREE RADICAL RESEARCH LA English DT Meeting Abstract CT Europe Meeting 2009 of the Society-for-Free-Radicals-Research CY AUG 26-29, 2009 CL Rome, ITALY SP Soc Free Rad Res C1 [Broedbaek, K.; Weimann, A.; Poulsen, H. E.] Rigshosp, Lab Clin Pharmacol, Copenhagen, Denmark. [Semba, R. D.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA. [Ferrucci, L.] NIA, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1071-5762 J9 FREE RADICAL RES JI Free Radic. Res. PY 2009 VL 43 BP 41 EP 42 PG 2 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 470KO UT WOS:000267973800051 ER PT J AU Pawlosky, RJ Hibbeln, JR Salem, N AF Pawlosky, R. J. Hibbeln, J. R. Salem, N., Jr. TI The effects of cigarette smoking and alcohol consumption on n-3 essential fatty acid metabolism in humans SO FREE RADICAL RESEARCH LA English DT Meeting Abstract CT Europe Meeting 2009 of the Society-for-Free-Radicals-Research CY AUG 26-29, 2009 CL Rome, ITALY SP Soc Free Rad Res C1 [Pawlosky, R. J.; Hibbeln, J. R.; Salem, N., Jr.] NIAAA, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1071-5762 J9 FREE RADICAL RES JI Free Radic. Res. PY 2009 VL 43 BP 50 EP 50 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 470KO UT WOS:000267973800085 ER PT J AU Juhasz, A Ge, Y Markel, S Chiu, A Matsumoto, L Van Balgooy, J Roy, K Doroshow, JH AF Juhasz, Agnes Ge, Yun Markel, Susan Chiu, Alice Matsumoto, Linda Van Balgooy, Josephus Roy, Krishnendu Doroshow, James H. TI Expression of NADPH oxidase homologues and accessory genes in human cancer cell lines, tumours and adjacent normal tissues SO FREE RADICAL RESEARCH LA English DT Article DE NADPH oxidase (NOX); reactive oxygen species (ROS); human cancer; human tumour cell lines; hydrogen peroxide ID HYDROGEN-PEROXIDE; NAD(P)H OXIDASE; PROSTATE-CANCER; GLUTATHIONE-PEROXIDASE; DUAL OXIDASES; HUMAN COLON; NOX1; APOPTOSIS; OVEREXPRESSION; ACTIVATION AB The family of NADPH oxidase (NOX) genes produces reactive oxygen species (ROS) pivotal for both cell signalling and host defense. To investigate whether NOX and NOX accessory gene expression might be a factor common to specific human tumour types, this study measured the expression levels of NOX genes 1-5, dual oxidase 1 and 2, as well as those of NOX accessory genes NoxO1, NoxA1, p47(phox), p67(phox) and p22(phox) in human cancer cell lines and in tumour and adjacent normal tissue pairs by quantitative, real-time RT-PCR. The results demonstrate tumour-specific patterns of NOX gene expression that will inform further studies of the role of NOX activity in tumour cell invasion, growth factor response and proliferative potential. C1 [Juhasz, Agnes; Ge, Yun; Roy, Krishnendu; Doroshow, James H.] NCI, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA. [Juhasz, Agnes; Ge, Yun; Roy, Krishnendu; Doroshow, James H.] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. [Markel, Susan; Chiu, Alice; Matsumoto, Linda; Van Balgooy, Josephus] City Hope Comprehens Canc Ctr, Dept Med Oncol & Therapeut Res, Duarte, CA 91010 USA. RP Doroshow, JH (reprint author), NCI, Div Canc Treatment & Diag, NIH, Bldg 31,Room 3A44,31 Ctr Dr, Bethesda, MD 20892 USA. EM doroshoj@mail.NIH.gov RI Bell, Tiffany/F-4403-2010 FU National Cancer Institute; National Institutes of Health [CA33572] FX We wish to thank Dr Mel Simpson and Dr Yvonne A. Evrard, SAIC-Frederick, Inc., for editorial assistance in the preparation of this manuscript. This project has been funded in whole or in part with federal funds from the National Cancer Institute, National Institutes of Health, Grant number CA33572. The content of this publication does not necessarily reflect the views or policies of the United States Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government. NR 41 TC 54 Z9 56 U1 1 U2 2 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1071-5762 J9 FREE RADICAL RES JI Free Radic. Res. PY 2009 VL 43 IS 6 BP 523 EP U5 DI 10.1080/10715760902918683 PG 14 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 457ZR UT WOS:000266979100001 PM 19431059 ER PT J AU Ito, S Miyoshi, N Degraff, WG Nagashima, K Kirschenbaum, LJ Riesz, P AF Ito, Shinji Miyoshi, Norio Degraff, William G. Nagashima, Kunio Kirschenbaum, Louis J. Riesz, Peter TI Enhancement of 5-Aminolevulinic acid-induced oxidative stress on two cancer cell lines by gold nanoparticles SO FREE RADICAL RESEARCH LA English DT Article DE Gold nanoparticles; 5-Aminolevulinic acid; cytotoxicity; reactive oxygen species ID DELTA-AMINOLEVULINIC-ACID; PHOTODYNAMIC THERAPY; FREE-RADICALS; CYTOTOXICITY; AUTOXIDATION; SIZE; MITOCHONDRIA; CONNECTIONS; GENERATION; CULTURE AB 5-Aminolevulinic acid (5-ALA) and its methyl ester (5-ALA-Me) at mM concentration levels induce oxidative stress via the production of reactive oxygen species (ROS). Human cancer cell lines (MCF-7 and HepG2) incubated in the dark in the simultaneous presence of 5.0 mM or more 5-ALA or 5-ALA-Me (for MCF-7) and 7 mu g/mL of 15 nm citrate capped gold nanoparticles (AuNPs) were damaged more seriously compared to those in the presence of the levulinic acid alone. Damage is visible in electron micrographs which reveal similar morphology both in the presence or absence of AuNPs. Cytotoxicity was observed irrespective of the presence of serum and medium. Production of ROS in cell free samples containing 5-ALA-Me was monitored by EPR as the DMPO-OH spin adduct and also showed a catalytic effect of AuNPs. Both SOD and CAT inhibited the production of ROS and also reduced cytotoxicity in the cell samples. These observations can be explained by initial attack on the cell membrane by ROS produced in the medium outside the cell and provide insight into possible uses of 5-ALA in cancer chemotherapy. C1 [Ito, Shinji; Degraff, William G.; Riesz, Peter] NCI, Radiat Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. [Miyoshi, Norio] Univ Fukui, Fac Med, Dept Pathol Sci, Div Tumor Pathol, Matsuoka, Fukui 9101193, Japan. [Nagashima, Kunio] NCI, Electron Microscope Lab, SAIC Frederick, NIH, Frederick, MD 21702 USA. [Kirschenbaum, Louis J.] Univ Rhode Isl, Dept Chem, Kingston, RI 02881 USA. RP Ito, S (reprint author), NCI, Radiat Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. EM itoshi@mail.nih.gov FU NIH; National Cancer Institute; Center for Cancer Reseach; National Institutes of Health [NOI-CO-12400] FX This research was supported by the Intramural Reseach Program of the NIH, National Cancer Institute, Center for Cancer Reseach, and was funded in part with federal funds from the National Cancer Institute, National Institutes of Health, under contract NOI-CO-12400. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government. NR 40 TC 26 Z9 29 U1 3 U2 20 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1071-5762 J9 FREE RADICAL RES JI Free Radic. Res. PY 2009 VL 43 IS 12 BP 1214 EP 1224 DI 10.3109/10715760903271249 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 532MP UT WOS:000272753100008 PM 19905984 ER PT S AU Vogel, SS Blank, PS Koushik, SV Thaler, C AF Vogel, Steven S. Blank, Paul S. Koushik, Srinagesh V. Thaler, Christopher BE Gadella, TWJ TI Spectral imaging and its use in the measurement of Forster resonance energy transfer in living cells SO FRET AND FLIM TECHNIQUES SE Laboratory Techniques in Biochemistry and Molecular Biology LA English DT Article; Book Chapter ID FLUORESCENCE MICROSCOPY; MEMBRANE MICRODOMAINS; 2-PHOTON EXCITATION; SPATIAL-RESOLUTION; FRET EFFICIENCY; LIVE CELLS; PROTEIN; FLIM; OLIGOMERIZATION; MOLECULES AB Forster resonance energy transfer (FRET) imaging is a form of microscopy that allows the visualization of interaction between two fluorophores on a 1-10 nm scale. FRET imaging is based on measuring subtle changes in fluorescence that arises from nonradiative energy transfer from a "donor'' fluorophore to an "acceptor.'' Interest in applying FRET to image molecular interactions inside living cells has been growing, but has been hampered by technical problems encountered when accurate and precise measurements of fluorescence is necessary. Ironically, a requirement for FRET to occur, spectral overlap of donor emission with acceptor absorption makes it technically difficult to accurately and efficiently measure the fluorescent signals required to quantify FRET. Spectral imaging is a relatively new form of fluorescence light microscopy where a fluorescent emission spectrum is recorded at each location in an image. Many of the technical problems encountered when acquiring FRET images can be eliminated by analyzing the data encoded in spectral images with an image analysis algorithm called linear unmixing. In this chapter, we will cover the theory of linear unmixing of spectral images, and describe how it can be used to acquire accurate FRET measurements. C1 [Vogel, Steven S.; Koushik, Srinagesh V.; Thaler, Christopher] NIAAA, NIH, Bethesda, MD 20892 USA. [Blank, Paul S.] NICHHD, NIH, Bethesda, MD 20892 USA. RP Vogel, SS (reprint author), NIAAA, NIH, 5625 Fishers Lane, Bethesda, MD 20892 USA. OI Vogel, Steven/0000-0002-3005-2667 NR 49 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0075-7535 BN 978-0-08-091512-8; 978-0-08-054958-3 J9 LAB TECH BIOCHEM MOL PY 2009 VL 33 BP 351 EP 394 DI 10.1016/S0075-7535(08)00008-9 PG 44 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BA3ZA UT WOS:000335187000009 ER PT B AU John, S Stuelten, CH Niederhuber, JE AF John, Simone Stuelten, Christina H. Niederhuber, John E. BE Leong, SPL TI Frontiers of Cancer Research: The Metastasis Challenge SO FROM LOCAL INVASION TO METASTATIC CANCER: INVOLVEMENT OF DISTANT SITES THROUGH THE LYMPHOVASCULAR SYSTEM SE Current Clinical Oncology Series LA English DT Article; Book Chapter DE metastasis; cancer; cancer stem cells; germline cancer risk; gene expression profiles; predictive profiles ID GROWTH-FACTOR-BETA; BREAST-CANCER; TUMOR-METASTASIS; TGF-BETA; CELLS; EZRIN; SURVIVAL; THERAPY; SIPA1; MMP-9 AB Greater than 90% of deaths in cancer patients are due to the metastatic spread of the tumor to vital organs, emphasizing the importance of efforts toward the prevention and treatment of this phenomenon. The ability to block the process of metastasis could have a significant impact on the mortality rates associated with malignancy. As a result, the study of metastasis has been a focus at numerous centers of research, including the National Cancer Institute (NCI). A plethora of new technologies developed over the last decade, including gene expression profiling, have allowed for the identification of a number of genes, many of them strictly confined to the stromal cells associated with the tumor that appear to be significantly involved in the metastatic process. This allows us to enhance our efforts at designing stromal directed therapies to be utilized in combination with more traditional regimens directed at tumor cells. This highly personalized signature of the tumor and tumor microenvironment provides the unprecedented opportunity to develop therapeutic solutions which are also designed to be preventive, in terms of the biologic processes that support development of tumor metastasis. In addition to new therapies, genetic profiling has also led to new ways of thinking about the origins and development of metastasis and metastatic potential. Research at the NCI provides an interesting perspective on inborn genetic traits that predispose an individual to metastasis, should a malignancy develop. The presence of these genetic traits has enormous implications for prophylactic therapy. Investigations such as these continually expand the frontiers of cancer research and hold the potential to contribute to the prevention and control of metastasis and its associated mortality. C1 [John, Simone; Stuelten, Christina H.] NCI, Cell & Canc Biol Branch, Ctr Canc Res, US Natl Inst Hlth, Bethesda, MD 20892 USA. RP John, S (reprint author), NCI, Cell & Canc Biol Branch, Ctr Canc Res, US Natl Inst Hlth, Bethesda, MD 20892 USA. NR 22 TC 0 Z9 0 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA BN 978-1-60327-086-1 J9 CURR CLIN ONCOL PY 2009 BP 3 EP 10 DI 10.1007/978-1-60327-087-8_1 D2 10.1007/978-1-60327-087-8 PG 8 WC Oncology SC Oncology GA BKF24 UT WOS:000267947100002 ER PT J AU Brigman, JL Ihne, J Saksida, LM Bussey, TJ Holmes, A AF Brigman, Jonathan L. Ihne, Jessica Saksida, Lisa M. Bussey, Timothy J. Holmes, Andrew TI Effects of subchronic phencyclidine (PCP) treatment on social behaviors, and operant discrimination and reversal learning in C57BL/6J mice SO FRONTIERS IN BEHAVIORAL NEUROSCIENCE LA English DT Article DE glutamate; mouse; schizophrenia; executive function; negative symptoms; NMDA; psychosis; prefrontal cortex AB Subchronic treatment with the psychotomimetic phencyclidine (PCP) has been proposed as a rodent model of the negative and cognitive/executive symptoms of schizophrenia. There has, however, been a paucity of studies on this model in mice, despite the growing use of the mouse as a subject in genetic and molecular studies of schizophrenia. In the present study, we evaluated the effects of subchronic PCP treatment (5 mg/kg twice daily x 7 days, followed by 7 days withdrawal) in C57BL/6J mice on (1) social behaviors using a sociability/social novelty-preference paradigm, and (2) pair wise visual discrimination and reversal learning using a touchscreen-based operant system. Results showed that mice subchronically treated with PCP made more visits to (but did not spend more time with) a social stimulus relative to an inanimate one, and made more visits and spent more time investigating a novel social stimulus over a familiar one. Subchronic PCP treatment did not significantly affect behavior in either the discrimination or reversal learning tasks. These data encourage further analysis of the potential utility of mouse subchronic PCP treatment for modeling the social withdrawal component of schizophrenia. They also indicate that the treatment regimen employed was insufficient to impair our measures of discrimination and reversal learning in the C57BL/6J strain. Further work will be needed to identify alternative methods (e.g., repeated cycles of subchronic PCP treatment, use of different mouse strains) that reliably produce discrimination and/or reversal impairment, as well as other cognitive/executive measures that are sensitive to chronic PCP treatment in mice. C1 [Brigman, Jonathan L.; Ihne, Jessica; Holmes, Andrew] NIAAA, Sect Behav Sci & Genet, Lab Integrat Neurosci, NIH, Rockville, MD 20852 USA. [Saksida, Lisa M.; Bussey, Timothy J.] Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. [Saksida, Lisa M.; Bussey, Timothy J.] MRC, Cambridge, England. [Saksida, Lisa M.; Bussey, Timothy J.] Wellcome Trust Behav & Clin Neurosci Inst, Cambridge, England. RP Brigman, JL (reprint author), NIAAA, Sect Behav Sci & Genet, Lab Integrat Neurosci, NIH, 5625 Fishers Lane,Room 2N09, Rockville, MD 20852 USA. EM brigmanj@mail.nih.gov RI Brigman, Jonathan/O-4978-2016; Saksida, Lisa/M-2753-2016; Bussey, Timothy/M-2758-2016; OI Saksida, Lisa/0000-0002-8416-8171; Bussey, Timothy/0000-0001-7518-4041; Reed, Jessica/0000-0003-0550-7284 FU National Institute of Alcohol Abuse and Alcoholism [Z01-AA000411] FX Research supported by the Intramural Research Program of the National Institute of Alcohol Abuse and Alcoholism (Z01-AA000411). NR 71 TC 38 Z9 38 U1 1 U2 7 PU FRONTIERS RES FOUND PI LAUSANNE PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND SN 1662-5153 J9 FRONT BEHAV NEUROSCI JI Front. Behav. Neurosci. PY 2009 VL 3 AR 2 DI 10.3389/neuro.08.002.2009 PG 11 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA V18VE UT WOS:000208031500002 PM 19255630 ER PT J AU Jia, R Zheng, ZM AF Jia, Rong Zheng, Zhi-Ming TI Regulation of bovine papillomavirus type 1 gene expression by RNA processing SO FRONTIERS IN BIOSCIENCE LA English DT Article DE Papillomaviruses; Gene expression; RNA splicing; RNA polyadenylation; Post-transcriptional regulation; Review ID PRE-MESSENGER-RNA; EXONIC SPLICING SUPPRESSOR; POLYADENYLATION FACTOR CPSF-73; LONG CONTROL REGION; TRANSFORMED-CELLS; U1 SNRNP; TRANSCRIPTIONAL REPRESSOR; CAENORHABDITIS-ELEGANS; E2 TRANSACTIVATOR; PREMESSENGER RNA AB Bovine papillomavirus type 1 (BPV-1) has served as a prototype for studying the molecular biology and pathogenesis of papillomaviruses. The expression of BPV-1 early and late genes is highly regulated at both transcription and post-transcriptional levels and strictly tied to the differentiation of keratinocytes. BPV-1 infects keratinocytes in the basal layer of the skin and replicates in the nucleus of infected cells in a differentiation-dependent manner. Although viral early genes begin to be expressed from the infected, undifferentiated basal cells, viral late genes are not expressed until the infected cells enter the terminal differentiation stage. Both BPV-1 early and late transcripts are intron-containing bicistronic or polycistronic RNAs, bearing more than one open reading frame and are polyadenylated at either an early or late poly ( A) site. Nuclear RNA processing of these transcripts by RNA splicing and poly ( A) site selection has been extensively analyzed in the past decade and various viral cis-elements and cellular factors involved in regulation of viral RNA processing were discovered, leading to our better understanding of the gene expression and biology of human papillomaviruses. C1 [Jia, Rong; Zheng, Zhi-Ming] NCI, HIV & AIDS Malignancy Branch, Ctr Canc Res, Natl Inst Hlth, Bethesda, MD 20892 USA. RP Zheng, ZM (reprint author), 10 Ctr Dr,Rm 6N106, Bethesda, MD 20892 USA. EM zhengt@exchange.nih.gov FU NIH, National Cancer Institute, Center for Cancer Research. FX We thank Barbara Spalholz and the NIH fellows editorial board for their critical reading of the manuscript. This research was supported by the Intramural Research Program of the NIH, National Cancer Institute, Center for Cancer Research. NR 84 TC 12 Z9 12 U1 1 U2 3 PU FRONTIERS IN BIOSCIENCE INC PI MANHASSET PA C/O NORTH SHORE UNIV HOSPITAL, BIOMEDICAL RESEARCH CENTER, 350 COMMUNITY DR, MANHASSET, NY 11030 USA SN 1093-9946 J9 FRONT BIOSCI JI Front. Biosci. PD JAN 1 PY 2009 VL 14 BP 1270 EP 1282 DI 10.2741/3307 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 393DZ UT WOS:000262352400080 PM 19273129 ER PT J AU Lin, L Park, S Lakatta, EG AF Lin, Li Park, Sungha Lakatta, Edward G. TI RAGE signaling in inflammation and arterial aging SO FRONTIERS IN BIOSCIENCE LA English DT Article DE receptor for advanced glycation end products; RAGE; RAGE Ligands; Toll-Like Receptors; Innate Immunity; Signaling; Inflammation; Aging; Vascular Diseases; Review ID GLYCATION END-PRODUCTS; TOLL-LIKE RECEPTORS; GROUP BOX-1 PROTEIN; NF-KAPPA-B; VASCULAR ENDOTHELIAL-CELLS; INNATE IMMUNE RECOGNITION; CROSS-LINK BREAKER; E-NULL MICE; SOLUBLE RECEPTOR; SCAVENGER RECEPTORS AB The receptor for advanced glycation end products ( RAGE) is a pattern recognition receptor (PRR) that interacts with diverse endogenous ligands. Ligation of RAGE triggers a series of cellular signaling events, including the activation of transcription factor NF-kappa B, leading to the production of pro-inflammatory cytokines, and causing inflammation. While acute inflammation serves to resolve pathogen infection and stresses, which promote tissue repair, persistent inflammation results in maladaptive tissue remodeling and damage. RAGE signaling has been implicated in multiple detrimental human illnesses including diabetes, atherosclerosis, arthritis, and Alzheimer's disease. In addition, prolonged inflammation often serves as the precursor for arterial remodeling that underlies the exponential increase of age-associated arterial diseases. Despite the significant progress and exciting discoveries in RAGE research, little is known on the biochemistry of RAGE and the signaling mechanism of RAGE remains poorly defined. The biological impact of RAGE signaling in clinical situations and aging-associated diseases also remains to be fully realized. This review attempts to provide a comprehensive summary on both recent findings and missing pieces of the RAGE puzzle. C1 [Lin, Li; Lakatta, Edward G.] NIA, Cardiovasc Sci Lab, Baltimore, MD 21224 USA. [Park, Sungha] Yonsei Univ, Coll Med, Cardiovasc Res Inst, Div Cardiol, Seoul, South Korea. RP Lin, L (reprint author), NIA, Cardiovasc Sci Lab, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. EM linli@mail.nih.gov FU NIH [RO1CA94102]; National Institute on Aging Intramural Research Program FX We thank Dr. Rui-Ping Xiao for a reading of the manuscript, and her encouragement for the RAGE project. We are grateful for Dr. Kenneth Boheler for his critical review and specific suggestions. Special thanks go to John Pang for editing the manuscript. Our research is supported by the NIH grant RO1CA94102 ( L. L.), and funding from the National Institute on Aging Intramural Research Program ( E. G. L). NR 97 TC 80 Z9 84 U1 1 U2 7 PU FRONTIERS IN BIOSCIENCE INC PI MANHASSET PA C/O NORTH SHORE UNIV HOSPITAL, BIOMEDICAL RESEARCH CENTER, 350 COMMUNITY DR, MANHASSET, NY 11030 USA SN 1093-9946 J9 FRONT BIOSCI JI Front. Biosci. PD JAN 1 PY 2009 VL 14 BP 1403 EP 1413 DI 10.2741/3315 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 393DZ UT WOS:000262352400088 PM 19273137 ER PT J AU Mbulaiteye, SM Hisada, M El-Omar, EM AF Mbulaiteye, Sam M. Hisada, Michie El-Omar, Emad M. TI Helicobacter Pylori associated global gastric cancer burden SO FRONTIERS IN BIOSCIENCE LA English DT Review DE Gastric Cancer; African Enigma; Parasites; Prevention; Review ID COST-EFFECTIVENESS ANALYSIS; LYMPHOID-TISSUE TYPE; HIGH-RISK POPULATION; VIRUS TYPE-I; FOLLOW-UP; VEGETABLE CONSUMPTION; GENE POLYMORPHISMS; ATROPHIC GASTRITIS; MONGOLIAN GERBILS; MOLECULAR-BIOLOGY AB Helicobacter pylori infection is ubiquitous, infecting close to one-half of the world's population, but its prevalence is declining in developed countries. Chronic H. pylori infection is etiologically linked to gastric adenocarcinoma, especially non-cardia type (63% of all stomach cancer or similar to 5.5% of the global cancer burden: similar to 25% of cancers associated with infectious etiology), and to gastric mucosal associated lymphoid tissue ( MALT) lymphoma, which accounts for up to 8% of all non-Hodgkin lymphoma. Epidemiological, clinical, and animal studies have established a central role for H. pylori in gastric carcinogenesis and provided insights into the mechanisms and biologic relationships between bacterial infection, host genetics, nutrition, and environmental factors. These discoveries invite strategies to prevent infection to be the logical primary goals in a multi-pronged effort to curtail suffering and death from H. pylori infection-associated cancers. C1 [Mbulaiteye, Sam M.] NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. [Hisada, Michie] TAP Pharmaceut Prod Inc, Lake Forest, IL USA. [El-Omar, Emad M.] Univ Aberdeen, Aberdeen, Scotland. [El-Omar, Emad M.] Aberdeen Royal Infirm, Aberdeen, Scotland. RP Mbulaiteye, SM (reprint author), 6120 Execut Blvd,Execut Plaza S,Rm 7080, Rockville, MD 20852 USA. EM mbulaits@mail.nih.gov FU Intramural NIH HHS [Z01 CP010150-08] NR 132 TC 40 Z9 44 U1 0 U2 4 PU FRONTIERS IN BIOSCIENCE INC PI MANHASSET PA C/O NORTH SHORE UNIV HOSPITAL, BIOMEDICAL RESEARCH CENTER, 350 COMMUNITY DR, MANHASSET, NY 11030 USA SN 1093-9946 J9 FRONT BIOSCI JI Front. Biosci. PD JAN 1 PY 2009 VL 14 BP 1490 EP 1504 DI 10.2741/3320 PG 15 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 393DZ UT WOS:000262352400093 PM 19273142 ER PT J AU Majerciak, V Zheng, ZM AF Majerciak, Vladimir Zheng, Zhi-Ming TI Kaposi's sarcoma-associated herpesvirus ORF57 in viral RNA processing SO FRONTIERS IN BIOSCIENCE LA English DT Article DE Kaposi's sarcoma-associated herpesvirus; Gene expression; ORF57; RNA splicing; Posttranscriptional regulation; Protein-RNA interaction; RNA export; Review ID REGULATORY PROTEIN ICP27; OPEN READING FRAME; VIRUS SM PROTEIN; KINASE CK2 PHOSPHORYLATION; ARGININE-RICH MOTIF; KH-DOMAIN PROTEINS; SIMPLEX-VIRUS; GENE-EXPRESSION; MESSENGER-RNA; NUCLEAR EXPORT AB Kaposi's sarcoma-associated herpesvirus ( KSHV) ORF57 (MTA, mRNA transcript accumulation) is a multifunctional regulator of the expression of viral lytic genes. KSHV ORF57 is expressed during viral lytic infection and is essential for virus production. Like its homologues in the herpesvirus family, ORF57 promotes the accumulation ( stabilization) and export of viral intronless RNA transcripts by a mechanism which remains to be defined. The ORF57-Aly/REF interaction plays only a small role in viral RNA export. Although other members of the family generally inhibit the splicing of cellular RNAs, KSHV ORF57 and EBV EB2, in sharp contrast, stimulate viral RNA splicing for the expression of viral intron-containing genes. The functions of KSHV ORF57 are independent of transcription and of other viral proteins; instead, these functions always rely on cellular components and occur in various protein-RNA complexes. ORF57 may synergize with KSHV ORF50 to transactivate a subset of viral promoters by an unknown mechanism. Thus, some functions of ORF57 have been conserved while others have diverged from its homologues as ORF57 adapted over evolution to KSHV biology and pathogenesis. C1 [Majerciak, Vladimir; Zheng, Zhi-Ming] NCI, HIV & AIDS Malignancy Branch, Ctr Canc Res, Natl Inst Hlth, Bethesda, MD 20892 USA. RP Zheng, ZM (reprint author), 10 Ctr Dr,Rm 6N106, Bethesda, MD 20892 USA. EM zhengt@exchange.nih.gov FU Center for Cancer Research,; National Cancer Institute; National Institutes of Health. FX This work was supported by the Intramural Research Program of the Center for Cancer Research, National Cancer Institute, National Institutes of Health. We thank Ren Sun for providing the gene structure information of MHV-68 ORF57. NR 84 TC 29 Z9 30 U1 0 U2 8 PU FRONTIERS IN BIOSCIENCE INC PI MANHASSET PA C/O NORTH SHORE UNIV HOSPITAL, BIOMEDICAL RESEARCH CENTER, 350 COMMUNITY DR, MANHASSET, NY 11030 USA SN 1093-9946 J9 FRONT BIOSCI JI Front. Biosci. PD JAN 1 PY 2009 VL 14 BP 1516 EP 1528 DI 10.2741/3322 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 393DZ UT WOS:000262352400095 PM 19273144 ER PT J AU Choi, EY Santoso, S Chavakis, T AF Choi, Eun Young Santoso, Sentot Chavakis, Triantafyllos TI Mechanisms of neutrophil transendothelial migration SO FRONTIERS IN BIOSCIENCE LA English DT Review DE Inflammation; Adhesion; Transmigration; Endothelial Cells; Junctions; Neutrophils; Review ID JUNCTIONAL-ADHESION-MOLECULE; VASCULAR ENDOTHELIAL PERMEABILITY; PERIVASCULAR BASEMENT-MEMBRANE; PROTEIN-TYROSINE-PHOSPHATASE; ISCHEMIA-REPERFUSION INJURY; INFLAMMATION IN-VIVO; CELL-CELL ADHESION; INTEGRIN ACTIVATION; LEUKOCYTE ADHESION; VE-CADHERIN AB Neutrophil recruitment is an integral part of the immune response to infection as well as of inflammatory disorders. The process of neutrophil extravasation comprises a complex multistep cascade that is orchestrated by a tightly coordinated sequence of adhesive interactions with vessel wall endothelial cells. Adhesion receptors as well as signaling molecules in both neutrophils and endothelial cells regulate the recruitment of neutrophils into the site of inflammation or infection. The present review will focus on novel aspects with regards to the last step of neutrophil recruitment, namely the transmigration of neutrophils through endothelial cells. C1 [Choi, Eun Young; Chavakis, Triantafyllos] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. [Santoso, Sentot] Univ Giessen, Inst Clin Immunol & Transfus Med, D-35392 Giessen, Germany. RP Chavakis, T (reprint author), NCI, Expt Immunol Branch, NIH, 10 Ctr Dr,Rm 4B17, Bethesda, MD 20892 USA. EM chavakist@mail.nih.gov FU Intramural NIH HHS [Z01 BC010663-03] NR 113 TC 32 Z9 33 U1 0 U2 6 PU FRONTIERS IN BIOSCIENCE INC PI MANHASSET PA C/O NORTH SHORE UNIV HOSPITAL, BIOMEDICAL RESEARCH CENTER, 350 COMMUNITY DR, MANHASSET, NY 11030 USA SN 1093-9946 J9 FRONT BIOSCI JI Front. Biosci. PD JAN 1 PY 2009 VL 14 BP 1596 EP 1605 DI 10.2741/3327 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 393DZ UT WOS:000262352400100 PM 19273149 ER PT J AU Frankel, AE Kuo, SR Dostal, D Watson, L Duesbery, NS Cheng, CP Cheng, HJ Tang, WJ Leppla, SH AF Frankel, Arthur E. Kuo, Shu-Ru Dostal, David Watson, Linley Duesbery, Nicholas S. Cheng, Che-Ping Cheng, Heng Jie Tang, Wei-Jen Leppla, Stephen H. TI Pathophysiology of anthrax SO FRONTIERS IN BIOSCIENCE LA English DT Article DE Anthrax; Heart Failure; Rats; Review ID DIRECTED MONOCLONAL-ANTIBODY; LETHAL TOXIN; BACILLUS-ANTHRACIS; PROTECTIVE ANTIGEN; INHALATIONAL ANTHRAX; CRYSTAL-STRUCTURE; SPORE CHALLENGE; HEART-FAILURE; RAT MODEL; MICE AB Infection by Bacillus anthracis in animals and humans results from accidental or intentional exposure, by oral, cutaneous or pulmonary routes, to spores, which are normally present in the soil. Treatment includes administration of antibiotics, vaccination or treatment with antibody to the toxin. A better understanding of the molecular basis of the processes involved in the pathogenesis of anthrax namely, spore germination in macrophages and biological effects of the secreted toxins on heart and blood vessels will lead to improved management of infected animals and patients. Controlling germination will be feasible by inhibiting macrophage paralysis and cell death. On the other hand, the control of terminal hypotension might be achieved by inhibition of cardiomyocyte mitogen-activated protein kinase and stimulation of vessel cAMP. C1 [Frankel, Arthur E.; Kuo, Shu-Ru; Dostal, David; Watson, Linley] Scott & White Mem Hosp & Clin, Temple, TX 76508 USA. [Duesbery, Nicholas S.] Van Andel Res Inst, Grand Rapids, MI USA. [Cheng, Che-Ping; Cheng, Heng Jie] Wake Forest Univ, Sch Med, Winston Salem, NC 27109 USA. [Tang, Wei-Jen] Univ Chicago, Chicago, IL 60637 USA. [Leppla, Stephen H.] NIAID, Bethesda, MD 20892 USA. RP Frankel, AE (reprint author), Scott & White Mem Hosp & Clin, 2401 S 31st St, Temple, TX 76508 USA. EM afrankel@swmail.sw.org OI DUESBERY, NICK/0000-0002-4258-5655 FU Van Andel Research Foundation; NSD [R21CA108438] FX This work was supported by the Van Andel Research Foundation and R21CA108438 (NSD). NR 44 TC 21 Z9 22 U1 1 U2 4 PU FRONTIERS IN BIOSCIENCE INC PI MANHASSET PA C/O NORTH SHORE UNIV HOSPITAL, BIOMEDICAL RESEARCH CENTER, 350 COMMUNITY DR, MANHASSET, NY 11030 USA SN 1093-9946 J9 FRONT BIOSCI JI Front. Biosci. PD JAN PY 2009 VL 14 BP 4516 EP 4524 DI 10.2741/3544 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 497LM UT WOS:000270060800060 PM 19273366 ER PT J AU Francischetti, IMB Sa-Nunes, A Mans, BJ Santos, IM Ribeiro, JMC AF Francischetti, Ivo M. B. Sa-Nunes, Anderson Mans, Ben J. Santos, Isabel M. Ribeiro, Jose M. C. TI The role of saliva in tick feeding SO FRONTIERS IN BIOSCIENCE-LANDMARK LA English DT Review DE Tick; Salivary Gland; Feeding; Hemostasis; Inflammation; Angiogenesis; Review ID LONE STAR TICK; TISSUE FACTOR PATHWAY; IXODES-RICINUS TICKS; ORNITHODOROS-SAVIGNYI ACARI; COAGULATION-FACTOR-XA; PLATELET-AGGREGATION INHIBITOR; CUTANEOUS BASOPHIL RESPONSES; SERINE PROTEINASE-INHIBITORS; AMBLYOMMA-AMERICANUM TICKS; ADULT FEMALE MOSQUITO AB When attempting to feed on their hosts, ticks face the problem of host hemostasis (the vertebrate mechanisms that prevent blood loss), inflammation (that can produce itching or pain and thus initiate defensive behavior on their hosts) and adaptive immunity (by way of both cellular and humoral responses). Against these barriers, ticks evolved a complex and sophisticated pharmacological armamentarium, consisting of bioactive lipids and proteins, to assist blood feeding. Recent progress in transcriptome research has uncovered that hard ticks have hundreds of different proteins expressed in their salivary glands, the majority of which have no known function, and include many novel protein families (e.g., their primary structure is unique to ticks). This review will address the vertebrate mechanisms of these barriers as a guide to identify the possible targets of these large numbers of known salivary proteins with unknown function. We additionally provide a supplemental Table that catalogues over 3,500 putative salivary proteins from various tick species, which might assist the scientific community in the process of functional identification of these unique proteins. This supplemental file is accessble from http://exon.niaid.nih.gov/transcriptome/tick_review/Sup-Table-1.x1s.gz. C1 [Francischetti, Ivo M. B.; Sa-Nunes, Anderson; Mans, Ben J.; Ribeiro, Jose M. C.] NIAID, Lab Malaria & Vector Res, Bethesda, MD 20892 USA. [Santos, Isabel M.] Ribeirao Preto Sch Med, Dept Biochem & Immunol, Ribeirao Preto, SP, Brazil. RP Ribeiro, JMC (reprint author), NIAID, Lab Malaria & Vector Res, 9000 Rockville Pike, Bethesda, MD 20892 USA. EM jribeiro@niaid.nih.gov RI Sa-Nunes, Anderson/D-8667-2012; de Miranda Santos, Isabel/B-7597-2012; de Miranda Santos, Isabel/D-5261-2016; OI Sa-Nunes, Anderson/0000-0002-1859-4973; de Miranda Santos, Isabel/0000-0002-0438-4430; Mans, Ben/0000-0002-0177-0029; Ribeiro, Jose/0000-0002-9107-0818 FU Intramural NIH HHS [ZIA AI000810-13] NR 406 TC 199 Z9 204 U1 5 U2 32 PU FRONTIERS IN BIOSCIENCE INC PI MANHASSET PA C/O NORTH SHORE UNIV HOSPITAL, BIOMEDICAL RESEARCH CENTER, 350 COMMUNITY DR, MANHASSET, NY 11030 USA SN 1093-9946 J9 FRONT BIOSCI-LANDMRK JI Front. Biosci. PD JAN 1 PY 2009 VL 14 BP 2051 EP 2088 DI 10.2741/3363 PG 38 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 393DZ UT WOS:000262352400136 PM 19273185 ER PT J AU Csiszar, A Podlutsky, A Wolin, MS Losonczy, G Pacher, P Ungvari, Z AF Csiszar, Anna Podlutsky, Andrej Wolin, Michael S. Losonczy, Gyorgy Pacher, Pal Ungvari, Zoltan TI Oxidative stress and accelerated vascular aging: implications for cigarette smoking SO FRONTIERS IN BIOSCIENCE-LANDMARK LA English DT Review DE Endothelium; Cigarette Smoking; Smokers; Tobacco; Senescence; Inflammation; Gene Expression; Redox Status; Peroxynitrite; PARP-1; poly polymerase; ADP-ribose; PARP ID NF-KAPPA-B; TUMOR-NECROSIS-FACTOR; ADP-RIBOSE-POLYMERASE; NITRIC-OXIDE SYNTHASE; ELECTRON-SPIN-RESONANCE; ENDOTHELIUM-DEPENDENT DILATION; ADHESION MOLECULE EXPRESSION; BRONCHIAL EPITHELIAL-CELLS; MESSENGER-RNA EXPRESSION; IL-8 GENE-EXPRESSION AB Cigarette smoking is the major cause of preventable morbidity and mortality in the United States and constitutes a major risk factor for atherosclerotic vascular disease, including coronary artery disease and stroke. Increasing evidence supports the hypothesis that oxidative stress and inflammation provide the pathophysiological link between cigarette smoking and CAD. Previous studies have shown that cigarette smoke activates leukocytes to release reactive oxygen and nitrogen species (ROS/RNS) and secrete pro-inflammatory cytokines, increases the adherence of monocytes to the endothelium and elicits airway inflammation. Here we present an overview of the direct effects of water-soluble cigarette smoke constituents on endothelial function, vascular ROS production and inflammatory gene expression. The potential pathogenetic role of peroxynitrite formation, and downstream mechanisms including poly (ADP-ribose) polymerase (PARP) activation in cardiovascular complications in smokers are also discussed. C1 [Csiszar, Anna; Wolin, Michael S.; Ungvari, Zoltan] New York Med Coll, Dept Physiol, Valhalla, NY 10595 USA. [Podlutsky, Andrej] Univ Texas Hlth Sci Ctr San Antonio, Sam & Ann Barshop Inst Longev & Aging Studies, San Antonio, TX 78245 USA. [Losonczy, Gyorgy] Semmelweis Univ, Pulmonol Klin, Budapest, Hungary. [Pacher, Pal] NIAAA, NIH, Bethesda, MD 20892 USA. RP Ungvari, Z (reprint author), New York Med Coll, Dept Physiol, Valhalla, NY 10595 USA. EM zoltan_ungvari@nymc.edu RI Pacher, Pal/B-6378-2008; Podlutsky, Andrej/F-5421-2015 OI Pacher, Pal/0000-0001-7036-8108; FU American Heart Association [0430108N, 0435140N]; NIH [HL077256, HL43023]; Philip Morris U.S.A. Inc.; Philip Morris International; San Antonio Area Foundation; National Institutes of Health/NIAAA FX This work was supported by grants from the American Heart Association (0430108N and 0435140N, to A.C. and Z.U.), the NIH (HL077256 and HL43023, to A. C. M.W. and Z.U.), Philip Morris U.S.A. Inc. and Philip Morris International (to Z.U.), the San Antonio Area Foundation (to A.P.) and in part funded by the Intramural Research Program of the National Institutes of Health/NIAAA (P.P. and P.M.). NR 181 TC 78 Z9 80 U1 1 U2 5 PU FRONTIERS IN BIOSCIENCE INC PI IRVINE PA 16471 SCIENTIFIC WAY, IRVINE, CA 92618 USA SN 1093-9946 EI 1093-4715 J9 FRONT BIOSCI-LANDMRK JI Front. Biosci. PD JAN 1 PY 2009 VL 14 BP 3128 EP 3144 DI 10.2741/4040 PG 17 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 393DZ UT WOS:000262352400213 PM 19273262 ER PT J AU Vanpouille, C Lisco, A Margolis, L AF Vanpouille, Christophe Lisco, Andrea Margolis, Leonid TI Off-label indication: acyclovir as an anti-HIV drug? SO Future Virology LA English DT Editorial Material ID HERPES-SIMPLEX-VIRUS; HUMAN-IMMUNODEFICIENCY-VIRUS; LYMPHOID-TISSUE; DNA-POLYMERASE; DOUBLE-BLIND; METAANALYSIS; SUPPRESSION; INFECTION; WOMEN; MEN C1 [Vanpouille, Christophe; Lisco, Andrea; Margolis, Leonid] NICHHD, Program Phys Biol, Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20892 USA. RP Vanpouille, C (reprint author), NICHHD, Program Phys Biol, Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, 10 Ctr Dr,Bldg 10,Room 9D58, Bethesda, MD 20892 USA. EM vanpouic@mail.nih.gov; liscoa@mail.nih.com; margolil@mail.nih.gov NR 37 TC 1 Z9 1 U1 1 U2 1 PU FUTURE MEDICINE LTD PI LONDON PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3 1QB, ENGLAND SN 1746-0794 J9 FUTURE VIROL JI Future Virol. PD JAN PY 2009 VL 4 IS 1 BP 1 EP 5 DI 10.2217/17460794.4.1.1 PG 5 WC Virology SC Virology GA 396PC UT WOS:000262602600001 ER PT J AU Lanford, RE Evans, MJ Lohmann, V Lindenbach, B Gale, M Rehermann, B Chang, KM Lemon, SM AF Lanford, Robert E. Evans, Matthew J. Lohmann, Volker Lindenbach, Brett Gale, Michael, Jr. Rehermann, Barbara Chang, Kyong-Mi Lemon, Stanley M. TI The Accelerating Pace of HCV Research: A Summary of the 15th International Symposium on Hepatitis C Virus and Related Viruses SO GASTROENTEROLOGY LA English DT Editorial Material C1 Univ Texas Med Branch, Inst Human Infect & Immun, 6200 Galveston Natl Lab, Galveston, TX 77555 USA. Southwest Fdn Biomed Res, San Antonio, TX USA. Mt Sinai Sch Med, Dept Microbiol, New York, NY USA. Univ Heidelberg, Dept Molec Virol, Heidelberg, Germany. Yale Univ, Sch Med, Sect Microbial Pathogenesis, New Haven, CT USA. Univ Washington, Dept Immunol, Seattle, WA USA. NIDDKD, Liver Dis Branch, Immunol Sect, Bethesda, MD USA. Univ Penn, Philadelphia, PA USA. Philadelphia VA Med Ctr, Philadelphia, PA USA. RP Lemon, SM (reprint author), Univ Texas Med Branch, Inst Human Infect & Immun, 6200 Galveston Natl Lab, 301 Univ Blvd, Galveston, TX 77555 USA. EM smlemon@utmb.edu OI Lohmann, Volker/0000-0001-8719-7608; Gale, Michael/0000-0002-6332-7436; Evans, Matthew/0000-0002-4991-3877 FU Intramural NIH HHS; NCI NIH HHS [K01 CA107092, K01-CA107092]; NIAID NIH HHS [R01-AI060389, K99 AI077800, K99-AI077800, R01 AI047519, R01 AI060389, R01-AI47519, U19 AI040035, U19-AI040035]; NIDA NIH HHS [R01 DA024563] NR 0 TC 10 Z9 11 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD JAN PY 2009 VL 136 IS 1 BP 9 EP 16 DI 10.1053/j.gastro.2008.11.019 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 388OG UT WOS:000262028500045 PM 19026648 ER PT J AU Gao, Y Kristinsson, SY Goldin, LR Bjorkholm, M Caporaso, NE Landgren, O AF Gao, Ying Kristinsson, Sigurdur Y. Goldin, Lynn R. Bjorkholm, Magnus Caporaso, Neil E. Landgren, Ola TI Increased Risk for Non-Hodgkin Lymphoma in Individuals With Celiac Disease and a Potential Familial Association SO GASTROENTEROLOGY LA English DT Article ID POPULATION-BASED COHORT; DERMATITIS-HERPETIFORMIS; MALIGNANCY; MORTALITY; DIAGNOSIS; CANCER; SUSCEPTIBILITY; AUTOIMMUNITY; MULTICENTER; CHILDHOOD AB Background & Aims: Celiac disease (CD), a common digestive disease, is well known to be associated with excess non-Hodgkin lymphoma (NHL) risk. However, there are only limited data on risk in the current era of serologic testing and human leukocytes antigen typing to screen for CD. There is also no information on the role of family history of CD in relation to lymphoma risk. Methods: We identified 37,869 NHL, 8323 Hodgkin lymphoma (HL), and 13,842 chronic lymphocytic leukemia patients diagnosed in Sweden between 1965 and 2004, as well as 236,408 matched controls and 613,961 first-degree relatives. Using logistic regression, we calculated odds ratios and 95% confidence intervals as measures of risks adjusted for matching factors. Results: Overall we found persons with a hospital discharge diagnosis of CD to have a 5.35-fold (95% CI, 3.56-8.06) increased NHL risk. Risk of HL was borderline increased (OR = 2.54, 95% CI, 0.99-6.56); however, there was no excess chronic lymphocytic leukemia risk. Persons diagnosed with CD in 1975-1984, 1985-1994, and 1995-2004 had a 13.2-fold (95% CI, 3.63- 48.0), 7.90-fold (95% CI, 3.38-18.5), and 3.84-fold (95% Cl, 2.28-6.45) increased risk of NHL, respectively (P(trend) < .0001). individuals with a sibling affected with CD had a 2.03-fold (95% CI, 1.29-3.19) increased NHL risk. Conclusions: Persons with CD have an increased NHL risk; however, the excess risk has tapered off substantially in the last 4 decades. The observed excess NHL risk among individuals with a sibling affected with CD suggests shared susceptibility. Future studies are needed to explore the roles of gluten intake, secondary intestinal inflammation, and susceptibility genes in relation to subsequent risk of developing lymphoma. C1 [Gao, Ying] NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. [Kristinsson, Sigurdur Y.; Bjorkholm, Magnus; Landgren, Ola] Karolinske Univ, Hosp Solna & Inst, Div Hematol, Dept Med, Stockholm, Sweden. RP Gao, Y (reprint author), NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd,Bldg EPS Room 7016, Bethesda, MD 20892 USA. EM gaoying@mail.nih.gov RI Kristinsson, Sigurdur /M-2910-2015 OI Kristinsson, Sigurdur /0000-0002-4964-7476 FU NIH; NCI; Swedish Cancer Society; Stockholm County Council; Karolinska Institutet Foundations FX Supported by grants from the Intramural Research Program of the NIH, NCI, Swedish Cancer Society, Stockholm County Council, and the Karolinska Institutet Foundations. The authors thank Ms Shiva Ayobi, the National Board of Health and Welfare, Stockholm, Sweden; Ms Susanne Dahilof, Statistics Sweden, Orebro, Sweden; and Ms Emily Steplowski, Information Management Services, Silver Spring, MD, for important efforts in the development of this database. NR 47 TC 46 Z9 47 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD JAN PY 2009 VL 136 IS 1 BP 91 EP 98 DI 10.1053/j.gastro.2008.09.031 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 388OG UT WOS:000262028500016 PM 18950631 ER PT J AU Lok, AS Seeff, LB Morgan, TR Di Bisceglie, AM Sterling, RK Curto, TM Everson, GT Lindsay, KL Lee, WM Bonkovsky, HL Dienstag, JL Ghany, MG Morishima, C Goodman, ZD AF Lok, Anna S. Seeff, Leonard B. Morgan, Timothy R. Di Bisceglie, Adrian M. Sterling, Richard K. Curto, Teresa M. Everson, Gregory T. Lindsay, Karen L. Lee, William M. Bonkovsky, Herbert L. Dienstag, Jules L. Ghany, Marc G. Morishima, Chihiro Goodman, Zachary D. CA HALT-C Trial Grp TI Incidence of Hepatocellular Carcinoma and Associated Risk Factors in Hepatitis C-Related Advanced Liver Disease SO GASTROENTEROLOGY LA English DT Article ID SUSTAINED VIROLOGICAL RESPONSE; INTERFERON THERAPY; NATURAL-HISTORY; VIRUS-INFECTION; UNITED-STATES; FOLLOW-UP; CIRRHOSIS; FIBROSIS; TRIAL; HEPATOCARCINOGENESIS AB Background & Aims: Although the incidence of hepatocellular carcinoma (HCC) is increasing in the United States, data from large prospective studies are limited. We evaluated the Hepatitis C Antiviral Long-Term Treatment Against Cirrhosis (HALT-C) cohort for the incidence of HCC and associated risk factors. Methods: Hepatitis C virus-positive patients with bridging fibrosis or cirrhosis who did not respond to peginterferon and ribavirin were randomized to groups that were given maintenance peginterferon for 3.5 years or no treatment. HCC incidence was determined by Kaplan-Meier analysis, and baseline factors associated with HCC were analyzed by Cox regression. Results: 1,005 patients (mean age, 50.2 years; 71% male; 72% white race) were studied; 59% had bridging fibrosis, and 41% had cirrhosis. During a median follow-up of 4.6 years (maximum, 6.7 years), HCC developed in 48 patients (4.8%). The cumulative 5-year HCC incidence was similar for peginterferontreated patients and controls, 5.4% vs 5.0%, respectively (P = .78), and was higher among patients with cirrhosis than those with bridging fibrosis, 7.0% vs 4.1%, respectively (P = .08). HCC developed in 8 (17%) patients whose serial biopsy specimens showed only fibrosis. A multivariate analysis model comprising older age, black race, lower platelet count, higher alkaline phosphatase, esophageal varices, and smoking was developed to predict the risk of HCC. Conclusions: We found that maintenance peginterferon did not reduce the incidence of HCC in the HALT-C cohort. Baseline clinical and laboratory features predicted risk for HCC. Additional studies are required to confirm our finding of HCC in patients with chronic hepatitis C and bridging fibrosis. C1 [Lok, Anna S.] Univ Michigan, Med Ctr, Div Gastroenterol, Ann Arbor, MI USA. [Seeff, Leonard B.] NIDDK, Div Digest Dis & Nutr, NIH, Dept Hlth & Human Serv, Bethesda, MD USA. [Morgan, Timothy R.] Univ Calif Irvine, Div Gastroenterol, Irvine, CA USA. [Morgan, Timothy R.] VA Long Beach Healthcare Syst, Gastroenterol Serv, Long Beach, CA USA. [Di Bisceglie, Adrian M.] St Louis Univ, Sch Med, Div Gastroenterol & Hepatol, St Louis, MO USA. [Sterling, Richard K.] Virginia Commonwealth Univ, Hepatol Sect, Med Ctr, Richmond, VA USA. [Curto, Teresa M.] New England Res Inst, Watertown, MA 02172 USA. [Everson, Gregory T.] Univ Colorado, Sch Med, Sect Hepatol, Div Gastroenterol & Hepatol, Denver, CO USA. [Lindsay, Karen L.] Univ So Calif, Keck Sch Med, Div Gastrointestinal & Liver Dis, Los Angeles, CA 90033 USA. [Lee, William M.] Univ Texas SW Med Ctr Dallas, Div Digest & Liver Dis, Dallas, TX 75390 USA. [Bonkovsky, Herbert L.] Univ Connecticut, Ctr Hlth, Dept Med, Farmington, CT USA. [Bonkovsky, Herbert L.] Univ Connecticut, Ctr Hlth, Dept Mol & Struct Biol, Farmington, CT USA. [Bonkovsky, Herbert L.] Univ Connecticut, Ctr Hlth, Liver Biliary Pancreat Ctr, Farmington, CT USA. [Dienstag, Jules L.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Gastrointestinal Unit,Med Serv, Boston, MA USA. [Dienstag, Jules L.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA. [Ghany, Marc G.] NIDDK, Liver Dis Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD USA. [Morishima, Chihiro] Univ Washington, Dept Lab Med, Div Virol, Seattle, WA 98195 USA. [Goodman, Zachary D.] Armed Forces Inst Pathol, Div Hepat Pathol, Washington, DC 20306 USA. [Goodman, Zachary D.] Armed Forces Inst Pathol, Vet Adm Special Reference Lab Pathol, Washington, DC 20306 USA. RP Lok, AS (reprint author), Univ Michigan Hosp, Div Gastroenterol, 3912 Taubman Ctr,SPC 5362, Ann Arbor, MI 48109 USA. EM aslok@umich.edu RI Lok, Anna /B-8292-2009; OI Yang, Shuman/0000-0002-9638-0890 FU National Institute of Diabetes and Digestive and Kidney Diseases; National Institute of Allergy and Infectious Diseases (NIAID); National Cancer Institute; National Center for Minority Health and Health Disparities; National Center for Research Resources; National Institutes of Health; Cooperative Research and Development Agreement (CRADA) FX Supported by the National Institute of Diabetes and Digestive and Kidney Diseases (contract numbers are listed in Appendix 1); the National Institute of Allergy and Infectious Diseases (NIAID); the National Cancer Institute; the National Center for Minority Health and Health Disparities; General Clinical Research Center grants from the National Center for Research Resources, National Institutes of Health (grant numbers are listed In Appendix 1); and by Hoffman-La Roche, Inc, through a Cooperative Research and Development Agreement (CRADA) with the National Institutes of Health. NR 54 TC 262 Z9 270 U1 1 U2 8 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD JAN PY 2009 VL 136 IS 1 BP 138 EP 148 DI 10.1053/j.gastro.2008.09.014 PG 11 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 388OG UT WOS:000262028500022 PM 18848939 ER PT S AU Luebke, AE Rova, C Von Doersten, PG Poulsen, DJ AF Luebke, Anne E. Rova, Cherokee Von Doersten, Peter G. Poulsen, David J. BE Ryan, AF TI Adenoviral and AAV-Mediated Gene Transfer to the Inner Ear: Role of Serotype, Promoter, and Viral Load on In Vivo and In Vitro Infection Efficiencies SO GENE THERAPY OF COCHLEAR DEAFNESS: PRESENT CONCEPTS AND FUTURE ASPECTS SE Advances in Oto-Rhino-Laryngology LA English DT Article; Book Chapter ID ADENOASSOCIATED VIRUS VECTORS; POSTTRANSCRIPTIONAL REGULATORY ELEMENT; CENTRAL-NERVOUS-SYSTEM; GUINEA-PIG COCHLEA; TRANSGENE EXPRESSION; HAIR-CELLS; MURINE COCHLEA; MIDDLE-EAR; THERAPY; TRANSDUCTION AB The lack of effective treatments for many forms of hearing and vestibular disorders has produced interest in virally mediated gene therapies. However, to develop a gene therapy strategy that would successfully treat inner ear disorders, appropriate viral vectors capable of transfecting cochlear and support cells must be identified. While virally mediated gene transfer into the inner ear has been accomplished using herpes simplex type I virus, vaccinia virus, retroviruses, adenovirus, and adeno-associated virus (AAV), we will restrict our discussion to AAV and adenoviral vectors. Issues such as vector toxicity and load, viral serotype and backbone, and promoter specificity are discussed and contrasted for both in vivo vs. in vitro inner ear gene transfer. Copyright (C) 2009 S. Karger AG, Basel C1 [Luebke, Anne E.] Univ Rochester, Med Ctr, Dept Biomed Engn, Rochester, NY 14642 USA. [Luebke, Anne E.] Univ Rochester, Med Ctr, Dept Neurobiol & Anat, Rochester, NY 14642 USA. [Rova, Cherokee; Von Doersten, Peter G.; Poulsen, David J.] Univ Montana, Dept Biomed & Pharmaceut Sci, COBRE Ctr Struct & Funct Neurosci, Missoula, MT 59812 USA. RP Luebke, AE (reprint author), Univ Rochester, Med Ctr, Dept Biomed Engn, Box 603,601 Elmwood Ave MC68547, Rochester, NY 14642 USA. EM Anne_Luebke@urmc.rochester.edu FU NIDCD NIH HHS [DC007217, DC003086] NR 41 TC 13 Z9 13 U1 2 U2 3 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 0065-3071 BN 978-3-8055-9035-8 J9 ADV OTO-RHINO-LARYNG JI Adv.Otorhinolaryngol. PY 2009 VL 66 BP 87 EP 98 PG 12 WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental; Otorhinolaryngology SC Biotechnology & Applied Microbiology; Research & Experimental Medicine; Otorhinolaryngology GA BKK42 UT WOS:000268380700006 PM 19494574 ER PT J AU Bleyer, AJ Hart, TC AF Bleyer, Anthony J. Hart, Thomas C. BE Lifton, RP Somlo, S Giebisch, GH Seldin, DW TI Medullary Cystic Disease SO GENETIC DISEASES OF THE KIDNEY LA English DT Article; Book Chapter ID JUVENILE HYPERURICEMIC NEPHROPATHY; TAMM-HORSFALL GLYCOPROTEIN; KIDNEY-DISEASE; RENAL-DISEASE; UROMODULIN GENE; GOUTY NEPHROPATHY; STORAGE DISEASES; CHROMOSOME 1Q21; UMOD GENE; MUTATIONS C1 [Bleyer, Anthony J.] Wake Forest Univ, Bowman Gray Sch Med, Nephrol Sect, Winston Salem, NC 27109 USA. [Hart, Thomas C.] Natl Inst Dent & Craniofacial Res, NIH, Div Intramural Res, Bethesda, MD USA. RP Bleyer, AJ (reprint author), Wake Forest Univ, Bowman Gray Sch Med, Nephrol Sect, Winston Salem, NC 27109 USA. NR 71 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA BN 978-0-08-092427-4 PY 2009 BP 447 EP 461 DI 10.1016/B978-0-12-449851-8.00026-7 PG 15 WC Urology & Nephrology SC Urology & Nephrology GA BEO63 UT WOS:000317591300027 ER PT J AU Grubb, RL Walther, MM Linehan, WM AF Grubb, Robert L., III Walther, McClellan M. Linehan, W. Marston BE Lifton, RP Somlo, S Giebisch, GH Seldin, DW TI The Genetic Basis of Cancer of the Kidney SO GENETIC DISEASES OF THE KIDNEY LA English DT Article; Book Chapter ID RENAL-CELL CARCINOMA; HOGG-DUBE-SYNDROME; VONHIPPEL-LINDAU-DISEASE; PARENCHYMAL SPARING SURGERY; GUIDED RADIOFREQUENCY ABLATION; TUMOR-SUPPRESSOR GENE; MET PROTOONCOGENE; SPONTANEOUS PNEUMOTHORAX; HEREDITARY LEIOMYOMATOSIS; CUTANEOUS LEIOMYOMATOSIS C1 [Grubb, Robert L., III; Walther, McClellan M.] NCI, Urol Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA. [Linehan, W. Marston] NCI, Urol Oncol Branch, Bethesda, MD 20892 USA. RP Grubb, RL (reprint author), NCI, Urol Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA. NR 82 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA BN 978-0-08-092427-4 PY 2009 BP 497 EP 508 DI 10.1016/B978-0-12-449851-8.00028-0 PG 12 WC Urology & Nephrology SC Urology & Nephrology GA BEO63 UT WOS:000317591300029 ER PT J AU Chou, JY Mansfield, BC Weinstein, DA AF Chou, Janice Y. Mansfield, Brian C. Weinstein, David A. BE Lifton, RP Somlo, S Giebisch, GH Seldin, DW TI Renal Disease in Type I Glycogen Storage Disease SO GENETIC DISEASES OF THE KIDNEY LA English DT Article; Book Chapter ID COLONY-STIMULATING FACTOR; MICROSOMAL GLUCOSE-6-PHOSPHATASE SYSTEM; CONTINUOUS GLUCOSE THERAPY; TERM CLINICAL-COURSE; LIVER-TRANSPLANTATION; TUBULAR-ACIDOSIS; MURINE GLUCOSE-6-PHOSPHATASE; CALCIUM NEPHROLITHIASIS; TRANSMEMBRANE TOPOLOGY; METABOLIC CONTROL C1 [Chou, Janice Y.] NICHD, Sect Cellular Differentiat, HDB, NIH, Bethesda, MD 20892 USA. [Mansfield, Brian C.] NICHHD, Sect Cellular Differentiat, Heritable Disorders Branch, NIH, Bethesda, MD USA. [Weinstein, David A.] Childrens Hosp, Div Endocrinol, Boston, MA 02115 USA. [Weinstein, David A.] Harvard Univ, Sch Med, Boston, MA USA. RP Chou, JY (reprint author), NICHD, Sect Cellular Differentiat, HDB, NIH, Bethesda, MD 20892 USA. NR 116 TC 1 Z9 1 U1 1 U2 1 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA BN 978-0-08-092427-4 PY 2009 BP 693 EP 708 DI 10.1016/B978-0-12-449851-8.00041-3 PG 16 WC Urology & Nephrology SC Urology & Nephrology GA BEO63 UT WOS:000317591300042 ER PT J AU Shibata, K Diatchenko, L Zaykin, DV AF Shibata, Kyoko Diatchenko, Luda Zaykin, Dmitri V. TI Haplotype Associations With Quantitative Traits in the Presence of Complex Multilocus and Heterogeneous Effects SO GENETIC EPIDEMIOLOGY LA English DT Article DE haplotype association; complex disease; epistasis; gene-gene interactions ID CATECHOL-O-METHYLTRANSFERASE; LIKELIHOOD-BASED INFERENCE; RNA SECONDARY STRUCTURE; COMBINING P-VALUES; UNRELATED INDIVIDUALS; MESSENGER-RNA; HUMAN BRAIN; INFERRED HAPLOTYPES; GENETIC-VARIATION; GENOTYPE DATA AB In genetic mapping of complex traits, scored haplotypes are likely to represent only a subset of all causal polymorphisms. At the extreme of this scenario, observed polymorphisms are not themselves functional, and only linked to causal ones via linkage disequilibrium (LD). We will demonstrate that due to Such incomplete knowledge regarding the underlying genetic mechanism, the variance of a trait may become different between the scored haplotypes. Thus, unequal variances between haplotypes may be indicative of additional functional polymorphisms affecting the trait. Methods accounting for such haplotype-specific variance may also provide an increased power to detect complex associations. We suggest ways to estimate and test these haplotypic variance contrasts, and incorporate them into the haplotypic tests for association. We further extend this approach to data with unknown gametic phase via likelihood-based simultaneous estimation of haplotypic effects and their frequencies. We find our approach to provide additional power, especially tinder the following types of models: (a) where scored and unobserved variants are epistatically interacting with each other; and (b) tinder heterogeneity models, where multiple unobserved mutations are linked to non-functional observed polymorphisms via LD. An illustrative example of usefulness of the method is discussed, utilizing analysis Of multilocus effects within the catechol-O-methyltransferase gene. Genet. Epidemiol. 33:63-78, 2009. Published 2008 Wiley-Liss, Inc. C1 [Shibata, Kyoko; Zaykin, Dmitri V.] NIEHS, NIH, Res Triangle Pk, NC 27709 USA. [Diatchenko, Luda] Univ N Carolina, Ctr Neurosensory Disorders, Chapel Hill, NC USA. RP Zaykin, DV (reprint author), NIEHS, NIH, 111 TW Alexander Dr,South Bldg 101,B356B,Mail Dro, Res Triangle Pk, NC 27709 USA. EM zaykind@niehs.nih.gov FU NIH [PO1NS045685, DE16558, DE017018] FX This research was supported in part by the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences. L.D. was supported by NIH grants PO1NS045685, DE16558, and DE017018. We thank Shyamal Peddada, Norman Kaplan, Rongheng Lin, Clare Weinberg, and David Umbach for stimulating discussion. We thank two reviewers for insightful suggestions. NR 53 TC 9 Z9 9 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PD JAN PY 2009 VL 33 IS 1 BP 63 EP 78 DI 10.1002/gepi.20358 PG 16 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 391PJ UT WOS:000262244900008 PM 18636529 ER PT J AU An, P Mukherjee, O Chanda, P Yao, L Engelman, CD Huang, CH Zheng, T Kovac, IP Dube, MP Liang, XY Li, J de Andrade, M Culverhouse, R Malzahn, D Manning, AK Clarke, GM Jung, J Province, MA AF An, Ping Mukherjee, Odity Chanda, Pritam Yao, Li Engelman, Corinne D. Huang, Chien-Hsun Zheng, Tian Kovac, Ilija P. Dube, Marie-Pierre Liang, Xueying Li, Jia de Andrade, Mariza Culverhouse, Robert Malzahn, Doerthe Manning, Alisa K. Clarke, Geraldine M. Jung, Jeesun Province, Michael A. TI The Challenge of Detecting Epistasis (G x G Interactions): Genetic Analysis Workshop 16 SO GENETIC EPIDEMIOLOGY LA English DT Article; Proceedings Paper CT 16th Genetic Analysis Workshop/17th Annual Meeting of the International-Genetic-Epidemiology-Society CY SEP 17-20, 2008 CL St Louis, MO SP Int Genet Epidemiol Soc DE generalized linear model; machine learning methods ID ASSOCIATION; TRAITS AB Interest is increasing in epistasis as a possible source of the unexplained variance missed by genome-wide association studies. The Genetic Analysis Workshop 16 Group 9 participants evaluated a wide variety of classical and novel analytical methods for detecting epistasis, in both the statistical and machine learning paradigms, applied to both real and simulated data. Because the magnitude of epistasis is clearly relative to scale of penetrance, and therefore to some extent, to the choice of model framework, it is not surprising that strong interactions under one model might be minimized or even disappear entirely under a different modeling framework. Genet. Epidetniol. 33 (Suppl. 1):S58-S67, 2009. (C) 2009 Wiley-Liss, Inc. C1 [An, Ping; Province, Michael A.] Washington Univ, Sch Med, Div Stat Genom, St Louis, MO 63108 USA. [An, Ping; Province, Michael A.] Washington Univ, Sch Med, Dept Genet, St Louis, MO 63108 USA. [Mukherjee, Odity] Natl Ctr Biol Sci, Bangalore, Karnataka, India. [Chanda, Pritam] SUNY Buffalo, Dept Comp Sci & Engn, Buffalo, NY 14260 USA. [Yao, Li; Engelman, Corinne D.] Univ Wisconsin, Dept Human Dev & Family Studies, Madison, WI USA. [Huang, Chien-Hsun; Zheng, Tian] Columbia Univ, Dept Stat, New York, NY USA. [Kovac, Ilija P.; Dube, Marie-Pierre] Montreal Heart Inst, Res Ctr, Montreal, PQ H1T 1C8, Canada. [Liang, Xueying] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA. [Li, Jia; de Andrade, Mariza] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA. [Culverhouse, Robert] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA. [Malzahn, Doerthe] Univ Gottingen, Dept Genet Epidemiol, Univ Med Ctr, Gottingen, Germany. [Manning, Alisa K.] Boston Univ, Sch Publ Hlth, Boston, MA USA. [Clarke, Geraldine M.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England. [Jung, Jeesun] Indiana Univ, Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA. RP Province, MA (reprint author), Washington Univ, Sch Med, Div Stat Genom, Box 8506,4444 Forest Pk Blvd, St Louis, MO 63108 USA. EM mprovince@wustl.edu RI Dube, Marie-Pierre/B-9364-2008 OI Dube, Marie-Pierre/0000-0001-8442-4393 FU FIC NIH HHS [TW0511-05]; NCRR NIH HHS [1U54RR023496]; NHLBI NIH HHS [HL087700, HL088215, HL088655, HL87660, N01 HC025195, R01 HL087660, R01 HL087700, R01 HL088215, R01 HL117078, U01 HL088655, U01 HL088655-02]; NIA NIH HHS [U01 AG023746]; NIAAA NIH HHS [AA01572]; NIAMS NIH HHS [AR44422, N01-AR-7-2232, R01 AR044422]; NIDA NIH HHS [DA023166, R03 DA023166]; NIGMS NIH HHS [GM070789, GM69590, K25 GM069590, R01 GM031575, R01 GM031575-25, R01 GM070789] NR 38 TC 9 Z9 10 U1 0 U2 2 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 2009 VL 33 BP S58 EP S67 DI 10.1002/gepi.20474 PG 10 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 529TL UT WOS:000272540700011 PM 19924703 ER PT J AU Sharma, D Stanley, RF Masison, DC AF Sharma, Deepak Stanley, Robert F. Masison, Daniel C. TI Curing of Yeast [URE3] Prion by the Hsp40 Cochaperone Ydj1p Is Mediated by Hsp70 SO GENETICS LA English DT Article ID ESCHERICHIA-COLI DNAJ; SACCHAROMYCES-CEREVISIAE; MOLECULAR CHAPERONES; SUBSTRATE-BINDING; J-DOMAIN; PEPTIDE SUBSTRATE; IN-VITRO; PROTEIN; PROPAGATION; SIS1 AB [URE3] is a prion of the yeast Ure2 protein. Hsp40 is a cochaperone that regulates Hsp70 chaperone activity. When overexpressed, the Hsp40 Ydj1p cures yeast of [URE3], but the Hsp40 Sis1p does not. On the basis of biochemical data Ydj1p has been proposed to cure [URE3] by binding soluble Ure2p and preventing it from joining priori aggregates. Here, we mutagenized Ydj1p and find that disrupting substrate binding, dimerization, membrane association, orability to transfer substrate to Hsp70 had little or no effect on curing. J-domain point mutations that disrupt functional interactions of Ydj1p with Hsp70 abolished curing, and the J domain alone cured [URE3]. Consistent with heterologous J domains possessing similar Hsp70 regulatory activity, the Sis1p J domain also cured [URE3]. We further show that. Ydj1p is not essential for [URE3] propagation and that depletion of Ure2p is lethal in cells lacking Ydj1p. Our data imply that curing of [URE3] by overproduced Ydj1p does not involve direct interaction of Ydj1p with Ure2p but rather works through regulation of Hsp70 through a specific J-protein/Hsp70 interaction. C1 [Sharma, Deepak; Stanley, Robert F.; Masison, Daniel C.] NIDDKD, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA. RP Masison, DC (reprint author), NIDDKD, Lab Biochem & Genet, NIH, 8 Ctr Dr,Bldg 8,Room 407, Bethesda, MD 20892 USA. EM masisond@helix.nih.gov FU National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health FX This research was supported by the intramural program of the National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health. NR 44 TC 21 Z9 23 U1 2 U2 3 PU GENETICS SOCIETY AMERICA PI BETHESDA PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA SN 0016-6731 EI 1943-2631 J9 GENETICS JI Genetics PD JAN PY 2009 VL 181 IS 1 BP 129 EP 137 DI 10.1534/genetics.108.098699 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 396MJ UT WOS:000262595500013 PM 19015537 ER PT S AU Pomeroy, J Soderberg, AM Franks, PW AF Pomeroy, Jeremy Soderberg, Anna M. Franks, Paul W. BE Collins, M TI Gene-Lifestyle Interactions and Their Consequences on Human Health SO GENETICS AND SPORTS SE Medicine and Sport Science LA English DT Article; Book Chapter ID BODY-MASS INDEX; DIABETES PREVENTION PROGRAM; IMPAIRED GLUCOSE-TOLERANCE; OBESITY-RELATED TRAITS; PHYSICAL-ACTIVITY; ENERGY-EXPENDITURE; FTO GENE; ENVIRONMENTAL-INFLUENCES; POSTMENOPAUSAL WOMEN; PREDATION RELEASE AB Our genes are the conduit through which the environment communicates to the cells in our bodies. The responses to these signals include hormonal, metabolic and neurological changes to tissues and organs that manifest as phenotypes - measurable responses to gene transcription and translation. Thus, the health consequences of lifestyle behaviors such as physical activity, which can be broadly defined as 'environmental' exposures, are channeled through our genes. The extent to which these signals are conveyed depends in part on the structure and function of our genome. Hence, even when exposed to the same exercise regimes or doses of physical activity, responses vary markedly from one person to the next; some experience marked changes in disease phenotypes such as lipid and glucose concentrations, adiposity, or blood pressure levels, whilst others appear unresponsive. It is this process that underlies the concept that we will discuss in this chapter, a concept termed gene-lifestyle interaction. The aims of this chapter are (a) to convey to the reader the fundamental principles of gene-lifestyle interaction; (b) to describe the historical basis to this area of research; (c) to explain how understanding gene-lifestyle interactions might enhance our knowledge of the molecular mechanisms of disease; (d) to speculate on the ways in which information of gene-lifestyle interactions might eventually facilitate disease prevention, and (e) to overview the published literature which has focused on obesity as an outcome. Copyright (C) 2009 S. Karger AG, Basel C1 [Pomeroy, Jeremy; Soderberg, Anna M.; Franks, Paul W.] Umea Univ Hosp, Genet Epidemiol & Clin Res Grp, Dept Publ Hlth & Clin Med, Div Med, SE-90187 Umea, Sweden. [Pomeroy, Jeremy] NIDDK, Phoenix Epidemiol & Clin Res Branch, NIH, Phoenix, AZ USA. RP Franks, PW (reprint author), Umea Univ Hosp, Genet Epidemiol & Clin Res Grp, Dept Publ Hlth & Clin Med, Div Med, SE-90187 Umea, Sweden. EM paul.franks@medicin.umu.se NR 62 TC 4 Z9 5 U1 0 U2 2 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 0254-5020 BN 978-3-8055-9027-3 J9 MED SPORT SCI JI Med.Sport Sci. PY 2009 VL 54 BP 110 EP 135 PG 26 WC Genetics & Heredity; Sport Sciences SC Genetics & Heredity; Sport Sciences GA BLF72 UT WOS:000270079000008 PM 19696511 ER PT J AU Kempf, L Weinberger, DR AF Kempf, Lucas Weinberger, Daniel R. BE Goldberg, TE Weinberger, DR TI Molecular Genetics and Bioinformatics: An Outline for Neuropsychological Genetics SO GENETICS OF COGNITIVE NEUROSCIENCE LA English DT Article; Book Chapter ID MESSENGER-RNA; HUMAN GENOME; POLYMORPHISM; IDENTIFICATION; SCHIZOPHRENIA; PROTEIN; ENCODE; BRAIN; COMT C1 [Kempf, Lucas; Weinberger, Daniel R.] NIMH, Genes Cognit & Psychosis Program, Bethesda, MD 20892 USA. RP Kempf, L (reprint author), NIMH, Genes Cognit & Psychosis Program, Bethesda, MD 20892 USA. NR 27 TC 0 Z9 0 U1 0 U2 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA BN 978-0-262-01307-9 PY 2009 BP 3 EP 26 PG 24 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA BPL47 UT WOS:000279150000002 ER PT J AU Nicodemus, KK Zhang, FY AF Nicodemus, Kristin K. Zhang, Fengyu BE Goldberg, TE Weinberger, DR TI Statistical Methods in Neuropsychiatric Genetics SO GENETICS OF COGNITIVE NEUROSCIENCE LA English DT Article; Book Chapter ID GENOME-WIDE ASSOCIATION; FALSE DISCOVERY RATES; QUANTITATIVE TRAIT; LINKAGE DISEQUILIBRIUM; LOGISTIC-MODELS; SIB-PAIRS; POWER; DISEASE; TESTS; STRATIFICATION C1 [Nicodemus, Kristin K.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England. [Zhang, Fengyu] NIMH, Genes Cognit & Psychosis Program, Bethesda, MD 20892 USA. RP Nicodemus, KK (reprint author), Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England. NR 51 TC 0 Z9 0 U1 0 U2 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA BN 978-0-262-01307-9 PY 2009 BP 27 EP 50 PG 24 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA BPL47 UT WOS:000279150000003 ER PT J AU Papaleo, F Weinberger, DR Chen, JS AF Papaleo, Francesco Weinberger, Daniel R. Chen, Jingshan BE Goldberg, TE Weinberger, DR TI Animal Models of Genetic Effects on Cognition SO GENETICS OF COGNITIVE NEUROSCIENCE LA English DT Article; Book Chapter ID RECEPTOR KNOCKOUT MICE; OVEREXPRESSING TRANSGENIC MICE; CANNABINOID CB1 RECEPTOR; MEDIAL FRONTAL-CORTEX; DOPAMINE D-1 RECEPTOR; REACTION-TIME-TASK; CORTICOTROPIN-RELEASING-FACTOR; GALANIN-TREATED RATS; CALMODULIN KINASE-II; MORRIS WATER MAZE C1 [Papaleo, Francesco] NIMH, Clin Brain Disorders Branch, Bethesda, MD 20892 USA. [Weinberger, Daniel R.; Chen, Jingshan] NIMH, Genes Cognit & Psychosis Program, Bethesda, MD 20892 USA. RP Papaleo, F (reprint author), NIMH, Clin Brain Disorders Branch, Bethesda, MD 20892 USA. NR 187 TC 2 Z9 2 U1 0 U2 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA BN 978-0-262-01307-9 PY 2009 BP 51 EP 94 PG 44 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA BPL47 UT WOS:000279150000004 ER PT J AU Hariri, AR Forbes, EE Bigos, KL AF Hariri, Ahmad R. Forbes, Erika E. Bigos, Kristin L. BE Goldberg, TE Weinberger, DR TI Genetics of Corticolimbic Function and Emotional Reactivity SO GENETICS OF COGNITIVE NEUROSCIENCE LA English DT Article; Book Chapter ID SEROTONIN TRANSPORTER GENE; 5-HT1A RECEPTOR-BINDING; MAJOR DEPRESSION; POLYMORPHISM 5-HTTLPR; AMYGDALA ACTIVATION; PERSONALITY-TRAITS; PROMOTER REGION; HUMAN BRAIN; ASSOCIATION; ANXIETY C1 [Hariri, Ahmad R.; Forbes, Erika E.] Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA 15260 USA. [Hariri, Ahmad R.; Forbes, Erika E.] Univ Pittsburgh, Sch Pharm, Dept Psychiat, Pittsburgh, PA USA. [Bigos, Kristin L.] NIMH, Genes Cognit & Psychosis Program, Bethesda, MD 20892 USA. RP Hariri, AR (reprint author), Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA 15260 USA. NR 50 TC 0 Z9 0 U1 0 U2 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA BN 978-0-262-01307-9 PY 2009 BP 145 EP 157 PG 13 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA BPL47 UT WOS:000279150000007 ER PT J AU Goldberg, TE Mattay, VS AF Goldberg, Terry E. Mattay, Venkata S. BE Goldberg, TE Weinberger, DR TI Genes Associated with Individual Differences in Cognitive Aging SO GENETICS OF COGNITIVE NEUROSCIENCE LA English DT Article; Book Chapter ID APOLIPOPROTEIN-E; ALZHEIMERS-DISEASE; EPSILON-4 ALLELE; EPISODIC MEMORY; WORKING-MEMORY; BRAIN-FUNCTION; POLYMORPHISM; DECLINE; AGE; GENOTYPE C1 [Goldberg, Terry E.] Litwin Zucker Alzheimers Dis Ctr, Great Neck, NY USA. [Goldberg, Terry E.; Mattay, Venkata S.] NIMH, Genes Cognit & Psychosis Program, Bethesda, MD 20892 USA. [Goldberg, Terry E.] Psychiat Res Feinstein Inst, Great Neck, NY USA. RP Goldberg, TE (reprint author), Litwin Zucker Alzheimers Dis Ctr, Great Neck, NY USA. NR 48 TC 3 Z9 3 U1 0 U2 2 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA BN 978-0-262-01307-9 PY 2009 BP 159 EP 174 PG 16 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA BPL47 UT WOS:000279150000008 ER PT J AU Cadet, JL AF Cadet, Jean Lud TI Amphetamine recapitulates developmental programs in the zebrafish SO GENOME BIOLOGY LA English DT Review ID CONDITIONED PLACE PREFERENCE; ADDICTION; GENES; BRAIN; MECHANISMS; BEHAVIOR; COCAINE; RERIO AB Addictive drugs hijack the human brain's 'reward' systems. A zebrafish model of addiction has recently been used to query changes in gene expression during this process. C1 NIDA, Mol Neuropsychiat Branch, IRP, NIH,Biomed Res Ctr, Baltimore, MD 21224 USA. RP Cadet, JL (reprint author), NIDA, Mol Neuropsychiat Branch, IRP, NIH,Biomed Res Ctr, 251 Bayview Blvd, Baltimore, MD 21224 USA. EM jcadet@intra.nida.nih.gov NR 19 TC 9 Z9 9 U1 5 U2 5 PU BIOMED CENTRAL LTD PI LONDON PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1474-760X J9 GENOME BIOL JI Genome Biol. PY 2009 VL 10 IS 7 AR 231 DI 10.1186/gb-2009-10-7-231 PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 487WV UT WOS:000269309600006 PM 19664194 ER PT J AU Church, DM Hillier, LW AF Church, Deanna M. Hillier, LaDeana W. TI Back to Bermuda: how is science best served? SO GENOME BIOLOGY LA English DT Editorial Material ID HUMAN GENOME; SEGMENTAL DUPLICATIONS; SEQUENCE; ASSEMBLER AB The independent announcements of two bovine genome assemblies from the same data suggest it is time to revisit the spirit of the Bermuda and Fort Lauderdale agreements and determine the policies for data release and distribution that will best serve both the producers of the data and the users. C1 [Church, Deanna M.] NCBI, Natl Lib Med, NIH, Bethesda, MD 20894 USA. [Hillier, LaDeana W.] Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA. RP Church, DM (reprint author), NCBI, Natl Lib Med, NIH, 8600 Rockville Pike, Bethesda, MD 20894 USA. EM church@ncbi.nlm.nih.gov FU Intramural NIH HHS [Z01 LM100604-04] NR 13 TC 2 Z9 2 U1 0 U2 2 PU BIOMED CENTRAL LTD PI LONDON PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1474-760X J9 GENOME BIOL JI Genome Biol. PY 2009 VL 10 IS 4 AR 105 DI 10.1186/gb-2009-10-4-105 PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 452MP UT WOS:000266544600002 PM 19435531 ER PT J AU Lal-Nag, M Morin, PJ AF Lal-Nag, Madhu Morin, Patrice J. TI The claudins SO GENOME BIOLOGY LA English DT Review ID RECESSIVE DEAFNESS DFNB29; JUNCTION BARRIER FUNCTION; OVARIAN-CANCER CELLS; HEPATITIS-C VIRUS; TIGHT-JUNCTION; EPITHELIAL-CELLS; MEMBRANE-PROTEINS; STRIA VASCULARIS; GENE FAMILY; EXPRESSION AB The claudin multigene family encodes tetraspan membrane proteins that are crucial structural and functional components of tight junctions, which have important roles in regulating paracellular permeability and maintaining cell polarity in epithelial and endothelial cell sheets. In mammals, the claudin family consists of 24 members, which exhibit complex tissue-specific patterns of expression. The extracellular loops of claudins from adjacent cells interact with each other to seal the cellular sheet and regulate paracellular transport between the luminal and basolateral spaces. The claudins interact with multiple proteins and are intimately involved in signal transduction to and from the tight junction. Several claudin mouse knockout models have been generated and the diversity of phenotypes observed clearly demonstrates their important roles in the maintenance of tissue integrity in various organs. In addition, mutation of some claudin genes has been causatively associated with human diseases and claudin genes have been found to be deregulated in various cancers. The mechanisms of claudin regulation and their exact roles in normal physiology and disease are being elucidated, but much work remains to be done. The next several years are likely to witness an explosion in our understanding of these proteins, which may, in turn, provide new approaches for the targeted therapy of various diseases. C1 [Morin, Patrice J.] Johns Hopkins Med Inst, Dept Pathol, Baltimore, MD 21287 USA. [Lal-Nag, Madhu; Morin, Patrice J.] Natl Inst Hlth Biomed Res Ctr, Lab Cellular & Mol Biol, NIA, Baltimore, MD 21224 USA. RP Morin, PJ (reprint author), Johns Hopkins Med Inst, Dept Pathol, Baltimore, MD 21287 USA. EM morinp@mail.nih.gov FU Intramural Research Program of the National Institutes of Health; National Institute on Aging FX We thank members of our laboratory for helpful comments on the manuscript. This work was supported entirely by the Intramural Research Program of the National Institutes of Health, National Institute on Aging. NR 47 TC 135 Z9 145 U1 0 U2 10 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1474-760X J9 GENOME BIOL JI Genome Biol. PY 2009 VL 10 IS 8 AR 235 DI 10.1186/gb-2009-10-8-235 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 492QA UT WOS:000269672900005 PM 19706201 ER PT J AU Ma, B Nussinov, R AF Ma, Buyong Nussinov, Ruth TI Regulating highly dynamic unstructured proteins and their coding mRNAs SO GENOME BIOLOGY LA English DT Review ID DISORDERED PROTEIN; TRANSLATION; P53; TUMORIGENESIS; EVOLUTION; SEQUENCE; REGIONS; BINDING AB The lifetimes and conformations of intrinsically unstructured proteins (IUPs) and their mRNAs are orchestrated to ensure precision, speed and flexibility in biological control. C1 [Ma, Buyong; Nussinov, Ruth] NCI, Basic Res Program, SAIC Frederick Inc, Ctr Canc Res Nanobiol Program, Frederick, MD 21702 USA. [Nussinov, Ruth] Tel Aviv Univ, Sackler Sch Med, Dept Human Genet & Mol Med, Sackler Inst Mol Med, IL-69978 Tel Aviv, Israel. RP Nussinov, R (reprint author), NCI, Basic Res Program, SAIC Frederick Inc, Ctr Canc Res Nanobiol Program, Frederick, MD 21702 USA. EM ruthnu@helix.nih.gov RI Ma, Buyong/F-9491-2011 OI Ma, Buyong/0000-0002-7383-719X FU National Cancer Institute; National Institutes of Health [NO1-CO-12400]; Intramural Research Program of the NIH; Center for Cancer Research. FX This project has been funded in whole or in part with Federal funds from the National Cancer Institute, National Institutes of Health, under contract number NO1-CO-12400. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government. This research was supported (in part) by the Intramural Research Program of the NIH, National Cancer Institute, Center for Cancer Research. NR 25 TC 15 Z9 15 U1 0 U2 2 PU BIOMED CENTRAL LTD PI LONDON PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1474-760X J9 GENOME BIOL JI Genome Biol. PY 2009 VL 10 IS 1 AR 204 DI 10.1186/gb-2009-10-1-204 PG 5 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 413WK UT WOS:000263823200005 PM 19226433 ER PT J AU Pankla, R Buddhisa, S Berry, M Blankenship, DM Bancroft, GJ Banchereau, J Lertmemongkolchai, G Chaussabel, D AF Pankla, Rungnapa Buddhisa, Surachat Berry, Matthew Blankenship, Derek M. Bancroft, Gregory J. Banchereau, Jacques Lertmemongkolchai, Ganjana Chaussabel, Damien TI Genomic transcriptional profiling identifies a candidate blood biomarker signature for the diagnosis of septicemic melioidosis SO GENOME BIOLOGY LA English DT Article ID REAL-TIME PCR; SYSTEMIC-LUPUS-ERYTHEMATOSUS; GENE-EXPRESSION; BURKHOLDERIA-PSEUDOMALLEI; PERIPHERAL-BLOOD; CLINICAL-EVALUATION; MONONUCLEAR-CELLS; SHOCK PATIENTS; T-CELLS; HLA-DR AB Background: Melioidosis is a severe infectious disease caused by Burkholderia pseudomallei, a Gram-negative bacillus classified by the National Institute of Allergy and Infectious Diseases (NIAID) as a category B priority agent. Septicemia is the most common presentation of the disease with a 40% mortality rate even with appropriate treatments. Better diagnostic tests are therefore needed to improve therapeutic efficacy and survival rates. Results: We have used microarray technology to generate genome-wide transcriptional profiles (>48,000 transcripts) from the whole blood of patients with septicemic melioidosis (n = 32), patients with sepsis caused by other pathogens (n = 31), and uninfected controls (n = 29). Unsupervised analyses demonstrated the existence of a whole blood transcriptional signature distinguishing patients with sepsis from control subjects. The majority of changes observed were common to both septicemic melioidosis and sepsis caused by other infections, including genes related to inflammation, interferon-related genes, neutrophils, cytotoxic cells, and T-cells. Finally, class prediction analysis identified a 37 transcript candidate diagnostic signature that distinguished melioidosis from sepsis caused by other organisms with 100% accuracy in a training set. This finding was confirmed in 2 independent validation sets, which gave high prediction accuracies of 78% and 80%, respectively. This signature was significantly enriched in genes coding for products involved in the MHC class II antigen processing and presentation pathway. Conclusions: Blood transcriptional patterns distinguish patients with septicemic melioidosis from patients with sepsis caused by other pathogens. Once confirmed in a large scale trial this diagnostic signature might constitute the basis of a differential diagnostic assay. C1 [Pankla, Rungnapa; Buddhisa, Surachat; Lertmemongkolchai, Ganjana] Khon Kaen Univ, Fac Associated Med Sci, Ctr Res & Dev Med Diagnost Labs, Dept Clin Immunol, Khon Kaen 40002, Thailand. [Pankla, Rungnapa; Banchereau, Jacques; Chaussabel, Damien] Baylor Inst Immunol Res, Cooperat Ctr Translat Res Human Immunol & Biodef, Baylor Natl Inst Allergy & Infect Dis NIAID, Dallas, TX 75204 USA. [Pankla, Rungnapa; Banchereau, Jacques; Chaussabel, Damien] Baylor Res Inst, Dallas, TX 75204 USA. [Berry, Matthew] Natl Inst Med Res, Ridgeway, Div Immunoregulat, London NW7 1AA, England. [Blankenship, Derek M.] Inst Hlth Care Res & Improvement, Dallas, TX 75206 USA. [Bancroft, Gregory J.] Univ London London Sch Hyg & Trop Med, Dept Infect & Trop Dis, London WC1E 7HT, England. RP Lertmemongkolchai, G (reprint author), Khon Kaen Univ, Fac Associated Med Sci, Ctr Res & Dev Med Diagnost Labs, Dept Clin Immunol, 123 Mittraparp Rd, Khon Kaen 40002, Thailand. EM ganja_le@kku.ac.th; DamienC@BaylorHealth.edu OI Lertmemongkolchai, Ganjana/0000-0001-6972-585X; Chaussabel, Damien/0000-0002-6131-7242 FU Baylor Health Care System foundation; National Institutes of Health [U19 AIO57234-02, U01 AI082110]; NIAID/NIH [AI-61363]; Commission of Higher Education, Ministry of Education PhD scholarship through Naresuan University, Thailand FX This work was funded by the Baylor Health Care System foundation and the National Institutes of Health (U19 AIO57234-02 and U01 AI082110 to JB) and the NIAID/NIH (AI-61363). RP was supported by the Commission of Higher Education, Ministry of Education PhD scholarship through Naresuan University, Thailand. We thank the staff of Khon Kaen Regional Hospital for patient recruitment; Quynh-Anh Nguyen, Indira Munagala, Chontida Supaprom, Maneerat Pinsiri, and Patcharaporn Tippayawat for their assistance throughout this project; Gordon Hayward for his help uploading the data into GEO; and Charles Quinn for setting up the companion website. NR 52 TC 68 Z9 68 U1 1 U2 11 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1474-760X J9 GENOME BIOL JI Genome Biol. PY 2009 VL 10 IS 11 AR R127 DI 10.1186/gb-2009-10-11-r127 PG 22 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 540OT UT WOS:000273344600014 PM 19903332 ER PT J AU Przytycka, TM AF Przytycka, Teresa M. TI Phenotypic variation meets systems biology SO GENOME BIOLOGY LA English DT Article AB A report of the 18th Annual Growth Factor and Signal Transduction Symposium, Ames, USA, 11-14 June 2009. C1 Natl Lib Med, NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA. RP Przytycka, TM (reprint author), Natl Lib Med, NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA. EM przytyck@ncbi.nlm.nih.gov NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1474-760X J9 GENOME BIOL JI Genome Biol. PY 2009 VL 10 IS 8 AR 313 DI 10.1186/gb-2009-10-8-313 PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 492QA UT WOS:000269672900006 PM 19664197 ER PT J AU Thomas, R Gohlke, JM Stopper, GF Parham, FM Portier, CJ AF Thomas, Reuben Gohlke, Julia M. Stopper, Geffrey F. Parham, Frederick M. Portier, Christopher J. TI Choosing the right path: enhancement of biologically relevant sets of genes or proteins using pathway structure SO GENOME BIOLOGY LA English DT Article ID MICROARRAY DATA; EXPRESSION DATA; FUNCTIONAL CATEGORIES; TESTING ASSOCIATION; STATISTICAL TESTS; LEVEL ANALYSIS; MIXED MODELS; ENRICHMENT; NETWORKS; ONTOLOGY AB A method is proposed that finds enriched pathways relevant to a studied condition using the measured molecular data and also the structural information of the pathway viewed as a network of nodes and edges. Tests are performed using simulated data and genomic data sets and the method is compared to two existing approaches. The analysis provided demonstrates the method proposed is very competitive with the current approaches and also provides biologically relevant results. C1 [Thomas, Reuben; Gohlke, Julia M.; Parham, Frederick M.; Portier, Christopher J.] NIEHS, Environm Syst Biol Grp, Mol Toxicol Lab, Res Triangle Pk, NC 27709 USA. [Stopper, Geffrey F.] Univ Cattolica Sacro Cuore, Dept Biol, Fairfield, CT 06825 USA. RP Portier, CJ (reprint author), NIEHS, Environm Syst Biol Grp, Mol Toxicol Lab, POB 12233, Res Triangle Pk, NC 27709 USA. EM portier@niehs.nih.gov RI Portier, Christopher/A-3160-2010; OI Portier, Christopher/0000-0002-0954-0279; Gohlke, Julia/0000-0002-6984-2893 FU Intramural Research Program of the NIH; National Institute of Environmental Health Sciences (NIEHS); NIH [P30 AR-46032]; National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) FX This research was supported by the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences (NIEHS). RT specially thanks Dr Shyamal Peddada of the Biostatistics Branch at NIEHS for valuable suggestions regarding the methodology. The Xenopus cyclopamine exposure experiments were performed by GFS in Yale University's Department of Ecology and Evolutionary Biology, and were supported in part by a grant to Gunter P Wagner by the Yale Core Center for Musculoskeletal Disorders, which is funded by NIH grant P30 AR-46032 from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). NR 52 TC 27 Z9 27 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 1474-760X J9 GENOME BIOL JI Genome Biol. PY 2009 VL 10 IS 4 AR R44 DI 10.1186/gb-2009-10-4-r44 PG 15 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 452MP UT WOS:000266544600016 PM 19393085 ER PT J AU Venancio, TM Balaji, S Iyer, LM Aravind, L AF Venancio, Thiago M. Balaji, S. Iyer, Lakshminarayan M. Aravind, L. TI Reconstructing the ubiquitin network - cross-talk with other systems and identification of novel functions SO GENOME BIOLOGY LA English DT Review ID BUDDING YEAST PROTEOME; SACCHAROMYCES-CEREVISIAE; DNA-DAMAGE; GLOBAL ANALYSIS; COMPARATIVE GENOMICS; INTERACTION DATABASE; SUMOYLATED PROTEINS; REGULATORY NETWORK; U-BOX; PROTEASOME AB Background: The ubiquitin system (Ub-system) can be defined as the ensemble of components including Ub/ubiquitin-like proteins, their conjugation and deconjugation apparatus, binding partners and the proteasomal system. While several studies have concentrated on structure-function relationships and evolution of individual components of the Ub-system, a study of the system as a whole is largely lacking. Results: Using numerous genome-scale datasets, we assemble for the first time a comprehensive reconstruction of the budding yeast Ub-system, revealing static and dynamic properties. We devised two novel representations, the rank plot to understand the functional diversification of different components and the clique-specific point-wise mutual-information network to identify significant interactions in the Ub-system. Conclusions: Using these representations, evidence is provided for the functional diversification of components such as SUMO-dependent Ub-ligases. We also identify novel components of SCF (Skp1-cullin-F-box)-dependent complexes, receptors in the ERAD (endoplasmic reticulum associated degradation) system and a key role for Sus1 in coordinating multiple Ub-related processes in chromatin dynamics. We present evidence for a major impact of the Ub-system on large parts of the proteome via its interaction with the transcription regulatory network. Furthermore, the dynamics of the Ub-network suggests that Ub and SUMO modifications might function cooperatively with transcription control in regulating cell-cycle-stage-specific complexes and in reinforcing periodicities in gene expression. Combined with evolutionary information, the structure of this network helps in understanding the lineage-specific expansion of SCF complexes with a potential role in pathogen response and the origin of the ERAD and ESCRT systems. C1 [Venancio, Thiago M.; Balaji, S.; Iyer, Lakshminarayan M.; Aravind, L.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA. RP Venancio, TM (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA. EM venancit@ncbi.nlm.nih.gov; aravind@ncbi.nlm.nih.gov RI Venancio, Thiago/B-5003-2011; Entomologiamolecular, Inct/J-8214-2013 FU Intramural Research Program of the National Institutes of Health, USA FX We acknowledge the Intramural Research Program of the National Institutes of Health, USA for funding our research. We also would like to acknowledge all the authors who have deposited their genome-scale datasets in public databases. NR 114 TC 23 Z9 26 U1 2 U2 10 PU BIOMED CENTRAL LTD PI LONDON PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1474-760X J9 GENOME BIOL JI Genome Biol. PY 2009 VL 10 IS 3 AR R33 DI 10.1186/gb-2009-10-3-r33 PG 18 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 452MO UT WOS:000266544500013 PM 19331687 ER PT J AU Zheng, DY Zhao, KJ Mehler, MF AF Zheng, Deyou Zhao, Keji Mehler, Mark F. TI Profiling RE1/REST-mediated histone modifications in the human genome SO GENOME BIOLOGY LA English DT Article ID RESTRICTIVE SILENCER FACTOR; NEURAL STEM-CELLS; SODIUM-CHANNEL GENE; NEURONAL GENES; TARGET GENES; TRANSCRIPTIONAL REPRESSION; CHROMATIN MODIFICATIONS; DEACETYLASE COMPLEX; IN-VIVO; REST AB Background: The transcriptional repressor REST (RE1 silencing transcription factor, also called NRSF for neuron-restrictive silencing factor) binds to a conserved RE1 motif and represses many neuronal genes in non-neuronal cells. This transcriptional regulation is transacted by several nucleosome-modifying enzymes recruited by REST to RE1 sites, including histone deacetylases (for example, HDAC1/2), demethylases (for example, LSD1), and methyltransferases (for example, G9a). Results: We have investigated a panel of 38 histone modifications by ChIP-Seq analysis for REST-mediated changes. Our study reveals a systematic decline of histone acetylations modulated by the association of RE1 with REST (RE1/REST). By contrast, alteration of histone methylations is more heterogeneous, with some methylations increased (for example, H3K27me3, and H3K9me2/ 3) and others decreased (for example, H3K4me, and H3K9me1). Furthermore, the observation of such trends of histone modifications in upregulated genes demonstrates convincingly that these changes are not determined by gene expression but are RE1/REST dependent. The outcomes of REST binding to canonical and non-canonical RE1 sites were nearly identical. Our analyses have also provided the first direct evidence that REST induces context-specific nucleosome repositioning, and furthermore demonstrate that REST-mediated histone modifications correlate with the affinity of RE1 motifs and the abundance of RE1-bound REST molecules. Conclusions: Our findings indicate that the landscape of REST-mediated chromatin remodeling is dynamic and complex, with novel histone modifying enzymes and mechanisms yet to be elucidated. Our results should provide valuable insights for selecting the most informative histone marks for investigating the mechanisms and the consequences of REST modulated nucleosome remodeling in both neural and non-neural systems. C1 [Zheng, Deyou; Mehler, Mark F.] Albert Einstein Coll Med, Rose F Kennedy Ctr Study Intellectual & Dev Disab, Dept Neurol, Inst Brain Disorders & Neural Regenerat, Bronx, NY 10461 USA. [Zheng, Deyou] Albert Einstein Coll Med, Dept Genet & Neurosci, Bronx, NY 10461 USA. [Zhao, Keji] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA. [Mehler, Mark F.] Albert Einstein Coll Med, Dept Neurosci, Bronx, NY 10461 USA. [Mehler, Mark F.] Albert Einstein Coll Med, Dept Psychiat & Behav Sci, Einstein Canc Ctr, Bronx, NY 10461 USA. RP Zheng, DY (reprint author), Albert Einstein Coll Med, Rose F Kennedy Ctr Study Intellectual & Dev Disab, Dept Neurol, Inst Brain Disorders & Neural Regenerat, Morris Pk Ave, Bronx, NY 10461 USA. EM dzheng@aecom.yu.edu OI Zheng, Deyou/0000-0003-4354-5337 FU Albert Einstein College of Medicine of Yeshiva University; Intramural Research Programs of National Heart, Lung, and Blood Institute; National Institutes of Health (NIH); NINDS; NIMH; Roslyn and Leslie Goldstein; Mildred and Bernard H Kayden; FM Kirby; Alpern Family; Rosanne H Silberman Foundations FX This work was supported by startup funds from Albert Einstein College of Medicine of Yeshiva University (to DZ), by research funds from the Intramural Research Programs of National Heart, Lung, and Blood Institute, National Institutes of Health (NIH) (to KZ), and by grants from the NINDS and NIMH, NIH and from the Roslyn and Leslie Goldstein, the Mildred and Bernard H Kayden, the FM Kirby, the Alpern Family and the Rosanne H Silberman Foundations (to MFM). NR 62 TC 46 Z9 47 U1 1 U2 5 PU BIOMED CENTRAL LTD PI LONDON PA CURRENT SCIENCE GROUP, MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1474-760X J9 GENOME BIOL JI Genome Biol. PY 2009 VL 10 IS 1 AR R9 DI 10.1186/gb-2009-10-1-r9 PG 20 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 413WK UT WOS:000263823200015 PM 19173732 ER PT J AU Rogozin, IB Basu, MK Csuros, M Koonin, EV AF Rogozin, Igor B. Basu, Malay Kumar Csueroes, Miklos Koonin, Eugene V. TI Analysis of Rare Genomic Changes Does Not Support the Unikont-Bikont Phylogeny and Suggests Cyanobacterial Symbiosis as the Point of Primary Radiation of Eukaryotes SO GENOME BIOLOGY AND EVOLUTION LA English DT Article ID AMINO-ACID REPLACEMENTS; EVOLUTIONARY RELATIONSHIPS; BACTERIAL PHYLOGENY; WIDE ANALYSIS; GENE FUSION; TREE; MITOCHONDRIA; POSITIONS; ORIGINS; LIFE AB The deep phylogeny of eukaryotes is an important but extremely difficult problem of evolutionary biology. Five eukaryotic supergroups are relatively well established but the relationship between these supergroups remains elusive, and their divergence seems to best fit a "Big Bang'' model. Attempts were made to root the tree of eukaryotes by using potential derived shared characters such as unique fusions of conserved genes. One popular model of eukaryotic evolution that emerged from this type of analysis is the unikont-bikont phylogeny: The unikont branch consists of Metazoa, Choanozoa, Fungi, and Amoebozoa, whereas bikonts include the rest of eukaryotes, namely, Plantae ( green plants, Chlorophyta, and Rhodophyta), Chromalveolata, excavates, and Rhizaria. We reexamine the relationships between the eukaryotic supergroups using a genome-wide analysis of rare genomic changes (RGCs) associated with multiple, conserved amino acids (RGC_CAMs and RGC_CAs), to resolve trifurcations of major eukaryotic lineages. The results do not support the basal position of Chromalveolata with respect to Plantae and unikonts or the monophyly of the bikont group and appear to be best compatible with the monophyly of unikonts and Chromalveolata. Chromalveolata show a distinct, additional signal of affinity with Plantae, conceivably, owing to genes transferred from the secondary, red algal symbiont. Excavates are derived forms, with extremely long branches that complicate phylogenetic inference; nevertheless, the RGC analysis suggests that they are significantly more likely to cluster with the unikont Chromalveolata assemblage than with the Plantae. Thus, the first split in eukaryotic evolution might lie between photosynthetic and nonphotosynthetic forms and so could have been triggered by the endosymbiosis between an ancestral unicellular eukaryote and a cyanobacterium that gave rise to the chloroplast. C1 [Rogozin, Igor B.; Basu, Malay Kumar; Koonin, Eugene V.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA. [Basu, Malay Kumar] J Craig Venter Inst, Rockville, MD USA. [Csueroes, Miklos] Univ Montreal, Dept Comp Sci & Operat Res, Montreal, PQ, Canada. RP Rogozin, IB (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bldg 10, Bethesda, MD 20892 USA. EM koonin@ncbi.nlm.nih.gov FU National Library of Medicine at National Institutes of Health/DHHS; National Sciences and Engineering Research Council of Canada FX Intramural Research Program of the National Library of Medicine at National Institutes of Health/DHHS; research grant from the National Sciences and Engineering Research Council of Canada. NR 86 TC 37 Z9 38 U1 4 U2 18 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1759-6653 J9 GENOME BIOL EVOL JI Genome Biol. Evol. PY 2009 VL 1 BP 99 EP 113 DI 10.1093/gbe/evp011 PG 15 WC Evolutionary Biology; Genetics & Heredity SC Evolutionary Biology; Genetics & Heredity GA 565DK UT WOS:000275269200011 PM 20333181 ER PT J AU Schneider, A Souvorov, A Sabath, N Landan, G Gonnet, GH Graur, D AF Schneider, Adrian Souvorov, Alexander Sabath, Niv Landan, Giddy Gonnet, Gaston H. Graur, Dan TI Estimates of Positive Darwinian Selection Are Inflated by Errors in Sequencing, Annotation, and Alignment SO GENOME BIOLOGY AND EVOLUTION LA English DT Article DE multiple sequence alignment; sequencing quality; gene annotation; positive Darwinian selection ID EVOLUTION; GENOME; GENES; LIKELIHOOD; MOUSE; OMA AB Published estimates of the proportion of positively selected genes (PSGs) in human vary over three orders of magnitude. In mammals, estimates of the proportion of PSGs cover an even wider range of values. We used 2,980 orthologous protein-coding genes from human, chimpanzee, macaque, dog, cow, rat, and mouse as well as an established phylogenetic topology to infer the fraction of PSGs in all seven terminal branches. The inferred fraction of PSGs ranged from 0.9% in human through 17.5% in macaque to 23.3% in dog. We found three factors that influence the fraction of genes that exhibit telltale signs of positive selection: the quality of the sequence, the degree of misannotation, and ambiguities in the multiple sequence alignment. The inferred fraction of PSGs in sequences that are deficient in all three criteria of coverage, annotation, and alignment is 7.2 times higher than that in genes with high trace sequencing coverage, "known'' annotation status, and perfect alignment scores. We conclude that some estimates on the prevalence of positive Darwinian selection in the literature may be inflated and should be treated with caution. C1 [Schneider, Adrian; Gonnet, Gaston H.] ETH, Zurich, Switzerland. [Souvorov, Alexander] NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA. [Sabath, Niv; Landan, Giddy; Graur, Dan] Univ Houston, Dept Biol & Biochem, Houston, TX 77004 USA. RP Schneider, A (reprint author), ETH, Zurich, Switzerland. EM dgraur@uh.edu OI Landan, Giddy/0000-0002-2502-8750 FU National Science Foundation [DBI-0543342] FX This work was supported by National Science Foundation grant [DBI-0543342 to D. G.]. NR 22 TC 50 Z9 51 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1759-6653 J9 GENOME BIOL EVOL JI Genome Biol. Evol. PY 2009 VL 1 BP 114 EP 118 DI 10.1093/gbe/evp012 PG 5 WC Evolutionary Biology; Genetics & Heredity SC Evolutionary Biology; Genetics & Heredity GA 565DK UT WOS:000275269200012 PM 20333182 ER PT J AU Carmel, L Koonin, EV AF Carmel, Liran Koonin, Eugene V. TI A Universal Nonmonotonic Relationship between Gene Compactness and Expression Levels in Multicellular Eukaryotes SO GENOME BIOLOGY AND EVOLUTION LA English DT Article DE eukaryotic gene structure; eukaryotic gene architecture; selection on gene compactness; genomic design; intron functionality; intron density ID HUMAN HOUSEKEEPING GENES; SEQUENCE EVOLUTION; MESSENGER-RNA; SHORT INTRONS; SELECTION; DROSOPHILA; SIGNATURE; ELEGANS; RATES; MPSS AB Analysis of gene architecture and expression levels of four organisms, Homo sapiens, Caenorhabditis elegans, Drosophila melanogaster, and Arabidopsis thaliana, reveals a surprising, nonmonotonic, universal relationship between expression level and gene compactness. With increasing expression level, the genes tend at first to become longer but, from a certain level of expression, they become more and more compact, resulting in an approximate bell-shaped dependence. There are two leading hypotheses to explain the compactness of highly expressed genes. The selection hypothesis predicts that gene compactness is predominantly driven by the level of expression, whereas the genomic design hypothesis predicts that expression breadth across tissues is the driving force. We observed the connection between gene expression breadth in humans and gene compactness to be significantly weaker than the connection between expression level and compactness, a result that is compatible with the selection hypothesis but not the genome design hypothesis. The initial gene elongation with increasing expression level could be explained, at least in part, by accumulation of regulatory elements enhancing expression, in particular, in introns. This explanation is compatible with the observed positive correlation between intron density and expression level of a gene. Conversely, the trend toward increasing compactness for highly expressed genes could be caused by selection for minimization of energy and time expenditure during transcription and splicing and for increased fidelity of transcription, splicing, and/or translation that is likely to be particularly critical for highly expressed genes. Regardless of the exact nature of the forces that shape the gene architecture, we present evidence that, at least, in animals, coding and noncoding parts of genes show similar architectonic trends. C1 [Carmel, Liran; Koonin, Eugene V.] Natl Lib Med, Natl Ctr Biotechnol Informat, Natl Inst Hlth, Bethesda, MD 20894 USA. [Carmel, Liran] Hebrew Univ Jerusalem, Dept Genet, Alexander Silberman Inst Life Sci, IL-91904 Jerusalem, Israel. RP Carmel, L (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, Natl Inst Hlth, Bethesda, MD 20894 USA. EM carmell@cc.huji.ac.il; koonin@ncbi.nlm.nih.gov FU US Department of Health and Human Services FX The authors would like to thank Miklos Csurors and Igor Rogozin for helpful discussions. The authors' research is supported by the intramural funds of the US Department of Health and Human Services (National Library of Medicine). NR 49 TC 25 Z9 26 U1 0 U2 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1759-6653 J9 GENOME BIOL EVOL JI Genome Biol. Evol. PY 2009 VL 1 BP 382 EP 390 DI 10.1093/gbe/evp038 PG 9 WC Evolutionary Biology; Genetics & Heredity SC Evolutionary Biology; Genetics & Heredity GA 565DK UT WOS:000275269200036 PM 20333206 ER PT J AU Goldin, LR Bjorkholm, M Kristinsson, SY Samuelsson, J Landgren, O AF Goldin, Lynn R. Bjoerkholm, Magnus Kristinsson, Sigurdur Y. Samuelsson, Jan Landgren, Ola TI Germline and somatic JAK2 mutations and susceptibility to chronic myeloproliferative neoplasms SO GENOME MEDICINE LA English DT Review AB Myeloproliferative neoplasms (MPNs) are a group of closely related stem-cell-derived clonal proliferative diseases. Most cases are sporadic but first-degree relatives of MPN patients have a five-to seven-fold increased risk for developing an MPN. The tumors of most patients carry a mutation in the Janus kinase 2 gene (JAK2(V617F)). Recently, three groups have described a strong association of JAK2 germline polymorphisms with MPN in patients positive for JAK2(V617F). The somatic mutation occurs primarily on one particular germline JAK2 haplotype, which may account for as much as 50% of the risk to first-degree relatives. This finding provides new directions for unraveling the pathogenesis of MPN. C1 [Goldin, Lynn R.] NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. [Bjoerkholm, Magnus; Kristinsson, Sigurdur Y.] Karolinska Univ Hosp Solna, Div Hematol, Dept Med, Stockholm, Sweden. [Bjoerkholm, Magnus; Kristinsson, Sigurdur Y.] Karolinska Inst, Stockholm, Sweden. [Samuelsson, Jan] Karolinska Inst, Dept Clin Sci & Educ, Stockholm, Sweden. [Samuelsson, Jan] Stockholm S Hosp, Dept Internal Med, Stockholm, Sweden. [Samuelsson, Jan] Swedish Myeloproliferat Disorder Study Grp, Stockholm, Sweden. [Landgren, Ola] NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Goldin, LR (reprint author), NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. EM goldinl@mail.nih.gov RI Kristinsson, Sigurdur /M-2910-2015 OI Kristinsson, Sigurdur /0000-0002-4964-7476 FU Intramural Research Program of the National Institutes of Health National Cancer Institute; Swedish Cancer Society; Stockholm County Council; Karolinska Institutet Foundations FX This research was supported by the Intramural Research Program of the National Institutes of Health National Cancer Institute and by grants from the Swedish Cancer Society, Stockholm County Council, the Karolinska Institutet Foundations. NR 18 TC 3 Z9 3 U1 0 U2 1 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1756-994X J9 GENOME MED JI Genome Med. PY 2009 VL 1 AR 55 DI 10.1186/gm55 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA V27QF UT WOS:000208627000055 PM 19490586 ER PT J AU Katayama, H Paczesny, S Prentice, R Aragaki, A Faca, VM Pitteri, SJ Zhang, Q Wang, H Silva, M Kennedy, J Rossouw, J Jackson, R Hsia, J Chlebowski, R Manson, J Hanash, S AF Katayama, Hiroyuki Paczesny, Sophie Prentice, Ross Aragaki, Aaron Faca, Vitor M. Pitteri, Sharon J. Zhang, Qing Wang, Hong Silva, Melissa Kennedy, Jacob Rossouw, Jacques Jackson, Rebecca Hsia, Judith Chlebowski, Rowan Manson, JoAnn Hanash, Samir TI Application of serum proteomics to the Women's Health Initiative conjugated equine estrogens trial reveals a multitude of effects relevant to clinical findings SO GENOME MEDICINE LA English DT Article AB Background: The availability of serum collections from the Women's Health Initiative (WHI) conjugated equine estrogens (CEE) randomized controlled trial provides an opportunity to test the potential of in-depth quantitative proteomics to uncover changes in the serum proteome related to CEE and to assess their relevance to trial findings, including elevations in the risk of stroke and venous thromboembolism and a reduction in fractures. Methods: Five independent large scale quantitative proteomics analyses were performed, each comparing a set of pooled serum samples collected from 10 subjects, 1 year following initiation of CEE at 0.625 mg/d, relative to their baseline pool. A subset of proteins that exhibited increased levels with CEE by quantitative proteomics was selected for validation studies. Results: Of 611 proteins quantified based on differential stable isotope labeling, the levels of 116 (19%) were changed after 1 year of CEE (nominal P < 0.05), while 64 of these had estimated false discovery rates < 0.05. Most of the changed proteins were not previously known to be affected by CEE and had relevance to processes that included coagulation, metabolism, osteogenesis, inflammation, and blood pressure maintenance. To validate quantitative proteomic data, 14 proteins were selected for ELISA. Findings for ten - IGF1, IGFBP4, IGFBP1, IGFBP2, F10, AHSG, GC, CP, MMP2, and PROZ - were confirmed in the initial set of 50 subjects and further validated in an independent set of 50 additional subjects who received CEE. Conclusions: CEE affected a substantial fraction of the serum proteome, including proteins with relevance to findings from the WHI CEE trial related to cardiovascular disease and fracture. C1 [Katayama, Hiroyuki; Paczesny, Sophie; Faca, Vitor M.; Pitteri, Sharon J.; Zhang, Qing; Wang, Hong; Silva, Melissa; Kennedy, Jacob; Hanash, Samir] Fred Hutchinson Canc Res Ctr, Mol Diagnost Program, Seattle, WA 98109 USA. [Katayama, Hiroyuki] Eisai & Co Ltd, Lab Core Technol, Tsukuba, Ibaraki 3002635, Japan. [Paczesny, Sophie] Univ Michigan, Dept Pediat, Ctr Canc, Ann Arbor, MI 48109 USA. [Prentice, Ross; Aragaki, Aaron] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98109 USA. [Rossouw, Jacques] NHLBI, Womens Hlth Initiat Branch, Bethesda, MD 20892 USA. [Jackson, Rebecca] Ohio State Univ, Div Endocrinol, Columbus, OH 43210 USA. [Hsia, Judith] AstraZeneca LP, Wilmington, DE 19850 USA. [Chlebowski, Rowan] Harbor UCLA Med Ctr, Los Angeles Biomed Res Inst, Torrance, CA 90502 USA. [Manson, JoAnn] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02215 USA. RP Hanash, S (reprint author), Fred Hutchinson Canc Res Ctr, Mol Diagnost Program, Fairview Ave N, Seattle, WA 98109 USA. EM shanash@fhcrc.org RI Faca, Vitor/A-3989-2013; OI FACA, VITOR MARCEL/0000-0003-3205-7944; Pitteri, Sharon/0000-0002-3119-873X FU National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services [N01WH22110, 24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-19, 32122, 42107-26, 42129-32, 44221]; National Cancer Institute [CA53996] FX This study was funded by the National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services (contracts N01WH22110, 24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-19, 32122, 42107-26, 42129-32, and 44221). The active study drug and placebo were supplied by Wyeth-Ayerst Research Laboratories, Philadelphia, Pennsylvania. Dr Prentice's work was partially supported by grant CA53996 from the National Cancer Institute. Decisions concerning study design, data collection and analysis, interpretation of the results, the preparation of the manuscript, or the decision to submit the manuscript for publication resided with committees composed of WHI investigators that included NHLBI representatives. The authors thank the WHI investigators and staff for their outstanding dedication and commitment. A list of key investigators involved in this research follows. A full listing of WHI investigators can be found at the WHI website [67]. Program Office: Elizabeth Nabel, Jacques Rossouw, Shari Ludlam, Linda Pottern, Joan McGowan, Leslie Ford, and Nancy Geller (National Heart, Lung, and Blood Institute, Bethesda, MD). Clinical Coordinating Center: Ross Prentice, Garnet Anderson, Andrea LaCroix, Charles L Kooperberg, Ruth E Patterson, Anne McTiernan (Fred Hutchinson Cancer Research Center, Seattle, WA); Sally Shumaker (Wake Forest University School of Medicine, Winston-Salem, NC); Evan Stein (Medical Research Labs, Highland Heights, KY); Steven Cummings (University of California at San Francisco, San Francisco, CA).; Clinical Centers: Sylvia Wassertheil-Smoller (Albert Einstein College of Medicine, Bronx, NY); Aleksandar Rajkovic (Baylor College of Medicine, Houston, TX); JoAnn Manson (Brigham and Women's Hospital, Harvard Medical School, Boston, MA); Annlouise R Assaf (Brown University, Providence, RI); Lawrence Phillips (Emory University, Atlanta, GA); Shirley Beresford (Fred Hutchinson Cancer Research Center, Seattle, WA); Judith Hsia (George Washington University Medical Center, Washington, DC); Rowan Chlebowski (Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA); Evelyn Whitlock (Kaiser Permanente Center for Health Research, Portland, OR); Bette Caan (Kaiser Permanente Division of Research, Oakland, CA); Jane Morley Kotchen (Medical College of Wisconsin, Milwaukee, WI); Barbara V Howard (MedStar Research Institute/Howard University, Washington, DC); Linda Van Horn (Northwestern University, Chicago/Evanston, IL); Henry Black (Rush Medical Center, Chicago, IL); Marcia L Stefanick (Stanford Prevention Research Center, Stanford, CA); Dorothy Lane (State University of New York at Stony Brook, Stony Brook, NY); Rebecca Jackson (The Ohio State University, Columbus, OH); Cora E Lewis (University of Alabama at Birmingham, Birmingham, AL); Tamsen Bassford (University of Arizona, Tucson/Phoenix, AZ); Jean Wactawski-Wende (University at Buffalo, Buffalo, NY); John Robbins (University of California at Davis, Sacramento, CA); F Allan Hubbell (University of California at Irvine, CA); Lauren Nathan (University of California at Los Angeles, Los Angeles, CA); Robert D Langer (University of California at San Diego, LaJolla/Chula Vista, CA); Margery Gass (University of Cincinnati, Cincinnati, OH); Marian Limacher (University of Florida, Gainesville/Jacksonville, FL); David Curb (University of Hawaii, Honolulu, HI); Robert Wallace (University of Iowa, Iowa City/Davenport, IA); Judith Ockene (University of Massachusetts/Fallon Clinic, Worcester, MA); Norman Lasser (University of Medicine and Dentistry of New Jersey, Newark, NJ); Mary Jo O'Sullivan (University of Miami, Miami, FL); Karen Margolis (University of Minnesota, Minneapolis, MN); Robert Brunner (University of Nevada, Reno, NV); Gerardo Heiss (University of North Carolina, Chapel Hill, NC); Lewis Kuller (University of Pittsburgh, Pittsburgh, PA); Karen C Johnson (University of Tennessee, Memphis, TN); Robert Brzyski (University of Texas Health Science Center, San Antonio, TX); Gloria E Sarto (University of Wisconsin, Madison, WI); Mara Vitolins (Wake Forest University School of Medicine, Winston-Salem, NC); Susan Hendrix (Wayne State University School of Medicine/Hutzel Hospital, Detroit, MI). NR 67 TC 25 Z9 26 U1 0 U2 3 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1756-994X J9 GENOME MED JI Genome Med. PY 2009 VL 1 AR 47 DI 10.1186/gm47 PG 16 WC Genetics & Heredity SC Genetics & Heredity GA V27QF UT WOS:000208627000047 PM 19402886 ER PT J AU Pitteri, SJ Hanash, SM Aragaki, A Amon, LM Chen, L Buson, TB Paczesny, S Katayama, H Wang, H Johnson, MM Zhang, Q McIntosh, M Wang, P Kooperberg, C Rossouw, JE Jackson, RD Manson, JE Hsia, J Liu, SM Martin, L Prentice, RL AF Pitteri, Sharon J. Hanash, Samir M. Aragaki, Aaron Amon, Lynn M. Chen, Lin Buson, Tina Busald Paczesny, Sophie Katayama, Hiroyuki Wang, Hong Johnson, Melissa M. Zhang, Qing McIntosh, Martin Wang, Pei Kooperberg, Charles Rossouw, Jacques E. Jackson, Rebecca D. Manson, JoAnn E. Hsia, Judith Liu, Simin Martin, Lisa Prentice, Ross L. TI Postmenopausal estrogen and progestin effects on the serum proteome SO GENOME MEDICINE LA English DT Article AB Background: Women's Health Initiative randomized trials of postmenopausal hormone therapy reported intervention effects on several clinical outcomes, with some important differences between estrogen alone and estrogen plus progestin. The biologic mechanisms underlying these effects, and these differences, have yet to be fully elucidated. Methods: Baseline serum samples were compared with samples drawn 1 year later for 50 women assigned to active hormone therapy in both the estrogen-plus-progestin and estrogen-alone randomized trials, by applying an in-depth proteomic discovery platform to serum pools from 10 women per pool. Results: In total, 378 proteins were quantified in two or more of the 10 pooled serum comparisons, by using strict identification criteria. Of these, 169 (44.7%) showed evidence (nominal P < 0.05) of change in concentration between baseline and 1 year for one or both of estrogen-plus-progestin and estrogen-alone groups. Quantitative changes were highly correlated between the two hormone-therapy preparations. A total of 98 proteins had false discovery rates < 0.05 for change with estrogen plus progestin, compared with 94 for estrogen alone. Of these, 84 had false discovery rates < 0.05 for both preparations. The observed changes included multiple proteins relevant to coagulation, inflammation, immune response, metabolism, cell adhesion, growth factors, and osteogenesis. Evidence of differential changes also was noted between the hormone preparations, with the strongest evidence in growth factor and inflammation pathways. Conclusions: Serum proteomic analyses yielded a large number of proteins similarly affected by estrogen plus progestin and by estrogen alone and identified some proteins and pathways that appear to be differentially affected between the two hormone preparations; this may explain their distinct clinical effects. C1 [Pitteri, Sharon J.; Hanash, Samir M.; Aragaki, Aaron; Amon, Lynn M.; Chen, Lin; Buson, Tina Busald; Paczesny, Sophie; Katayama, Hiroyuki; Wang, Hong; Johnson, Melissa M.; Zhang, Qing; McIntosh, Martin; Wang, Pei; Kooperberg, Charles; Prentice, Ross L.] Fred Hutchinson Canc Res Ctr, Publ Hlth Sci Div, Seattle, WA 98109 USA. [Paczesny, Sophie] Univ Michigan, Ctr Comprehens Canc, Dept Pediat, Ann Arbor, MI 48109 USA. [Katayama, Hiroyuki] Eisai Inc, Biomarkers & Personalized Med Unit, Andover, MA 01810 USA. [Rossouw, Jacques E.] NHLBI, WHI Project Off, NIH, Bethesda, MD 20892 USA. [Jackson, Rebecca D.] Ohio State Univ, Div Endocrinol, Columbus, OH 43210 USA. [Manson, JoAnn E.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA. [Hsia, Judith] AstraZeneca LP, Res & Dev, Wilmington, DE 19803 USA. [Liu, Simin] Div Publ Hlth, Los Angeles, CA 90095 USA. [Liu, Simin] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90095 USA. [Martin, Lisa] George Washington Univ, Dept Med, Washington, DC 20052 USA. RP Prentice, RL (reprint author), Fred Hutchinson Canc Res Ctr, Publ Hlth Sci Div, 1100 Fairview Ave N, Seattle, WA 98109 USA. EM rprentic@fhcrc.org RI Liu, Simin/I-3689-2014; OI Liu, Simin/0000-0003-2098-3844; Pitteri, Sharon/0000-0002-3119-873X FU National Heart, Lung, and Blood Institute, National Institutes of Health, U. S. Department of Health and Human Services [HHSN268200764314C, N01WH22110, 24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-19, 32122, 42107-26, 42129-32, 44221]; National Cancer Institute [CA53996] FX Funding/Support: This work was supported by the National Heart, Lung, and Blood Institute, National Institutes of Health, U. S. Department of Health and Human Services [contracts HHSN268200764314C, N01WH22110, 24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-19, 32122, 42107-26, 42129-32, and 44221]. Clinical Trials Registration: ClinicalTrials.gov identifier: NCT00000611. The work of Dr. Prentice was partially supported by grant CA53996 from the National Cancer Institute. NR 41 TC 22 Z9 22 U1 0 U2 1 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1756-994X J9 GENOME MED JI Genome Med. PY 2009 VL 1 AR 121 DI 10.1186/gm121 PG 14 WC Genetics & Heredity SC Genetics & Heredity GA V27QF UT WOS:000208627000121 PM 20034393 ER PT J AU Van, QN Veenstra, TD AF Van, Que N. Veenstra, Timothy D. TI How close is the bench to the bedside? Metabolic profiling in cancer research SO GENOME MEDICINE LA English DT Review AB Metabolic profiling using mass spectrometry (MS) and nuclear magnetic resonance spectroscopy (NMR) is integral to the rapidly expanding field of metabolomics, which is making progress in toxicology, plant science and various diseases, including cancer. In the area of oncology and metabolic phenotyping, researchers have probed the known changes in malignant cellular pathways using new experimental techniques to gain more insights, and others are exploiting these same cellular pathways for therapeutic drug targets and for novel cancer biomarkers, with the ultimate goal of translation to the clinic. Here, we discuss the challenges and opportunities in metabolic phenotyping for discovering novel cancer biomarkers, and we assess the clinical applicability of MS and NMR. C1 [Van, Que N.; Veenstra, Timothy D.] NCI, Lab Prote & Analyt Technol, Adv Technol Program, SAIC Frederick Inc, Frederick, MD 21702 USA. RP Veenstra, TD (reprint author), NCI, Lab Prote & Analyt Technol, Adv Technol Program, SAIC Frederick Inc, Frederick, MD 21702 USA. EM veenstra@ncifcrf.gov FU National Cancer Institute, National Institutes of Health [N01-CO-12400] FX This project has been funded in whole or in part with federal funds from the National Cancer Institute, National Institutes of Health, under contract N01-CO-12400. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government. NR 29 TC 16 Z9 17 U1 0 U2 2 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1756-994X J9 GENOME MED JI Genome Med. PY 2009 VL 1 AR 5 DI 10.1186/gm5 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA V27QF UT WOS:000208627000005 PM 19348692 ER PT J AU Veenstra, TD AF Veenstra, Timothy D. TI Using a global proteomic approach to identify proteins affected by estrogen therapy SO GENOME MEDICINE LA English DT Article AB With the increase in technological capabilities for measuring biological molecules, there is a greater trend to conduct non-biased, discovery-driven studies that collect information on hundreds of molecules in a single study. The hope is that novel findings can be detected within these large datasets. For protein analysis, these non-biased studies are particularly challenging as no technology is presently capable of providing a view of the entire proteome. The ability of non-biased studies to accurately detect specific differences within the proteomes of samples obtained from differentially treated individuals must be conclusively demonstrated before investigators will routinely adopt these methods as part of their experimental protocols. This need is especially true for clinical and epidemiological studies in which limited amounts of samples are available. C1 NCI, Lab Prote & Analyt Technol, Adv Technol Program, SAIC Frederick Inc, Frederick, MD 21702 USA. RP Veenstra, TD (reprint author), NCI, Lab Prote & Analyt Technol, Adv Technol Program, SAIC Frederick Inc, Frederick, MD 21702 USA. EM veenstra@ncifcrf.gov FU National Cancer Institute, National Institutes of Health [HHSN261200800001E] FX This project has been funded in whole or in part with federal funds from the National Cancer Institute, National Institutes of Health, under Contract HHSN261200800001E. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government. NR 6 TC 0 Z9 0 U1 0 U2 1 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1756-994X J9 GENOME MED JI Genome Med. PY 2009 VL 1 AR 58 DI 10.1186/gm58 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA V27QF UT WOS:000208627000058 PM 19519954 ER PT J AU Cuddapah, S Jothi, R Schones, DE Roh, TY Cui, KR Zhao, KJ AF Cuddapah, Suresh Jothi, Raja Schones, Dustin E. Roh, Tae-Young Cui, Kairong Zhao, Keji TI Global analysis of the insulator binding protein CTCF in chromatin barrier regions reveals demarcation of active and repressive domains SO GENOME RESEARCH LA English DT Article ID ENHANCER-BLOCKING ACTIVITY; HUMAN GENOME; C-MYC; NUCLEAR-ORGANIZATION; H19 GENE; SITES; TRANSCRIPTION; METHYLATION; DNA; WIDE AB Insulators are DNA elements that prevent inappropriate interactions between the neighboring regions of the genome. They can be functionally classified as either enhancer blockers or domain barriers. CTCF ( CCCTC-binding factor) is the only known major insulator-binding protein in the vertebrates and has been shown to bind many enhancer-blocking elements. However, it is not clear whether it plays a role in chromatin domain barriers between active and repressive domains. Here, we used ChIP-seq to map the genome-wide binding sites of CTCF in three cell types and identified significant binding of CTCF to the boundaries of repressive chromatin domains marked by H3K27me3. Although we find an extensive overlapping of CTCF-binding sites across the three cell types, its association with the domain boundaries is cell-type-specific. We further show that the nucleosomes flanking CTCF-binding sites are well positioned. Interestingly, we found a complementary pattern between the repressive H3K27me3 and the active H2AK5ac regions, which are separated by CTCF. Our data indicate that CTCF may play important roles in the barrier activity of insulators, and this study provides a resource for further investigation of the CTCF function in organizing chromatin in the human genome. C1 [Cuddapah, Suresh; Jothi, Raja; Schones, Dustin E.; Roh, Tae-Young; Cui, Kairong; Zhao, Keji] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA. RP Zhao, KJ (reprint author), NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA. RI Jothi, Raja/G-3780-2015 FU National Heart, Lung, and Blood Institute, National Institutes of Health FX This work was supported by the Intramural Research Program of the National Heart, Lung, and Blood Institute, National Institutes of Health. The gene expression analysis using Affymetrix DNA microarrays was performed by NHLBI DNA microarray Core Facility. We thank Artem Barski, Andrew Smith, and L. Aravind for helpful comments and discussions. NR 45 TC 338 Z9 349 U1 0 U2 23 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT PI WOODBURY PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA SN 1088-9051 J9 GENOME RES JI Genome Res. PD JAN PY 2009 VL 19 IS 1 BP 24 EP 32 DI 10.1101/gr.082800.108 PG 9 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA 390YQ UT WOS:000262200000003 PM 19056695 ER PT J AU Rudd, MK Endicott, RM Friedman, C Walker, M Young, JM Osoegawa, K de Jong, PJ Green, ED Trask, BJ AF Rudd, M. Katharine Endicott, RaeLynn M. Friedman, Cynthia Walker, Megan Young, Janet M. Osoegawa, Kazutoyo de Jong, Pieter J. Green, Eric D. Trask, Barbara J. CA NISC Comparative Sequencing Progra TI Comparative sequence analysis of primate subtelomeres originating from a chromosome fission event SO GENOME RESEARCH LA English DT Article ID FACIOSCAPULOHUMERAL MUSCULAR-DYSTROPHY; OLFACTORY RECEPTOR GENE; DNA REARRANGEMENTS; 4Q SUBTELOMERE; EVOLUTIONARY; COMMON; REGION; D4Z4; HYBRIDIZATION; ORGANIZATION AB Subtelomeres are concentrations of interchromosomal segmental duplications capped by telomeric repeats at the ends of chromosomes. The nature of the segments shared by different sets of human subtelomeres reflects their high rate of recent interchromosomal exchange. Here, we characterize the rearrangements incurred by the 15q subtelomere after it arose from a chromosome fission event in the common ancestor of great apes. We used FISH, sequencing of genomic clones, and PCR to map the breakpoint of this fission and track the fate of flanking sequence in human, chimpanzee, gorilla, orangutan, and macaque genomes. The ancestral locus, a cluster of olfactory receptor (OR) genes, lies internally on macaque chromosome 7. Sequence originating from this fission site is split between the terminus of 15q and the pericentromere of 14q in the great apes. Numerous structural rearrangements, including interstitial deletions and transfers of material to or from other subtelomeres, occurred subsequent to the fission, such that each species has a unique 15q structure and unique collection of ORs derived from the fission locus. The most striking rearrangement involved transfer of at least 200 kb from the fission-site region to the end of chromosome 4q, where much still resides in chimpanzee and gorilla, but not in human. This gross structural difference places the subtelomeric defect underlying facioscapulohumeral muscular dystrophy ( FSHD) much closer to the telomere in human 4q than in the hybrid 4q-15q subtelomere of chimpanzee. C1 [Rudd, M. Katharine; Endicott, RaeLynn M.; Friedman, Cynthia; Walker, Megan; Young, Janet M.; Trask, Barbara J.] Fred Hutchinson Canc Res Ctr, Div Human Biol, Seattle, WA 98109 USA. [Osoegawa, Kazutoyo; de Jong, Pieter J.] Childrens Hosp & Res Ctr Oakland, Childrens Hosp Oakland Res Inst, Ctr Genet, Oakland, CA 94609 USA. [Green, Eric D.] NHGRI, NISC Comparat Sequencing Program, Genome Technol Branch, NIH, Bethesda, MD 20892 USA. [Green, Eric D.; NISC Comparative Sequencing Progra] NHGRI, NIH, Intramural Sequencing Ctr, Rockville, MD 20852 USA. RP Trask, BJ (reprint author), Fred Hutchinson Canc Res Ctr, Div Human Biol, Seattle, WA 98109 USA. EM btrask@fhcrc.org FU NIH [RO1-GM057070, RO1-DC004209, T32-HG00035, U01 HG002523] FX We thank Elena Linardopoulou for advice, Baoli Zhu and Mikhail Nefedov for construction of BAC libraries, and Yoko Kuroki and Asao Fujiyama for chimpanzee BACs. This work was supported by NIH grants RO1-GM057070 and RO1-DC004209 ( B. J. T.), T32-HG00035 ( M. K. R.), and U01 HG002523 ( P. d. J.). The following individuals were key contributors within the NISC Comparative Sequencing Program: Robert Blakesley, Gerard Bouffard, Shelise Brooks, Jyoti Gupta, Jacquelyn Idol, Jennifer McDowell, Baishali Maskeri, Jennifer Vogt, and Alice Young. NR 35 TC 11 Z9 12 U1 1 U2 5 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT PI WOODBURY PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA SN 1088-9051 J9 GENOME RES JI Genome Res. PD JAN PY 2009 VL 19 IS 1 BP 33 EP 41 DI 10.1101/gr.083170.108 PG 9 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA 390YQ UT WOS:000262200000004 PM 18952852 ER PT J AU Olden, K AF Olden, Kenneth BE Willard, HF Ginsburg, GS TI Human Health and Disease: Interaction Between the Genome and the Environment SO GENOMIC AND PERSONALIZED MEDICINE, VOL 1 LA English DT Article; Book Chapter ID S-TRANSFERASE M1; LUNG-CANCER RISK; ACUTE LYMPHOBLASTIC-LEUKEMIA; GENETIC POLYMORPHISMS; N-ACETYLTRANSFERASE; QUINONE OXIDOREDUCTASE; GSTT1 POLYMORPHISMS; ALLERGIC RESPONSES; HIV-1 INFECTION; BLADDER-CANCER C1 NIEHS, Mol Carcinogenesis Lab, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. RP Olden, K (reprint author), NIEHS, Mol Carcinogenesis Lab, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. NR 102 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA BN 978-0-12-370888-5 PY 2009 BP 47 EP 59 DI 10.1016/B978-0-12-369420-1.00004-4 PG 13 WC Genetics & Heredity; Medicine, Research & Experimental SC Genetics & Heredity; Research & Experimental Medicine GA BCX27 UT WOS:000311822400006 ER PT J AU Antonellis, A Green, ED AF Antonellis, Anthony Green, Eric D. BE Willard, HF Ginsburg, GS TI Inter-Species Comparative Sequence Analysis: A Tool for Genomic Medicine SO GENOMIC AND PERSONALIZED MEDICINE, VOL 1 LA English DT Article; Book Chapter ID CYSTIC-FIBROSIS GENE; WIDE ASSOCIATION; HIRSCHSPRUNG-DISEASE; NONCODING SEQUENCES; NUCLEOTIDE-BINDING; DNA-SEQUENCES; MOUSE MODEL; CFTR GENE; IDENTIFICATION; MUTATIONS C1 [Antonellis, Anthony; Green, Eric D.] NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA. RP Antonellis, A (reprint author), NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA. NR 54 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA BN 978-0-12-370888-5 PY 2009 BP 120 EP 130 DI 10.1016/B978-0-12-369420-1.00010-X PG 11 WC Genetics & Heredity; Medicine, Research & Experimental SC Genetics & Heredity; Research & Experimental Medicine GA BCX27 UT WOS:000311822400012 ER PT J AU Yu, LR Stewart, NA Veenstra, TD AF Yu, Li-Rong Stewart, Nicolas A. Veenstra, Timothy D. BE Willard, HF Ginsburg, GS TI Proteomics: The Deciphering of the Functional Genome SO GENOMIC AND PERSONALIZED MEDICINE, VOL 1 LA English DT Article; Book Chapter ID MASS-SPECTROMETRY; PEPTIDES; ELECTROPHORESIS; PROTEINS; SPECTRA C1 [Yu, Li-Rong; Stewart, Nicolas A.; Veenstra, Timothy D.] NCI, SAIC Frederick Inc, Frederick, MD 21702 USA. RP Yu, LR (reprint author), NCI, SAIC Frederick Inc, Frederick, MD 21702 USA. NR 27 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA BN 978-0-12-370888-5 PY 2009 BP 173 EP 179 DI 10.1016/B978-0-12-369420-1.00014-7 PG 7 WC Genetics & Heredity; Medicine, Research & Experimental SC Genetics & Heredity; Research & Experimental Medicine GA BCX27 UT WOS:000311822400016 ER PT J AU Crawford, NPS Hunter, KW AF Crawford, Nigel P. S. Hunter, Kent W. BE Willard, HF Ginsburg, GS TI Emerging Concepts in Metastasis SO GENOMIC AND PERSONALIZED MEDICINE, VOL 2 LA English DT Article; Book Chapter ID BREAST-CANCER METASTASIS; COMPARATIVE GENOMIC HYBRIDIZATION; TRANSGENIC MOUSE MODEL; TUMOR PROGRESSION; IMPORTANT DETERMINANT; COLORECTAL-CANCER; MULTIPLE CROSS; MESSENGER-RNA; SOLID TUMORS; ARRAY CGH C1 [Crawford, Nigel P. S.; Hunter, Kent W.] NCI, CCR, NIH, Lab Canc Biol & Genet, Bethesda, MD 20892 USA. RP Crawford, NPS (reprint author), NCI, CCR, NIH, Lab Canc Biol & Genet, Bethesda, MD 20892 USA. NR 61 TC 0 Z9 1 U1 1 U2 1 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA BN 978-0-12-370889-2 PY 2009 BP 977 EP 989 DI 10.1016/B978-0-12-369420-1.00081-0 PG 13 WC Genetics & Heredity; Medicine, Research & Experimental SC Genetics & Heredity; Research & Experimental Medicine GA BCU33 UT WOS:000311433700030 ER PT J AU Jain, S Singleton, AB AF Jain, Shushant Singleton, Andrew B. BE Willard, HF Ginsburg, GS TI Parkinson's Disease: Genomic Perspectives SO GENOMIC AND PERSONALIZED MEDICINE, VOL 2 LA English DT Article; Book Chapter ID MITOCHONDRIAL-DNA DELETIONS; SUBSTANTIA-NIGRA NEURONS; ALPHA-SYNUCLEIN; NEURODEGENERATIVE DISEASES; RECESSIVE PARKINSONISM; LOCUS TRIPLICATION; MUTATIONS; GENE; ASSOCIATION; LRRK2 C1 [Jain, Shushant; Singleton, Andrew B.] NIA, Neurogenet Lab, Mol Genet Unit, NIH, Bethesda, MD 20892 USA. [Jain, Shushant] UCL, Reta Lila Weston Inst Neurol Studies, London W1T 4JF, England. [Jain, Shushant] UCL, Inst Neurol, Dept Mol Neurosci, London W1T 4JF, England. RP Jain, S (reprint author), NIA, Neurogenet Lab, Mol Genet Unit, NIH, Bethesda, MD 20892 USA. NR 48 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA BN 978-0-12-370889-2 PY 2009 BP 1233 EP 1242 DI 10.1016/B978-0-12-369420-1.00100-1 PG 10 WC Genetics & Heredity; Medicine, Research & Experimental SC Genetics & Heredity; Research & Experimental Medicine GA BCU33 UT WOS:000311433700049 ER PT J AU Weinberg, CR AF Weinberg, C. R. TI Less is more, except when less is less: Studying joint effects SO GENOMICS LA English DT Article DE Synergy; Interaction; joint effects ID LOGISTIC-REGRESSION; DISEQUILIBRIUM; EXPOSURE; DISEASE; DESIGN; TRIADS; GENES AB Most diseases are complex in that they are caused by the joint action of multiple factors, both genetic and environmental. Over the past few decades, the mathematical convenience of logistic regression has served to enshrine the Multiplicative model, to the point where many epidemiologists believe that departure from additivity on a log scale implies that two factors interact in causing disease. Other terminology in epidemiology, where students are told that inequality of relative risks across levels of a second factor should be seen as "effect modification," reinforces an uncritical acceptance of multiplicative joint effect as the biologically meaningful no-interaction null. Our first task, when studying joint effects, is to understand the limitations of our definitions for "interaction," and recognize that what statisticians mean and what biologists might want to mean by interaction may not coincide. joint effects are notoriously hard to identify and characterize, even when asking a simple and unsatisfying question, like whether two effects are log-additive. The rule of thumb for such efforts is that a factor-of-four sample size is needed, compared with that needed to demonstrate main effects of either genes or exposures. So strategies have been devised that focus on the most informative individuals, either through risk-based sampling for a cohort, or case-control sampling, extreme phenotype sampling, pooling, two-stage sampling, exposed-only, or case-only designs. These designs gain efficiency, but at a cost of flexibility in models for joint effects. A relatively new approach avoids population controls by genotyping case-parent triads. Because it requires parents, the method works best for diseases with onset early in life. With this design, the role of autosomal genetic variants is assessed by in effect treating the nontransmitted parental alleles as controls for affected offspring. Despite advantages for looking at genetic effects, the triad design faces limitations when examining joint effects of genetic and environmental factors. Because population-based controls are not included, main effects for exposures cannot be estimated, and consequently one only has access to inference related to a multiplicative null. We have proposed a hybrid approach that offers the best features of both case-parent and case-control designs. Through genotyping of parents of population-based controls and assuming Mendelian transmission, power is markedly enhanced. One can also estimate main effects for exposures and now flexibly assess models for joint effects. Published by Elsevier Inc. C1 NIEHS, Res Triangle Pk, NC 27709 USA. RP Weinberg, CR (reprint author), NIEHS, MD A3-03,POB 12233, Res Triangle Pk, NC 27709 USA. EM weinber2@niehs.nih.gov FU NIH; National Institute of Environmental Health Sciences [Z01 ES 040006-11] FX This work was supported by the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences (Z01 ES 040006-11). NR 13 TC 16 Z9 16 U1 1 U2 6 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0888-7543 J9 GENOMICS JI Genomics PD JAN PY 2009 VL 93 IS 1 BP 10 EP 12 DI 10.1016/j.ygeno.2008.06.002 PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 394ZP UT WOS:000262492000003 PM 18598750 ER PT J AU Hou, Z Romero, R Uddin, M Than, NG Wildman, DE AF Hou, Zhuocheng Romero, Roberto Uddin, Monica Than, Nandor Gabor Wildman, Derek E. TI Adaptive history of single copy genes highly expressed in the term human placenta SO GENOMICS LA English DT Article DE Evolution; Positive selection; Gene expression; Eutheria; Mouse gene phenotypes; Pregnancy; Comparative genomics ID PHYLOGENETIC ANALYSIS; MAXIMUM-LIKELIHOOD; POSITIVE SELECTION; EUTHERIAN MAMMALS; EVOLUTION; TROPHOBLAST; MOUSE; PREGNANCY; DATABASE; PRETERM AB The chorioallantoic placenta is a shared derived feature of "placental" mammals essential for the success of eutherian reproduction. Identifying the genes involved in the emergence of the placenta may provide clues for understanding the biology of this organ. Here we identify among 4960 single copy genes in mammals, 222 that show high expression levels in human placentas at term. Further, we present evidence that 94 of these 222 genes evolved adaptively during human evolutionary history since the time of the last common ancestor of eutherian mammals. Remarkably, the majority of positive selection occurred on the eutherian stem lineage suggesting that ancient adaptations have been retained in the human placenta. Of these positively selected genes, 28 have been shown to play a role in human pregnancy and placental biology, and at least 26 have important pregnancy-related phenotypes in mice. Adaptations in genes highly expressed in human placenta are attractive candidates for functional and clinical studies. Published by Elsevier Inc. C1 [Hou, Zhuocheng; Romero, Roberto; Than, Nandor Gabor; Wildman, Derek E.] Wayne State Univ, Perinatol Res Branch, NICHD, NIH,DHHS, Detroit, MI 48201 USA. [Hou, Zhuocheng; Romero, Roberto; Uddin, Monica; Wildman, Derek E.] Wayne State Univ, Sch Med, Ctr Mol Med & Genet, Detroit, MI 48201 USA. [Wildman, Derek E.] Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA. [Than, Nandor Gabor] Semmelweis Univ, Dept Obstet & Gynecol 1, H-1088 Budapest, Hungary. [Hou, Zhuocheng] China Agr Univ, Dept Anim Genet, Beijing 100094, Peoples R China. RP Romero, R (reprint author), Wayne State Univ, Perinatol Res Branch, NICHD, NIH,DHHS,Hutzel Womens Hosp, 3990 John R, Detroit, MI 48201 USA. EM prbchiefstaff@med.wayne.edu; dwildman@med.wayne.edu FU Eunice Kennedy Shriver National Institute of Child Health; Human Development/NIH/DHHS FX This research was supported in part by the Intramural Research program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development/NIH/DHHS. We thank Morris Goodman (Wayne State University) for insightful comments on a draft of this manuscript, and we acknowledge Munirul Islam (Wayne State University) for computational assistance. We thank two anonymous reviewer's for their valuable comments. NR 63 TC 12 Z9 12 U1 0 U2 4 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0888-7543 EI 1089-8646 J9 GENOMICS JI Genomics PD JAN PY 2009 VL 93 IS 1 BP 33 EP 41 DI 10.1016/j.ygeno.2008.09.005 PG 9 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 394ZP UT WOS:000262492000008 PM 18848617 ER PT J AU Pascual, I Larrayoz, IM Rodriguez, IR AF Pascual, Iranzu Larrayoz, Ignacio M. Rodriguez, Ignacio R. TI Retinoic acid regulates the human methionine sulfoxide reductase A (MSRA) gene via two distinct promoters SO GENOMICS LA English DT Article DE Methionine sulfoxide reductase; Dual promoters; Retinoic acid; Retinoic acid receptors; Promoters; Regulatory elements; RPE ID OXIDATIVE STRESS; SACCHAROMYCES-CEREVISIAE; A MSRA; CELLS; EXPRESSION; MITOCHONDRIAL; PROTEINS; PROTECTS; MAMMALS; CLONING AB MSRAs (methionine sulfoxide reductases A) are enzymes that reverse the effects of oxidative damage by reducing methionine sulfoxide back to methionine and recovering protein function. In this study we demonstrate that the transcriptional regulation of the human MSRA gene is complex and driven by two distinct promoters. Both promoters demonstrate high expression in human brain and kidney tissues. The upstream (promoter I) regulates the msrA1 transcript that codes for the mitochondrial form of MSRA and is highly active in a broad range of cell lines. The downstream promoter (promoter 2) regulates the msrA2/3 transcripts that code for the cytosolic/nuclear forms of MSRA and is generally less active. Promoter 2 contains a 65 bp putative enhancer region that is very active in the retinal pigment epithelium-derived D407 cell line. Both promoters are partially regulated by all-trans retinoic acid via RARA and other RARs. Published by Elsevier Inc. C1 [Pascual, Iranzu; Larrayoz, Ignacio M.; Rodriguez, Ignacio R.] NEI, NIH, Retinal Cell & Mol Biol Lab, Mech Retinal Dis Sect, Bethesda, MD 20892 USA. RP Rodriguez, IR (reprint author), 7 Mem Dr MSC 0706, Bethesda, MD 20892 USA. EM rodriguezi@nei.nih.gov RI Larrayoz, Ignacio/I-5613-2012 OI Larrayoz, Ignacio/0000-0003-1629-152X FU National Eye Institute intramural Research program FX This work was supported by the National Eye Institute intramural Research program. NR 38 TC 7 Z9 7 U1 1 U2 2 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0888-7543 J9 GENOMICS JI Genomics PD JAN PY 2009 VL 93 IS 1 BP 62 EP 71 DI 10.1016/j.ygeno.2008.09.002 PG 10 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 394ZP UT WOS:000262492000011 PM 18845237 ER PT J AU Wu, ZJ Yuan, LX Jia, N Wang, YH Sun, LG AF Wu, Zijun Yuan, Linxi Jia, Nan Wang, Yuhong Sun, Liguang TI Microbial biomineralization of iron seepage water: Implication for the iron ores formation in intertidal zone of Zhoushan Archipelago, East China Sea SO GEOCHEMICAL JOURNAL LA English DT Article DE ancient wood layer; seepage water; biomineralization; iron ores; intertidal zone ID SUBSURFACE GRANITIC ENVIRONMENTS; NORTHEAST PACIFIC-OCEAN; SUBTERRANEAN ENVIRONMENT; FOSSIL BACTERIA; FE-OXIDES; BOG-IRON; MINERALS; MICROORGANISMS; PRECIPITATION; STROMATOLITES AB The biogeochemcical reactions responsible for fossilized minerals preservation in ancient geological conditions are very often debatable, because little is known about the in situ processes at geo-historical period. In the present study, we describe the formation of iron ores collected in the intertidal zone of the Zhujiajian Island, Zhoushan Archipelago in the East China Sea. Morphological, mineralogical and geochemical analyses were performed on the iron ores and the surrounding geological materials. The results show that the iron ores, composed of spherical ferrihydrite and fibrous aggregates of goethite, presented morphological characteristics reminiscent of bacterial activity. The biominerization process in the seepage system is believed to represent an analogue mechanism for the biogenic formation of iron ores. The degradation of the ancient wood layer provided humic Substances which accelerated the leaching process of iron from the Surrounding bedrock and soils. The abundant leaching iron not only provided the sufficient iron material source, but also created the ideal conditions for the survival of the iron-oxidizing bacteria. The presence of Leptothrix-like sheaths and Gallionella-like stalks in the present-day seepage environment promoted the oxidization of Fe2+ to Fe3+ and the rapid precipitation of bacteriogenic iron oxides (BIOS) oil bacterial sheaths and stalks, allowing the preservation of the morphological characteristics of the bacteria. As time went by, the amorphous biomineralization product (ferrihydrite) call further transfer to more crystalline goethite and therefore be preserved in the ores permanently, representing as the imprints of bacterial activity during the formation of iron ores. The present findings should help elucidate the role of bacteria in the formation of biogenic iron ores in different environments during geo-historical context. C1 [Wu, Zijun; Yuan, Linxi; Jia, Nan; Sun, Liguang] Univ Sci & Technol China, Inst Polar Environm, Hefei 230026, Anhui, Peoples R China. [Wang, Yuhong] NIH, Bethesda, MD 20892 USA. RP Sun, LG (reprint author), Univ Sci & Technol China, Inst Polar Environm, Hefei 230026, Anhui, Peoples R China. EM slg@ustc.edu.cn FU Projects of the Knowledge Innovation of CAS [KZCX3-SW-151]; Chinese Postdoctoral Science Foundation [20060400723] FX The authors would like to thank Dr. D. Fortin for valuable suggestions in preparing this manuscript. We also thank Dr. Tazaki and an anonymous reviewer for their valuable critical comments in improving manuscript. We also acknowledge Dr. Watanabe, associate editor of Geochemical Journal for his effort on dealing with our manuscript. This research was financed by the Projects of the Knowledge Innovation of CAS (Grant No. KZCX3-SW-151) and the Chinese Postdoctoral Science Foundation (Grant No. 20060400723). NR 55 TC 8 Z9 8 U1 1 U2 17 PU GEOCHEMICAL SOC JAPAN PI TOKYO PA 358-5 YAMABUKI-CHO, SHINJUKU-KU, TOKYO, 162-0801, JAPAN SN 0016-7002 EI 1880-5973 J9 GEOCHEM J JI Geochem. J. PY 2009 VL 43 IS 3 BP 167 EP 177 PG 11 WC Geochemistry & Geophysics SC Geochemistry & Geophysics GA 467IB UT WOS:000267730900003 ER PT B AU Kanapuru, B Ershler, WB AF Kanapuru, Bindu Ershler, William B. BE Hurria, A Balducci, L TI Physiological Consequences of Aging SO GERIATRIC ONCOLOGY: TREATMENT, ASSESSMENT AND MANAGEMENT LA English DT Article; Book Chapter ID AGE-RELATED-CHANGES; D-DIMER LEVELS; SUBCLINICAL CARDIOVASCULAR-DISEASE; INTERLEUKIN-6 GENE-EXPRESSION; MILD COGNITIVE IMPAIRMENT; DWELLING ELDERLY PERSONS; BODY-COMPOSITION CHANGES; AFRICAN-AMERICAN WOMEN; CORONARY-HEART-DISEASE; SKELETAL-MUSCLE MASS C1 [Kanapuru, Bindu; Ershler, William B.] Harbor Hosp, NIH, Baltimore, MD 21225 USA. RP Ershler, WB (reprint author), Harbor Hosp, NIH, NM545, Baltimore, MD 21225 USA. EM ershlerwi@grc.nia.nih.gov NR 145 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES BN 978-0-387-89069-2 PY 2009 BP 71 EP 93 DI 10.1007/978-0-387-89070-8_4 D2 10.1007/978-0-387-89070-8 PG 23 WC Oncology; Geriatrics & Gerontology SC Oncology; Geriatrics & Gerontology GA BLV49 UT WOS:000271172100004 ER PT J AU Cesari, M Pahor, M Marzetti, E Zamboni, V Colloca, G Tosato, M Patel, KV Tovar, JJ Markides, K AF Cesari, Matteo Pahor, Marco Marzetti, Emanuele Zamboni, Valentina Colloca, Giuseppe Tosato, Matteo Patel, Kushang V. Tovar, Jennifer J. Markides, Kyriakos TI Self-Assessed Health Status, Walking Speed and Mortality in Older Mexican-Americans SO GERONTOLOGY LA English DT Article DE Self-assessed health status; Walking speed; Mortality; Hispanic EPESE ID LOWER-EXTREMITY FUNCTION; PHYSICAL PERFORMANCE BATTERY; RATED HEALTH; SUBSEQUENT DISABILITY; GAIT SPEED; FOLLOW-UP; ASSOCIATION; PREDICTOR; PEOPLE; WOMEN AB Background: Self-assessed health status (SAHS) and physical performance measures ( in particular, walking speed) are strong predictors of health-related events. Nevertheless, the possible interaction between them in predicting major outcomes has not been clearly explored. Objective: The aim of the study is to evaluate the predictive and additive value for mortality of a SAHS measure and a walking speed test. Methods: Data are from 2,139 Mexican-Americans aged >= 65 years enrolled in the Hispanic Established Populations for Epidemiologic Studies of the Elderly, and followed for 5.8 years. At the baseline visit, participants were asked to answer to the question 'How is your health in general?' presented as a four-level Likert item (i.e., poor, fair, good, excellent). They were also asked to 'walk down and back as fast as it felt safe and comfortable' along an 8-ft track. Cox proportional hazard models, receiver operating characteristic (ROC) curve, and specificity/sensitivity analyses were performed to evaluate the predictive value of SAHS and walking speed for mortality. Results: The mean age of the sample was 72.1 years. Participants reporting 'poor' SAHS were more likely to die compared to those with 'excellent' SAHS, even after adjustment for potential confounders (HR 1.52, 95% CI 1.10-2.10). Similar results were obtained for participants with slow walking speed (<0.29 m/s; HR 1.68, 95% CI 1.27-2.24; reference group: walking speed >= 0.81 m/s). A statistically significant, but weak, correlation between SAHS and walking speed was observed (Pearson's r = 0.069, p = 0.001). No significant differences in areas under curves from ROC analyses were reported for the prediction of mortality when the SAHS and walking speed were tested ( alone or in combination). Both tests presented high specificity (>= 80%) for the prediction of mortality. Conclusion: SAHS and walking speed are not only significant and independent predictors of mortality in older Mexican-Americans, but also present a similar predictive value. The additive prognostic value of the two measures is limited. Copyright (c) 2008 S. Karger AG, Basel C1 [Cesari, Matteo; Pahor, Marco; Marzetti, Emanuele] Univ Florida, Inst Aging, Dept Aging & Geriatr Res, Gainesville, FL 32611 USA. [Zamboni, Valentina; Colloca, Giuseppe; Tosato, Matteo] Univ Cattolica Sacro Cuore, Dept Gerontol Geriatr & Psychiat, I-00168 Rome, Italy. [Patel, Kushang V.] NIA, NIH, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA. [Tovar, Jennifer J.; Markides, Kyriakos] Univ Texas Med Branch, Dept Prevent Med & Community Hlth, Galveston, TX USA. RP Cesari, M (reprint author), Univ Florida, Inst Aging, Dept Aging & Geriatr Res, POB 112610, Gainesville, FL 32611 USA. EM macesari@gmail.com RI Cesari, Matteo/A-4649-2008; Marzetti, Emanuele/A-9430-2010; OI Cesari, Matteo/0000-0002-0348-3664; Marzetti, Emanuele/0000-0001-9567-6983; Tosato, Matteo/0000-0001-5750-9746 FU National Institute on Aging [AG10939, AG17638]; National Institutes of Health [1P30AG028740]; University of Texas Medical Branch Center for Population Health and Health Disparities [1P50CA105631-02]; University of Florida-Institute on Aging; Claude D. Pepper Older Americans Independence Center FX This research was supported, in part, by the Intramural Research Program of the National Institute on Aging, National Institutes of Health. This study was supported by grants AG10939 and AG17638 from the National Institute on Aging and, in part, by the University of Texas Medical Branch Center for Population Health and Health Disparities (1P50CA105631-02). This work was also supported by the University of Florida-Institute on Aging and the Claude D. Pepper Older Americans Independence Center (NIH grant 1P30AG028740). NR 32 TC 16 Z9 17 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0304-324X J9 GERONTOLOGY JI Gerontology PY 2009 VL 55 IS 2 BP 194 EP 201 DI 10.1159/000174824 PG 8 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA 433GH UT WOS:000265191800010 PM 19018125 ER PT J AU Taaffe, DR Henwood, TR Nalls, MA Walker, DG Lang, TF Harris, TB AF Taaffe, Dennis R. Henwood, Tim R. Nalls, Michael A. Walker, Duncan G. Lang, Thomas F. Harris, Tamara B. TI Alterations in Muscle Attenuation following Detraining and Retraining in Resistance-Trained Older Adults SO GERONTOLOGY LA English DT Article DE Intramuscular fat; Hounsfield units; Computed tomography; Muscle ID HUMAN SKELETAL-MUSCLE; KIDNEY-DISEASE PEAK; INSULIN SENSITIVITY; COMPUTED-TOMOGRAPHY; ELDERLY-MEN; BODY-COMPOSITION; PROGRESSIVE EXERCISE; PHYSICAL-ACTIVITY; CONTROLLED-TRIAL; GROWTH-HORMONE AB Background: Aging skeletal muscle is characterized not only by a reduction in size (sarcopenia) and strength but also by an increase in fatty infiltration (myosteatosis). An effective countermeasure to sarcopenia is resistance exercise; however, its effect on fatty infiltration is less clear. Objective: To examine in resistance-trained older persons whether muscle attenuation, a noninvasive measure of muscle density reflecting intramuscular lipid content, is altered with training status. Methods: Thirteen healthy community-dwelling men and women aged 65-83 years (body mass index 27.0 +/- 1.2, mean +/- SE) had computed-tomography scans of the mid-thigh performed following 24 weeks of training, 24 weeks of detraining, and 12 weeks of retraining. Training and retraining were undertaken twice weekly for several upper-and lower-body muscle groups. Skeletal muscle attenuation in Hounsfield units (HU) as well as mid-thigh muscle volume was obtained for the quadriceps and hamstrings. Muscle strength was assessed by 1-repetition maximum and physical function by a battery of tests. Results: The average change in muscle strength following training, detraining and retraining was 48.8 +/- 2.9%, -17.6 +/- 1.3%, and 19.8 +/- 2.0%, respectively. Strength changes were accompanied by significant alterations in muscle density ( p<0.001), with the quadriceps HU decreasing by 7.7 +/- 1.0% following detraining and increasing by 5.4 +/- 0.5% with retraining. For the hamstrings HU measure, detraining and retraining resulted in an 11.9 +/- 1.4% loss and a 5.5 +/- 1.8% gain, respectively. There was no significant change in muscle volume. Conclusion: Cessation of resistance exercise in trained older persons increases the fatty infiltration of muscle, while resumption of exercise decreases it. Monitoring changes in both muscle size and fat infiltration may enable a more comprehensive assessment of exercise in combating age-related muscular changes. Copyright (c) 2008 S. Karger AG, Basel C1 [Taaffe, Dennis R.] Univ Queensland, Fac Hlth Sci, Sch Human Movement Studies, Brisbane, Qld 4072, Australia. [Walker, Duncan G.] Wesley Hosp, So Xray Clin, Brisbane, Qld, Australia. [Nalls, Michael A.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD USA. [Lang, Thomas F.] Univ Calif San Francisco, Dept Radiol, San Francisco, CA 94143 USA. RP Taaffe, DR (reprint author), Univ Queensland, Fac Hlth Sci, Sch Human Movement Studies, Brisbane, Qld 4072, Australia. EM dtaaffe@hms.uq.edu.au RI Henwood, Tim/F-2762-2010; Lang, Thomas/B-2685-2012; OI Lang, Thomas/0000-0002-3720-8038; Henwood, Tim/0000-0002-6836-6733 FU Intramural NIH HHS [Z01 AG007400-02] NR 42 TC 74 Z9 75 U1 2 U2 12 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0304-324X J9 GERONTOLOGY JI Gerontology PY 2009 VL 55 IS 2 BP 217 EP 223 DI 10.1159/000182084 PG 7 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA 433GH UT WOS:000265191800013 PM 19060453 ER PT B AU Krafft, A Salomon, R Crumrine, M AF Krafft, Amy Salomon, Rachelle Crumrine, Martin BE Mitrasinovic, PM TI NIAID RESOURCES FOR THE GLOBAL RESEARCH COMMUNITY TO SUPPORT DEVELOPMENT OF NEW INFLUENZA THERAPEUTICS SO GLOBAL VIEW OF THE FIGHT AGAINST INFLUENZA LA English DT Article; Book Chapter ID CYCLOPENTANE NEURAMINIDASE INHIBITORS; IN-VIVO ACTIVITIES; A VIRUS-INFECTION; COMBINATION THERAPY; PROTECTS FERRETS; PANDEMIC VIRUS; MICE; H5N1; RWJ-270201; OSELTAMIVIR AB With the threat of pandemic influenza still looming, preparedness efforts to develop new diagnostics, vaccines, and therapeutics have expanded to help control the persistent threat of seasonal and novel influenza viruses. The National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health (NIH), has issued solicitations for proposals to fund development of new influenza therapeutics and optimization of existing antivirals. NIAID has also implemented programs designed to support qualified researchers worldwide who may not be funded by NIAID but who are engaged in discovery, early development, and evaluation of new influenza therapeutics. These programs are designed to foster development of antivirals with novel mechanisms of action and immunotherapeutics to prevent or treat influenza. These support services are also part of a larger NIAID effort to build a comprehensive set of research resources to facilitate efforts to develop the next generation of vaccines, diagnostics, and therapeutics. Resources available to influenza researchers at different stages of the product development path include support of the following: Early development of new therapeutic compounds ranging from monoclonal antibodies to novel small molecules with antiviral or immunomodulatory activity against influenza infection; Preclinical evaluation services, for example, in vitro assessment of antiviral activity, followed by in vivo efficacy testing in animal models; Advanced preclinical services, if warranted, to provide data to inform regulatory review and approval processes; Clinical testing units for Phase I studies, for the most promising therapeutic candidates. NIAID's research resources are intended to help researchers navigate the various complexities and challenges inherent in the scientific and regulatory process of discovery and early development of new influenza therapeutics. This chapter will also illustrate how these resources have been used for the early development of peramivir and T-705, two promising new drugs that are currently in clinical trials. For more information on NIAID's research resources, including eligibility requirements and contact information, visit www.niaid.nih.gov/research/resources. C1 [Krafft, Amy; Salomon, Rachelle; Crumrine, Martin] NIAID, Div Microbiol & Infect Dis, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. [Krafft, Amy] NIAID, SARS & Related Viral Resp Dis Sect, RDB DMID DHHS, NIH, Bethesda, MD 20892 USA. RP Krafft, A (reprint author), NIAID, Div Microbiol & Infect Dis, NIH, Dept Hlth & Human Serv, 9000 Rockville Pike, Bethesda, MD 20892 USA. EM kraffta@niaid.nih.gov NR 93 TC 0 Z9 0 U1 0 U2 0 PU NOVA SCIENCE PUBLISHERS, INC PI HAUPPAUGE PA 400 OSER AVE, STE 1600, HAUPPAUGE, NY 11788-3635 USA BN 978-1-60741-952-5 PY 2009 BP 223 EP 247 PG 25 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA BLU87 UT WOS:000271109400014 ER PT S AU Marques, AH Silverman, MN Sternberg, EM AF Marques, Andrea H. Silverman, Marni N. Sternberg, Esther M. BE Judd, LL Sternberg, EM TI Glucocorticoid Dysregulations and Their Clinical Correlates From Receptors to Therapeutics SO GLUCOCORTICOIDS AND MOOD CLINICAL MANIFESTATIONS, RISK FACTORS, AND MOLECULAR MECHANISMS SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on Glucocorticoids and Mood - Clinical Manifestations, Risk Factors and Molecular Mechanisms CY JUN 20-21, 2008 CL San Diego, CA DE cortisol; HPA axis; glucocorticoid resistance; depression; psychosis; inflammation; cytokines ID CORTICOTROPIN-RELEASING HORMONE; MAJOR DEPRESSIVE DISORDER; CORTICOSTEROID-BINDING GLOBULIN; TREATMENT-RESISTANT DEPRESSION; PITUITARY-ADRENOCORTICAL AXIS; STEROID DEMENTIA SYNDROME; NECROSIS-FACTOR-ALPHA; FUNCTION IN-VITRO; CUSHINGS-SYNDROME; ANTIDEPRESSANT TREATMENT AB Clinicians have long known that a substantial proportion of patients treated with high-dose glucocorticoids experience a variety of serious side effects, including metabolic syndrome, bone loss, and mood shifts, such as depressive symptomatology, manic or hypomanic symptoms, and even suicide. The reason for individual variability in expression or severity of these side effects is not clear. However, recent emerging literature is beginning to shed light on possible mechanisms of these effects. As an introduction to this volume, this chapter will review the basic biology of glucocorticoid release and molecular mechanisms of glucocorticoid receptor function, and will discuss how dysregulation of glucocorticoid action at all levels could contribute to such side effects. At the molecular level, glucocorticoid receptor polymorphisms may be associated either with receptor hypofunction or hyperfunction and could thus contribute to differential individual sensitivity to the effects of glucocorticoid treatment. Numerous factors regulate hypothalamic-pituitary-adrenal (HPA) axis responsiveness, which could also contribute to individual differences in glucocorticoid side effects. One of these is sex hormone status and the influence of estrogen and progesterone on HPA axis function and mood. Another is immune system activity, in which immune molecules, such as interleukins and cytokines, activate the HPA axis and alter brain function, including memory, cognition, and mood. The effects of cytokines in inducing sickness behaviors, which overlap with depressive symptomatology, could also contribute to individual differences in such symptomatology. Taken together, this knowledge will have important relevance for identifying at-risk patients to avoid or minimize such side effects when they are treated with glucocorticoids. A framework for assessment of patients is proposed that incorporates functional, physiological, and molecular biomarkers to identify subgroups of patients at risk for depressive symptomatology associated with glucocorticoid treatment, and for prevention of side effects, which in many cases can be life-threatening. C1 [Marques, Andrea H.; Silverman, Marni N.; Sternberg, Esther M.] NIMH, Integrat Neural Immune Program, Sect Neuroendocrine Immunol & Behav, NIH, Rockville, MD 20852 USA. RP Sternberg, EM (reprint author), NIMH, Integrat Neural Immune Program, Sect Neuroendocrine Immunol & Behav, NIH, 5625 Fishers Lane,MSC 9401, Rockville, MD 20852 USA. EM sternbee@mail.nih.gov; sternbee@mail.nih.gov RI marques, andrea/H-5297-2012 FU Intramural NIH HHS [ZIA MH002585-19] NR 152 TC 60 Z9 62 U1 1 U2 15 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN STREET, MALDEN 02148, MA USA SN 0077-8923 BN 978-1-57331-748-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2009 VL 1179 BP 1 EP 18 DI 10.1111/j.1749-6632.2009.04987.x PG 18 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BMJ24 UT WOS:000272551200001 PM 19906229 ER PT S AU Schmidt, PJ Rubinow, DR AF Schmidt, Peter J. Rubinow, David R. BE Judd, LL Sternberg, EM TI Sex Hormones and Mood in the Perimenopause SO GLUCOCORTICOIDS AND MOOD CLINICAL MANIFESTATIONS, RISK FACTORS, AND MOLECULAR MECHANISMS SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on Glucocorticoids and Mood - Clinical Manifestations, Risk Factors and Molecular Mechanisms CY JUN 20-21, 2008 CL San Diego, CA DE menopause transition; depression; estrogen ID PITUITARY-ADRENAL AXIS; ESTROGEN-RECEPTOR-BETA; MENSTRUAL-CYCLE PHASE; POSITRON-EMISSION-TOMOGRAPHY; FORCED SWIM TEST; ELEMENT-BINDING PROTEIN; MENOPAUSAL TRANSITION; RAT-BRAIN; GONADAL-STEROIDS; POSTMENOPAUSAL WOMEN AB The focus of this chapter is the relationship between the onset of depression in women and the reproductive events of the menopause transition. Epidemiologic studies have documented that the majority of women do not become depressed during the menopause transition. However, recent longitudinal studies suggest that in some women, the reproductive events related to the menopause transition could play a role in the onset of depression. No abnormality of ovarian hormones has been identified that distinguishes women with depression from those who remain asymptomatic during the menopause transition. Nonetheless, several findings suggest a role of ovarian hormones in the onset of these depressions. First, episodes of depression cluster during the stage of the menopause transition that is accompanied by estradiol withdrawal. Second, randomized controlled trials have documented the short-term (3-6 weeks) antidepressant efficacy of estradiol in depressed perimenopausal women. Third, experimentally induced estradiol withdrawal triggers mood symptoms in some women. Thus, although depression is not a uniform accompaniment of the menopause transition, in some women, age-related changes in ovarian estrogen production may alter central nervous system function and predispose them to develop depression. C1 [Schmidt, Peter J.] NIMH, Behav Endocrinol Branch, Dept Hlth & Human Serv, Bethesda, MD USA. [Rubinow, David R.] Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA. RP Schmidt, PJ (reprint author), Bldg 10 CRC,Room 65340,10 Ctr Dr,MSC 1276, Bethesda, MD 20892 USA. EM peterschmidt@mail.nih.gov FU Intramural NIH HHS [Z01 MH002537-19] NR 169 TC 55 Z9 55 U1 3 U2 7 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN STREET, MALDEN 02148, MA USA SN 0077-8923 BN 978-1-57331-748-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2009 VL 1179 BP 70 EP 85 DI 10.1111/j.1749-6632.2009.04982.x PG 16 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BMJ24 UT WOS:000272551200005 PM 19906233 ER PT S AU Hauger, RL Risbrough, V Oakley, RH Olivares-Reyes, JA Dautzenberg, FM AF Hauger, Richard L. Risbrough, Victoria Oakley, Robert H. Alberto Olivares-Reyes, J. Dautzenberg, Frank M. BE Judd, LL Sternberg, EM TI Role of CRF Receptor Signaling in Stress Vulnerability, Anxiety, and Depression SO GLUCOCORTICOIDS AND MOOD CLINICAL MANIFESTATIONS, RISK FACTORS, AND MOLECULAR MECHANISMS SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on Glucocorticoids and Mood - Clinical Manifestations, Risk Factors and Molecular Mechanisms CY JUN 20-21, 2008 CL San Diego, CA DE corticotropin releasing factor, CRF; urocortin 2, UCN2; urocortin 3, UCN3; CRF receptor type 1, CRF(1) receptor; CRF receptor type 2, CRF(2) receptor; G protein-coupled receptor, GPCR; GPCR kinase, GRK; cyclic 3 ', 5 '-adenosine monophosphate; cyclic AMP; extracellular signal-regulated kinase, ERK; mitogen-activated protein kinase; MAPK; brain-derived neurotrophic factor, BDNF ID CORTICOTROPIN-RELEASING-FACTOR; PROTEIN-COUPLED RECEPTORS; NEUROTROPHIC FACTOR EXPRESSION; MECHANISM REGULATING STRESS; TEENAGE SUICIDE VICTIMS; ELEMENT-BINDING PROTEIN; BETA-ARRESTIN; BASOLATERAL AMYGDALA; FACTOR TYPE-1; HOMOLOGOUS DESENSITIZATION AB Markers of hyperactive central corticotropin releasing factor (CRF) systems and CRF-related single nucleotide polymorphisms (SN-Ps) have been identified in patients with anxiety and depressive disorders. Designing more effective antagonists may now be guided by data showing that small molecules bind to transmembrane domains. Specifically, CRF(1) receptor antagonists have been developed as novel anxiolytic and antidepressant treatments. Because CRF(1) receptors become rapidly desensitized by G protein-coupled receptor kinase (GRK) and beta-arrestin mechanisms in the presence of high agonist concentrations, neuronal hypersecretion of synaptic CRF alone may be insufficient to account for excessive central CRE neurotransmission in stress-induced affective pathophysiology. In addition to desensitizing receptor function, GRK phosphorylation and beta-arrestin binding can shift a G protein-coupled receptor (GPCR) to signal selectively via the extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK-MAPK) or Akt pathways independent of G proteins. Also, Epac-dependent CRF(1) receptor signaling via the ERK-MAPK pathway has been found to potentiate brain-derived neurotrophic factor (BDNF)-stimulated TrkB signaling. Thus, genetic or acquired abnormalities in GRK and beta-arrestin function may be involved in the pathophysiology of stress-induced anxiety and depression. C1 [Hauger, Richard L.] Univ Calif San Diego, Sch Med, Dept Psychiat, La Jolla, CA 92093 USA. [Hauger, Richard L.] Univ Calif San Diego, VA Healthcare Syst, Psychiat Serv, La Jolla, CA 92093 USA. [Oakley, Robert H.] NIEHS, Lab Signal Transduct, NIH, Res Triangle Pk, NC 27709 USA. [Alberto Olivares-Reyes, J.] IPN, CINVESTAV, Dept Biochem, Ctr Res & Adv Studies, Mexico City 07738, DF, Mexico. [Dautzenberg, Frank M.] Nycomed GmbH, Constance, Germany. RP Hauger, RL (reprint author), Univ Calif San Diego, Sch Med, Dept Psychiat, 9500 Gillman Dr, La Jolla, CA 92093 USA. EM rhauger@ucsd.edu FU Department of Veterans Affairs; VA Center of Excellence for Stress and Mental Health (CESAMH); Mental Illness Research, Education and Clinical Center (MIRECC) [VISN22]; NIH/NIA [AG022982]; NIH/NIMH [MH074697]; Center for Research and Advanced Studies of the National Polytechnic Institute (CINVESTAV-IPN); CONACYT-SEP [CB-2005-01-48777]; National Institute of Environmental Health Sciences FX R. L. Hauger was supported by a Merit Review grant from the Department of Veterans Affairs; the VA Center of Excellence for Stress and Mental Health (CESAMH) and Mental Illness Research, Education and Clinical Center (MIRECC) of VISN22; and NIH/NIA (AG022982) and NIH/NIMH (MH074697) RO1 grants. J. A. Olivares-Reyes was supported by the Center for Research and Advanced Studies of the National Polytechnic Institute (CINVESTAV-IPN) and a CONACYT-SEP research grant (CB-2005-01-48777). V Risbrough was Supported by an NIH/NIMH (MH074697) RO1 grant. R. H. Clakley was supported by the National Institute of Environmental Health Sciences. We gratefully acknowledge Susan Shew for editorial assistance. NR 121 TC 95 Z9 100 U1 1 U2 11 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN STREET, MALDEN 02148, MA USA SN 0077-8923 BN 978-1-57331-748-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2009 VL 1179 BP 120 EP 143 DI 10.1111/j.1749-6632.2009.05011.x PG 24 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BMJ24 UT WOS:000272551200008 PM 19906236 ER PT S AU Chrousos, GP Kino, T AF Chrousos, George P. Kino, Tomoshige BE Judd, LL Sternberg, EM TI Glucocorticoid Signaling in the Cell Expanding Clinical Implications to Complex Human Behavioral and Somatic Disorders SO GLUCOCORTICOIDS AND MOOD CLINICAL MANIFESTATIONS, RISK FACTORS, AND MOLECULAR MECHANISMS SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on Glucocorticoids and Mood - Clinical Manifestations, Risk Factors and Molecular Mechanisms CY JUN 20-21, 2008 CL San Diego, CA DE metabolic syndrome; osteoporosis; CDK5; GR phosphorylation; stress system; glucocorticoid resistance; glucocorticoid hypersensitivity ID CYCLIN-DEPENDENT KINASE-5; PITUITARY-ADRENAL AXIS; FRAGMENT-LENGTH-POLYMORPHISM; RECEPTOR GENE; TRANSCRIPTIONAL ACTIVITY; N363S POLYMORPHISM; METABOLIC SYNDROME; IN-VIVO; BODY-COMPOSITION; STRESS SYSTEM AB Glucocorticoids contribute to the maintenance of basal and stress-related homeostasis in all higher organisms, and influence a large proportion of the expressed human genome, and their effects spare almost no organs or tissues. Glucocorticoids regulate many functions of the central nervous system, such as arousal, cognition, mood, sleep, the activity and direction of intermediary metabolism, the maintenance of a proper cardiovascular tone, the activity and quality of the immune and inflammatory reaction, including the manifestations of the sickness syndrome, and growth and reproduction. The numerous actions of glucocorticoids are mediated by a set of at least 16 glucocorticoid receptor (GR) isoforms forming homo- or hetero-dimers. The GRs consist of multifunctional domain proteins operating as ligand-dependent transcription factors that interact with many other cell signaling systems, including large and small G proteins. The presence of multiple GR monomers and homo- or hetero-dimers expressed in a cell-specific fashion at different quantities with quantitatively and qualitatively different transcriptional activities suggest that the glucocorticoid signaling system is highly stochastic. Glucocorticoids are heavily involved in human pathophysiology and influence life expectancy. Common behavioral and/or somatic complex disorders, such as anxiety, depression, insomnia, chronic pain and fatigue syndromes, obesity, the metabolic syndrome, essential hypertension, diabetes type 2, atherosclerosis with its cardiovascular sequelae, and osteoporosis, as well as autoimmune inflammatory and allergic disorders, all appear to have a glucocorticoid-regulated component. C1 [Chrousos, George P.] Univ Athens, Sch Med, Dept Pediat 1, GR-11527 Athens, Greece. [Chrousos, George P.; Kino, Tomoshige] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pediat Endocrinol Sect, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA. RP Chrousos, GP (reprint author), Univ Athens, Sch Med, Aghia Sophia Childrens Hosp, Dept Pediat 1, GR-11527 Athens, Greece. EM chrousge@med.uoa.gr FU University of Athens, Athens, Greece; Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD FX This is a synoptic review of work supported by the University of Athens, Athens, Greece, and the Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD. NR 77 TC 86 Z9 89 U1 1 U2 9 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN STREET, MALDEN 02148, MA USA SN 0077-8923 BN 978-1-57331-748-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2009 VL 1179 BP 153 EP 166 DI 10.1111/j.1749-6632.2009.04988.x PG 14 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BMJ24 UT WOS:000272551200010 PM 19906238 ER PT S AU Revollo, JR Cidlowski, JA AF Revollo, Javier R. Cidlowski, John A. BE Judd, LL Sternberg, EM TI Mechanisms Generating Diversity in Glucocorticoid Receptor Signaling SO GLUCOCORTICOIDS AND MOOD CLINICAL MANIFESTATIONS, RISK FACTORS, AND MOLECULAR MECHANISMS SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on Glucocorticoids and Mood - Clinical Manifestations, Risk Factors and Molecular Mechanisms CY JUN 20-21, 2008 CL San Diego, CA DE glucocorticoids; signaling; glucocorticoid receptor ID NF-KAPPA-B; NITRIC-OXIDE SYNTHASE; TRANSCRIPTIONAL ACTIVATION; BETA-ISOFORM; HORMONE RECEPTORS; NUCLEAR RECEPTORS; GENE-REGULATION; TATA BOX; EXPRESSION; DOMAIN AB Glucocorticoids regulate diverse biological processes throughout the body via the glucocorticoid receptor (GR). Ligand-bound GR translocates into the nucleus and can elicit changes in gene expression by direct contact with the DNA or by protein-protein interactions with other transcription factors. The GR can also mediate rapid nongenomic signaling events initiated in the cytoplasm. In this chapter, we review the biological and physiological implications of glucocorticoids, the GR, and many of the signal transduction mechanisms that mediate their action. C1 [Revollo, Javier R.; Cidlowski, John A.] NIEHS, Mol Endocrinol Grp, Lab Signal Transduct, NIH, Res Triangle Pk, NC 27709 USA. RP Cidlowski, JA (reprint author), NIEHS, Mol Endocrinol Grp, Lab Signal Transduct, NIH, MD F3-07,POB 12233, Res Triangle Pk, NC 27709 USA. EM cidlows1@niehs.nih.gov NR 69 TC 96 Z9 100 U1 1 U2 7 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN STREET, MALDEN 02148, MA USA SN 0077-8923 BN 978-1-57331-748-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2009 VL 1179 BP 167 EP 178 DI 10.1111/j.1749-6632.2009.04986.x PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BMJ24 UT WOS:000272551200011 PM 19906239 ER PT S AU Sternberg, EM Judd, LL AF Sternberg, Esther M. Judd, Lewis L. BE Judd, LL Sternberg, EM TI Conference Summary and Conclusions A Comprehensive Approach to Predicting and Managing Mood Effects of Glucocorticoids SO GLUCOCORTICOIDS AND MOOD CLINICAL MANIFESTATIONS, RISK FACTORS, AND MOLECULAR MECHANISMS SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Conference on Glucocorticoids and Mood - Clinical Manifestations, Risk Factors and Molecular Mechanisms CY JUN 20-21, 2008 CL San Diego, CA DE glucocorticoids; mood; stress; suicidal ideation ID ORAL CORTICOSTEROIDS AB The discovery of glucocorticoids and their enormous therapeutic benefits led to the use of these compounds as valuable medications for a wide variety of diseases. In 1950 this effort was ushered in by a landmark event-the awarding of the 1950 Nobel Prize in Physiology and Medicine to Drs. Phillip Hench, Edward Kendall, and Tadeus Reichstein. It was Hench who described and researched the successful use of the glucocorticoid, cortisone, and pituitary adrenocorticotrophic hormones to treat rheumatoid arthritis. Significant scientific discovery preceded Hench and colleagues' efforts, but the revolutionary accumulation of discovery in glucocorticoids since then is one of the unique scientific stories in the history of medicine. The scientific conference upon which this volume is based represents an attempt to convene a state-of-the-science meeting on the current understanding and scientific status of this fascinating, far-reaching, and fast-moving field. This last chapter will summarize the exciting presentations of this 2-day conference. C1 [Judd, Lewis L.] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA. [Sternberg, Esther M.] NIMH, NIH, Bethesda, MD 20892 USA. RP Judd, LL (reprint author), Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA. EM ljudd@ucsd.edu; ljudd@ucsd.edu FU Intramural NIH HHS [ZIA MH002585-21, Z01 MH002585-18] NR 19 TC 5 Z9 5 U1 0 U2 1 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN STREET, MALDEN 02148, MA USA SN 0077-8923 BN 978-1-57331-748-1 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2009 VL 1179 BP 229 EP 233 DI 10.1111/j.1749-6632.2009.05059.x PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BMJ24 UT WOS:000272551200015 PM 19906243 ER PT J AU Wang, XB Song, YJ Jacobi, JL Tuan, RS AF Wang, Xibin Song, Yingjie Jacobi, Jennifer L. Tuan, Rocky S. TI Inhibition of histone deacetylases antagonized FGF2 and IL-1 beta effects on MMP expression in human articular chondrocytes SO GROWTH FACTORS LA English DT Article DE Fibroblast growth factor; interleukin-1 beta; histone deacetylase; matrix metalloproteinase; articular chondrocyte; trichostatin A ID OSTEOARTHRITIC CARTILAGE; GENE-EXPRESSION; MATRIX METALLOPROTEINASE-13; HUMAN COLLAGENASE-3; SIGNALING PATHWAY; PROMOTER ACTIVITY; II COLLAGEN; IN-VITRO; CELLS; ARTHRITIS AB Fibroblast growth factor-2 (FGF2) and interleukin-1 beta (IL-1 beta) stimulate the expression of matrix metalloproteinases ( MMPs) in articular chondrocytes, which may contribute to cartilage degradation and development of osteoarthritis. Histone deacetylases (HDACs) have recently been implicated in the regulation of MMP gene expression. To investigate the functional involvement of HDACs in the signaling pathway of FGF2 and IL-1 beta, we examined the effects of HDAC inhibition on activities of FGF2 or IL-1 beta on gene expression of MMP-1, MMP-3, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs-5 (ADAMTS5), collagen type II, and aggrecan. Human articular chondrocyte cultures were treated with FGF2 or IL-1 beta in the presence or absence of HDAC inhibitor (trichostatin A, TSA). Gene expression levels after treatments were assessed using quantitative real time PCR. Results showed that FGF2 and IL-1 beta both increased MMP-1 and - 13 expression, while IL-1 beta also increased MMP-3 mRNA levels. These effects were attenuated in the presence of TSA in a dose dependent manner. In contrast to the effects on MMPs, FGF2 decreased mRNA levels of ADAMTS-5, which was not affected by HDAC inhibition. FGF2, IL-1 beta, and TSA inhibited expression of aggrecan, while TSA also decreased mRNA levels of collagen type II. These findings showed that HDAC inhibition antagonized FGF2 and IL-1 beta induced MMP expression. Combination of FGF2 and the HDAC inhibitor decreases both anabolic and catabolic genes, which may slow the cartilage turnover and be beneficial for maintaining cartilage integrity. C1 [Wang, Xibin; Song, Yingjie; Jacobi, Jennifer L.; Tuan, Rocky S.] NIAMSD, Cartilage Biol & Orthopaed Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP Tuan, RS (reprint author), NIAMSD, Cartilage Biol & Orthopaed Branch, NIH, Dept Hlth & Human Serv, Bldg 50,Room 1523, Bethesda, MD 20892 USA. EM tuanr@mail.nih.gov FU Intramural Research Program [Z01 AR41131]; National Institute of Arthritis, and Musculoskeletal and Skin Diseases; NIH FX The authors thank Dr. Paul Manner, George Washington University and University of Washington, for providing human tissue specimens. This research was supported by the Intramural Research Program (Z01 AR41131), National Institute of Arthritis, and Musculoskeletal and Skin Diseases, NIH. NR 42 TC 29 Z9 31 U1 6 U2 8 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 0897-7194 J9 GROWTH FACTORS JI Growth Factors PY 2009 VL 27 IS 1 BP 40 EP 49 DI 10.1080/08977190802625179 PG 10 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA 387FS UT WOS:000261937700005 PM 19107653 ER PT J AU Fukuda, T Iwata, M Kitazoe, M Maeda, T Salomon, D Hirohata, S Tanizawa, K Kuroda, S Seno, M AF Fukuda, Takayuki Iwata, Miki Kitazoe, Midori Maeda, Takashi Salomon, David Hirohata, Satoshi Tanizawa, Katsuyuki Kuroda, Shun'ichi Seno, Masaharu TI Human eosinophil cationic protein enhances stress fiber formation in Balb/c 3T3 fibroblasts and differentiation of rat neonatal cardiomyocytes SO GROWTH FACTORS LA English DT Article DE ECP; fibroblast; stress fiber; cardiomyocyte; beating rate ID EMBRYONIC STEM-CELLS; SCHISTOSOMA-MANSONI; GRANULE PROTEINS; GENE-EXPRESSION; GROWTH-FACTOR; IN-VITRO; RNASE 3; SERUM; RHO; CHILDREN AB We found that eosinophil cationic protein (ECP) stimulated the growth of mouse Balb/c 3T3 fibroblasts. ECP-treated 3T3 cells were more flattened and exhibited enhanced stress fiber formation. The enhancement of cytoskeleton after addition of recombinant ECP appeared stable and was able to inhibit disassembly of actin filaments that was induced by fibroblast growth factor-2. The ROCK inhibitor, Y-27632, abrogated this enhancement on stress fiber formation that was induced by ECP indicating the involvement of Rho/ROCK signaling pathway. The effect of ECP was assessed on the differentiation of primary cardiomyocytes derived from rat neonatal heart since the development of actin filaments is significantly related with organization of stress fibers. As the result, both beating rate and the expression of cardiac muscle specific markers such as atrial natriuretic factor were enhanced in the presence of ECP. Thus ECP may also function as a cardiomyocyte differentiation factor. C1 [Seno, Masaharu] Okayama Univ, Grad Sch Nat Sci & Technol, Dept Med & Bioengn Sci, Lab Nanobiotechnol,Kita Ku, Okayama 7008530, Japan. [Iwata, Miki; Tanizawa, Katsuyuki; Kuroda, Shun'ichi] Osaka Univ, Dept Struct Mol Biol, Inst Sci & Ind Res, Osaka 5670047, Japan. [Salomon, David] Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Mol Biol & Biochem, Okayama 7008558, Japan. [Hirohata, Satoshi] NCI, Tumor Gwowth Fator Sect, Mammary Biol & Tumorigenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA. RP Seno, M (reprint author), Okayama Univ, Grad Sch Nat Sci & Technol, Dept Med & Bioengn Sci, Lab Nanobiotechnol,Kita Ku, Room 361,Bldg Eng 6,3-1-1 Tsushima Naka, Okayama 7008530, Japan. EM mseno@cc.okayama-u.ac.jp RI Hirohata, Satoshi/B-2253-2011; SENO, Masaharu /B-2092-2011 OI Hirohata, Satoshi/0000-0002-4815-5891; SENO, Masaharu /0000-0001-8547-6259 FU Ministry of Education, Culture, Sports, Science and Technology Grant-in-Aid for Scientific Research; Japan Science and Technology Agency (JST); Chugoku Industrial Innovation Center FX We thank Drs Koichi Igarashi, Hiroko Tada, and Hidenori Yamada for their precious advices and discussions through this study. This research was supported in part by the Ministry of Education, Culture, Sports, Science and Technology Grant-in-Aid for Scientific Research, by Japan Science and Technology Agency (JST), and by Chugoku Industrial Innovation Center. NR 41 TC 6 Z9 6 U1 0 U2 1 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 0897-7194 J9 GROWTH FACTORS JI Growth Factors PY 2009 VL 27 IS 4 BP 228 EP 236 AR PII 912343689 DI 10.1080/08977190902987149 PG 9 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA 468MK UT WOS:000267823100003 PM 19521893 ER PT S AU Grisshammer, R AF Grisshammer, Reinhard BE Burgess, RR Deutscher, MP TI PURIFICATION OF RECOMBINANT G-PROTEIN-COUPLED RECEPTORS SO GUIDE TO PROTEIN PURIFICATION, SECOND EDITION SE Methods in Enzymology LA English DT Review; Book Chapter ID RAT NEUROTENSIN RECEPTOR; INTEGRAL MEMBRANE-PROTEINS; LARGE-SCALE PURIFICATION; ESCHERICHIA-COLI; EXPRESSION SYSTEM; CRYSTAL-STRUCTURE; BOVINE RHODOPSIN; INSECT CELLS; OVEREXPRESSION; STABILITY AB Structural and functional analysis of most G-protein-coupled receptors (GPCRs) requires their expression and purification in functional form. The produced amount of recombinant membrane-inserted receptors depends on the optimal combination of a particular GPCR and production host; optimization of expression is still a matter of trial-and-error. Prior to purification, receptors must be extracted from the membranes by use of detergent(s). The choice of an appropriate detergent for solubilization and purification is crucial to maintain receptors in their functional state. The initial enrichment can be carried out by affinity chromatography using a general affinity tag (e.g., poly-histidine tag). If the first purification step does not yield pure receptor protein, purification to homogeneity can often be achieved by use of a subsequent receptor-specific ligand column. If suitable immobilized ligands are not available, size exclusion chromatography or other techniques need to be applied. Many GPCRs become unstable upon detergent extraction from lipid membranes, and measures for stabilization are discussed. As an example, the purification of a functional neurotensin receptor to homogeneity in milligram quantities is given below. C1 NINDS, US Dept HHS, NIH, Rockville, MD USA. RP Grisshammer, R (reprint author), NINDS, US Dept HHS, NIH, Rockville, MD USA. RI Grisshammer, Reinhard/C-3089-2015 FU Intramural NIH HHS [Z01 NS003016-02] NR 47 TC 32 Z9 32 U1 0 U2 10 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 BN 978-0-12-374536-1 J9 METHOD ENZYMOL JI Methods Enzymol. PY 2009 VL 463 BP 631 EP 645 DI 10.1016/S0076-6879(09)63036-6 PG 15 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BMF70 UT WOS:000272201000036 PM 19892196 ER PT J AU Patel, KV Guralnik, JM AF Patel, Kushang V. Guralnik, Jack M. TI Prognostic implications of anemia in older adults SO Haematologica-The Hematology Journal LA English DT Editorial Material ID HEMOGLOBIN CONCENTRATION; CARDIOVASCULAR HEALTH; PHYSICAL PERFORMANCE; MORTALITY; IMPACT; WOMEN; HOSPITALIZATION; DISABILITY; DISEASE; MUSCLE C1 [Patel, Kushang V.; Guralnik, Jack M.] NIA, Lab Epidemiol Demog & Biometry, Intramural Res Program, Bethesda, MD 20892 USA. RP Patel, KV (reprint author), NIA, Lab Epidemiol Demog & Biometry, Intramural Res Program, Bethesda, MD 20892 USA. EM patelku@mail.nih.gov NR 21 TC 15 Z9 16 U1 0 U2 0 PU FERRATA STORTI FOUNDATION PI PAVIA PA VIA GIUSEPPE BELLI 4, 27100 PAVIA, ITALY SN 0390-6078 J9 HAEMATOL-HEMATOL J JI Haematol-Hematol. J. PD JAN PY 2009 VL 94 IS 1 BP 1 EP 2 DI 10.3324/haematol.2008.001289 PG 2 WC Hematology SC Hematology GA 396LL UT WOS:000262593100001 PM 19118372 ER PT J AU Young, NS AF Young, Neal S. TI Paroxysmal nocturnal hemoglobinuria and myelodysplastic syndromes: clonal expansion of PIG-A-mutant hematopoietic cells in bone marrow failure SO Haematologica-The Hematology Journal LA English DT Editorial Material ID COMPLEMENT INHIBITOR ECULIZUMAB; TRANSPLANTATION; MANAGEMENT; RECEPTOR; DISEASE C1 NHLBI, Hematol Branch, Bethesda, MD 20892 USA. RP Young, NS (reprint author), NHLBI, Hematol Branch, Bethesda, MD 20892 USA. EM youngns@mail.nih.gov NR 25 TC 10 Z9 13 U1 0 U2 0 PU FERRATA STORTI FOUNDATION PI PAVIA PA VIA GIUSEPPE BELLI 4, 27100 PAVIA, ITALY SN 0390-6078 J9 HAEMATOL-HEMATOL J JI Haematol-Hematol. J. PD JAN PY 2009 VL 94 IS 1 BP 3 EP 7 DI 10.3324/haematol.2008.001297 PG 5 WC Hematology SC Hematology GA 396LL UT WOS:000262593100002 PM 19118373 ER PT J AU Nichols, WL Hultln, MB James, AH Manco-Johnson, MJ Montgomery, RR Ortel, TL Rick, ME Sadler, JE Weinstein, M Yawn, BP AF Nichols, W. L. Hultln, M. B. James, A. H. Manco-Johnson, M. J. Montgomery, R. R. Ortel, T. L. Rick, M. E. Sadler, J. E. Weinstein, M. Yawn, B. P. TI von Willebrand factor content in Alphanate((R)) (Laurence J. Logan) - reply SO HAEMOPHILIA LA English DT Letter ID FACTOR CONCENTRATE; DISEASE C1 [Nichols, W. L.] Mayo Clin, Special Coagulat Lab, Coll Med, Div Hematopathol,Dept Lab Med & Pathol, Rochester, MN 55905 USA. [Nichols, W. L.] Mayo Clin, Coagulat Clin, Coll Med, Rochester, MN 55905 USA. [Nichols, W. L.] Mayo Clin, Comprehens Hemophilia Ctr, Coll Med, Div Hematol & Internal Med, Rochester, MN 55905 USA. [Hultln, M. B.] SUNY Stony Brook, Dept Med, Stony Brook, NY 11794 USA. [James, A. H.] Duke Univ, Med Ctr, Dept Obstet & Gynecol, Durham, NC 27710 USA. [Manco-Johnson, M. J.] Univ Colorado Denver, Dept Pediat, Aurora, CO USA. [Manco-Johnson, M. J.] Childrens Hosp, Ctr Canc & Blood Disorders, Denver, CO 80218 USA. [Montgomery, R. R.] Med Coll Wisconsin, BloodCtr Wisconsin, Blood Res Inst, Milwaukee, WI 53226 USA. [Montgomery, R. R.] Med Coll Wisconsin, Sect Pediat Hematol, Dept Pediat, Milwaukee, WI 53226 USA. [Ortel, T. L.] Duke Univ, Med Ctr, Dept Pathol, Clin Coagulat Lab, Durham, NC 27710 USA. [Ortel, T. L.] Duke Univ, Dept Med, Div Hematol, Durham, NC 27710 USA. [Rick, M. E.] NIH, Warren G Magnuson Clin Ctr, Hematol Serv, Bethesda, MD 20892 USA. [Sadler, J. E.] Washington Univ, Dept Med, St Louis, MO USA. [Weinstein, M.] US FDA, Off Blood Res & Review, Ctr Biol Evaluat & Res, Rockville, MD 20857 USA. [Yawn, B. P.] Univ Minnesota, Dept Family & Community Med, Minneapolis, MN USA. [Yawn, B. P.] Olmsted Med Ctr, Dept Res, Rochester, MN USA. RP Nichols, WL (reprint author), Mayo Clin, Special Coagulat Lab, Coll Med, Div Hematopathol,Dept Lab Med & Pathol, Hilton 200, Rochester, MN 55905 USA. EM nichols.william@mayo.edu RI Sadler, Evan/D-8556-2011; OI Sadler, J. Evan/0000-0001-5705-469X NR 4 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 1351-8216 J9 HAEMOPHILIA JI Haemophilia PD JAN PY 2009 VL 15 IS 1 BP 370 EP 371 DI 10.1111/j.1365-2516.2008.01903.x PG 2 WC Hematology SC Hematology GA 394TK UT WOS:000262470600053 ER PT B AU Costello, RB Leser, M Coates, PM AF Costello, Rebecca B. Leser, Maureen Coates, Paul M. BE Bales, CW Ritchie, CS TI Dietary Supplements: Current Knowledge and Future Frontiers SO HANDBOOK OF CLINICAL NUTRITION AND AGING, SECOND EDITION SE Nutrition and Health Series LA English DT Article; Book Chapter DE Dietary supplements; nutrients; botanicals; DSHEA; needs assessment; evidence-based guidelines; health claims ID RANDOMIZED CONTROLLED-TRIALS; VITAMIN-E SUPPLEMENTATION; BENIGN PROSTATIC HYPERPLASIA; PLACEBO-CONTROLLED TRIAL; BILOBA SPECIAL EXTRACT; HEALTHY OLDER-ADULTS; PERIPHERAL ARTERIAL-DISEASE; POLYUNSATURATED FATTY-ACIDS; CONTROLLED CLINICAL-TRIALS; HERB-DRUG INTERACTIONS AB The evidence base for the use of dietary supplements is well documented for some, such as the essential nutrients, but it is scant for others, such as some designer supplements and botanicals. Popular dietary supplements consumed by older Americans that have national public health recommendations and established guidelines for use include omega-3 fatty acids; the B vitamins, folic acid, vitamins 136, and 1312; vitamins D and E; and the minerals, calcium, potassium, and magnesium. Dietary supplements not endorsed by national public health recommendations but with a considerable evidence base upon which randomized clinical trials can be planned or guidelines for use might be formulated include coenzyme Q10, creatine, and the botanicals black cohosh, French pine bark, Ginkgo biloba, and saw palmetto. A clinical deficiency of vitamins or minerals, other than iron and possibly vitamin D, is uncommon in the United States, except for certain high-risk groups. In situations when recommended nutrients cannot be obtained by food alone or retained by the body because of impaired absorption or other physiologic limitations, dietary supplements can provide benefit. When taken, multivitamin preparations should include 100% of the daily value for vitamins B12, B6, D, and folic acid. C1 [Costello, Rebecca B.; Coates, Paul M.] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA. [Leser, Maureen] NIH, Ctr Clin, Dept Nutr, Bethesda, MD 20892 USA. RP Costello, RB (reprint author), NIH, Off Dietary Supplements, Bldg 10, Bethesda, MD 20892 USA. NR 269 TC 0 Z9 0 U1 4 U2 4 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA BN 978-1-60327-384-8 J9 NUTR HEALTH SER JI Nutr. Health Ser. PY 2009 BP 553 EP 633 DI 10.1007/978-1-60327-385-5_28 PG 81 WC Geriatrics & Gerontology; Gerontology; Public, Environmental & Occupational Health; Medicine, General & Internal; Nutrition & Dietetics SC Geriatrics & Gerontology; Public, Environmental & Occupational Health; General & Internal Medicine; Nutrition & Dietetics GA BJT85 UT WOS:000267149000028 ER PT B AU Merikangas, KR Knight, E AF Merikangas, Kathleen Ries Knight, Erin BE NolenHoeksema, S Hilt, LM TI The Epidemiology of Depression in Adolescents SO HANDBOOK OF DEPRESSION IN ADOLESCENTS LA English DT Article; Book Chapter ID DSM-III-R; NATIONAL-COMORBIDITY-SURVEY; GREAT SMOKY MOUNTAINS; MENTAL-HEALTH-SERVICES; PSYCHIATRIC-DISORDERS; MAJOR DEPRESSION; BIPOLAR SPECTRUM; YOUNG-ADULTS; BIRTH COHORT; RISK-FACTORS C1 [Merikangas, Kathleen Ries; Knight, Erin] NIMH, Bethesda, MD 20892 USA. RP Merikangas, KR (reprint author), NIMH, Bethesda, MD 20892 USA. NR 88 TC 7 Z9 7 U1 1 U2 1 PU ROUTLEDGE PI LONDON PA 11 NEW FETTER LANE, LONDON EC4P 4EE, ENGLAND BN 978-1-136-67586-7; 978-0-8058-6235-5 PY 2009 BP 53 EP 73 PG 21 WC Psychology, Clinical; Psychology, Developmental; Psychiatry SC Psychology; Psychiatry GA BA1WQ UT WOS:000333146100004 ER PT B AU de Falco, S Venuti, P Esposito, G Bornstein, MH AF de Falco, Simona Venuti, Paola Esposito, Gianluca Bornstein, Marc H. BE Jelinek, D Dvorak, G TI Mother-Child and Father-Child Interaction in Families of Children with Down Syndrome SO HANDBOOK OF DOWN SYNDROME RESEARCH SE Neurodevelopmental Diseases Laboratory and Clinical Research Series LA English DT Article; Book Chapter ID EMOTIONAL AVAILABILITY SCALES; TYPICALLY DEVELOPING-CHILDREN; YOUNG-CHILDREN; SYMBOLIC PLAY; ATTACHMENT REPRESENTATIONS; NONVERBAL-COMMUNICATION; INFANT INTERACTION; JOINT ATTENTION; STILL-FACE; PARENTS AB Healthy parent-child interaction is as essential to the early development of children with Down Syndrome as it is for typically developing children. In early childhood, this transaction is largely regulated by reciprocal emotional exchanges between partners. Through their caregiving, parents supply their children with the experiences they need for both physical and psychological growth. Contemporary opinion is that positive emotional sharing is an indispensable frame to effective caregiving of children with an intellectual disability, but at the same time specific cognitive and/or motor impairments may short-circuit the child's ability to understand and exchange emotions. In this chapter we first outline the current findings about parent-child interaction in children with Down Syndrome. Then we report in details the results of two studies about children with Down Syndrome in which we compared mother-child and father-child dyads with respect to some pivotal aspects of parent-child interaction, namely affective quality and play behaviours; for each study, the differences and similarities between mothers and fathers as well as the children's contribution to relationship functioning are presented. The discussion of the findings refer to the theoretical perspective according to which dyadic interactions based on emotional involvement may lead to enhanced cognitive functioning in children with Down Syndrome. Finally, the clinical implications of this framework are discussed. C1 [de Falco, Simona; Venuti, Paola; Esposito, Gianluca] Univ Trent, Dept Cognit Sci & Educ, I-38100 Trento, Italy. [Bornstein, Marc H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP de Falco, S (reprint author), Univ Trent, Dept Cognit Sci & Educ, I-38100 Trento, Italy. NR 97 TC 0 Z9 0 U1 1 U2 9 PU NOVA SCIENCE PUBLISHERS, INC PI HAUPPAUGE PA 400 OSER AVE, STE 1600, HAUPPAUGE, NY 11788-3635 USA BN 978-1-60741-690-6 J9 NEURODEV DIS LAB CLI PY 2009 BP 249 EP 265 PG 17 WC Genetics & Heredity; Psychology, Developmental; Neurosciences; Psychiatry SC Genetics & Heredity; Psychology; Neurosciences & Neurology; Psychiatry GA BMS09 UT WOS:000273435800009 ER PT B AU Charles, N Rivera, J AF Charles, Nicolas Rivera, Juan BE Hagg, R Kohlund, S TI Basophil Granulocytes: Small in Numbers, Mighty in Immune Regulation SO HANDBOOK OF GRANULOCYTES : CLASSIFICATION, TOXIC MATERIALS PRODUCED AND PATHOLOGY SE Human Anatomy and Physiology LA English DT Article; Book Chapter ID LYN-DEFICIENT MICE; CHRONIC ALLERGIC INFLAMMATION; AUTOIMMUNE-DISEASE; MAST-CELLS; T-CELLS; RESPONSES; SYSTEM; ASTHMA; ROLES; PLAY C1 [Charles, Nicolas; Rivera, Juan] NIAMSD, Lab Immune Cell Signaling, NIH, Bethesda, MD 20895 USA. RP Charles, N (reprint author), NIAMSD, Lab Immune Cell Signaling, NIH, Bethesda, MD 20895 USA. NR 29 TC 0 Z9 0 U1 0 U2 0 PU NOVA SCIENCE PUBLISHERS, INC PI HAUPPAUGE PA 400 OSER AVE, STE 1600, HAUPPAUGE, NY 11788-3635 USA BN 978-1-60741-582-4 J9 HUM ANAT PHYSIOL PY 2009 BP 317 EP 324 PG 8 WC Anatomy & Morphology; Physiology SC Anatomy & Morphology; Physiology GA BPC23 UT WOS:000278499700013 ER PT B AU Huang, A Summers, RM AF Huang, Adam Summers, Ronald M. BE Bankman, IN TI Computer Processing Methods for Virtual Endoscopy SO HANDBOOK OF MEDICAL IMAGE PROCESSING AND ANALYSIS, 2ND EDITION LA English DT Article; Book Chapter ID AIDED POLYP DETECTION; TRANSBRONCHIAL NEEDLE ASPIRATION; SURFACE CURVATURE ESTIMATION; CURVED CROSS-SECTIONS; CT-COLONOGRAPHY; COLONIC POLYPS; COLORECTAL POLYPS; SPIRAL-CT; TOMOGRAPHIC COLONOGRAPHY; CENTERLINE EXTRACTION C1 [Huang, Adam; Summers, Ronald M.] NIH, Ctr Clin, Dept Diagnost Radiol, Bethesda, MD 20892 USA. RP Huang, A (reprint author), NIH, Ctr Clin, Dept Diagnost Radiol, Bethesda, MD 20892 USA. NR 113 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA BN 978-0-08-055914-8; 978-0-12-373904-9 PY 2009 BP 833 EP 845 DI 10.1016/B978-012373904-9.50059-3 PG 13 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA BCS43 UT WOS:000311277600055 ER PT B AU Esposito, G Venuti, P de Falco, S Bornstein, MH AF Esposito, G. Venuti, P. de Falco, S. Bornstein, M. H. BE Krause, PH Dailey, TM TI MATERNAL EMOTIONAL AVAILABILITY AND INFANT SMILING AND CRYING AT 5 MONTHS OF AGE SO HANDBOOK OF PARENTING: STYLES, STRESSES AND STRATEGIES SE Family Issues in the 21st Century LA English DT Article; Book Chapter DE Smile; Cry; Emotional Availability ID ATTACHMENT REPRESENTATIONS; MOTHERS; BEHAVIOR; CONTINUITY; GENDER; SCALES; CRIES AB In this observational study, we examined relations of maternal emotional availability with infant smiling and crying, two behaviors that represent infants' principal social communicative functions. Fifty-four mother-infant dyads were analyzed using two independent observation systems: (a) the infant socioemotional behaviors and (b) the Emotional Availability Scales. The amount of infant smiling differentiated dyads with different levels of maternal emotional availability. The more infants smile, the greater the odds that their mothers will be more emotionally available. By contrast, no association for cry was found with maternal emotional availability. These results are consistent with the burgeoning literature on the Emotional Availability construct that stresses the importance of expressed positive emotions as determinants of the quality of mother-infant interaction. C1 [Esposito, G.; Venuti, P.; de Falco, S.] Univ Trent, Dept Cognit Sci & Educ, I-38068 Rovereto, TN, Italy. [Bornstein, M. H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Dept Hlth & Human Serv, Bethesda, MD USA. RP Esposito, G (reprint author), Univ Trent, Dept Cognit Sci & Educ, Via Matteo Del Ben 5, I-38068 Rovereto, TN, Italy. EM gianluca.esposito@unitn.it NR 46 TC 0 Z9 0 U1 0 U2 3 PU NOVA SCIENCE PUBLISHERS, INC PI HAUPPAUGE PA 400 OSER AVE, STE 1600, HAUPPAUGE, NY 11788-3635 USA BN 978-1-60741-766-8 J9 FAM ISS 21ST CENTURY PY 2009 BP 111 EP 123 PG 13 WC Family Studies; Psychology, Developmental SC Family Studies; Psychology GA BNV83 UT WOS:000275677100009 ER PT S AU Frey, AJ Boyce, CA Tarullo, LB AF Frey, Andy J. Boyce, Cheryl Anne Tarullo, Louisa Banks BE Sailor, W Dunlap, G Sugai, G Horner, R TI Integrating a Positive Behavior Support Approach Within Head Start SO HANDBOOK OF POSITIVE BEHAVIOR SUPPORT SE Issues in Clinical Child Psychology LA English DT Article; Book Chapter ID EARLY-CHILDHOOD SETTINGS; YOUNG-CHILDREN; CHALLENGING BEHAVIOR; EARLY INTERVENTION; SCHOOL; PRESCHOOLERS; PREVALENCE; PREVENTION; SERVICES; CLIMATE C1 [Frey, Andy J.] Univ Louisville, Louisville, KY 40292 USA. [Boyce, Cheryl Anne] NIMH, Bethesda, MD USA. RP Frey, AJ (reprint author), Univ Louisville, Louisville, KY 40292 USA. NR 78 TC 4 Z9 4 U1 0 U2 1 PU SPRINGER PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 1574-0471 BN 978-0-387-09631-5 J9 ISSUES CLIN CHILD PS PY 2009 BP 125 EP 148 D2 10.1007/978-0-387-09632-2 PG 24 WC Psychology, Clinical; Education, Special; Psychology, Developmental; Psychology SC Psychology; Education & Educational Research GA BJX48 UT WOS:000267357000006 ER PT J AU Jett, DA Yeung, DT AF Jett, David A. Yeung, David T. BE Gupta, RC TI Strategies to Enhance Medical Countermeasures After the Use of Chemical Warfare Agents on Civilians SO HANDBOOK OF TOXICOLOGY OF CHEMICAL WARFARE AGENTS LA English DT Article; Book Chapter ID INDUCED PULMONARY-FIBROSIS; BAL FLUID; EXPOSURE; SARIN; PYRIDOSTIGMINE; ANTIDOTES; TOXICITY AB The information in this chapter is provided for educational purposes only and does not necessarily represent endorsement by, or an official position of, the National Institute of Neurological Disorders and Stroke or any other Federal agency. C1 [Jett, David A.; Yeung, David T.] NINDS, NIH, NSC, Bethesda, MD 20892 USA. RP Jett, DA (reprint author), NINDS, NIH, NSC, 6001 Execut Blvd,Room 2177,MSC 9527, Bethesda, MD 20892 USA. OI /0000-0001-5692-0170 NR 15 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA BN 9780-0-80-92273-7 PY 2009 BP 889 EP 895 DI 10.1016/B978-012374484-5.00059-6 PG 7 WC Toxicology SC Toxicology GA BFT95 UT WOS:000321306800060 ER PT J AU Harsh, V Meltzer-Brody, S Rubinow, DR Schmidt, PJ AF Harsh, Veronica Meltzer-Brody, Samantha Rubinow, David R. Schmidt, Peter J. TI Reproductive Aging, Sex Steroids, and Mood Disorders SO HARVARD REVIEW OF PSYCHIATRY LA English DT Review DE depression; estrogen; menopause transition ID POSTMENOPAUSAL HORMONE-THERAPY; ESTROGEN REPLACEMENT THERAPY; RANDOMIZED CONTROLLED-TRIAL; LATE MENOPAUSAL TRANSITION; ELEMENT-BINDING PROTEIN; MIDLIFE WOMENS HEALTH; MIDDLE-AGED WOMEN; QUALITY-OF-LIFE; HOT FLASHES; PERIMENOPAUSAL WOMEN AB Epidemiologic studies have documented that the majority of women do not become depressed during the menopause transition. However, recent longitudinal studies suggest that in some women, the events related to the menopause transition could play a role in the onset of depression. In this article we review evidence suggesting a relationship between the menopause transition and depression. Additionally, we describe several findings that suggest a role of ovarian hormones in the onset of these depressions, including the clustering of episodes of depression during the stage of the menopause transition that is accompanied by estradiol withdrawal, and the therapeutic effects of short-term estradiol in depressed perimenopausal women. Finally, we discuss possible causes of affective disturbances during the menopause transition. C1 [Harsh, Veronica; Schmidt, Peter J.] NIMH, Sect Behav Endocrinol, Bethesda, MD 20892 USA. [Meltzer-Brody, Samantha; Rubinow, David R.] Univ N Carolina Chapel Hill Psychiat, Chapel Hill, NC USA. RP Schmidt, PJ (reprint author), NIMH, Sect Behav Endocrinol, 10 Ctr Dr,MSC 1276, Bethesda, MD 20892 USA. EM PeterSchmidt@mail.nih.gov FU Intramural NIH HHS [Z01 MH002865-03] NR 178 TC 23 Z9 24 U1 5 U2 8 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1067-3229 EI 1465-7309 J9 HARVARD REV PSYCHIAT JI Harv. Rev. Psychiatr. PY 2009 VL 17 IS 2 BP 87 EP 102 AR PII 910510948 DI 10.1080/10673220902891877 PG 16 WC Psychiatry SC Psychiatry GA 434SO UT WOS:000265294600003 PM 19373618 ER PT J AU Persky, S McBride, CM AF Persky, Susan McBride, Colleen M. TI Immersive Virtual Environment Technology: A Promising Tool for Future Social and Behavioral Genomics Research and Practice SO HEALTH COMMUNICATION LA English DT Article ID REALITY; SUSCEPTIBILITY; COMMUNICATION; PERFORMANCE; PSYCHOLOGY; FEEDBACK; SMOKERS AB Social and behavioral research needs to get started now if scientists are to direct genomic discoveries to address pressing public health problems. Advancing social and behavioral science will require innovative and rigorous communication methodologies that move researchers beyond reliance on traditional tools and their inherent limitations. One such emerging research tool is immersive virtual environment technology (virtual reality), a methodology that gives researchers the ability to maintain high experimental control and mundane realism of scenarios; portray and manipulate complex, abstract objects and concepts; and implement innovative implicit behavioral measurement. This report suggests the role that immersive virtual environment technology can play in furthering future research in genomics-related education, decision making, test intentions, behavior change, and health-care provider behaviors. Practical implementation and challenges are also discussed. C1 [Persky, Susan; McBride, Colleen M.] NHGRI, Social & Behav Res Branch, Bethesda, MD 20892 USA. RP Persky, S (reprint author), NHGRI, Social & Behav Res Branch, 31 Ctr Dr,Bldg 31,Rm B1B54D, Bethesda, MD 20892 USA. EM perskys@mail.nih.gov FU Intramural NIH HHS [Z99 HG999999] NR 27 TC 9 Z9 9 U1 1 U2 4 PU LAWRENCE ERLBAUM ASSOC INC-TAYLOR & FRANCIS PI PHILADELPHIA PA 325 CHESTNUT STREET, STE 800, PHILADELPHIA, PA 19106 USA SN 1041-0236 J9 HEALTH COMMUN JI Health Commun. PY 2009 VL 24 IS 8 BP 677 EP 682 DI 10.1080/10410230903263982 PG 6 WC Communication; Health Policy & Services SC Communication; Health Care Sciences & Services GA 557CA UT WOS:000274644600001 PM 20183376 ER PT J AU Han, PKJ Moser, RP Klein, WMP Beckjord, EB Dunlavy, AC Hesse, BW AF Han, Paul K. J. Moser, Richard P. Klein, William M. P. Beckjord, Ellen Burke Dunlavy, Andrea C. Hesse, Bradford W. TI Predictors of Perceived Ambiguity About Cancer Prevention Recommendations: Sociodemographic Factors and Mass Media Exposures SO HEALTH COMMUNICATION LA English DT Article ID SCREENING MAMMOGRAPHY; BREAST-CANCER; DECISION-MAKING; RISK; WOMEN; INFORMATION; COVERAGE; NEWS; COMMUNICATION; PERCEPTIONS AB Cancer prevention recommendations reaching the public today are often ambiguous-that is, of uncertain reliability, credibility, or adequacy-yet little is known about the factors that influence public perceptions of this ambiguity. We used data from the 2005 Health Information National Trends Survey, conducted by the U.S. National Cancer Institute, to explore how sociodemographic characteristics and self-reported mass media exposures relate to perceptions of ambiguity regarding recommendations for the prevention of colon, skin, and lung cancer. Various sociodemographic characteristics (age, education, race) and mass media exposures (television, radio, Internet, health news) were found to be associated with perceived ambiguity about cancer prevention recommendations, and many of these associations varied by cancer type. These findings have important implications for future health communication research and practice. C1 [Han, Paul K. J.] NCI, Outcomes Res Branch, Div Canc Control & Populat Sci, Rockville, MD 20892 USA. [Klein, William M. P.] Univ Pittsburgh, Dept Psychol, Pittsburgh, PA 15260 USA. [Beckjord, Ellen Burke] RAND Corp, Pittsburgh, PA USA. [Dunlavy, Andrea C.] Univ Washington, Sch Publ Hlth, Seattle, WA 98195 USA. RP Han, PKJ (reprint author), NCI, Outcomes Res Branch, Div Canc Control & Populat Sci, 6130 Execut Blvd,EPN 4091,MSC 7344, Rockville, MD 20892 USA. EM hanp@mail.nih.gov OI Han, Paul/0000-0003-0165-1940; Hesse, Bradford/0000-0003-1142-1161 FU Intramural NIH HHS [Z99 HG999999] NR 38 TC 13 Z9 14 U1 1 U2 11 PU LAWRENCE ERLBAUM ASSOC INC-TAYLOR & FRANCIS PI PHILADELPHIA PA 325 CHESTNUT STREET, STE 800, PHILADELPHIA, PA 19106 USA SN 1041-0236 J9 HEALTH COMMUN JI Health Commun. PY 2009 VL 24 IS 8 BP 764 EP 772 DI 10.1080/10410230903242242 PG 9 WC Communication; Health Policy & Services SC Communication; Health Care Sciences & Services GA 557CA UT WOS:000274644600010 PM 20183385 ER PT J AU Schwartz, MD Valdimarsdottir, HB DeMarco, TA Peshkin, BN Lawrence, W Rispoli, J Brown, K Isaacs, C O'Neill, S Shelby, R Grumet, SC McGovern, MM Garnett, S Bremer, H Leaman, S O'Mara, K Kelleher, S Komaridis, K AF Schwartz, Marc D. Valdimarsdottir, Heiddis B. DeMarco, Tiffani A. Peshkin, Beth N. Lawrence, William Rispoli, Jessica Brown, Karen Isaacs, Claudine O'Neill, Suzanne Shelby, Rebecca Grumet, Sherry C. McGovern, Margaret M. Garnett, Sarah Bremer, Heather Leaman, Suzanne O'Mara, Kathryn Kelleher, Sarah Komaridis, Kathryn TI Randomized Trial of a Decision Aid for BRCA1/BRCA2 Mutation Carriers: Impact on Measures of Decision Making and Satisfaction SO HEALTH PSYCHOLOGY LA English DT Article DE BRCA1; BRCA2; decision aid; risk reducing mastectomy ID CONTRALATERAL PROPHYLACTIC MASTECTOMY; BREAST-CANCER; BRCA2 MUTATION; WOMEN; KNOWLEDGE; SUPPORT; SURGERY; SUSCEPTIBILITY; OOPHORECTOMY; CONFLICT AB Objective: Genetic testing is increasingly part of routine clinical care for women with a family history of breast cancer. Given their substantially elevated risk for breast cancer, BRCA1/BRCA2 mutation carriers must make the difficult decision whether or not to opt for risk reducing mastectomy. To help BRCA1/2 carriers make this decision, the authors developed a computer-based interactive decision aid that was tested against usual care in a randomized controlled trial. Design: After the completion of genetic counseling, 214 female (aged 21-75) BRCA1/BRCA2 mutation carriers were randomized to Usual Care (UC; N = 114) or Usual Care plus Decision Aid (DA; N = 100) arms. UC participants received no additional intervention. DA participants were sent the CD-ROM DA to view at home. Main Outcome Measures: The authors measured final management decision, decisional conflict, decisional satisfaction, and receipt of risk reducing mastectomy at 1-, 6-, and 12-months postrandomization. Results: Longitudinal analyses revealed that the DA was effective among carriers who were initially undecided about how to manage their breast cancer risk. Within this group, the DA led to an increased likelihood of reaching a management decision (OR = 3.09, 95% CI = 1.62, 5.90; p < .001), decreased decisional conflict (B = -.46, z = -3.1, p < .002), and increased satisfaction (B = .27, z = 3.1, p = .002) compared to UC. Among carriers who had already made a management decision by the time of randomization, the DA had no benefit relative to UC. Conclusion: These results demonstrate that BRCA1/BRCA2 mutation carriers who are having difficulty making a breast cancer risk management decision can benefit from adjunct decision support. C1 [Schwartz, Marc D.; DeMarco, Tiffani A.; Peshkin, Beth N.; Lawrence, William; Isaacs, Claudine; Garnett, Sarah; Bremer, Heather; Leaman, Suzanne; O'Mara, Kathryn; Kelleher, Sarah; Komaridis, Kathryn] Georgetown Univ, Lombardi Comprehens Canc Ctr, Dept Oncol, Canc Control Program, Washington, DC 20007 USA. [Schwartz, Marc D.; DeMarco, Tiffani A.; Peshkin, Beth N.; Lawrence, William; Isaacs, Claudine; Garnett, Sarah; Bremer, Heather; Leaman, Suzanne; O'Mara, Kathryn; Kelleher, Sarah; Komaridis, Kathryn] Georgetown Univ, Lombardi Comprehens Canc Ctr, Dept Oncol, Fisher Ctr Familial Canc Res, Washington, DC 20007 USA. [Valdimarsdottir, Heiddis B.] Mt Sinai Sch Med, Dept Oncol Sci, New York, NY USA. [Rispoli, Jessica; Brown, Karen; McGovern, Margaret M.] Mt Sinai Sch Med, Dept Genet & Genom Sci, New York, NY USA. [O'Neill, Suzanne] NHGRI, Social & Behav Res Branch, NIH, Bethesda, MD 20892 USA. [Shelby, Rebecca] Duke Univ, Dept Psychiat & Behav Sci, Durham, NC 27706 USA. RP Schwartz, MD (reprint author), Georgetown Univ, Lombardi Comprehens Canc Ctr, Dept Oncol, Canc Control Program, 3300 Whitehaven St NW,Suite 4100, Washington, DC 20007 USA. EM schwartm@georgetown.edu OI Garnett, Sarah/0000-0001-7552-0789 FU National Cancer Institute [RO1 CA01846] FX IRB approval was granted for this study and all participants provided informed consent. This research was supported by National Cancer Institute Grant RO1 CA01846. NR 36 TC 47 Z9 47 U1 0 U2 6 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0278-6133 J9 HEALTH PSYCHOL JI Health Psychol. PD JAN PY 2009 VL 28 IS 1 BP 11 EP 19 DI 10.1037/a0013147 PG 9 WC Psychology, Clinical; Psychology SC Psychology GA 394EA UT WOS:000262427200002 PM 19210013 ER PT J AU Kim, KHC Bursac, Z DiLillo, V White, DB West, DS AF Kim, Karen Hye-cheon Bursac, Zoran DiLillo, Vicki White, Della Brown West, Delia Smith TI Stress, Race, and Body Weight SO HEALTH PSYCHOLOGY LA English DT Article DE stress; race; body weight; obesity; health disparities ID PERCEIVED STRESS; SOCIOECONOMIC-STATUS; AFRICAN-AMERICANS; EATING INVENTORY; LOSS MAINTENANCE; UNITED-STATES; WOMEN; HEALTH; OBESITY; ADULTS AB Objective: Stress has been identified as a significant factor in health and in racial/ethnic health disparities. A potential mediator in these relationships is body weight. Design: Cross-sectional and longitudinal relationships between stress, race, and body weight were examined in an ethnically diverse sample of overweight and obese women with Type 2 diabetes (n = 217) enrolled in a behavioral weight loss program. Main Outcome Measures: Stress (Perceived Stress Scale) was assessed at baseline only and body weight (body mass index) was assessed at baseline and 6 months. Results: Stress was not related to baseline body weight. With every 1 unit lower scored on the baseline stress measure, women lost 0.10 kg +/- .04 more at 6 months (p < .05). When women were divided into tertiles based on baseline stress scores, those in the lowest stress group had significantly greater weight loss (5.2 kg +/- 4.9) compared with those in the highest stress group (3.0 kg +/- 4.0) (p < .05). There was a trend for African Americans to report higher levels of stress (20.7 +/- 8.8) than Whites (18.3 +/- 8.3) (p = .08). Conclusion: The association between higher stress and diminished weight loss has implications for enhancing weight loss programs for women with Type 2 diabetes. C1 [Kim, Karen Hye-cheon; West, Delia Smith] Univ Arkansas Med Sci, Dept Hlth Behav & Hlth Educ, Little Rock, AR 72202 USA. [Bursac, Zoran] Univ Arkansas Med Sci, Dept Biostat, Little Rock, AR 72202 USA. [DiLillo, Vicki] Ohio Wesleyan Univ, Dept Psychol, Delaware, OH USA. [White, Della Brown] NHGRI, NIH, Bethesda, MD 20892 USA. RP Kim, KHC (reprint author), Univ Arkansas Med Sci, Fay W Boozman Coll Publ Hlth, 4301 W Markham 820, Little Rock, AR 72202 USA. EM khk@uarns.edu FU NIDDK NIH HHS [R01 DK054041] NR 41 TC 13 Z9 13 U1 2 U2 3 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0278-6133 J9 HEALTH PSYCHOL JI Health Psychol. PD JAN PY 2009 VL 28 IS 1 BP 131 EP 135 DI 10.1037/a0012648 PG 5 WC Psychology, Clinical; Psychology SC Psychology GA 394EA UT WOS:000262427200016 PM 19210027 ER PT J AU Yoon, JC Shiina, M Ahlenstiel, G Rehermann, B AF Yoon, Joo Chun Shiina, Musaaki Ahlenstiel, Golo Rehermann, Barbara TI Natural Killer Cell Function Is Intact After Direct Exposure to Infectious Hepatitis C Virions SO HEPATOLOGY LA English DT Article ID VIRUS ENVELOPE PROTEIN; HUMAN NK CELLS; HUMAN CYTOMEGALOVIRUS; HEPATOMA-CELLS; CORE PROTEIN; CLASS-I; CYTOTOXICITY; CULTURE; RESPONSES; REPLICATION AB Although hepatitis C virus (HCV) has been shown to readily escape from virus-specific T and B cell responses, its effects on natural killer (NK) cells are less clear. Based on two previous reports that recombinant, truncated HCV E2 protein inhibits NK cell functions via crosslinking of CD81, it is now widely believed that HCV impairs NK cells as a means to establish persistence. However, the relevance of these findings has not been verified with HCV E2 expressed as part of intact virions. Here we employed a new cell culture system generating infectious HCV particles with genotype I a and 2a structural proteins, and analyzed direct and indirect effects of HCV on human NK cells. Antibody-mediated crosslinking of CD16 stimulated and antibody-mediated crosslinking of CD81 inhibited NK cell activation and interferon gamma (IFN-gamma) production. However, infectious HCV itself had no effect even at titers that far exceeded HCV RNA and protein concentrations in the blood of infected patients. Consistent with these results, anti-CD81 but not HCV inhibited NK cell cytotoxicity. These results were independent of the presence or absence of HCV-binding antibodies and independent of the presence or absence of other peripheral blood mononuclear cell populations. Conclusion: HCV la or 2a envelope proteins do not modulate NK cell function when expressed as a part of infectious HCV particles. Without direct inhibition by HCV, NK cells may become activated by cytokines in acute HCV infection and contribute to infection outcome and disease pathogenesis. (HEPATOLOGY 2009;49:12-21.) C1 [Yoon, Joo Chun; Shiina, Musaaki; Ahlenstiel, Golo; Rehermann, Barbara] NIDDK, Immunol Sect, Liver Dis Branch, NIH, Bethesda, MD 20892 USA. RP Rehermann, B (reprint author), NIDDK, Immunol Sect, Liver Dis Branch, NIH, 10 Ctr Dr,Room 9B16, Bethesda, MD 20892 USA. EM rehermann@nih.gov RI Yoon, Joo Chun/D-3675-2012; OI Yoon, Joo Chun/0000-0001-9395-8418; Ahlenstiel, Golo/0000-0003-0026-1457 FU National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health; Deutsche Forschungsgemeinschaft (DFG), Bonn, Germany [AH173/1-1] FX Supported by the National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health intramural research program. G.A. was supported by grant AH173/1-1 from Deutsche Forschungsgemeinschaft (DFG), Bonn, Germany. NR 37 TC 69 Z9 73 U1 0 U2 3 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD JAN PY 2009 VL 49 IS 1 BP 12 EP 21 DI 10.1002/hep.22624 PG 10 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 389WX UT WOS:000262127400005 PM 19085909 ER PT J AU El-Serag, HB Engels, EA Landgren, O Chiao, E Henderson, L Amaratunge, HC Giordano, TP AF El-Serag, Hashem B. Engels, Eric A. Landgren, Ola Chiao, Elizabeth Henderson, Louise Amaratunge, Harshinie C. Giordano, Thomas P. TI Risk of Hepatobiliary and Pancreatic Cancers After Hepatitis C Virus Infection: A Population-Based Study of US Veterans SO HEPATOLOGY LA English DT Article ID ADMINISTRATION MEDICAL SYSTEM; UNITED-STATES; INTRAHEPATIC CHOLANGIOCARCINOMA; EXTRAHEPATIC CHOLANGIOCARCINOMA; LIVER; CIRRHOSIS; ASCERTAINMENT; PREVALENCE; CARCINOMA; AFFAIRS AB Hepatitis C virus (HCV) may increase the risk of hepatopancreaticobiliary tumors other than hepatocellular carcinoma (HCC). Previous case control studies indicated a possible association between HCV and intrahepatic cholangiocarcinoma (ICC). Little is known about the association between HCV and extrahepatic cholangiocarcinoma (ECC) or pancreatic cancer. We conducted a cohort study including 146,394 HCV-infected and 572,293 HCV-uninfected patients who received care at Veterans Affairs health care facilities. Patients with two visits between 1996 and 2004 with HCV infection were included, as were up to four matched HCV-uninfected subjects for each HCV-infected subject. Risks of ICC, ECC, pancreatic cancer, and HCC were assessed using proportional hazards regression. In the 1.37 million person-years of follow-up, which began 6 months after the baseline visit, there were 75 cases of ECC, 37 cases of ICC, 617 cases of pancreatic cancer, and 1679 cases of HCC. As expected, the risk of HCC associated with HCV was very high (hazard ratio [HR], 15.09; 95% confidence interval [95% CI], 13.44, 16.94). Risk for ICC was elevated with HCV infection 2.55; 1.31, 4.95), but risk for ECC was not significantly increased (1.50; 0.60, 1.85). Adjustments for cirrhosis, diabetes, inflammatory bowel disease, hepatitis B, alcoholism, and alcoholic liver disease did not reduce the risk for ICC below twofold. The risk of pancreatic cancer was slightly elevated (1.23; 1.02, 1.49), but was attenuated after adjusting for alcohol use, pancreatitis, and other variables. Conclusions. Findings indicated that HCV infection conferred a more than twofold elevated risk of ICC. Absence of an association with ECC was consistent in adjusted and unadjusted models. A significant association with pancreatic cancer was erased by alcohol use and other variables. (HEPATOLOGY 2009;49:116-123.) C1 [El-Serag, Hashem B.; Chiao, Elizabeth; Henderson, Louise; Amaratunge, Harshinie C.; Giordano, Thomas P.] Baylor Coll Med, Dept Med, Houston, TX 77030 USA. [El-Serag, Hashem B.; Chiao, Elizabeth; Henderson, Louise; Amaratunge, Harshinie C.; Giordano, Thomas P.] Dept Vet Affairs Med Ctr, Hlth Serv Res & Dev Serv, Houston Ctr Qual Care & Utilizat Studies, Houston, TX USA. [Engels, Eric A.; Landgren, Ola] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD USA. RP El-Serag, HB (reprint author), Houston VA Med Ctr 152, 2002 Holcombe Blvd, Houston, TX 77030 USA. EM hasheme@bcm.tmc.edu FU National Cancer Institute, National Institutes of Health; Michael E. DeBakey Veterans Affairs Medical Center; Department of Veterans Affairs, Houston; NIH [K24 DK078154-01] FX Supported by the Intramural Program of the National Cancer Institute, National Institutes of Health, and the Michael E. DeBakey Veterans Affairs Medical Center, Department of Veterans Affairs, Houston, TX. Dr. El-Sang is supported by NIH grant K24 DK078154-01. NR 25 TC 134 Z9 141 U1 0 U2 1 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD JAN PY 2009 VL 49 IS 1 BP 116 EP 123 DI 10.1002/hep.22606 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 389WX UT WOS:000262127400016 PM 19085911 ER PT J AU Brinker, AD Wassel, RT Lyndly, J Serrano, J Avigan, M Lee, WM Seeff, LB AF Brinker, Allen D. Wassel, Ronald T. Lyndly, Jenna Serrano, Jose Avigan, Mark Lee, William M. Seeff, Leonard B. TI Telithromycin-Associated Hepatotoxicity: Clinical Spectrum and Causality Assessment of 42 Cases SO HEPATOLOGY LA English DT Article ID FULMINANT HEPATIC-FAILURE; INDUCED LIVER-INJURY; ADVERSE REACTIONS; CLARITHROMYCIN; THERAPY; DISEASE; DRUGS AB Telithromycin is the first of a new class of ketolide antibiotics with increased activity against penicillin-resistant and erythromycin-resistant pneumococci. This agent received approval by the United States Food and Drug Administration (FDA) in 2004 for treatment of upper and lower respiratory infections. Following market introduction, spontaneous reports of telithromycin-associated hepatotoxicity, including frank liver failure, were received. To address these reports, an ad hoc group with expertise in spontaneous adverse events reporting and experience in evaluating drug-induced liver injury was formed, including members of the FDA, other federal agencies, and academia. The primary objective of this group was to adjudicate case reports of hepatic toxicity for causal attribution to telithromycin. After an initial screening of all cases of liver injury associated with telithromycin reported to FDA as of April 2006 by one of the authors, 42 cases were comprehensively reviewed and adjudicated. Five cases included a severe outcome of either death (n = 4) or liver transplantation (n = 1); more than half were considered highly likely or probable in their causal association with telithromycin. Typical clinical features were: short latency (median, 10 days) and abrupt onset of fever, abdominal pain, and jaundice, sometimes with the presence of ascites; even in cases that resolved. Concurrence in assignment of causality increased after agreement on definitions of categories and interactive discussions. Conclusion: Telithromycin is a rare cause of drug-induced liver injury that may have a distinctive clinical signature and associated high mortality rate. Consensus for attribution of liver injury to a selected drug exposure by individual experts can be aided by careful definition of terminology and discussion. (HEPATOLOGY 2009;49:250-257.) C1 [Brinker, Allen D.; Wassel, Ronald T.; Lyndly, Jenna; Avigan, Mark] US FDA, Ctr Drug Evaluat & Res, Off Surveillance & Epidemiol, Silver Spring, MD 20993 USA. [Serrano, Jose; Seeff, Leonard B.] NIDDKD, NIH, Liver Dis Res Branch, Div Digest Dis & Nutr, Bethesda, MD 20892 USA. [Lee, William M.] Univ Texas SW Med Ctr Dallas, Meredith Mosley Chair Liver Dis, Dallas, TX 75390 USA. RP Brinker, AD (reprint author), US FDA, Ctr Drug Evaluat & Res, Off Surveillance & Epidemiol, 10903 New Hampshire Ave,Bldg 22, Silver Spring, MD 20993 USA. EM allen.brinker@fda.hhs.gov NR 44 TC 55 Z9 60 U1 2 U2 4 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD JAN PY 2009 VL 49 IS 1 BP 250 EP 257 DI 10.1002/hep.22620 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 389WX UT WOS:000262127400029 PM 19085949 ER PT J AU Snyder, JS Radik, R Wojtowicz, JM Cameron, HA AF Snyder, Jason S. Radik, Ruvim Wojtowicz, J. Martin Cameron, Heather A. TI Anatomical Gradients of Adult Neurogenesis and Activity: Young Neurons in the Ventral Dentate Gyrus Are Activated by Water Maze Training SO HIPPOCAMPUS LA English DT Article DE dorsal; spatial memory; hippocampus; immediate-early gene; c-fos ID GENERATED GRANULE CELLS; HIPPOCAMPAL NEUROGENESIS; SPATIAL MEMORY; SYNAPTIC PLASTICITY; ENTORHINAL CORTEX; MESSENGER-RNA; RAT; DORSAL; EXPRESSION; DEPRESSION AB Hippocampal function varies in a subregion-specific fashion: spatial processing is thought to rely on the dorsal hippocampus, whereas anxiety-related behavior relies more on the ventral hippocampus. During development, neurogenesis in the dentate gyrus (DG) proceeds along ventral to dorsal as well as suprapyramidal to infrapyramidal gradients, but it is unclear whether regional differences in neurogenesis are maintained in adulthood. Moreover, it is unknown whether young neurons in the adult exhibit subregion-specific patterns of activation. We therefore examined the magnitude of neurogenesis and the activation of young and mature granule cells in DG subregions in adult rats that learned a spatial water maze task, swam with no platform, or were left untouched. We found that both adult neurogenesis and granule cell activation, as defined by c-fos expression in the granule cell population as a whole, were higher in the dorsal than the ventral DG. In contrast, c-fos expression in adult-born granule cells, identified by PSA-NCAM or location in the subgranular zone, occurred at a higher rate in the opposite subregion, the ventral DG. Interestingly, c-fos expression in the entire granule cell population was equivalent in water maze-trained rats and swim control rats, but was increased in the young granule cells only in the learning condition. These results provide new evidence that hippocampally-relevant experience activates young and mature neurons in different DG subregions and with different experiential specificity, and suggest that adult-born neurons may play a specific role in anxiety-related behavior or other nonspatial aspects of hippocampal function. (C) 2008 Wiley-Liss, Inc. C1 [Snyder, Jason S.; Cameron, Heather A.] NIH, Bethesda, MD 20892 USA. [Snyder, Jason S.; Radik, Ruvim; Wojtowicz, J. Martin] Univ Toronto, Dept Physiol, Toronto, ON, Canada. RP Snyder, JS (reprint author), NIH, Bldg 35-3C911,MSC3718, Bethesda, MD 20892 USA. EM snyderjason@mail.nih.gov RI Snyder, Jason/F-3435-2011; Cameron, Heather/E-6221-2011; OI Cameron, Heather/0000-0002-3245-5777; Snyder, Jason/0000-0002-5509-0272 FU National Institute of Mental Health [Z01-MH002784]; Ontario Graduate Scholarship; CIHR; National Institutes of Health FX Grant sponsor: National Institute of Mental Health; Grant number: Z01-MH002784; Grant sponsors: Ontario Graduate Scholarship, CIHR grant, The Intramural Program of the National Institutes of Health. NR 75 TC 96 Z9 96 U1 0 U2 4 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1050-9631 J9 HIPPOCAMPUS JI Hippocampus PY 2009 VL 19 IS 4 BP 360 EP 370 DI 10.1002/hipo.20525 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 435KI UT WOS:000265342400004 PM 19004012 ER PT J AU Snyder, JS Glover, LR Sanzone, KM Kamhi, JF Cameron, HA AF Snyder, Jason S. Glover, Lucas R. Sanzone, Kaitlin M. Kamhi, J. Frances Cameron, Heather A. TI The Effects of Exercise and Stress on the Survival and Maturation of Adult-Generated Granule Cells SO HIPPOCAMPUS LA English DT Article DE dentate gyrus; running; adult neurogenesis; immediate-early gene; Arc ID MOUSE DENTATE GYRUS; RUNNING WHEEL EXERCISES; CHRONIC MILD STRESS; HIPPOCAMPAL NEUROGENESIS; SYNAPTIC PLASTICITY; VOLUNTARY EXERCISE; NEURONAL DIFFERENTIATION; RAT HIPPOCAMPUS; GENE-EXPRESSION; PROLIFERATION AB Stress strongly inhibits proliferation of granule cell precursors in the adult dentate gyros, whereas voluntary running has the opposite effect. Few studies, however, have examined the possible effects of these environmental manipulations on the maturation and survival of young granule cells. We examined the number of surviving granule cells and the proportion of young neurons that were functionally mature, as defined by seizure-induced immediate-early gene (IEG) expression, in 14- and 21-day-old granule cells in mice that were given access to a running wheel, restrained daily for 2 h, or given no treatment during this period. Treatments began 2 days after BrdU injection, to isolate effects on survival from those on cell proliferation. We found a large increase in granule cell survival in running mice when compared with controls at both time points. In addition, running increased the proportion of granule cells expressing the IEG Arc in response to seizures, suggesting that it speeds incorporation into circuits, i.e., functional maturation. Stressed mice showed no change in Arc expression, compared with control animals, but, surprisingly, showed a transient increase in survival of 14-day-old granule cells, which was gone 7 days later. Examination of cell proliferation, using the endogenous mitotic marker PCNA showed an increase in cell proliferation after 12 days of running but not after 19 days of running. The number of proliferating cells was unchanged 24 h after the 12th or 19th episode of daily restraint stress. These findings demonstrate that running has strong effects on survival and maturation of young granule cells as well as their birth and that stress can have positive but short-lived effects on granule cell survival. Published 2009 Wiley-Liss, Inc.(dagger) C1 [Snyder, Jason S.; Glover, Lucas R.; Sanzone, Kaitlin M.; Kamhi, J. Frances; Cameron, Heather A.] NIMH, Unit Neuroplast, Mood & Anxiety Disorders Program, NIH, Bethesda, MD 20892 USA. RP Snyder, JS (reprint author), NIMH, Unit Neuroplast, Mood & Anxiety Disorders Program, NIH, Bldg 35-3C911,MSC3718, Bethesda, MD 20892 USA. EM snyderjason@mail.nih.gov RI Snyder, Jason/F-3435-2011; Cameron, Heather/E-6221-2011; OI Cameron, Heather/0000-0002-3245-5777; Kamhi, J. Frances/0000-0002-3806-0506; Snyder, Jason/0000-0002-5509-0272 FU National Institute of Mental Health [Z01-MH002784] FX Grant sponsor: Intramural Program of the National Institute of Mental Health; Grant number: Z01-MH002784; Grant sponsor: Intramural Program of the National Institutes of Health NR 59 TC 82 Z9 87 U1 0 U2 6 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1050-9631 J9 HIPPOCAMPUS JI Hippocampus PY 2009 VL 19 IS 10 BP 898 EP 906 DI 10.1002/hipo.20552 PG 9 WC Neurosciences SC Neurosciences & Neurology GA 508VP UT WOS:000270965800003 PM 19156854 ER PT J AU Stranahan, AM Lee, K Martin, B Maudsley, S Golden, E Cutler, RG Mattson, MP AF Stranahan, Alexis M. Lee, Kim Martin, Bronwen Maudsley, Stuart Golden, Erin Cutler, Roy G. Mattson, Mark P. TI Voluntary Exercise and Caloric Restriction Enhance Hippocampal Dendritic Spine Density and BDNF Levels in Diabetic Mice SO HIPPOCAMPUS LA English DT Article DE diabetes; dendrite; hippocampus; exercise; dietary restriction ID MEDIATED SYNAPTIC PLASTICITY; INSULIN-RESISTANCE SYNDROME; NEUROTROPHIC FACTOR; DIETARY RESTRICTION; COGNITIVE FUNCTION; DENTATE GYRUS; GROWTH-FACTOR; GLUCOSE-METABOLISM; ENERGY-METABOLISM; CORTICAL-NEURONS AB Diabetes may adversely affect cognitive function, but the underlying mechanisms are unknown. To investigate whether manipulations that enhance neurotrophin levels will also restore neuronal structure and function in diabetes, we examined the effects of wheel running and dietary energy restriction on hippocampal neuron morphology and brain-derived neurotrophic factor (BDNF) levels in db/db mice, a model of insulin resistant diabetes. Running wheel activity, caloric restriction, or the combination of the two treatments increased levels of BDNF in the hippocampus of db/db mice. Enhancement of hippocampal BDNF was accompanied by increases in dendritic spine density on the secondary and tertiary dendrites of dentate granule neurons. These studies suggest that diabetes exerts detrimental effects on hippocampal structure, and that this state can be attenuated by increasing energy expenditure and decreasing energy intake. Published 2009 Wiley-Liss, Inc.(dagger) C1 [Stranahan, Alexis M.; Lee, Kim; Martin, Bronwen; Golden, Erin; Cutler, Roy G.; Mattson, Mark P.] NIA, Cellular & Mol Neurosci Sect, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA. [Stranahan, Alexis M.] Princeton Univ, Dept Psychol, Princeton, NJ 08544 USA. [Maudsley, Stuart] NIA, Receptor Pharmacol Unit, Neurosci Lab, Baltimore, MD 21224 USA. [Mattson, Mark P.] Johns Hopkins Univ, Dept Neurosci, Baltimore, MD USA. RP Mattson, MP (reprint author), NIA, Cellular & Mol Neurosci Sect, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA. EM mattsonm@grc.nia.nih.gov RI Mattson, Mark/F-6038-2012; OI Lee, Kim/0000-0002-5675-1896 FU NIH NRSA F31 [AG024690-03]; National Institute on Aging FX Grant sponsor: NIH NRSA F31; Grant number: AG024690-03; Grant sponsor: National Institute on Aging Intramural Research Program. NR 46 TC 136 Z9 138 U1 0 U2 5 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1050-9631 J9 HIPPOCAMPUS JI Hippocampus PY 2009 VL 19 IS 10 BP 951 EP 961 DI 10.1002/hipo.20577 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 508VP UT WOS:000270965800008 PM 19280661 ER PT B AU Cargill, V Fenton, KA AF Cargill, Victoria Fenton, Kevin A. BE Stone, V Ojikutu, B Rawlings, MK Smith, KY TI The Epidemiology, Prevention, and Control of HIV/AIDS Among African Americans SO HIV/AIDS IN U.S. COMMUNITIES OF COLOR LA English DT Article; Book Chapter ID HUMAN-IMMUNODEFICIENCY-VIRUS; ACTIVE ANTIRETROVIRAL THERAPY; RISKY SEXUAL-BEHAVIOR; HIV-INFECTED ADULTS; UNITED-STATES; MEDICAL-CARE; SERVICES UTILIZATION; RACIAL DISPARITIES; SOCIAL-CONTEXT; HEALTH C1 [Cargill, Victoria] NIH, Off AIDS Res, Bethesda, MD 20892 USA. [Fenton, Kevin A.] Ctr Dis Control & Prevent, Natl Ctr HIV AIDS Viral Hepatitis STD & TB Preven, Atlanta, GA USA. RP Cargill, V (reprint author), NIH, Off AIDS Res, 5635 Fishers Lane,Suite 4000, Bethesda, MD 20892 USA. EM vc52x@nih.gov NR 66 TC 2 Z9 2 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES BN 978-0-387-98151-2 PY 2009 BP 1 EP 21 DI 10.1007/978-0-387-98152-9_1 D2 10.1007/978-0-387-98152-9 PG 21 WC Ethnic Studies; Public, Environmental & Occupational Health; Infectious Diseases SC Ethnic Studies; Public, Environmental & Occupational Health; Infectious Diseases GA BKW34 UT WOS:000269460200001 ER PT B AU Jones, DJ Roberts, GW AF Jones, Dionne J. Roberts, George W. BE Stone, V Ojikutu, B Rawlings, MK Smith, KY TI Substance Abuse, HIV, and Mental Health Issues: Prevention and Treatment Challenges SO HIV/AIDS IN U.S. COMMUNITIES OF COLOR LA English DT Article; Book Chapter ID AFRICAN-AMERICAN WOMEN; ACTIVE ANTIRETROVIRAL THERAPY; HUMAN-IMMUNODEFICIENCY-VIRUS; RISK REDUCTION INTERVENTION; INJECTION-DRUG USERS; PSYCHIATRIC-DISORDERS; UNITED-STATES; DEPRESSIVE SYMPTOMS; POSITIVE PATIENTS; ILLNESS C1 [Jones, Dionne J.] Natl Inst Drug Abuse, Serv Res Branch, Div Epidemiol Serv & Prevent Res, Bethesda, MD 20892 USA. [Roberts, George W.] Ctr Dis Control & Prevent, Div Partnerships & Strateg Alliances, Atlanta, GA USA. RP Jones, DJ (reprint author), Natl Inst Drug Abuse, Serv Res Branch, Div Epidemiol Serv & Prevent Res, Bethesda, MD 20892 USA. EM djones1@nida.nih.gov NR 81 TC 0 Z9 0 U1 2 U2 3 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES BN 978-0-387-98151-2 PY 2009 BP 227 EP 244 DI 10.1007/978-0-387-98152-9_12 D2 10.1007/978-0-387-98152-9 PG 18 WC Ethnic Studies; Public, Environmental & Occupational Health; Infectious Diseases SC Ethnic Studies; Public, Environmental & Occupational Health; Infectious Diseases GA BKW34 UT WOS:000269460200012 ER PT J AU Sahasrabuddhe, VV Vermund, SH AF Sahasrabuddhe, Vikrant V. Vermund, Sten H. BE Mayer, KH Pizer, HF TI Current and future trends: implications for HIV prevention SO HIV PREVENTION: A COMPREHENSIVE APPROACH LA English DT Article; Book Chapter ID SEXUALLY-TRANSMITTED INFECTIONS; IMMUNODEFICIENCY-VIRUS TYPE-1; RANDOMIZED CONTROLLED-TRIAL; INJECTION-DRUG USERS; SUB-SAHARAN AFRICA; ANTIRETROVIRAL THERAPY; DEVELOPING-COUNTRIES; COST-EFFECTIVENESS; MALE CIRCUMCISION; RISK BEHAVIORS C1 [Sahasrabuddhe, Vikrant V.] Vanderbilt Univ, Sch Med, Dept Pediat, Div Infect Dis, Nashville, TN 37235 USA. [Sahasrabuddhe, Vikrant V.] Inst Global Hlth, Vanderbilt India Programs, Nashville, TN USA. [Sahasrabuddhe, Vikrant V.] Vanderbilt Meharry Framework Program Global Hlth, Nashville, TN USA. [Vermund, Sten H.] Vanderbilt Univ, Sch Med, Nashville, TN 37235 USA. [Vermund, Sten H.] Vanderbilt Univ, Sch Med, Inst Global Hlth, Nashville, TN 37235 USA. [Vermund, Sten H.] NIAID, NIH, Vaccine Trials & Epidemiol Branch, Div Aids, Bethesda, MD 20892 USA. RP Sahasrabuddhe, VV (reprint author), Vanderbilt Univ, Sch Med, Dept Pediat, Div Infect Dis, Nashville, TN 37235 USA. NR 113 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 978-0-08-092129-7 PY 2009 BP 11 EP 30 PG 20 WC Public, Environmental & Occupational Health; Immunology; Infectious Diseases SC Public, Environmental & Occupational Health; Immunology; Infectious Diseases GA BEK32 UT WOS:000317059400003 ER PT J AU Anderson, DJ AF Anderson, Deborah J. BE Mayer, KH Pizer, HF TI Understanding the biology of HIV-1 transmission: the foundation for prevention SO HIV PREVENTION: A COMPREHENSIVE APPROACH LA English DT Article; Book Chapter ID HUMAN-IMMUNODEFICIENCY-VIRUS; SEXUALLY-TRANSMITTED INFECTIONS; CELL-MEDIATED CYTOTOXICITY; HUMAN CERVICAL TISSUE; FEMALE GENITAL-TRACT; SUB-SAHARAN AFRICA; CD4(+) T-CELLS; VAGINAL TRANSMISSION; MALE CIRCUMCISION; ANTIRETROVIRAL THERAPY C1 [Anderson, Deborah J.] Boston Univ, Sch Med, Dept Microbiol, Boston, MA 02118 USA. [Anderson, Deborah J.] Boston Univ, Sch Med, Dept Obstet & Gynecol, Boston, MA 02118 USA. [Anderson, Deborah J.] WHO, Human Reprod Programme, Geneva, Switzerland. [Anderson, Deborah J.] NIH, Study Sect, Bethesda, MD 20892 USA. RP Anderson, DJ (reprint author), Boston Univ, Sch Med, Dept Microbiol, Boston, MA 02118 USA. NR 122 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 978-0-08-092129-7 PY 2009 BP 31 EP 52 DI 10.1016/B978-0-12-374235-3.00002-9 PG 22 WC Public, Environmental & Occupational Health; Immunology; Infectious Diseases SC Public, Environmental & Occupational Health; Immunology; Infectious Diseases GA BEK32 UT WOS:000317059400004 ER PT J AU Gay, CL Kashuba, AD Cohen, MS AF Gay, Cynthia L. Kashuba, Angela D. Cohen, Myron S. BE Mayer, KH Pizer, HF TI Using antiretrovirals to prevent HIV transmission SO HIV PREVENTION: A COMPREHENSIVE APPROACH LA English DT Article; Book Chapter ID HUMAN-IMMUNODEFICIENCY-VIRUS; SEXUAL RISK BEHAVIOR; NONOCCUPATIONAL POSTEXPOSURE PROPHYLAXIS; TENOFOVIR DISOPROXIL FUMARATE; FEMALE GENITAL-TRACT; HEALTH-CARE WORKERS; RANDOMIZED CONTROLLED-TRIAL; NON-OCCUPATIONAL EXPOSURE; DRUG-RESISTANT VARIANTS; TO-CHILD TRANSMISSION C1 [Gay, Cynthia L.; Cohen, Myron S.] Univ N Carolina, Chapel Hill, NC 27515 USA. [Kashuba, Angela D.] Univ N Carolina, Sch Pharm, Div Pharmacotherapy & Expt Therapeut, Chapel Hill, NC USA. [Kashuba, Angela D.] UNC Ctr AIDS Res Clin Pharmacol & Analyt Chem Cor, Charlotte, NC USA. [Cohen, Myron S.] UNC Div Infect Dis, Charlotte, NC USA. [Cohen, Myron S.] UNC Inst Global Hlth & Infect Dis, Charlotte, NC USA. [Cohen, Myron S.] UNC Ctr AIDS Res, Charlotte, NC USA. [Cohen, Myron S.] NIH Ctr HIV Vaccine Immunol CHAVI, Senior Leadership Grp, Bethesda, MD 20892 USA. [Cohen, Myron S.] NIH HIV Prevent Trials Network HPTN, Leadership Grp, Bethesda, MD 20892 USA. RP Gay, CL (reprint author), Univ N Carolina, Chapel Hill, NC 27515 USA. NR 194 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 978-0-08-092129-7 PY 2009 BP 107 EP 145 DI 10.1016/B978-0-12-374235-3.00005-4 PG 39 WC Public, Environmental & Occupational Health; Immunology; Infectious Diseases SC Public, Environmental & Occupational Health; Immunology; Infectious Diseases GA BEK32 UT WOS:000317059400007 ER PT B AU Pequegnat, W Stover, E AF Pequegnat, Willo Stover, Ellen BE Mayer, KH Pizer, HF TI Payoff from AIDS behavioral prevention research SO HIV PREVENTION: A COMPREHENSIVE APPROACH LA English DT Article; Book Chapter ID HUMAN-IMMUNODEFICIENCY-VIRUS; SEXUAL-RISK BEHAVIOR; RANDOMIZED CONTROLLED-TRIAL; HIV-PREVENTION; UNITED-STATES; TRANSMITTED-DISEASES; SAN-FRANCISCO; BISEXUAL MEN; METHAMPHETAMINE USE; MALE CIRCUMCISION C1 [Pequegnat, Willo] NIMH, Mental Hlth Res Ctr, Bethesda, MD USA. [Stover, Ellen] NIMH, Div AIDS & Hlth & Behav Res, Bethesda, MD USA. RP Pequegnat, W (reprint author), NIMH, Mental Hlth Res Ctr, Bethesda, MD USA. NR 136 TC 2 Z9 2 U1 2 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 978-0-08-092129-7; 978-0-12-374235-3 PY 2009 BP 169 EP 202 PG 34 WC Public, Environmental & Occupational Health; Immunology; Infectious Diseases SC Public, Environmental & Occupational Health; Immunology; Infectious Diseases GA BEK32 UT WOS:000317059400009 ER PT J AU Beyrer, C Sherman, SG Baral, S AF Beyrer, Chris Sherman, Susan G. Baral, Stefan BE Mayer, KH Pizer, HF TI Harm reduction, human rights and public health SO HIV PREVENTION: A COMPREHENSIVE APPROACH LA English DT Article; Book Chapter ID FEMALE SEX WORKERS; SEXUALLY-TRANSMITTED INFECTIONS; INJECTION-DRUG USERS; HUMAN-IMMUNODEFICIENCY-VIRUS; MIDDLE-INCOME COUNTRIES; HEPATITIS-C INFECTION; PACIFIC ISLANDER MEN; HIV-INFECTION; SYRINGE EXCHANGE; RISK BEHAVIOR C1 [Beyrer, Chris; Sherman, Susan G.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA. [Beyrer, Chris] US NIH, Off AIDS Res, Bethesda, MD 20892 USA. [Beyrer, Chris] World Bank Inst, Washington, DC USA. [Beyrer, Chris] World Bank, Thailand Off, Washington, DC USA. [Baral, Stefan] Univ Toronto, Toronto, ON M5S 1A1, Canada. [Baral, Stefan] Johns Hopkins Sch Publ Hlth, Ctr Publ Hlth & Human Rights, Dept Epidemiol, Baltimore, MD USA. [Baral, Stefan] HIV Vaccine Trial Network, IDU Working Grp, Seattle, WA USA. RP Beyrer, C (reprint author), HIV Vaccine Trials Network, Injecting Drug Use Working Grp, Seattle, WA USA. NR 109 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 978-0-08-092129-7 PY 2009 BP 501 EP 523 PG 23 WC Public, Environmental & Occupational Health; Immunology; Infectious Diseases SC Public, Environmental & Occupational Health; Immunology; Infectious Diseases GA BEK32 UT WOS:000317059400020 ER PT J AU Kamari, Y Peleg, E Herman, MO Bursztyn, M Grossman, E Sharabi, Y AF Kamari, Y. Peleg, E. Herman, M. -O. Bursztyn, M. Grossman, E. Sharabi, Y. TI The Effect of Chronic Hyperinsulinemia on Plasma Adiponectin Levels in Sprague-Dawley Rats SO HORMONE AND METABOLIC RESEARCH LA English DT Article DE adiponectin; insulin; Sprague-Dawley rats ID 3T3-L1 ADIPOCYTES; METABOLIC SYNDROME; GENE-EXPRESSION; HEART-DISEASE; INSULIN-RESISTANCE; ADIPOSE-TISSUE; RISK FACTOR; SECRETION; OBESITY; PROTEIN AB Adiponectin is an important vascular protective substance whose levels are reduced in states of insulin resistance. The relationships between plasma insulin levels and adiponectin are not fully understood, and it is not known whether it is the elevated circulating levels of insulin or insulin resistance that directly affects adiponectin levels. The present study evaluates the direct effect of chronic hyperinsulinemia on plasma adiponectin levels. Male Sprague-Dawley rats were treated with insulin (n=15) administered by a sustained-release implant or were given a sham implantation (n=10) as a control group. Body weight, systolic blood pressure, plasma glucose, triglycerides, insulin, and adiponectin were measured at baseline and after 20 and 40 d of treatment. insulin-treated rats and controls showed a similar increase in body weight. The insulin-treated group had a significant increase in plasma insulin levels and a decrease in plasma glucose levels compared with the sham group, with no change in blood pressure or triglyceride levels. Adiponectin levels remained unchanged despite the significant increase in insulin levels. High circulating insulin levels do not affect plasma adiponectin levels. These results support the concept that the primary defect that results in insulin resistance and hyperinsulinemia is responsible for the altered plasma adiponectin levels in the metabolic syndrome and type 2 diabetes. C1 [Kamari, Y.; Peleg, E.; Herman, M. -O.; Grossman, E.; Sharabi, Y.] Chaim Sheba Med Ctr, Hypertens Unit, IL-52621 Tel Hashomer, Israel. [Kamari, Y.; Peleg, E.; Herman, M. -O.; Grossman, E.; Sharabi, Y.] Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel. [Bursztyn, M.] Hadassah Univ Hosp, Hypertens Unit, IL-91120 Jerusalem, Israel. [Sharabi, Y.] NIH, Bethesda, MD 20892 USA. RP Kamari, Y (reprint author), Chaim Sheba Med Ctr, Hypertens Unit, IL-52621 Tel Hashomer, Israel. EM yehuda.kamari@sheba.health.gov.il OI Grossman, Ehud/0000-0001-8353-0661 FU Talpiot Medical Leadership Program Award; Sheba Medical Center, Tel Hashomer, Israel; Sami and Angela Shamoon Diabetes; Athero-sclerosis Research Fund FX This work was funded in part by the Talpiot Medical Leadership Program Award, Sheba Medical Center, Tel Hashomer, Israel (Y. Kamari), the Sami and Angela Shamoon Diabetes and Athero-sclerosis Research Fund (Y. Kamari). The authors thank Mrs. Zehava Shabtai for her technical assistance. NR 37 TC 5 Z9 5 U1 0 U2 5 PU GEORG THIEME VERLAG KG PI STUTTGART PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY SN 0018-5043 J9 HORM METAB RES JI Horm. Metab. Res. PD JAN PY 2009 VL 41 IS 1 BP 46 EP 49 DI 10.1055/s-0028-1087207 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 399CO UT WOS:000262778200009 PM 18949682 ER PT J AU Knowler, WC AF Knowler, William C. TI Diabetes in American Indian populations SO HORMONE RESEARCH LA English DT Meeting Abstract C1 [Knowler, William C.] NIDDK, NIH, Phoenix, AZ USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 BP 13 EP 13 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 502WB UT WOS:000270489900045 ER PT J AU Stratakis, CA AF Stratakis, Constantine A. TI Molecular mechanism of adrenal tumorigenesis SO HORMONE RESEARCH LA English DT Meeting Abstract C1 NICHD, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 BP 18 EP 18 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 502WB UT WOS:000270489900063 ER PT J AU Baron, J AF Baron, Jeffrey TI Bone development, growth and structure SO HORMONE RESEARCH LA English DT Meeting Abstract C1 NICHD, Sect Growth & Dev, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 BP 21 EP 21 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 502WB UT WOS:000270489900070 ER PT J AU Lui, J Forcinito, P Chang, M Chen, WP Barnes, KM Baron, J AF Lui, Julian Forcinito, Patricia Chang, Maria Chen, Weiping Barnes, Kevin M. Baron, Jeffrey TI A genetic program limiting body size in mammals SO HORMONE RESEARCH LA English DT Meeting Abstract C1 [Lui, Julian; Forcinito, Patricia; Chang, Maria; Barnes, Kevin M.; Baron, Jeffrey] NICHD, Program Dev Endocrinol & Genet, Bethesda, MD USA. [Chen, Weiping] NIDDK, Microarray Core Facil, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 BP 25 EP 25 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 502WB UT WOS:000270489900085 ER PT J AU Rezvani, G Lui, JCK Barnes, KM Baron, J AF Rezvani, Geoffrey Lui, Julian C. K. Barnes, Kevin M. Baron, Jeffrey TI Imprinted genes that affect body size promote growth of embryonal malignancies SO HORMONE RESEARCH LA English DT Meeting Abstract C1 [Rezvani, Geoffrey; Lui, Julian C. K.; Barnes, Kevin M.; Baron, Jeffrey] NICHD, PDEGEN, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 BP 25 EP 25 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 502WB UT WOS:000270489900084 ER PT J AU Chagin, AS Hirai, T Weinstein, LS Chen, M Kronenberg, HM AF Chagin, Andrei S. Hirai, Takao Weinstein, Lee S. Chen, Min Kronenberg, Henry M. TI Postnatal deletion of the G-protein subunit alpha (G(s)alpha) in epiphyseal chondrocytes inhibits longitudinal bone growth SO HORMONE RESEARCH LA English DT Meeting Abstract C1 [Chagin, Andrei S.; Hirai, Takao; Kronenberg, Henry M.] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA. [Chagin, Andrei S.; Hirai, Takao; Kronenberg, Henry M.] Harvard Univ, Sch Med, Boston, MA USA. [Weinstein, Lee S.; Chen, Min] NIDDKD, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 SU 3 BP 27 EP 27 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 502WB UT WOS:000270489900090 ER PT J AU Gafni, RI Brahim, J Andreopoulou, P Bhattacharyya, N Kelly, MH Brillante, BA Reynolds, JC Zhou, H Dempster, DW Collins, MT AF Gafni, Rachel I. Brahim, Jaime Andreopoulou, Panagiota Bhattacharyya, Nisan Kelly, Marilyn H. Brillante, Beth A. Reynolds, James C. Zhou, Hua Dempster, David W. Collins, Michael T. TI Treatment of hypoparathyroid adults and adolescents with parathyroid hormone (PTH) 1-34 induces marked changes in bone turnover and structure: a biochemical and histomorphometric study SO HORMONE RESEARCH LA English DT Meeting Abstract C1 [Gafni, Rachel I.; Andreopoulou, Panagiota; Bhattacharyya, Nisan; Kelly, Marilyn H.; Brillante, Beth A.; Reynolds, James C.; Collins, Michael T.] NIH, Bethesda, MD 20892 USA. [Brahim, Jaime] Univ Maryland Med Syst, Baltimore, MD USA. Helen Hayes Hosp, W Haverstraw, NY USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 BP 29 EP 29 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 502WB UT WOS:000270489900095 ER PT J AU Han, J Damaso, L Welch, S Sweeten, S Balagopal, P Mauras, N AF Han, Joan Damaso, Ligeia Welch, Susan Sweeten, Shawn Balagopal, Prabhakaran (Babu) Mauras, Nelly TI Effects of GH and nutritional therapy in boys with constitutional growth delay: a randomized controlled trial SO HORMONE RESEARCH LA English DT Meeting Abstract C1 [Han, Joan; Damaso, Ligeia; Welch, Susan; Sweeten, Shawn; Mauras, Nelly] Nemours Childrens Clin, Div Endocrinol, Jacksonville, FL USA. [Han, Joan] NICHD, Program Dev Endocrinol & Genet, NIH, Bethesda, MD USA. [Balagopal, Prabhakaran (Babu)] Nemours Childrens Clin, Biomed Anal Lab, Jacksonville, FL USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 BP 45 EP 45 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 502WB UT WOS:000270489900140 ER PT J AU Lodish, MB Kim, SY Raygada, M Huynh, TT Faucz, F Horvath, A Pacak, K Helman, L Stratakis, CA AF Lodish, Maya B. Kim, Su Y. Raygada, Margarita Huynh, Thanh T. Faucz, Fabio Horvath, Anelia Pacak, Karl Helman, Lee Stratakis, Constantine A. TI Succinate dehydrogenase mutations are present in pediatric and adult wild-type gists occurring in patients without associated paraganglioma SO HORMONE RESEARCH LA English DT Meeting Abstract C1 [Lodish, Maya B.; Raygada, Margarita; Faucz, Fabio; Horvath, Anelia; Stratakis, Constantine A.] NICHD, SEGEN, NIH, Bethesda, MD USA. [Huynh, Thanh T.; Pacak, Karl] NICHD, DIR, RBMB, Bethesda, MD USA. [Kim, Su Y.; Helman, Lee] NCI, DBS, POB, Bethesda, MD 20892 USA. RI Faucz, Fabio/C-1607-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 BP 95 EP 95 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 502WB UT WOS:000270489900282 ER PT J AU Lodish, MB Adams, KT Huynh, TT Prodanov, T Ling, A Shusterman, S Basu, E Jimenez, C Stratakis, CA Pacak, K AF Lodish, Maya B. Adams, Karen T. Huynh, Thanh T. Prodanov, Tamara Ling, Alex Shusterman, Suzanne Basu, Ellen Jimenez, Camilo Stratakis, Constantine A. Pacak, Karel TI Succinate dehydrogenase mutations are strongly associated with paraganglioma of the organ of Zuckerkandl in pediatric and adult patients SO HORMONE RESEARCH LA English DT Meeting Abstract C1 [Lodish, Maya B.; Stratakis, Constantine A.] NICHD, SEGEN, NIH, Bethesda, MD USA. [Adams, Karen T.; Huynh, Thanh T.; Prodanov, Tamara; Pacak, Karel] NICHD, DIR, RBMB, NIH, Bethesda, MD USA. [Ling, Alex] NIH, CC, DRD, Bethesda, MD 20892 USA. [Shusterman, Suzanne; Basu, Ellen] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. [Jimenez, Camilo] Univ Texas MD Anderson Canc Ctr, Dept Endocrine Neoplasia & Hormonal Disorders, Houston, TX 77030 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 BP 96 EP 96 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 502WB UT WOS:000270489900283 ER PT J AU Brown, RJ Walter, M Rother, KI AF Brown, Rebecca J. Walter, Mary Rother, Kristina I. TI Diet soda increases early insulin and GLP-1 secretion in healthy volunteers SO HORMONE RESEARCH LA English DT Meeting Abstract C1 [Brown, Rebecca J.; Walter, Mary; Rother, Kristina I.] NIDDKD, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 BP 159 EP 159 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 502WB UT WOS:000270489900465 ER PT J AU Keselman, A Chiesa, A Malozowski, S Vieytes, A Heinrich, JJ de Papendieck, LG AF Keselman, Ana Chiesa, Ana Malozowski, Saul Vieytes, Ana Heinrich, Juan Jorge de Papendieck, Laura Gruneiro TI Abnormal Responses to TRH in Children Born Small for Gestational Age That Failed to Catch Up SO HORMONE RESEARCH LA English DT Article DE Thyroid impairment; Thyroid-stimulating hormone; Small for gestational age ID INTRAUTERINE GROWTH; FETAL-GROWTH; NEURON AB Background: Fifteen percent of small for gestational age (SGA) children remain short and undergo thyroid axis evaluations. Methods: We analyzed data on thyroid assessment of 58 SGA children. Five had primary autoimmune hypothyroidism. In the remaining 53 patients, TSH, free T4 (FT4), antithyroid antibodies and 90-min TRH test results were analyzed. Patients were grouped into G1 (n = 27; normal) and G2 (n = 26; abnormal) according to their response to the TRH test compared with 30 normal children. Results: No differences were found in chronological age, gestational age, or birth weight standard deviation score (SDS) between groups. G2 showed higher SDS BMI at consultation (p < 0.05). FT4 (ng/dl) levels were similar in all groups, while basal TSH levels were statistically different in G2 compared with G1 and controls. In 21 G2 patients treated with thyroxine, FT4 levels did not change, TSH normalized, BMI SDS and height remained unchanged. Conclusion: These data suggest that in SGA short children thyroid abnormalities may occur. Some of them may be due to a different setting of the hypothalamic-hypophyseal-thyroid axis during intrauterine life. Intrauterine growth retardation may permanently influence endocrine systems by affecting their programming during development. Further follow-up is needed to confirm these findings and to assess their natural history and potential clinical impact. Copyright (C) 2009 S. Karger AG, Basel C1 [Keselman, Ana; Chiesa, Ana; Vieytes, Ana; Heinrich, Juan Jorge; de Papendieck, Laura Gruneiro] Hosp Ninos Dr Ricardo Gutierrez, CEDIE, Buenos Aires, DF, Argentina. [Malozowski, Saul] NIDDKD, Div Diabet Endocrinol & Metab Dis, Bethesda, MD 20892 USA. RP Keselman, A (reprint author), Gallo 1360, RA-1425 Buenos Aires, DF, Argentina. EM akeselman@cedie.org.ar NR 27 TC 1 Z9 1 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 IS 3 BP 167 EP 171 DI 10.1159/000232492 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 491IS UT WOS:000269572700006 PM 19729948 ER PT J AU Dinauer, C Korelitz, JJ Mattison, DR Zito, J Rivkees, SA AF Dinauer, Catherine Korelitz, James J. Mattison, Donald R. Zito, Julie Rivkees, Scott A. TI Prevalence and treatment of childhood Graves' disease in the United States SO HORMONE RESEARCH LA English DT Meeting Abstract C1 [Dinauer, Catherine; Rivkees, Scott A.] Yale Univ, Sch Med, New Haven, CT USA. [Korelitz, James J.] Westat Corp, Rockville, MD USA. [Mattison, Donald R.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA. [Zito, Julie] Univ Maryland, Baltimore, MD 21201 USA. RI Mattison, Donald/C-2015-2009; Mattison, Donald/L-4661-2013 OI Mattison, Donald/0000-0001-5623-0874 NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 BP 172 EP 172 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 502WB UT WOS:000270489900506 ER PT J AU Finkielstain, GP Hanna, RM Van Ryzin, C Chen, WY McDonnell, NB Merke, DP AF Finkielstain, Gabriela P. Hanna, Reem M. Van Ryzin, Carol Chen, Wuyan McDonnell, Nazli B. Merke, Deborah P. TI Comprehensive genetic analysis of 183 unrelated patients with congenital adrenal hyperplasia due to 21-hydroxylase deficiency SO HORMONE RESEARCH LA English DT Meeting Abstract C1 [Finkielstain, Gabriela P.] NICHD, Program Dev Endocrinol & Genet, NIH, Bethesda, MD USA. [Hanna, Reem M.; Van Ryzin, Carol] NIH, Ctr Clin, Bethesda, MD USA. [Chen, Wuyan] NIA, Clin Invest Lab, NIH, Baltimore, MD 21224 USA. [McDonnell, Nazli B.] NIA, Clin Res Branch, NIH, Baltimore, MD 21224 USA. [Merke, Deborah P.] NICHD, Reprod Biol & Med Branch, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 BP 196 EP 196 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 502WB UT WOS:000270489900579 ER PT J AU Keil, MF Lange, E Stratakis, CA AF Keil, Margaret F. Lange, Eileen Stratakis, Constantine A. TI Atypical Cushings presentation in a child with Carney's complex SO HORMONE RESEARCH LA English DT Meeting Abstract C1 [Keil, Margaret F.; Lange, Eileen; Stratakis, Constantine A.] NICHD, Sect Endocrinol Genet, Program Dev Endocrinol Genet, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 BP 205 EP 205 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 502WB UT WOS:000270489900608 ER PT J AU Andrade, AC Lui, JL Nilsson, O AF Andrade, Anenisia C. Lui, Julian Nilsson, Ola TI Temporal and spatial expression of a growth-regulated network of imprinted genes in growth plate cartilage SO HORMONE RESEARCH LA English DT Meeting Abstract C1 [Andrade, Anenisia C.; Nilsson, Ola] Karolinska Inst, Pediat Endocrinol Unit, Stockholm, Sweden. [Andrade, Anenisia C.; Nilsson, Ola] Karolinska Inst, Ctr Mol Med, Dept Woman & Child Hlth, Stockholm, Sweden. [Andrade, Anenisia C.] Dept Pediat, Pediat Endocrinol Unit, Sao Paulo, Brazil. [Lui, Julian] NICHHD, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 BP 273 EP 273 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 502WB UT WOS:000270489900806 ER PT J AU Lee, PA Gollenberg, AL Hediger, ML Himes, JH Louis, GM AF Lee, Peter A. Gollenberg, Audra L. Hediger, Mary L. Himes, John H. Louis, Germaine M. TI Inhibin-B levels higher among non-Hispanic black than Mexican-American and non-Hispanic white prepubertal and pubertal boys SO HORMONE RESEARCH LA English DT Meeting Abstract C1 [Lee, Peter A.] Penn State Coll Med, Hershey, PA USA. [Gollenberg, Audra L.; Hediger, Mary L.; Louis, Germaine M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Rockville, MD USA. [Himes, John H.] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 SU 3 BP 336 EP 337 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 502WB UT WOS:000270489900999 ER PT J AU Rothenbuhler, A Horvath, A Faucz, FR Almeida, M Lodish, M Libe, R Bertherat, J Sratakis, CA AF Rothenbuhler, Anya Horvath, Analia Faucz, Fabio R. Almeida, Madson Lodish, Maya Libe, Rossella Bertherat, Jerome Sratakis, Constantine A. TI Two novel mutations in PDE8B, a cAMP phosphodiasterase highly expressed in the adrenal cortex, in a cohort of patients with adrenal tumors SO HORMONE RESEARCH LA English DT Meeting Abstract C1 [Rothenbuhler, Anya; Horvath, Analia; Faucz, Fabio R.; Almeida, Madson; Lodish, Maya; Sratakis, Constantine A.] NICHHD, Endocrinol Sect, Genet & Pediat Endocrinol Training Program, NIH, Bethesda, MD 20892 USA. [Libe, Rossella; Bertherat, Jerome] Inst Cochin, Endocrinol Metab & Canc Dept, CNRS UMR8104, INSERM U567, Paris, France. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 72 BP 346 EP 346 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 502WB UT WOS:000270489901028 ER PT J AU Bondy, CA AF Bondy, Carolyn A. TI Turner Syndrome 2008 SO HORMONE RESEARCH LA English DT Article; Proceedings Paper CT 40th International Symposium on Endocrinology and Metabolism CY APR 23-MAY 24, 2008 CL Paris, FRANCE DE Turner syndrome; Sex chromosome anomaly; Pubertal induction; Short stature; Congenital heart disease ID GROWTH-HORMONE; PRENATAL-DIAGNOSIS; PREVALENCE; DISSECTION; MOSAICISM; TRIAL; GIRLS; WOMEN; 45,X AB Background: Fetuses with prenatal diagnoses of 45, X Turner syndrome (TS) and abnormal fetal ultrasounds have poor prognoses for survival, but with modern medical management, those that do survive to birth may have good clinical outcomes. Fetuses with incidental diagnoses of mosaicism for 45, X associated with normal ultrasounds have a high survival rate and may have no or only mild features of TS. Current Guidelines: At present, appropriate treatment for girls with TS may include growth-promoting therapy and pubertal induction with the dual aims of optimizing adult height and facilitating psychosocial adjustment. Current recommendations advocate mimicking normal physiology as much as possible, with use of microdose estradiol to initiate puberty. Healthcare providers should play a role in helping girls psychosocially adapt to ovarian failure. We now recognize there is an unacceptably high rate of premature mortality in adults with TS, mainly because of complications from congenital heart disease. Cardiac magnetic resonance imaging is recommended to screen for individuals at high risk for serious complications. Copyright (C) 2009 S. Karger AG, Basel C1 NICHHD, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA. RP Bondy, CA (reprint author), NICHHD, Dev Endocrinol Branch, NIH, CRC 1-3330,10 Ctr Dr, Bethesda, MD 20892 USA. EM bondyc@mail.nih.gov FU Intramural NIH HHS NR 19 TC 26 Z9 30 U1 0 U2 4 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 71 BP 52 EP 56 DI 10.1159/000178039 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 395UI UT WOS:000262548600013 PM 19153507 ER PT J AU Agarwal, SK Ozawa, A Mateo, CM Marx, SJ AF Agarwal, Sunita K. Ozawa, Atsushi Mateo, Carmen M. Marx, Stephen J. TI The MEN1 Gene and Pituitary Tumours SO HORMONE RESEARCH LA English DT Article; Proceedings Paper CT 10th KIGS/KIMS Expert Meeting on Growth Hormone and Growth Disorders CY APR, 2008 CL Florence, ITALY SP KIGS, KIMS DE Angiogenesis; MEN1; Mouse; p27(Kip1); Pituitary tumour; Prolactinoma; Tumour suppressor ID MULTIPLE ENDOCRINE NEOPLASIA; FAMILIAL ISOLATED HYPERPARATHYROIDISM; DEPENDENT KINASE INHIBITORS; CARCINOID-TUMORS; MOUSE MODEL; TYPE-1 MEN1; GROWTH; ADENOMAS; MUTATION; MICE AB Sporadic multiple endocrine neoplasia type 1 (MEN1) is defined as the occurrence of tumours in two of three main endocrine tissue types: parathyroid, pituitary and pancreaticoduodenal. A prolactinoma variant or Burin variant of MEN1 was found to occur in three large kindreds, with more prolactinomas and fewer gastrinomas than typical MEN1. MEN1 tumours differ from common tumours by showing features from the MEN1 gene (e.g. larger pituitary tumours). They also show various expressions of tumour multiplicity; however, pituitary tumour in MEN1 is usually solitary. Diagnosis in MEN1 carriers during childhood is not directed at cancers but at benign morbid tumours. Morbid prolactinoma occurred at the age of 5 years in one MEN1 individual; hence, this is the earliest age at which to recommend tumour surveillance in carriers. The MEN I gene shows biallelic inactivation in 30% of some types of common variety endocrine tumours (e.g. parathyroid adenoma, gastrinoma, insulinoma and bronchial carcinoid), but in only 1-5% of common pituitary tumours. Heterozygous knockout of MEN1 in mice provides a robust model of MEN1 and has been found to support further research on anti-angiogenesis therapy for pituitary tumours. The rarity of MEN1 mutations in some MEN1-like states aids the identification of other mutated genes, such as AIP, HRPT2 and p27(Kip1). We present recent clinical and basic findings about the MEN1 gene, particularly concerning hereditary vs. common variety pituitary tumours. copyright (C) 2009 S. Karger AG, Basel C1 [Agarwal, Sunita K.; Ozawa, Atsushi; Mateo, Carmen M.; Marx, Stephen J.] NIDDK, Metab Dis Branch, NIH, Bethesda, MD 20892 USA. RP Marx, SJ (reprint author), NIDDK, Metab Dis Branch, NIH, Bldg 10,Room 9C-103, Bethesda, MD 20892 USA. EM marxs@mail.nih.gov RI Agarwal, Sunita/D-1428-2016 OI Agarwal, Sunita/0000-0002-7557-3191 FU Intramural NIH HHS NR 53 TC 23 Z9 24 U1 0 U2 4 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 2009 VL 71 BP 131 EP 138 DI 10.1159/000192450 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 443VF UT WOS:000265938200021 PM 19407509 ER PT J AU Hager, GL Stavreva, DA Voss, TC AF Hager, G. L. Stavreva, D. A. Voss, T. C. BE Pfaff, DW Arnold, AP Etgen, AM Fahrbach, SE Rubin, RT TI Nuclear Mechanisms of Glucocorticoid Action SO HORMONES, BRAIN AND BEHAVIOR, VOLS 1-5, 2ND EDITION LA English DT Article; Book Chapter ID CHROMATIN-REMODELING COMPLEX; ESTROGEN-RECEPTOR-ALPHA; DNA-BINDING DOMAIN; RNA-POLYMERASE-II; NF-KAPPA-B; TUMOR VIRUS PROMOTER; HEAT-SHOCK-PROTEIN; TERMINAL ACTIVATION DOMAIN; STEROID-HORMONE RECEPTORS; HSP90 MOLECULAR CHAPERONE C1 [Hager, G. L.; Stavreva, D. A.; Voss, T. C.] NCI, NIH, Bethesda, MD 20892 USA. RP Hager, GL (reprint author), NCI, NIH, Bethesda, MD 20892 USA. NR 325 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA BN 978-0-08-088783-8 PY 2009 BP 1329 EP 1364 PG 36 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA BCV83 UT WOS:000311627101020 ER PT J AU Brinton, RD Gore, AC Schmidt, PJ Morrison, JH AF Brinton, R. D. Gore, A. C. Schmidt, P. J. Morrison, J. H. BE Pfaff, DW Arnold, AP Etgen, AM Fahrbach, SE Rubin, RT TI Reproductive Aging of Females: Neural Systems SO HORMONES, BRAIN AND BEHAVIOR, VOLS 1-5, 2ND EDITION LA English DT Article; Book Chapter ID GONADOTROPIN-RELEASING-HORMONE; ESTROGEN REPLACEMENT THERAPY; DENDRITIC SPINE DENSITY; METHYL-D-ASPARTATE; RANDOMIZED CONTROLLED-TRIAL; HEALTH INITIATIVE MEMORY; CONJUGATED EQUINE ESTROGENS; MILD COGNITIVE IMPAIRMENT; MIDDLE-AGED RATS; RECEPTOR-DEPENDENT MECHANISM C1 [Brinton, R. D.] Univ So Calif, Los Angeles, CA 90089 USA. [Gore, A. C.] Univ Texas Austin, Austin, TX 78712 USA. [Schmidt, P. J.] NIMH, NIH, Bethesda, MD 20892 USA. [Morrison, J. H.] Mt Sinai Sch Med, New York, NY USA. RP Brinton, RD (reprint author), Univ So Calif, Los Angeles, CA 90089 USA. NR 203 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA BN 978-0-08-088783-8 PY 2009 BP 2199 EP 2222 PG 24 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA BCV83 UT WOS:000311627103005 ER PT J AU Rubinow, DR Schmidt, PJ Meltzer-Brody, S Harsh, VL AF Rubinow, D. R. Schmidt, P. J. Meltzer-Brody, S. Harsh, V. L. BE Pfaff, DW Arnold, AP Etgen, AM Fahrbach, SE Rubin, RT TI Gonadal Hormones and Behavior in Women: Concentrations versus Context SO HORMONES, BRAIN AND BEHAVIOR, VOLS 1-5, 2ND EDITION LA English DT Article; Book Chapter ID PITUITARY-ADRENAL AXIS; MENSTRUAL-CYCLE PHASE; PREMENSTRUAL DYSPHORIC DISORDER; CEREBRAL-BLOOD-FLOW; CORTICOTROPIN-RELEASING HORMONE; NATIONAL COMORBIDITY SURVEY; PLASMA BETA-ENDORPHIN; LATE LUTEAL-PHASE; SEROTONIN-REUPTAKE INHIBITORS; AFFECTIVE PUERPERAL PSYCHOSIS C1 [Rubinow, D. R.; Meltzer-Brody, S.] Univ N Carolina, Chapel Hill, NC 27599 USA. [Schmidt, P. J.; Harsh, V. L.] NIH, Bethesda, MD 20892 USA. RP Rubinow, DR (reprint author), Univ N Carolina, Chapel Hill, NC 27599 USA. NR 403 TC 0 Z9 0 U1 2 U2 5 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA BN 978-0-08-088783-8 PY 2009 BP 2395 EP 2428 PG 34 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA BCV83 UT WOS:000311627103013 ER PT J AU Lenroot, RK Schmitt, JE Ordaz, SJ Wallace, GL Neale, MC Lerch, JP Kendler, KS Evans, AC Giedd, JN AF Lenroot, Rhoshel K. Schmitt, James E. Ordaz, Sarah J. Wallace, Gregory L. Neale, Michael C. Lerch, Jason P. Kendler, Kenneth S. Evans, Alan C. Giedd, Jay N. TI Differences in Genetic and Environmental Influences on the Human Cerebral Cortex Associated With Development During Childhood and Adolescence SO HUMAN BRAIN MAPPING LA English DT Article DE brain; twin study; genetics; growth and development; child; adolescent; magnetic resonance imaging ID AUTOMATED 3-D EXTRACTION; HUMAN BRAIN; CORTICAL THICKNESS; EXPRESSION PROFILES; MONOZYGOTIC TWINS; HOMO-SAPIENS; MRI DATA; EVOLUTION; MODELS; HERITABILITY AB In this report, we present the first regional quantitative analysis of age-related differences in the heritability of cortical thickness using anatomic MRI with a large pediatric sample of twins, twin siblings, and singletons (n = 600, mean age 11.1 years, range 5-19). Regions of primary sensory and motor cortex, which develop earlier, both phylogenetically and ontologically, show relatively greater genetic effects earlier in childhood. Later developing regions within the dorsal prefrontal cortex and temporal lobes conversely show increasingly prominent genetic effects with maturation. The observation that regions associated with complex cognitive processes such as language, tool use, and executive function are more heritable in adolescents than children is consistent with previous studies showing that IQ becomes increasingly heritable with maturity(Plomin et al. [1997]: Psychol Sci 8:442-447). These results suggest that both the specific cortical region and the age of the population should be taken into account when using cortical thickness as an intermediate phenotype to link genes, environment, and behavior. Hum Brain Mapp 30:163-174, 2009. (c) 2007 Wiley-Liss, Inc. C1 [Lenroot, Rhoshel K.; Ordaz, Sarah J.; Wallace, Gregory L.; Giedd, Jay N.] NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA. [Schmitt, James E.; Neale, Michael C.; Kendler, Kenneth S.] Virginia Commonwealth Univ, Virginia Inst Psychiat & Behav Genet, Richmond, VA USA. [Ordaz, Sarah J.] Univ Pittsburgh, Lab Neurocognit Dev, Pittsburgh, PA USA. [Lerch, Jason P.] Hosp Sick Children, Mouse Imaging Ctr, Toronto, ON M5G 1X8, Canada. [Evans, Alan C.] McGill Univ, Montreal Neurol Inst, McConnell Brain Imaging Ctr, Montreal, PQ, Canada. RP Lenroot, RK (reprint author), NIMH, Child Psychiat Branch, NIH, 10 Ctr Dr,Room 4C110,MSC 1367, Bethesda, MD 20892 USA. EM lenrootr@mail.nih.gov RI Giedd, Jay/A-3080-2008; Giedd, Jay/B-7302-2012; Giedd, Jay/J-9644-2015; OI Giedd, Jay/0000-0003-0827-3460; Giedd, Jay/0000-0003-2002-8978; Wallace, Gregory/0000-0003-0329-5054 FU NIH [MI-1-20030, M H-65329] FX Contract grant sponsor: NIH; Contract grant numbers: MI-1-20030, M H-65329. NR 71 TC 146 Z9 149 U1 4 U2 21 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1065-9471 J9 HUM BRAIN MAPP JI Hum. Brain Mapp. PD JAN PY 2009 VL 30 IS 1 BP 163 EP 174 DI 10.1002/hbm.20494 PG 12 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 393TW UT WOS:000262397000014 PM 18041741 ER PT J AU Hester, SD Drobna, Z Andrews, DMK Liu, J Waalkes, MP Thomas, DJ Styblo, M AF Hester, S. D. Drobna, Z. Andrews, D. M. K. Liu, J. Waalkes, M. P. Thomas, D. J. Styblo, M. TI Expression of AS3MT alters transcriptional profiles in human urothelial cells exposed to arsenite SO HUMAN & EXPERIMENTAL TOXICOLOGY LA English DT Article DE arsenite; AS3MT; human urothelial cells; transcriptional profiles ID MONOMETHYLARSONOUS ACID MMA(III); INDUCED MALIGNANT-TRANSFORMATION; PENTAVALENT ARSENICALS; HUMAN HEPATOCYTES; METHYLATION; TOXICITY; METABOLISM; TRIVALENT; RAT; METHYLTRANSFERASE AB Inorganic arsenic (iAs) is an environmental toxicant and human carcinogen. The enzymatic methylation of iAs that is catalyzed by arsenic (+3 oxidation state)methyltransferase (AS3MT) generates reactive methylated intermediates that contribute to the toxic and carcinogenic effects of iAs. We have shown that clonal human urothelial cells (UROtsa/F35) that express rat AS3MT and methylate iAs are more susceptible to acute toxicity of arsenite (iAs(III)) than parental UROtsa cells that do not express AS3MT and do not methylate iAs. The current work examines transcriptional changes associated with AS3MT expression and identifies specific categories of genes expressed in UROtsa and UROtsa/F35 cells in response to a 24-h exposure to 1 or 50 mu M iAs(III). Here, the expression of 21,073 genes was assessed using Agilent Human 1A(V2) arrays. Venn analysis showed marked concentration-dependent differences between gene expression patterns in UROtsa and UROTsa/F35 cells exposed to iAs(III). Among 134 genes altered by exposure to subtoxic 1 mu M iAs(III), only 14 were shared by both cell lines. Exposure to cytotoxic 50 mu M iAs(III) uniquely altered 1389 genes in UROtsa/F35 and 649 genes in UROtsa cells; 5033 altered genes were associated with the chemical alone. In UROtsa, but not UROtsa/F35 cells exposure to 1 mu M iAs(III) altered expression of genes associated with cell adhesion. In contrast, expression of genes involved in cell cycle regulation was significantly altered in UROtsa/F35 cells at this exposure level. At 50 mu M iAs(III), pathways regulating cell cycle, cell death, transcription, and metabolism were affected in both cell lines. However, only Urotsa/F35 cells showed numerous G-protein and kinase pathway alterations as well as alterations in pathways involved in cell growth and differentiation. These data link the AS3MT-catalyzed methylation of iAs to specific genomic responses in human cells exposed to iAs(III). Further analysis of these responses will help to characterize the role of AS3MT-catalyzed methylation in modulation of iAs(III) toxicity. C1 [Hester, S. D.] US EPA, NHEERL, ECD, Canc Biol Branch, Res Triangle Pk, NC 27711 USA. [Drobna, Z.; Styblo, M.] Univ N Carolina, Dept Nutr, Chapel Hill, NC USA. [Liu, J.; Waalkes, M. P.] NIEHS, LCC, NCI, Res Triangle Pk, NC 27709 USA. [Thomas, D. J.] US EPA, NHEERL, ETD, Pharmacokinet Branch, Res Triangle Pk, NC 27711 USA. [Styblo, M.] Univ N Carolina, Ctr Environm Med Asthma & Lung Biol, Chapel Hill, NC USA. RP Hester, SD (reprint author), US EPA, Cellular Toxicol Branch, Div Environm Carcinogenesis, B143-06,109 TW Alexander Dr, Res Triangle Pk, NC 27711 USA. EM hester.susan@epa.gov FU NIH, National Cancer Institute, Center for Cancer Research FX The research described in this article has been reviewed by the National Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, and approved for publication. Approval does not signify that the contents necessarily reflect the views and the policies of the Agency, nor does mention of trade names or commercial products constitute endorsement or recommendation for use. The authors wish to thank Dr Ram Ramabhadran and Dr Kirk Kitchin for review of this manuscript. The work was supported [in part] by the Intramural Research Program of the NIH, National Cancer Institute, Center for Cancer Research. NR 27 TC 7 Z9 7 U1 1 U2 1 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 0960-3271 J9 HUM EXP TOXICOL JI Hum. Exp. Toxicol. PD JAN PY 2009 VL 28 IS 1 BP 49 EP 61 DI 10.1177/0960327109102368 PG 13 WC Toxicology SC Toxicology GA 449HY UT WOS:000266322700009 PM 19411561 ER PT J AU McArdle, PF Whitcomb, BW AF McArdle, P. F. Whitcomb, B. W. TI Improper Adjustment for Baseline in Genetic Association Studies of Change in Phenotype SO HUMAN HEREDITY LA English DT Article DE Cold pressor test; DAG; Vasoconstriction; Bias; Regression ID COLD-PRESSOR TEST; BLOOD-PRESSURE; MODELS; EPIDEMIOLOGY; HYPERTENSION; REACTIVITY; DESIGN; BIASES AB Objective: In studies of associations between genetic factors and outcomes where change in phenotype is of interest, proper modeling of the data, particularly the treatment of baseline trait values, is required to draw valid conclusions. Methods: The authors compared models of blood pressure response to a cold pressor test with and without inclusion of baseline blood pressure as a regressor and evaluate the resultant biases. Results: Adjustment for baseline presents a potential source of bias for assessment of genotype-phenotype associations. This bias was observed to occur both under the absence of a true effect, as well when a relation between genotype and change in phenotype was simulated. In simulations that incorporated measurement error, estimates were as great as two fold the true parameter values when unmeasured confounding was a factor. Conclusions: Adjusting for baseline introduces bias in genetic association studies when change in phenotype is the outcome of interest. Model misspecification bias may impact inference and provide one possible source of non-replication of findings in the literature. Copyright (C) 2008 S. Karger AG, Basel C1 [McArdle, P. F.] Univ Maryland, Sch Med, Div Endocrinol Diabet & Nutr, Baltimore, MD 21201 USA. [Whitcomb, B. W.] NICHHD, Div Epidemiol Stat & Prevent Res, Natl Inst Hlth, Rockville, MD USA. RP McArdle, PF (reprint author), Univ Maryland, Sch Med, Div Endocrinol Diabet & Nutr, 660 W Redwood St,Room 492, Baltimore, MD 21201 USA. EM pmcardle@epi.umaryland.edu FU Eunice Kennedy Shriver National Institute of Child Health and Human Development; [U01 HL72515] FX This research was supported in part by the Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development. NR 21 TC 4 Z9 4 U1 2 U2 5 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0001-5652 J9 HUM HERED JI Hum. Hered. PY 2009 VL 67 IS 3 BP 176 EP 182 DI 10.1159/000181156 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 395TM UT WOS:000262546400005 PM 19077436 ER PT J AU Bekker, V O'Brien, TR Chanock, S AF Bekker, Vincent O'Brien, Thomas R. Chanock, Stephen TI Population Genetics and Comparative Genetics of CLDN1, a Gene Involved in Hepatitis C Virus Entry SO HUMAN HEREDITY LA English DT Article DE Hepatitis C virus; Population genetics; Evolution; Selection; Conservation; Tight junctions; Viral receptor ID INTERNATIONAL METAANALYSIS; DISEASE PROGRESSION; NATURAL-SELECTION; DNA POLYMORPHISM; GENOTYPE DATA; CLAUDIN-1; INFECTION; CCR5-DELTA-32; ALLELES; GENOME AB The claudin-1 gene (CLDN1) is a member of a family of genes that encodes proteins found in tight junctions and it has recently been implicated as one of several receptors for late stage binding of hepatitis C virus (HCV). Exploration of the population genetics of this gene could be informative, especially in the investigation of a possible genetic contribution to HCV infection. Comparison to a highly similar gene, claudin-7 (CLDN7) could provide insight into the recent molecular evolution of CLDN1. Mean interspecies conservation score was 0.11 (SD 0.28) for CLDN1 and 0.31 (SD 0.43) for CLDN7. Resequence analysis was performed across all exons and evolutionarily conserved regions in CLDN1 (13 kb in total) and CLDN7 (2 kb in total) in 204 chromosomes drawn from the SNP500Cancer resource of four self-described ethnic groups in the US. For CLDN1, 133 SNPs were identified as well as 8 indels and an AC repeat length polymorphism. For CLDN7, 5 SNPs were identified. Assessment of nucleotide diversity (including F(st), theta and pi statistics) did not show evidence for recent positive or negative selection in either gene. The pattern of linkage disequilibrium was determined for each group and there is substantial difference for common SNPS (>5%) between populations as well as genes, further supporting the absence of signatures of recent selection. Copyright (C) 2008 S. Karger AG, Basel C1 [O'Brien, Thomas R.; Chanock, Stephen] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20852 USA. [Bekker, Vincent; Chanock, Stephen] Ctr Canc Res, Pediat Oncol Branch, Sect Genom Variat, Bethesda, MD USA. [Chanock, Stephen] NCI, NIH, Gaithersburg, MD USA. RP O'Brien, TR (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, 6120 Executive Blvd,Room 7082, Rockville, MD 20852 USA. EM obrient@exchange.nih.gov NR 34 TC 1 Z9 2 U1 1 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0001-5652 J9 HUM HERED JI Hum. Hered. PY 2009 VL 67 IS 3 BP 206 EP 216 DI 10.1159/000181159 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA 395TM UT WOS:000262546400008 PM 19077439 ER PT J AU Boehringer, S Pfeiffer, RM AF Boehringer, Stefan Pfeiffer, Ruth M. TI A Model for Fine Mapping in Family Based Association Studies SO HUMAN HEREDITY LA English DT Article DE Family data; Likelihood; Haplotypes; Latent disease locus; Alzheimer ID GENOME-WIDE ASSOCIATION; LINKAGE DISEQUILIBRIUM; ALZHEIMER-DISEASE; UNIFIED APPROACH; CANCER; TESTS; RISK; LOCI AB Genome wide association studies for complex diseases are typically followed by more focused characterization of the identified genetic region. We propose a latent class model to evaluate a candidate region with several measured markers using observations on families. The main goal is to estimate linkage disequilibrium (LD) between the observed markers and the putative true but unobserved disease locus in the region. Based on this model, we estimate the joint distribution of alleles at the observed markers and the unobserved true disease locus, and a penetrance parameter measuring the impact of the disease allele on disease risk. A family specific random effect allows for varying baseline disease prevalences for different families. We present a likelihood framework for our model and assess its properties in simulations. We apply the model to an Alzheimer data set and confirm previous findings in the ApoE region. Copyright (C) 2009 S. Karger AG, Basel C1 [Boehringer, Stefan] Univ Klinikum Essen, Inst Humangenet, D-45122 Essen, Germany. [Pfeiffer, Ruth M.] NCI, Biostat Branch, Bethesda, MD 20892 USA. RP Boehringer, S (reprint author), Univ Klinikum Essen, Inst Humangenet, Hufelandstr 55, D-45122 Essen, Germany. EM correspondence@s-boehringer.org RI Pfeiffer, Ruth /F-4748-2011 FU DFG [BO 1955/2-3] FX Part of this work was supported by DFG grant BO 1955/2-3. NR 25 TC 0 Z9 0 U1 1 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0001-5652 J9 HUM HERED JI Hum. Hered. PY 2009 VL 67 IS 4 BP 226 EP 236 DI 10.1159/000194976 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA 428QR UT WOS:000264864500002 PM 19172082 ER PT J AU Jeffries, NO AF Jeffries, Neal O. TI Ranking Bias in Association Studies SO HUMAN HEREDITY LA English DT Article DE Estimation bias; Multiple comparisons ID GENOME SCANS AB Background: It is widely appreciated that genomewide association studies often yield overestimates of the association of a marker with disease when attention focuses upon the marker showing the strongest relationship. For example, in a case-control setting the largest (in absolute value) estimated odds ratio has been found to typically overstate the association as measured in a second, independent set of data. The most common reason given for this observation is that the choice of the most extreme test statistic is often conditional upon first observing a significant p value associated with the marker. A second, less appreciated reason is described here. Under common circumstances it is the multiple testing of many markers and subsequent focus upon those with most extreme test statistics (i.e. highly ranked results) that leads to bias in the estimated effect sizes. Conclusions: This bias, termed ranking bias, is separate from that arising from conditioning on a significant p value and may often be a more important factor in generating bias. An analytic description of this bias, simulations demonstrating its extent, and identification of some factors leading to its exacerbation are presented. Copyright (C) 2009 S. Karger AG, Basel C1 NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA. RP Jeffries, NO (reprint author), NHLBI, Off Biostat Res, NIH, MSC 7913,6701 Rockledge Dr, Bethesda, MD 20892 USA. EM nealjeff@nhlbi.nih.gov NR 12 TC 7 Z9 7 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0001-5652 J9 HUM HERED JI Hum. Hered. PY 2009 VL 67 IS 4 BP 267 EP 275 DI 10.1159/000194979 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 428QR UT WOS:000264864500005 PM 19172085 ER PT J AU Uribe, M Adams, S Stringaris, K Chouchane, L Marincola, F AF Uribe, M. Adams, S. Stringaris, K. Chouchane, L. Marincola, F. TI HLA AND KIR IN TUNISIANS WITH NPC SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract CT 35th Annual Meeting of the American-Society-for-Histocompatibility-and-Immunogenetics CY NOV 02-06, 2009 CL San Francisco, CA SP Amer Soc Histocompatibil & Immunogenet C1 [Uribe, M.; Adams, S.; Marincola, F.] NIH, HLA Lab, Bethesda, MD 20892 USA. [Stringaris, K.] NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PY 2009 VL 70 BP S138 EP S138 PG 1 WC Immunology SC Immunology GA 517KB UT WOS:000271611200265 ER PT J AU Ranganathan, S Harmison, GG Meyertholen, K Pennuto, M Burnett, BG Fischbeck, KH AF Ranganathan, Srikanth Harmison, George G. Meyertholen, Kristin Pennuto, Maria Burnett, Barrington G. Fischbeck, Kenneth H. TI Mitochondrial abnormalities in spinal and bulbar muscular atrophy SO HUMAN MOLECULAR GENETICS LA English DT Article ID TRANSGENIC MOUSE MODEL; POLYGLUTAMINE ANDROGEN RECEPTOR; AMYOTROPHIC-LATERAL-SCLEROSIS; CREB-BINDING PROTEIN; HUNTINGTONS-DISEASE; EXPANDED POLYGLUTAMINE; ENERGY-METABOLISM; OXIDATIVE STRESS; CELL-DEATH; TRANSCRIPTIONAL COACTIVATOR AB Spinal and bulbar muscular atrophy (SBMA) is a motor neuron disease caused by polyglutamine expansion mutation in the androgen receptor (AR). We investigated whether the mutant protein alters mitochondrial function. We found that constitutive and doxycycline-induced expression of the mutant AR in MN-1 and PC12 cells, respectively, are associated with depolarization of the mitochondrial membrane. This was mitigated by cyclosporine A, which inhibits opening of the mitochondrial permeability transition pore. We also found that the expression of the mutant protein in the presence of ligand results in an elevated level of reactive oxygen species, which is blocked by the treatment with the antioxidants co-enzyme Q10 and idebenone. The mutant protein in MN-1 cells also resulted in increased Bax, caspase 9 and caspase 3. We assessed the effects of mutant AR on the transcription of mitochondrial proteins and found altered expression of the peroxisome proliferator-activated receptor gamma coactivator 1 and the mitochondrial specific antioxidant superoxide dismutase-2 in affected tissues of SBMA knock-in mice. In addition, we found that the AR associates with mitochondria in cultured cells. This study thus provides evidence for mitochondrial dysfunction in SBMA cell and animal models, either through indirect effects on the transcription of nuclear-encoded mitochondrial genes or through direct effects of the mutant protein on mitochondria or both. These findings indicate possible benefit from mitochondrial therapy for SBMA. C1 [Ranganathan, Srikanth; Harmison, George G.; Meyertholen, Kristin; Pennuto, Maria; Burnett, Barrington G.; Fischbeck, Kenneth H.] NINDS, Neurogenet Branch, Bethesda, MD 20892 USA. RP Ranganathan, S (reprint author), NINDS, Neurogenet Branch, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA. EM ranganas@ninds.nih.gov OI Pennuto, Maria/0000-0001-8634-0767 FU NINDS; Fondazione Telethon [GFP04005]; Kennedy's Disease Association FX The work was supported by intramural research funds from the NINDS, and by Fondazione Telethon ( GFP04005) and a Kennedy's Disease Association research grant ( to M. P.). Funding to pay the open access charges was provided by the intramural research funds from the NINDS. NR 81 TC 74 Z9 76 U1 1 U2 6 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD JAN 1 PY 2009 VL 18 IS 1 BP 27 EP 42 DI 10.1093/hmg/ddn310 PG 16 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 383NM UT WOS:000261680300003 PM 18824496 ER PT S AU Kapoor, A Wood, B Mazilu, D Horvath, KA Li, M AF Kapoor, Ankur Wood, Brad Mazilu, Dumitru Horvath, Keith A. Li, Ming GP IEEE TI MRI-compatible Hands-on Cooperative Control of a Pneumatically Actuated Robot SO ICRA: 2009 IEEE INTERNATIONAL CONFERENCE ON ROBOTICS AND AUTOMATION, VOLS 1-7 SE IEEE International Conference on Robotics and Automation ICRA LA English DT Proceedings Paper CT IEEE International Conference on Robotics and Automation CY MAY 12-17, 2009 CL Kobe, JAPAN SP IEEE ID SURGERY; INTERVENTIONS; SYSTEM AB MRI compatible robots are emerging as useful tools for image guided interventions. A shared control between a user and the MRI compatible robot makes it more intuitive instrument especially during setup phases of interventions. We present a MRI compatible, hands-on cooperative system using Innomotion robotic arm. An economic MM compatible user input sensor was developed and its functionality was tested under typical application conditions. Performance improvement in phantom tasks shows promise of adding hands-on interface in MRI compatible robots. C1 [Kapoor, Ankur; Wood, Brad] NIH, Ctr Clin, Bethesda, MD 20892 USA. [Mazilu, Dumitru; Horvath, Keith A.; Li, Ming] Natl Inst Hlth, Natl Heart Lung & Blood Inst, Bethesda, MD 20892 USA. RP Kapoor, A (reprint author), NIH, Ctr Clin, Bethesda, MD 20892 USA. EM kapooran@mail.nih.gov; bwood@mail.nih.gov; mazilud@mail.nih.gov; horvathka@mail.nih.gov; lim2@mail.nih.gov FU Intramural Research Program of the National Institutes of Health (NIH); Clinical Center; National Heart, Lung, and Blood Institute FX This research was supported by the the Intramural Research Program of the National Institutes of Health (NIH), Clinical Center, and National Heart, Lung, and Blood Institute. NR 18 TC 0 Z9 0 U1 0 U2 0 PU IEEE PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 USA SN 1050-4729 BN 978-1-4244-2788-8 J9 IEEE INT CONF ROBOT PY 2009 BP 2281 EP + PG 2 WC Automation & Control Systems; Robotics SC Automation & Control Systems; Robotics GA BOB06 UT WOS:000276080401057 ER PT J AU Chen, J Wong, S Chang, J Chung, PC Li, H Koc, UV Prior, FW Newcomb, R AF Chen, Jie Wong, Stephen Chang, Joseph Chung, Pau-Choo Li, Huai Koc, Ut-Va Prior, Fred W. Newcomb, Robert TI A Wake-Up Call for the Engineering and Biomedical Science Communities SO IEEE CIRCUITS AND SYSTEMS MAGAZINE LA English DT Article AB With the burst of Information Technology (IT) bubble at the beginning of this century, people are looking for the next wave of technology in which to invest. While we believe that biomedical applications and systems are this next stage, unfortunately, the engineering and bioscience communities are unprepared for the many challenges. In order to connect the engineering and the biomedical science communities, we established the LifeScience Systems and Applications (LiSSA) Technical Committee within IEEE Circuits and Systems Society in 2005-an initiative supported by the National Institutes of Health (NIH) through a conference grant to enable dialogue between the engineering and biomedical science communities. Henceforth, we have organized several annual workshops with different themes on the NIH campus. After each workshop, a white paper is published in IEEE circuits and systems magazine to present the major challenges in various chosen theme areas. Recently, we chose "Biomarker Development and Applications" as our workshop theme. For the first time, we invited eight IEEE societies and various NIH institutes to send their representatives for face-to-face dialogue. This article presents the major challenges in biomarker development and applications based on the general consensus of the conference. The aim of the article is to serve as a wake-up call for more engineers to participate in crucial life-science application and systems research. C1 [Chen, Jie] Univ Alberta, Dept Biomed Engn & Elect & Comp Engn, Edmonton, AB, Canada. [Chang, Joseph] Nanyang Technol Univ, Sch Elect & Elect Engn, Singapore, Singapore. [Chung, Pau-Choo] Natl Cheng Kung Univ, Dept Elect Engn, Tainan 70101, Taiwan. [Li, Huai] NIA, NIH, Bethesda, MD 20892 USA. [Prior, Fred W.] Washington Univ, Sch Med, Mallinckrodt Inst Radiol, Elect Radiol Lab, St Louis, MO USA. [Newcomb, Robert] Univ Maryland, Dept Elect & Comp Engn, College Pk, MD 20742 USA. [Chen, Jie] Univ Alberta, Dept Elect & Comp Engn, Edmonton, AB, Canada. [Chen, Jie] Univ Alberta, Dept Biomed Engn, Edmonton, AB, Canada. RP Chen, J (reprint author), Univ Alberta, Dept Biomed Engn & Elect & Comp Engn, Edmonton, AB, Canada. NR 0 TC 1 Z9 1 U1 0 U2 2 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI PISCATAWAY PA 445 HOES LANE, PISCATAWAY, NJ 08855 USA SN 1531-636X J9 IEEE CIRC SYST MAG JI IEEE Circuits Syst. Mag. PY 2009 VL 9 IS 2 BP 69 EP 77 DI 10.1109/MCAS.2009.932557 PG 9 WC Engineering, Electrical & Electronic SC Engineering GA 502CV UT WOS:000270432900006 ER PT J AU Barrett, T Ravizzini, G Choyke, PL Kobayashi, H AF Barrett, Tristan Ravizzini, Gregory Choyke, Peter L. Kobayashi, Hisataka TI Dendrimers in Medical Nanotechnology Application of Dendrimer Molecules in Bioimaging and Cancer Treatment SO IEEE ENGINEERING IN MEDICINE AND BIOLOGY MAGAZINE LA English DT Review ID NEUTRON-CAPTURE THERAPY; IN-VIVO EVALUATION; MAGNETIC-RESONANCE; CONTRAST AGENTS; MONOCLONAL-ANTIBODY; POLYAMIDOAMINE DENDRIMERS; STARBURST DENDRIMERS; POLYETHYLENE-GLYCOL; GOLD NANOPARTICLES; PAMAM DENDRIMERS C1 [Kobayashi, Hisataka] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA. [Choyke, Peter L.] NIH, Ctr Clin, Dept Diagnost Radiol, Bethesda, MD 20892 USA. RP Kobayashi, H (reprint author), NCI, Mol Imaging Program, NIH, Bldg 10,Room 1B40,MSC 1088, Bethesda, MD 20892 USA. EM kobayash@mail.nih.gov FU Intramural NIH HHS [Z99 CA999999] NR 105 TC 36 Z9 38 U1 2 U2 22 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI PISCATAWAY PA 445 HOES LANE, PISCATAWAY, NJ 08855 USA SN 0739-5175 J9 IEEE ENG MED BIOL JI IEEE Eng. Med. Biol. Mag. PD JAN-FEB PY 2009 VL 28 IS 1 BP 12 EP 22 DI 10.1109/MEMB.2008.931012 PG 11 WC Engineering, Biomedical; Medical Informatics SC Engineering; Medical Informatics GA 395RU UT WOS:000262542000005 PM 19150767 ER PT S AU Gandhi, R Kim, YA Lee, S Ryu, J Wan, PJ AF Gandhi, Rajiv Kim, Yoo-Ah Lee, Seungjoon Ryu, Jiho Wan, Peng-Jun GP IEEE TI Approximation Algorithms for Data Broadcast in Wireless Networks SO IEEE INFOCOM 2009 - IEEE CONFERENCE ON COMPUTER COMMUNICATIONS, VOLS 1-5 SE IEEE INFOCOM LA English DT Proceedings Paper CT IEEE INFOCOM Conference 2009 CY APR 19-25, 2009 CL Rio de Janeiro, BRAZIL SP IEEE AB Broadcasting is a fundamental operation in wireless networks and plays an important role in the communication protocol design. In multihop wireless networks, however, interference at a node due to simultaneous transmissions from its neighbors makes it non-trivial to design a minimum-latency broadcast algorithm, which is known to be NP-complete. We present a simple 12-approximation algorithm for the one-to-all broadcast problem that improves all previously known guarantees for this problem. We then consider the all-to-all broadcast problem where each node sends its own message to all other nodes. For the all-to-all broadcast problem, we present two algorithms with approximation ratios of 20 and 34, improving the best result available in the literature. Finally, we report experimental evaluation of our algorithms. Our studies indicate that our algorithms perform much better in practice than the worst-case guarantees provided in the theoretical analysis and achieve up to 37% performance improvement over existing schemes. C1 [Gandhi, Rajiv] Rutgers State Univ, Dept Comp Sci, Camden, NJ 08102 USA. [Kim, Yoo-Ah] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA. [Lee, Seungjoon] AT&T Labs Res, Florham Pk, NJ 07932 USA. [Ryu, Jiho] UNIST, Ulsan 330708, South Korea. [Wan, Peng-Jun] IIT, Dept Comp Sci, Chicago, IL 60616 USA. RP Gandhi, R (reprint author), Rutgers State Univ, Dept Comp Sci, Camden, NJ 08102 USA. EM rajivg@camden.rutgers.edu; ykim@engr.uconn.edu; slee@research.att.com; jhryu@mmlab.snu.ac.kr; wan@cs.iit.edu FU US National Science Foundation [CCF-0830569, CCF-1048606]; National Research Foundation of Korea - Korean Government [NRF-2012R1A6A3A01012020] FX A preliminary version of this paper appeared in the Proceedings of the 28th IEEE INFOCOM, 2009. This work was supported by US National Science Foundation Awards CCF-0830569 and CCF-1048606. This work was supported in part by the National Research Foundation of Korea Grant funded by the Korean Government (NRF-2012R1A6A3A01012020). NR 19 TC 6 Z9 7 U1 0 U2 0 PU IEEE PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 USA SN 0743-166X BN 978-1-4244-3512-8 J9 IEEE INFOCOM SER PY 2009 BP 2681 EP + DI 10.1109/INFCOM.2009.5062211 PG 2 WC Computer Science, Hardware & Architecture; Engineering, Electrical & Electronic; Telecommunications SC Computer Science; Engineering; Telecommunications GA BNS10 UT WOS:000275366201111 ER PT J AU Li, RJ Principe, JC Bradley, M Ferrari, V AF Li, Ruijiang Principe, Jose C. Bradley, Margaret Ferrari, Vera TI A Spatiotemporal Filtering Methodology for Single-Trial ERP Component Estimation SO IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING LA English DT Article DE Event-related potentials (ERPs); single-trial estimation; spatiotemporal filtering ID EEG; CLASSIFICATION; LOCALIZATION; HABITUATION; BRAIN AB A new spatiotemporal filtering method for single-trial event-related potential (EPP) estimation is proposed. Instead of attempting to model the entire ERP waveform, the method relies on modeling ERP component descriptors (amplitude and latency) thru the spatial diversity of multichannel recordings, and thus, it is tailored to extract signals in negative SNR conditions. The model allows for both amplitude and latency variability in the ERP component under investigation. The extracted ERP component is constrained through a spatial filter to have minimal distance (with respect to some metric) in the temporal domain from a user-designed template component. The spatial filter may be interpreted as a noise canceller in the spatial domain. Study with both simulated data and real cognitive ERP data shows the effectiveness of the proposed method. C1 [Li, Ruijiang; Principe, Jose C.] Univ Florida, Dept Elect & Comp Engn, Computat NeuroEngn Lab, Gainesville, FL 32611 USA. [Bradley, Margaret; Ferrari, Vera] Univ Florida, Ctr Study Emot & Attent, NIMH, Gainesville, FL 32611 USA. RP Li, RJ (reprint author), Univ Florida, Dept Elect & Comp Engn, Computat NeuroEngn Lab, Gainesville, FL 32611 USA. EM ruijiang@cnel.ufl.edu; principe@cnel.ufl.edu; bradley@ufl.edu; vferrari@ufl.edu FU Graduate Alumni Fellowship from the University of Florida; National Institute of Mental Health (NIMH) [P50 MH072850-01] FX This work was supported in part by Graduate Alumni Fellowship from the University of Florida and in part by the National Institute of Mental Health (NIMH) under Grant P50 MH072850-01. NR 31 TC 16 Z9 19 U1 0 U2 3 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI PISCATAWAY PA 445 HOES LANE, PISCATAWAY, NJ 08855 USA SN 0018-9294 J9 IEEE T BIO-MED ENG JI IEEE Trans. Biomed. Eng. PD JAN PY 2009 VL 56 IS 1 BP 83 EP 92 DI 10.1109/TBME.2008.2002153 PG 10 WC Engineering, Biomedical SC Engineering GA 411HR UT WOS:000263640900011 PM 19224722 ER PT J AU Wang, ZS Maier, A Logothetis, NK Liang, HL AF Wang, Zhisong Maier, Alexander Logothetis, Nikos K. Liang, Hualou TI Relaxation-Based Feature Selection for Single-Trial Decoding of Bistable Perception SO IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING LA English DT Article DE Bistable stimuli; feature selection; local field potential (LFP); middle temporal (MT); multitaper spectral analysis; perception; redundancy; relaxation (RELAX); relevance; sequential forward selection (SFS); single-trial decoding; structure-from-motion (SFM); support vector machines (SVMs) ID FEATURE SUBSET-SELECTION; GAMMA-OSCILLATIONS; EVOKED-POTENTIALS; DECISION-MAKING; CORTEX; BRAIN; ALGORITHMS; ATTENTION; CHOICE AB Bistable perception refers to the phenomenon of spontaneously alternating percepts while viewing the same stimulus continuously. Bistable stimuli allow dissociation between stimuli and perception, and thus, provide a unique opportunity for understanding the neural basis of visual perception. In this paper, we focus on a relaxation (RELAX) based algorithm to select features from the multitaper spectral estimates of the multichannel intracortical local field potential (UP), simultaneously collected from the middle temporal visual cortex of a macaque monkey, for decoding its bistable structure-from-motion (SFM) perception. We demonstrate that RELAX surpasses the conventional sequential forward selection (SFS) by offering the flexibility of modifying selected features. We propose a redundancy reduction preprocessing technique to significantly reduce the computational load for both SFS and RELAX. We exploit the support vector machines classifier based on the selected features for single-trial decoding the reported perception. Our results demonstrate the excellent performance of the RELAX feature selection algorithm. Furthermore, we find that the features in the gamma frequency band (30-100 Hz) of LFP are most relevant to bistable SFM perception. This finding is novel in awake monkey studies and suggests that gamma oscillations carry the most discriminative information for bistable perception of SFM stimuli. C1 [Wang, Zhisong; Liang, Hualou] Univ Texas Houston, Hlth Sci Ctr, Sch Hlth Informat Sci, Houston, TX 77030 USA. [Maier, Alexander] NIMH, Unit Cognit Neurophysiol & Imaging, Bethesda, MD 20892 USA. [Logothetis, Nikos K.] Max Planck Inst Biol Cybernet, D-72076 Tubingen, Germany. RP Liang, HL (reprint author), Drexel Univ, Sch Biomed Engn, Philadelphia, PA 19104 USA. EM hualou.liang@drexel.edu RI Maier, Alexander/B-7489-2009 OI Maier, Alexander/0000-0002-7250-502X FU National Institutes of Health (NIH) [R01MH072034]; Max Planck Society FX This work was supported in part by the National Institutes of Health (NIH) under Grant R01MH072034 and in part by the Max Planck Society. NR 43 TC 1 Z9 1 U1 0 U2 0 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI PISCATAWAY PA 445 HOES LANE, PISCATAWAY, NJ 08855 USA SN 0018-9294 J9 IEEE T BIO-MED ENG JI IEEE Trans. Biomed. Eng. PD JAN PY 2009 VL 56 IS 1 BP 101 EP 110 DI 10.1109/TBME.2008.2003260 PG 10 WC Engineering, Biomedical SC Engineering GA 411HR UT WOS:000263640900013 PM 19224724 ER PT J AU Zhou, QF Cha, JH Huang, YH Zhang, R Cao, WW Shung, KK AF Zhou, Qifa Cha, Jung Hyui Huang, Yuhong Zhang, Rui Cao, Wenwu Shung, K. Kirk TI Alumina/Epoxy Nanocomposite Matching Layers for High-Frequency Ultrasound Transducer Application SO IEEE TRANSACTIONS ON ULTRASONICS FERROELECTRICS AND FREQUENCY CONTROL LA English DT Article ID MHZ AB Mismatch of acoustic impedance at the interface between a piezoelectric transducer and the medium to he probed will substantially reduce the amount of ultrasound energy being transmitted into the medium. Therefore, matching layer is a critical component of air ultrasonic transducer. A spin-coating process was used to fabricate alumina/polymer nanocomposite films with alumina volume fractions ranging from 14 to 32%. The particle size of alumina is in tire range of 10 to 40 nm. The thicknesses of the matching layer can be controlled trolled by the spinning speed and the concentration of solution Acoustic impedances of these nanocomposite matching layers are in the range, of 2.8 to 5.1 MRayls with different alumina contents, which meet, Hie matching layer requirement. The attenuation of a nanocomposite matching layer with smooth surface is about 15 dB/mm at 40 MHz. The pulse-echo spectrum and frequency spectrum of a high-frequency transducer using this nanocomposite matching layer are reported. C1 [Zhou, Qifa; Cha, Jung Hyui; Shung, K. Kirk] Univ So Calif, Dept Biomed Engn, Los Angeles, CA 90089 USA. [Zhou, Qifa; Cha, Jung Hyui; Shung, K. Kirk] Univ So Calif, NIH, Transducer Resource Ctr, Los Angeles, CA 90089 USA. [Huang, Yuhong] Chemat Technol Inc, Northridge, CA USA. [Zhang, Rui; Cao, Wenwu] Penn State Univ, Mat Res Lab, University Pk, PA 16802 USA. RP Zhou, QF (reprint author), Univ So Calif, Dept Biomed Engn, Los Angeles, CA 90089 USA. RI Cao, Wenwu/F-6091-2012 OI Cao, Wenwu/0000-0002-2447-1486 FU NIH [P41-EB2182, 1 R43 EB003244-01A1] FX The authors gratefully acknowledge the financial support from the NIH under Grant, #P41-EB2182 and 1 R43 EB003244-01A1. NR 9 TC 15 Z9 15 U1 5 U2 29 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI PISCATAWAY PA 445 HOES LANE, PISCATAWAY, NJ 08855 USA SN 0885-3010 J9 IEEE T ULTRASON FERR JI IEEE Trans. Ultrason. Ferroelectr. Freq. Control PD JAN PY 2009 VL 56 IS 1 BP 213 EP 219 DI 10.1109/TUFFC.2009.1021 PG 7 WC Acoustics; Engineering, Electrical & Electronic SC Acoustics; Engineering GA 395ZI UT WOS:000262561600024 PM 19213648 ER PT S AU Wang, SJ Summers, RM Zhang, CS AF Wang, Shijun Summers, Ronald M. Zhang, Changshui GP IEEE TI A Fast Mean-field Method for Large-scale High-dimensional data and its Application in Colonic Polyp Detection at CT Colonography SO IJCNN: 2009 INTERNATIONAL JOINT CONFERENCE ON NEURAL NETWORKS, VOLS 1- 6 SE IEEE International Joint Conference on Neural Networks (IJCNN) LA English DT Proceedings Paper CT International Joint Conference on Neural Networks CY JUN 14-19, 2009 CL Atlanta, GA SP Int Neural Network Soc, IEEE Computat Intelligence Soc ID DIFFUSION MAPS; REDUCTION; FRAMEWORK AB In this paper, we propose a fast mean-field method called LHMF to handle probabilistic models of large-scale data in high dimensional space. By using diffusion map locally linear embedding method which is a non-linear dimensionality reduction method, we first embed the high dimensional data into a low dimensional space. Then we construct a coarse-grained graph which preserves the spectral properties of original weighted graph in the high dimensional space by clustering. A new spin model is defined in the diffusion space and the geometric centroids of clusters represent variables in the new spin model. The calculation demand of mean-field methods can be reduced greatly on the coarse-grained spin model. The final marginal moments of original variables are derived from the states of geometric centroids by using geometric harmonics. We first tested the proposed method on the MNIST hand-written digits dataset. Experimental results show that the LHMF method is competent with consistency approach, a state-of-the-art semi-supervised learning method. Then we applied the proposed method to a large-scale colonic polyp dataset from computed tomography (CT) scans. Free-response operator characteristic analysis shows that our method achieves higher sensitivity with lower false positive rate compared with support vector machines. C1 [Wang, Shijun; Summers, Ronald M.] NIH, Dept Radiol & Imaging Sci, Bethesda, MD 20892 USA. [Zhang, Changshui] Tsinghua Univ, Dept Automat, Tsinghua Natl Lab Informat Sci & Technol TNList, State Key Lab Informat Technol & Syst, Beijing 100084, Peoples R China. RP Wang, SJ (reprint author), NIH, Dept Radiol & Imaging Sci, Bethesda, MD 20892 USA. FU Intramural Research Program of the NIH Clinical Center; National Natural Science Foundation of China [60835002] FX This research was supported by the Intramural Research Program of the NIH Clinical Center and National Natural Science Foundation of China (NSFC Grant No. 60835002 ). This study utilized the high-performance computational capabilities of the NIH Biowulf PClLinux cluster. We also thank Drs. Perry Pickhardt, Richard Choi and William Schindler for CT colonography data. NR 24 TC 0 Z9 0 U1 0 U2 0 PU IEEE PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 USA SN 2161-4393 BN 978-1-4244-3549-4 J9 IEEE IJCNN PY 2009 BP 402 EP + PG 3 WC Computer Science, Artificial Intelligence; Computer Science, Hardware & Architecture; Engineering, Electrical & Electronic SC Computer Science; Engineering GA BQB78 UT WOS:000280591600059 ER PT S AU DeLeo, J Leonard, C Sumner, AE AF DeLeo, Jim Leonard, Carl Sumner, Anne E. GP IEEE TI Constructing Clinical Scoring Systems to Determine the Need for an Oral Glucose Tolerance Test SO IJCNN: 2009 INTERNATIONAL JOINT CONFERENCE ON NEURAL NETWORKS, VOLS 1- 6 SE IEEE International Joint Conference on Neural Networks (IJCNN) LA English DT Proceedings Paper CT International Joint Conference on Neural Networks CY JUN 14-19, 2009 CL Atlanta, GA SP Int Neural Network Soc, IEEE Computat Intelligence Soc ID INSULIN-RESISTANCE; LIFE-STYLE AB We developed a methodology for constructing scoring systems to support bivalent decision making in clinical medicine. Such systems could be of great benefit in forced-choice decision-making situations as well as in triaging, screening, and diagnostic applications. Our methodology combines medical judgment with explicit computer-derived information to identify an optimum parsimonious set of variables for predicting bivalent (2-class) outcomes. It includes a process for using these variables to produce scores for each negative (d=0) and positive (d=1) class entity and for using these scores in decision making. We produced this methodology while attempting to devise a system that determines which African Americans are most likely to be glucose intolerant (i.e. pre-diabetic) and hence would benefit by taking an oral glucose tolerance test. We achieved excellent results as evidenced by ROC plot areas of .85 for men alone and .94 for women alone. We anticipate actual clinical use of the scoring systems that we constructed. We also anticipate constructing and deploying other similar useful clinical decision support systems with our methodology. C1 [DeLeo, Jim; Leonard, Carl] NIH, Ctr Clin, Bethesda, MD 20892 USA. [Sumner, Anne E.] Natl Inst Diabetes & Digest & Kidney Diseases, Bethesda, MD 20892 USA. RP DeLeo, J (reprint author), NIH, Ctr Clin, Bethesda, MD 20892 USA. EM jdeleo@nih.gov; cleonard@lired.com; AnneS@niddk.nih.gov NR 12 TC 0 Z9 0 U1 0 U2 0 PU IEEE PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 USA SN 2161-4393 BN 978-1-4244-3549-4 J9 IEEE IJCNN PY 2009 BP 2490 EP + PG 2 WC Computer Science, Artificial Intelligence; Computer Science, Hardware & Architecture; Engineering, Electrical & Electronic SC Computer Science; Engineering GA BQB78 UT WOS:000280591601104 ER PT J AU Bauer, TR Adler, RL Hickstein, DD AF Bauer, Thomas R., Jr. Adler, Rima L. Hickstein, Dennis D. TI Potential Large Animal Models for Gene Therapy of Human Genetic Diseases of Immune and Blood Cell Systems SO ILAR JOURNAL LA English DT Review DE anemia; gene therapy; genetic disease; hematopoietic; immunodeficiency; integrin; leukocyte; transplantation ID CHEDIAK-HIGASHI-SYNDROME; SEVERE COMBINED IMMUNODEFICIENCY; LEUKOCYTE ADHESION DEFICIENCY; BONE-MARROW-TRANSPLANTATION; PYRUVATE-KINASE DEFICIENCY; DEPENDENT PROTEIN-KINASE; HEREDITARY HEMOLYTIC-ANEMIA; I GLANZMANNS-THROMBASTHENIA; HERMANSKY-PUDLAK-SYNDROME; COLONY-STIMULATING FACTOR AB Genetic mutations involving the cellular components of the hematopoietic system-red blood cells, white blood cells, and platelets-manifest clinically as anemia, infection, and bleeding. Although gene targeting has recapitulated many of these diseases in mice, these murine homologues are limited as translational models by their small size and brief life span as well as the fact that mutations induced by gene targeting do not always faithfully reflect the clinical manifestations of such mutations in humans. Many of these limitations can be overcome by identifying large animals with genetic diseases of the hematopoietic system corresponding to their human disease counterparts. In this article, we describe human diseases of the cellular components of the hematopoietic system that have counterparts in large animal species, in most cases carrying mutations in the same gene (CD18 in leukocyte adhesion deficiency) or genes in interacting proteins (DNA cross-link repair 1C protein and protein kinase, DNA-activated catalytic polypeptide in radiation-sensitive severe combined immunodeficiency). Furthermore, we describe the potential of these animal models to serve as disease-specific preclinical models for testing the efficacy and safety of clinical interventions such as hematopoietic stem cell transplantation or gene therapy before their use in humans with the corresponding disease. C1 [Bauer, Thomas R., Jr.; Hickstein, Dennis D.] NCI, Mol Oncol & Gene Transfer Sect, ETIB, Ctr Canc Res,Natl Inst Hlth, Bethesda, MD 20892 USA. RP Bauer, TR (reprint author), NCI, Mol Oncol & Gene Transfer Sect, ETIB, Ctr Canc Res,Natl Inst Hlth, 10 Ctr Dr,MSC1203,Bldg 10 CRC,Rm 3-3264, Bethesda, MD 20892 USA. EM bauert@mail.nih.gov FU Intramural Research Program of the US National Institutes of Health; National Cancer Institute, Center for Cancer Research FX This work was supported by the Intramural Research Program of the US National Institutes of Health, National Cancer Institute, Center for Cancer Research. NR 207 TC 15 Z9 15 U1 0 U2 5 PU INST LABORATORY ANIMAL RESEARCH, NATL RES COUNCIL PI WASHINGTON PA 500 FIFTH ST, N W, WASHINGTON, DC 20001 USA SN 1084-2020 J9 ILAR J JI ILAR J. PY 2009 VL 50 IS 2 BP 168 EP 186 PG 19 WC Veterinary Sciences SC Veterinary Sciences GA 448ZW UT WOS:000266301500006 PM 19293460 ER PT S AU Frenkel, V AF Frenkel, Victor BE Vaezy, S Zderic, V TI Ultrasound Mediated Drug and Gene Delivery SO IMAGE-GUIDED THERAPY SYSTEMS SE Engineering in Medicine and Biology LA English DT Article; Book Chapter ID INTENSITY FOCUSED ULTRASOUND; TEMPERATURE-SENSITIVE LIPOSOMES; LOW-FREQUENCY ULTRASOUND; BLOOD-BRAIN-BARRIER; TISSUE-PLASMINOGEN ACTIVATOR; MR CONTRAST AGENT; IN-VIVO; RADIATION-FORCE; SOLID TUMORS; THERMOSENSITIVE LIPOSOMES AB Therapeutic ultrasound is best known for its ability to thermally ablate tissue, which has been shown to be effective for the treatment of tumors and uterine fibroids. Nondestructive exposures, however, may be used for enhancing drug and gene delivery, where the mechanisms for doing so are predominantly nonthermal. Presently, low intensity, nonfocused beams are being used in physical therapy for enhancing local transdermal delivery of therapeutically beneficial agents. However, there is a multitude of preclinical examples in the literature demonstrating how focused ultrasound beams can be used to generate increases in the permeability of deeper tissues for enhancing the delivery of conventional agents, as well as for deploying and activating drugs and genes using specially tailored vehicles and formulations. In this chapter, the development of these applications will be described and an emphasis will be placed on the relevant ultrasound mechanisms involved. By using image guidance to deliver the ultrasound energy safely and efficiently for these applications, therapeutic ultrasound holds much promise to further the treatment of cancer and other diseases. C1 NIH, Radiol & Imaging Sci Clin Ctr, Bethesda, MD 20892 USA. RP Frenkel, V (reprint author), NIH, Radiol & Imaging Sci Clin Ctr, 10 Ctr Dr, Bethesda, MD 20892 USA. EM vfrenkel@cc.nih.gov NR 126 TC 0 Z9 0 U1 0 U2 3 PU ARTECH HOUSE PI NORWOOD PA 685 CANTON ST, NORWOOD, MA 02062 USA SN 0278-0054 BN 978-1-59693-109-1 J9 ENG MED BIOL JI Eng. Med. Biol. PY 2009 BP 177 EP 196 PG 20 WC Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging SC Engineering; Radiology, Nuclear Medicine & Medical Imaging GA BKL87 UT WOS:000268458600010 ER PT S AU Kwan, JY AF Kwan, Justin Y. BE Pourmand, R TI Dysimmune Neuropathy SO IMMUNE-MEDIATED NEUROMUSCULAR DISEASES SE Frontiers of Neurology and Neuroscience LA English DT Article; Book Chapter ID MYELIN-ASSOCIATED GLYCOPROTEIN; IGM MONOCLONAL GAMMOPATHY; ENDOTHELIAL GROWTH-FACTOR; PLASMA-CELL DYSCRASIA; ANTI-MAG POLYNEUROPATHY; CROW-FUKASE-SYNDROME; UNDETERMINED SIGNIFICANCE; PERIPHERAL NEUROPATHY; POEMS SYNDROME; MULTIPLE-MYELOMA AB Dysimmune neuropathy is an etiologically heterogeneous entity with diverse clinical presentations. The underlying causes encompass several different benign and neoplastic syndromes. Peripheral nervous system manifestations are common, and in some cases, the initial symptom of the abnormal immune system. Early recognition of the immunologic disturbance or malignancy as the cause of neuropathy with appropriate diagnostic testing is necessary so that potentially effective therapies can be initiated. This review discusses evaluation, differential diagnosis, clinical findings, pathophysiology, and treatment of disease states with abnormal immunoglobulin production that are associated with peripheral neuropathies. Copyright (C) 2009 S. Karger AG, Basel C1 NINDS, EMG Sect, NIH, Bethesda, MD 20892 USA. RP Kwan, JY (reprint author), NINDS, EMG Sect, NIH, Bldg 10 CRC Room 7-5680,10 Ctr Dr MSC 1404, Bethesda, MD 20892 USA. EM kwanjy@ninds.nih.gov NR 114 TC 2 Z9 2 U1 0 U2 0 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 1660-4431 BN 978-3-8055-9141-6 J9 FRONT NEUROL NEUROSC JI Front. Neurol. Neurosci. PY 2009 VL 26 BP 67 EP 84 PG 18 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA BKL49 UT WOS:000268434800004 PM 19349705 ER PT J AU Jiang, CC Zhao, ML Diaz, M AF Jiang, Chuancang Zhao, Ming Lang Diaz, Marilyn TI Activation-induced deaminase heterozygous MRL/lpr mice are delayed in the production of high-affinity pathogenic antibodies and in the development of lupus nephritis SO IMMUNOLOGY LA English DT Article DE affinity maturation; autoantibodies; autoimmunity; B cells; immunogenetics ID INDUCED CYTIDINE DEAMINASE; CLASS SWITCH RECOMBINATION; DNA B-CELLS; MRL-LPR/LPR MICE; SOMATIC HYPERMUTATION; GENETIC DISSECTION; RHEUMATOID FACTORS; MURINE LUPUS; PRONE MICE; DEFICIENCY CAUSES AB We previously reported that activation-induced deaminase (AID) heterozygous MRL/lpr mice have substantially lower levels of serum anti-dsDNA autoantibodies than AID wild-type littermates. Given the known functions of AID, here we examined whether this decrease in pathogenic autoantibodies in the heterozygotes was the result of a defect in class switch recombination, somatic hypermutation, or both. We report significant impairment of switch recombination to most isotypes except immunoglobulin G3 (IgG3) in vitro. However, serum levels of IgG were similar to AID wild-type levels even in very young mice. Mutation accumulation in the B cells from Peyer's patches also revealed reduced somatic hypermutation in the heterozygotes. Unlike the switch defect, the hypermutation defect probably resulted in an in vivo effect because the serum IgG antibodies from the heterozygotes were of strikingly lower affinity to dsDNA than serum IgG antibodies from wild-type littermates. This suggests that the somatic hypermutation defect resulted in impaired affinity maturation of autoantibodies in these mice and explains the low levels of specific anti-dsDNA antibodies in the heterozygotes. This correlated with a delay in the development of kidney damage. These results imply that AID levels impact the class switch recombination and somatic hypermutation mechanisms and directly implicate affinity maturation of autoantibodies in autoimmunity. C1 [Jiang, Chuancang; Zhao, Ming Lang; Diaz, Marilyn] D3 01 Natl Inst Environm Hlth Sci, Mol Genet Lab, NIH, Res Triangle Pk, NC 27709 USA. RP Diaz, M (reprint author), D3 01 Natl Inst Environm Hlth Sci, Mol Genet Lab, NIH, 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA. EM diaz@niehs.nih.gov FU National Institutes of Health; National Institute of Environmental Health Sciences FX We are grateful to John W. Drake, Laurent Verkoczy and Tom Kunkel for editing and commenting on the manuscript. We also thank Ron Herbert, Natasha Clayton and Warren Lieuallen for histological and electron microscopy analyses and Carl Bortner and Maria Sifre for assistance with flow cytometry. This research was supported by the Intramural Research Program of the National Institutes of Health, National Institute of Environmental Health Sciences. NR 63 TC 27 Z9 27 U1 0 U2 2 PU WILEY-BLACKWELL PUBLISHING, INC PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0019-2805 J9 IMMUNOLOGY JI Immunology PD JAN PY 2009 VL 126 IS 1 BP 102 EP 113 DI 10.1111/j.1365-2567.2008.02882.x PG 12 WC Immunology SC Immunology GA 381ID UT WOS:000261528300012 PM 18624728 ER PT J AU Wang, RX Han, GC Song, L Wang, JA Chen, GJ Xu, RA Yu, M Qian, JH Shen, BF Li, Y AF Wang, Renxi Han, Gencheng Song, Lun Wang, Jianan Chen, Guojiang Xu, Ruonan Yu, Ming Qian, Jiahua Shen, Beifen Li, Yan TI CD8(+) regulatory T cells are responsible for GAD-IgG gene-transferred tolerance induction in NOD mice SO IMMUNOLOGY LA English DT Article DE CD8(+) regulatory T cells; diabetes; gene therapy; NOD mice; tolerance ID GLUTAMIC-ACID DECARBOXYLASE; TGF-BETA; FUSION PROTEINS; B-CELLS; IMMUNE-RESPONSES; FOXP3; CD4(+); EXPRESSION; AUTOIMMUNITY; MAINTENANCE AB Our previous studies demonstrated that lipopolysaccharide (LPS)-stimulated splenocytes, retrovirally transduced with a glutamate decarboxylate 65 (GAD) and immunoglobulin G (IgG) fusion construct, can protect non-obese diabetic (NOD) mice from diabetes by inducing GAD-specific tolerance, and also that there are increased numbers of CD4(+) regulatory T cells (Tregs) in GAD-IgG-treated NOD mice. However, little is known about the role of CD8(+) Tregs in GAD-IgG gene-transferred tolerance induction in NOD mice. Here, we found that GAD-IgG-transduced splenocytes induced an increase in the number of CD8(+) Foxp3(+) Tregs in vitro. Using a T-cell depletion assay, we found that, compared with undepleted groups, NOD recipients transfused with CD8(-) or CD8(-) CD25(-) GAD-IgG-transduced splenocytes showed a decrease in the percentage of CD8(+) Foxp3(+) T cells, a high incidence of diabetes, serious insulitis, GAD-specific hyperresponsiveness at both the cellular and humoral levels, and changes in cytokine expression. These results indicate that CD8(+) Tregs, which were induced in vitro by GAD-IgG-transduced splenocytes, were also responsible for GAD-IgG gene-transferred tolerance induction in NOD mice. C1 [Wang, Renxi; Han, Gencheng; Song, Lun; Wang, Jianan; Chen, Guojiang; Xu, Ruonan; Yu, Ming; Shen, Beifen; Li, Yan] Inst Basic Med Sci, Dept Mol Immunol, Beijing 100850, Peoples R China. [Qian, Jiahua] NCI, NIH, Bethesda, MD 20892 USA. RP Li, Y (reprint author), Inst Basic Med Sci, Dept Mol Immunol, Tai Ping Rd 27, Beijing 100850, Peoples R China. EM liyan62033@yahoo.com.cn FU National Nature and Science Funds [30571732]; National '973' Fund [2007CB512406] FX We gratefully acknowledge Dr Jiannan Feng for useful advice. This work was supported by National Nature and Science Funds (30571732) and National '973' Fund Grant 2007CB512406. NR 39 TC 10 Z9 11 U1 1 U2 5 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0019-2805 J9 IMMUNOLOGY JI Immunology PD JAN PY 2009 VL 126 IS 1 BP 123 EP 131 DI 10.1111/j.1365-2567.2008.02884.x PG 9 WC Immunology SC Immunology GA 381ID UT WOS:000261528300014 PM 18624731 ER PT J AU Marincola, FM AF Marincola, Francesco M. TI Future of immunotherapy: a call for comparative immunology FOREWORD SO IMMUNOTHERAPY LA English DT Editorial Material ID OVARIAN-CANCER; REJECTION; RELEVANCE; TISSUE; TUMORS; CELLS C1 NIH, IDIS, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA. RP Marincola, FM (reprint author), NIH, IDIS, Dept Transfus Med, Ctr Clin, 9000 Rockville Pike, Bethesda, MD 20892 USA. EM fmarincola@mail.cc.nih.gov NR 21 TC 5 Z9 5 U1 0 U2 3 PU FUTURE MEDICINE LTD PI LONDON PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3 1QB, ENGLAND SN 1750-743X J9 IMMUNOTHERAPY JI Immunotherapy PD JAN PY 2009 VL 1 IS 1 BP 1 EP 3 DI 10.2217/1750-743X.1.1.1 PG 3 WC Immunology SC Immunology GA 541IV UT WOS:000273409400001 PM 20635965 ER PT J AU Chase, JC Celli, J Bosio, CM AF Chase, Jennifer C. Celli, Jean Bosio, Catharine M. TI Direct and Indirect Impairment of Human Dendritic Cell Function by Virulent Francisella tularensis Schu S4 SO INFECTION AND IMMUNITY LA English DT Article ID PATHOGENICITY ISLAND; ENDOTOXIN TOLERANCE; PORPHYROMONAS-GINGIVALIS; MOLECULAR-MECHANISMS; BURKHOLDERIA-MALLEI; MEASLES-VIRUS; INFECTION; ACTIVATION; MICE; LIPOPOLYSACCHARIDE AB The gram-negative, facultative intracellular bacterium Francisella tularensis causes acute, lethal pneumonic disease following infection with only 10 CFU. The mechanisms used by the bacterium to accomplish this in humans are unknown. Here, we demonstrate that virulent, type A F. tularensis strain Schu S4 efficiently infects and replicates in human myeloid dendritic cells (DCs). Despite exponential replication over time, Schu S4 failed to stimulate transforming growth factor beta, interleukin-10 (IL-10), IL-6, IL-1 beta, IL-12, tumor necrosis factor alpha, alpha interferon (IFN-alpha), and IFN-beta throughout the course of infection. Schu S4 also suppressed the ability of directly infected DCs to respond to different Toll-like receptor agonists. Furthermore, we also observed functional inhibition of uninfected bystander cells. This inhibition was mediated, in part, by a heat-stable bacterial component. Lipopolysaccharide (LPS) from Schu S4 was present in Schu S4-conditioned medium. However, Schu S4 LPS was weakly inflammatory and failed to induce suppression of DCs at concentrations below 10 mu g/ml, and depletion of Schu S4 LPS did not significantly alleviate the inhibitory effect of Schu S4-conditioned medium in uninfected human DCs. Together, these data show that type A F. tularensis interferes with the ability of a central cell type of the immune system, DCs, to alert the host of infection both intra-and extracellularly. This suggests that immune dysregulation by F. tularensis operates on a broader and more comprehensive scale than previously appreciated. C1 [Chase, Jennifer C.; Bosio, Catharine M.] NIAID, Immun Pulm Pathogens Sect, Intracellular Parasites Lab, Rocky Mt Labs,NIH, Hamilton, MT 59840 USA. [Celli, Jean] NIAID, Tularemia Pathogenesis Sect, Intracellular Parasites Lab, Rocky Mt Labs,NIH, Hamilton, MT 59840 USA. RP Bosio, CM (reprint author), NIAID, Immun Pulm Pathogens Sect, Intracellular Parasites Lab, Rocky Mt Labs,NIH, 303 S 4th St, Hamilton, MT 59840 USA. EM bosioc@niaid.nih.gov RI Bosio, Catharine/D-7456-2015 FU Intramural Research Program of the National Institutes of Health; National Institute of Allergy and Infectious Diseases FX This work was supported by the Intramural Research Program of the National Institutes of Health, National Institute of Allergy and Infectious Diseases. NR 52 TC 58 Z9 58 U1 0 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 2009 VL 77 IS 1 BP 180 EP 195 DI 10.1128/IAI.00879-08 PG 16 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 399BT UT WOS:000262776100017 PM 18981246 ER PT J AU Voth, DE Heinzen, RA AF Voth, Daniel E. Heinzen, Robert A. TI Sustained Activation of Akt and Erk1/2 Is Required for Coxiella burnetii Antiapoptotic Activity SO INFECTION AND IMMUNITY LA English DT Article ID MONOCYTE-DERIVED MACROPHAGES; NF-KAPPA-B; HOST-CELL; LEGIONELLA-PNEUMOPHILA; PROTEIN-KINASE; MALIGNANT-TRANSFORMATION; CHLAMYDIA-TRACHOMATIS; SIGNALING PATHWAY; DRUG-RESISTANCE; APOPTOSIS AB Coxiella burnetii is an obligate intracellular bacterial pathogen that directs biogenesis of a lysosome-like, parasitophorous vacuole in mammalian cells. We recently reported that C. burnetii inhibits apoptotic cell death in macrophages, presumably as a mechanism to sustain the host for completion of its lengthy infectious cycle. In the current study, we further investigated C. burnetii manipulation of host cell signaling and apoptosis by examining the effect of C. burnetii infection on activation of 15 host proteins involved in stress responses, cytokine production, and apoptosis. C. burnetii infection of THP-1 human macrophage-like cells caused increased levels of phosphorylated c-Jun, Hsp27, Jun N-terminal protein kinase, and p38 at 2 h postinfection (hpi), and this activation rapidly decreased to near basal levels by 24 hpi. The prosurvival kinases Akt and Erk1/2 (extracellular signal-regulated kinases 1 and 2) were also activated at 2 to 6 hpi; however, the phosphorylation of these proteins increased coincident with C. burnetii replication through at least 72 hpi. Sustained phosphorylation of Akt and Erk1/2 was abolished by treatment of infected cells with rifampin, indicating their activation is a C. burnetii-directed event requiring pathogen RNA synthesis. Moreover, pharmacological inhibition of Akt or Erk1/2 significantly decreased C. burnetii antiapoptotic activity. Collectively, these results indicate the importance of C. burnetii modulation of host signaling and demonstrate a critical role for Akt and Erk1/2 in successful intracellular parasitism and maintenance of host cell viability. C1 [Voth, Daniel E.; Heinzen, Robert A.] NIAID, Coxiella Pathogenesis Sect, Intracellular Parasites Lab, Rocky Mt Labs,NIH, Hamilton, MT 59840 USA. RP Heinzen, RA (reprint author), NIAID, Coxiella Pathogenesis Sect, Intracellular Parasites Lab, Rocky Mt Labs,NIH, 903 S 4th St, Hamilton, MT 59840 USA. EM rheinzen@niaid.nih.gov FU Intramural Research Program of the National Institutes of Health; National Institute of Allergy and Infectious Diseases FX This research was supported by the Intramural Research Program of the National Institutes of Health, National Institute of Allergy and Infectious Diseases. NR 48 TC 51 Z9 51 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 2009 VL 77 IS 1 BP 205 EP 213 DI 10.1128/IAI.01124-08 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 399BT UT WOS:000262776100019 PM 18981248 ER PT J AU Swanson, KA Taylor, LD Frank, SD Sturdevant, GL Fischer, ER Carlson, JH Whitmire, WM Caldwell, HD AF Swanson, Kena A. Taylor, Lacey D. Frank, Shaun D. Sturdevant, Gail L. Fischer, Elizabeth R. Carlson, John H. Whitmire, William M. Caldwell, Harlan D. TI Chlamydia trachomatis Polymorphic Membrane Protein D Is an Oligomeric Autotransporter with a Higher-Order Structure SO INFECTION AND IMMUNITY LA English DT Article ID PYLORI-VACUOLATING-CYTOTOXIN; HOST-CELLS; SURFACE PROJECTIONS; GENOME SEQUENCE; INTRACELLULAR PATHOGEN; ELECTRON-MICROSCOPY; INFECTED CELLS; PSITTACI; PNEUMONIAE; ACTIVATION AB Chlamydia trachomatis is a globally important obligate intracellular bacterial pathogen that is a leading cause of sexually transmitted disease and blinding trachoma. Effective control of these diseases will likely require a preventative vaccine. C. trachomatis polymorphic membrane protein D (PmpD) is an attractive vaccine candidate as it is conserved among C. trachomatis strains and is a target of broadly cross-reactive neutralizing antibodies. We show here that immunoaffinity-purified native PmpD exists as an oligomer with a distinct 23-nm flower-like structure. Two-dimensional blue native-sodium dodecyl sulfate-polyacrylamide gel electrophoresis analyses showed that the oligomers were composed of full-length PmpD (p155) and two proteolytically processed fragments, the p73 passenger domain (PD) and the p82 translocator domain. We also show that PmpD undergoes an infection-dependent proteolytic processing step late in the growth cycle that yields a soluble extended PD (p111) that was processed into a p73 PD and a novel p30 fragment. Interestingly, soluble PmpD peptides possess putative eukaryote-interacting functional motifs, implying potential secondary functions within or distal to infected cells. Collectively, our findings show that PmpD exists as two distinct forms, a surface-associated oligomer exhibiting a higher-order flower-like structure and a soluble form restricted to infected cells. We hypothesize that PmpD is a multifunctional virulence factor important in chlamydial pathogenesis and could represent novel vaccine or drug targets for the control of human chlamydial infections. C1 [Swanson, Kena A.; Taylor, Lacey D.; Frank, Shaun D.; Sturdevant, Gail L.; Carlson, John H.; Whitmire, William M.; Caldwell, Harlan D.] NIAID, Rocky Mt Labs, Intracellular Parasites Lab, NIH, Hamilton, MT 59840 USA. [Fischer, Elizabeth R.] NIAID, Rocky Mt Labs, Res Technol Branch, NIH, Hamilton, MT 59840 USA. RP Caldwell, HD (reprint author), NIAID, Rocky Mt Labs, Intracellular Parasites Lab, NIH, 903 S 4th St, Hamilton, MT 59840 USA. EM hcaldwell@niaid.nih.gov FU NIH; NIAID FX This research was supported by the Intramural Research Program of the NIH, NIAID. NR 57 TC 44 Z9 51 U1 0 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 2009 VL 77 IS 1 BP 508 EP 516 DI 10.1128/IAI.01173-08 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 399BT UT WOS:000262776100053 PM 19001072 ER PT J AU Weinstein, RA Henderson, DK AF Weinstein, Robert A. Henderson, David K. TI A Double-Edged Sword and a Golden Opportunity for Healthcare Epidemiology SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY LA English DT Editorial Material ID SAFETY NETWORK; INFECTIONS C1 [Henderson, David K.] NIH, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA. [Weinstein, Robert A.] John H Stroger Jr Hosp Cook Cty, Div Med, Chicago, IL USA. [Weinstein, Robert A.] Rush Med Coll, Chicago, IL 60612 USA. RP Henderson, DK (reprint author), NIH, Warren G Magnuson Clin Ctr, Bldg 10,Rm 6-1480,10 Ctr Dr,MSC 1504, Bethesda, MD 20892 USA. EM dkh@nih.gov NR 11 TC 6 Z9 6 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0899-823X J9 INFECT CONT HOSP EP JI Infect. Control Hosp. Epidemiol. PD JAN PY 2009 VL 30 IS 1 BP 1 EP 3 DI 10.1086/596559 PG 3 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA 381OV UT WOS:000261546700001 PM 19067597 ER PT S AU Nunez, NP Hursting, SD Yakar, S Fowler, D Vinson, C AF Nunez, Nomeli P. Hursting, Stephen D. Yakar, Shoshana Fowler, Dan Vinson, Charles BE Kozlov, SV TI Obesity Provides a Permissive Milieu in Inflammation-Associated Carcinogenesis: Analysis of Insulin and IGF Pathways SO INFLAMMATION AND CANCER: METHODS AND PROTOCOLS, VOL 2: MOLECULAR ANALYSIS AND PATHWAYS SE Methods in Molecular Biology LA English DT Article; Book Chapter DE Cancer; Diabetes; Lypodystraphy; Lypoatrophy; Insulin; Inflammation ID GROWTH-FACTOR-I; BREAST-CANCER; T-CELLS; OVERWEIGHT; DISEASE; MOUSE; RISK; MICE AB Current dogma suggests that the positive correlation between obesity and cancer is driven by white adipose tissue that accompanies obesity, possibly through excess secretion of adipokines. However, recent studies in fatless A-Zip/F-1 mice, which have undetectable adipokine levels but display accelerated tumor formation, suggest that adipokines are not required for the enhanced tumor development. The A-Zip/F-1 m ice are also diabetic and display elevated circulating levels of other molecules frequently associated with obesity and carcinogenesis: insulin, insulin-like growth factor-1, and inflammatory cytokines. Therefore, we postulate that the pathways associated with insulin resistance and inflammation, rather than adipocyte-derived factors, may represent key prevention or therapeutic targets for disrupting the obesity-cancer link. C1 [Nunez, Nomeli P.; Hursting, Stephen D.] Univ Texas Austin, Div Nutr Sci, Austin, TX 78712 USA. [Yakar, Shoshana] Mt Sinai Sch Med, Dept Med, Div Endocrinol Diabet & Bone Dis, New York, NY USA. [Vinson, Charles] NCI, Lab Metab, NIH, Bethesda, MD 20892 USA. [Fowler, Dan] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA. RP Nunez, NP (reprint author), Univ Texas Austin, Div Nutr Sci, Austin, TX 78712 USA. FU NIAMS NIH HHS [R01 AR055141, R01 AR054919] NR 27 TC 8 Z9 8 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA SN 1064-3745 BN 978-1-60327-529-3 J9 METHODS MOL BIOL JI Methods Mol. Biol. PY 2009 VL 512 BP 29 EP 37 DI 10.1007/978-1-60327-530-9_3 D2 10.1007/978-1-60327-530-9 PG 9 WC Biochemical Research Methods SC Biochemistry & Molecular Biology GA BKJ98 UT WOS:000268336200003 PM 19347271 ER PT S AU Kozlov, SV AF Kozlov, Serguei V. BE Kozlov, SV TI Development of a Cell-Based Assay to Quantify the Inflammatory Potential of Test Substances and Screen Compound Libraries for Anti-cancer Drug Candidates in a High-Throughput Format SO INFLAMMATION AND CANCER: METHODS AND PROTOCOLS, VOL 2: MOLECULAR ANALYSIS AND PATHWAYS SE Methods in Molecular Biology LA English DT Article; Book Chapter DE Inflammation; Cell-based assays; Cancer; NF-kappa B; High-throughput screening ID NF-KAPPA-B; TUMOR-NECROSIS-FACTOR; CANCER; ACTIVATION; EXPRESSION; INHIBITORS; SYSTEM AB Despite the current availability of an impressive in vitro assay battery developed to quantitatively analyze the broad panel of small compounds and macromolecules that possess the inflammatory potential, little methodology exists nowadays that affords a researcher or clinician to quantify the ultimate output on the level of cell signaling response caused by inflammatory pathway stimulation. As a matter of fact, majority of analytical tools measure bona fide inflammatory substances (e.g., cytokines or chemokines) by their direct binding to secondary reagents such as specific antibodies or other selectively affine substrates with the final readout generated via quantification of the resulting complexes. Although specific and highly reproducible, this approach provides no discrimination between biologically active versus inactive input analyte nor does it address the differential biological potential for the questioned substances related to their in vivo stability and biodistribution. In a search for alternative solutions, a novel strategy is emerging that employs cell-based methods of inflammatory substance measurements allowing to detect and quantify the downstream effects of analyte's activity translated in terms of inflammatory pathways stimulation. In addition, application of cell based assays simultaneously permits entry level evaluation of compound toxicity and endows with a powerful approach to perform high-throughput screenings of, e.g., small molecule libraries in a quest for novel compounds capable of influencing the inflammation process. C1 Natl Canc Inst Frederick, Canc & Dev Biol Lab, Frederick, MD USA. RP Kozlov, SV (reprint author), Natl Canc Inst Frederick, Canc & Dev Biol Lab, Frederick, MD USA. NR 20 TC 1 Z9 1 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA SN 1064-3745 BN 978-1-60327-529-3 J9 METHODS MOL BIOL JI Methods Mol. Biol. PY 2009 VL 512 BP 159 EP 167 DI 10.1007/978-1-60327-530-9_9 D2 10.1007/978-1-60327-530-9 PG 9 WC Biochemical Research Methods SC Biochemistry & Molecular Biology GA BKJ98 UT WOS:000268336200009 PM 19347277 ER PT B AU Miller, FW AF Miller, Frederick W. BE Kagen, LJ TI Classification of Idiopathic Inflammatory Myopathies SO INFLAMMATORY MYOPATHIES LA English DT Article; Book Chapter DE Clinicopathologic; Serologic; Myositis-specific autoantibodies; Environmental; Genetic; Phenotypes ID MYOSITIS-SPECIFIC AUTOANTIBODIES; INCLUSION-BODY MYOSITIS; CLASS-II HAPLOTYPE; DISTINCT HLA-A; JUVENILE DERMATOMYOSITIS; PROTECTIVE FACTORS; MACROPHAGIC MYOFASCIITIS; IMMUNOGENETIC RISK; ALLELIC PROFILES; OVERDIAGNOSED ENTITY AB Although it has been long recognized that inflammatory muscle disease of unknown etiology may present clinically and respond to therapy in a variety of ways, our approaches regarding how to best classify or divide these entities into more understandable groups of patients has evolved as larger series have been studied using advanced laboratory, immunopathologic, and genetic technologies. In addition to the traditional clinicopathologic classifications of these entities, there is increasing interest in using newer methods, including serology, environmental exposures, and molecular genetics, to divide these syndromes into more homogeneous subsets. While our understanding of these disorders is far from complete, it is clear that the inflammatory myopathies are composed of many separate and distinct disorders with widely divergent clinical signs, symptoms, pathology, laboratory abnormalities, immune responses, genetic and environmental risk factors, and prognoses. Classification of the inflammatory myopathies remains unsatisfactory and controversial, with a number of competing approaches currently in use. Nonetheless, while many different schemes have been proposed, this chapter focuses on the classifications based on clinical signs, pathology, and autoantibodies that today are useful in assessing subjects, as well as possible new approaches that take into account environmental exposures and immunogenetics. Our understanding of the pathogenesis, classification, and prognosis of the inflammatory myopathies will become more complete as we decipher the interrelationships among all the critical features of disease-including the genetic and environmental risk factors necessary and sufficient for the induction of myositis-and develop more rational ways of dividing and treating these increasingly recognized syndromes. C1 NIEHS, Environm Autoimmun Grp, Off Clin Res, NIH,HHS,Natl Inst Hlth Clin Res Ctr, Bethesda, MD 20892 USA. RP Miller, FW (reprint author), NIEHS, Environm Autoimmun Grp, Off Clin Res, NIH,HHS,Natl Inst Hlth Clin Res Ctr, Bethesda, MD 20892 USA. EM millerf@mail.nih.gov OI Miller, Frederick/0000-0003-2831-9593 NR 62 TC 0 Z9 0 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA BN 978-1-60327-828-7 PY 2009 BP 15 EP 28 DI 10.1007/978-1-60327-827-0_2 D2 10.1007/978-1-60327-827-0 PG 14 WC Neurosciences; Rheumatology SC Neurosciences & Neurology; Rheumatology GA BKY22 UT WOS:000269607000002 ER PT B AU Rider, LG AF Rider, Lisa G. BE Kagen, LJ TI Outcomes and Assessment for Inflammatory Muscle Disease SO INFLAMMATORY MYOPATHIES LA English DT Article; Book Chapter DE Outcome assessment; Disease activity; Disease damage; Quality of life ID QUALITY-OF-LIFE; CUTANEOUS ASSESSMENT-TOOL; HEALTH ASSESSMENT QUESTIONNAIRE; MYOSITIS ASSESSMENT SCALE; JUVENILE DERMATOMYOSITIS; SKELETAL-MUSCLE; INTERNATIONAL CONSENSUS; CORE SET; CLINICAL CHARACTERISTICS; PRELIMINARY DEFINITIONS AB This chapter describes the development and preliminary validation of measures to evaluate myositis disease activity, damage, and health-related quality of life for the adult and juvenile idiopathic inflammatory myopathies. The focus is primarily on the core set measures that have been developed through consensus methods by multidisciplinary collaborative study groups as well as new definitions of improvement that provide a composite response measure that combines the core set tools. Additional approaches that are not as fully validated but may also be important in the evaluation of individual myositis patients or useful in certain myositis studies are also reviewed. The utilization of standardized, validated approaches to assess myositis disease activity, damage, and health-related quality of life is enhancing the conduct of myositis clinical studies and therapeutic trials. C1 NIEHS, Environm Autoimmun Grp, Off Clin Res, NIH, Bethesda, MD USA. RP Rider, LG (reprint author), NIEHS, Environm Autoimmun Grp, Off Clin Res, NIH, Bethesda, MD USA. OI Rider, Lisa/0000-0002-6912-2458 NR 98 TC 0 Z9 0 U1 0 U2 1 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA BN 978-1-60327-828-7 PY 2009 BP 253 EP 276 DI 10.1007/978-1-60327-827-0_15 D2 10.1007/978-1-60327-827-0 PG 24 WC Neurosciences; Rheumatology SC Neurosciences & Neurology; Rheumatology GA BKY22 UT WOS:000269607000015 ER PT S AU Geng, XJ Ross, TJ Zhan, W Gu, H Chao, YP Lin, CP Christensen, GE Schuff, N Yang, YH AF Geng, Xiujuan Ross, Thomas J. Zhan, Wang Gu, Hong Chao, Yi-Ping Lin, Ching-Po Christensen, Gary E. Schuff, Norbert Yang, Yihong BE Prince, JL Pham, DL Myers, KJ TI Diffusion MRI Registration Using Orientation Distribution Functions SO INFORMATION PROCESSING IN MEDICAL IMAGING, PROCEEDINGS SE Lecture Notes in Computer Science LA English DT Proceedings Paper CT 21st International Conference on Information Processing in Medical Imaging CY JUL 05-10, 2009 CL Coll William & Mary, Williamsburg, VA SP Natl Inst Biomed Imaging & Biengn, Natl Canc Inst, Natl Inst Neurol Disorders & Stroke, Natl Inst Aging, Johns Hopkins Univ HO Coll William & Mary AB We propose a linear-elastic registration method to register diffusion-weighted MRI (DW-MRI) data sets by mapping their diffusion orientation distribution functions (ODFs). The ODFs were reconstructed using a q-ball imaging (QBI) technique to resolve intravoxel fiber crossing. The registration method is based on mapping the ODF maps represented by spherical harmonics which yield analytic solutions and reduce the computational complexity. ODF reorientation is required to maintain the consistency with transformed local fiber directions. The reorientation matrices are extracted from the local Jacobian and directly applied to the coefficients of spherical harmonics. The similarity cost of the registration is defined by the ODF shape distance calculated from the spherical harmonic coefficients. The transformation fields are regularized by linear elastic constraints. The proposed method was validated using both synthetic and real data sets. Experimental results show that the elastic registration improved the affine alignment by further reducing the ODF shape difference; reorientation during the registration produced registered ODF maps with more consistent principle directions compared to registrations without reorientation or simultaneous reorientation. C1 [Geng, Xiujuan; Ross, Thomas J.; Gu, Hong; Yang, Yihong] NIDA, NIH, Bethesda, MD 20892 USA. [Chao, Yi-Ping] Natl Taiwan Univ, Dept Elect Engn, Taipei, Taiwan. [Lin, Ching-Po] Natl Yang Ming Univ, Inst Neurosci, Taipei 112, Taiwan. [Zhan, Wang; Schuff, Norbert] Univ Calif San Francisco, Dept Radiol, San Francisco, CA 94143 USA. [Christensen, Gary E.] Univ Iowa, Dept Elect & Comp Engn, Iowa City, IA USA. RP Geng, XJ (reprint author), NIDA, NIH, Bethesda, MD 20892 USA. EM gengx@mail.nih.gov OI Ross, Thomas/0000-0002-7745-3572 FU Intramural Research Program of the National Institute on Drug Abuse (NIDA); National Institute of Health (NIH) FX This work was supported by the Intramural Research Program of the National Institute on Drug Abuse (NIDA), National Institute of Health (NIH). NR 15 TC 8 Z9 8 U1 0 U2 0 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0302-9743 BN 978-3-642-02497-9 J9 LECT NOTES COMPUT SC PY 2009 VL 5636 BP 626 EP + PG 2 WC Computer Science, Information Systems; Computer Science, Theory & Methods; Medical Informatics SC Computer Science; Medical Informatics GA BLR60 UT WOS:000270886300052 ER PT B AU Watson, KD Wexler, P AF Watson, Katherine D. Wexler, Philip BE Wexler, P TI History of Toxicology SO INFORMATION RESOURCES IN TOXICOLOGY, 4TH EDITION LA English DT Article; Book Chapter ID OCCUPATIONAL-MEDICINE; RADIATION PROTECTION; PERSONAL PERSPECTIVE; LANDMARK ARTICLE; WORLD-WAR; LEAD; DISEASES; HEALTH; PATTERSON,CLAIR; EPIDEMIOLOGY C1 [Watson, Katherine D.] Oxford Brookes Univ, Dept Hist, Oxford OX3 0BP, England. [Wexler, Philip] NIH, Natl Lib Med, Bethesda, MD 20894 USA. RP Watson, KD (reprint author), Oxford Brookes Univ, Dept Hist, Gipsy Lane, Oxford OX3 0BP, England. NR 199 TC 2 Z9 2 U1 2 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 9780-0-80-92003-0; 9780-1-23-73593-5 PY 2009 BP 11 EP 29 DI 10.1016/B978-0-12-373593-5.00002-1 PG 19 WC Toxicology SC Toxicology GA BEI30 UT WOS:000316691900007 ER PT J AU Holmgren, S AF Holmgren, Stephanie BE Wexler, P TI Development of Toxicoinformatics SO INFORMATION RESOURCES IN TOXICOLOGY, 4TH EDITION LA English DT Article; Book Chapter ID TOXICOLOGY INFORMATION; SYSTEMS BIOLOGY; DATABASE; CHEMOINFORMATICS; TOXICITY; RESOURCES; FUTURE; TOXICOGENOMICS; BIOINFORMATICS; IMPLEMENTATION C1 [Holmgren, Stephanie] NIEHS, Lib Serv, Res Triangle Pk, NC 27709 USA. [Holmgren, Stephanie] NIEHS, Informat Serv, Res Triangle Pk, NC USA. RP Holmgren, S (reprint author), NIEHS, Lib Serv, Rall Bldg 101,111 Alexander Dr, Res Triangle Pk, NC 27709 USA. NR 90 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 9780-0-80-92003-0 PY 2009 BP 31 EP 48 DI 10.1016/B978-0-12-373593-5.00003-3 PG 18 WC Toxicology SC Toxicology GA BEI30 UT WOS:000316691900008 ER PT J AU Wexler, P AF Wexler, Philip BE Wexler, P TI Information Resources in Toxicology Fourth Edition Preface SO INFORMATION RESOURCES IN TOXICOLOGY, 4TH EDITION LA English DT Editorial Material; Book Chapter C1 NIH, Natl Lib Med, Bethesda, MD 20894 USA. RP Wexler, P (reprint author), NIH, Natl Lib Med, Bethesda, MD 20894 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 9780-0-80-92003-0 PY 2009 BP XXXI EP XXXII DI 10.1016/B978-0-12-373593-5.00116-6 PG 2 WC Toxicology SC Toxicology GA BEI30 UT WOS:000316691900002 ER PT J AU Wexler, P AF Wexler, Philip BE Wexler, P TI Information Resources in Toxicology Fourth Edition Preface to the Third Edition SO INFORMATION RESOURCES IN TOXICOLOGY, 4TH EDITION LA English DT Editorial Material; Book Chapter C1 NIH, Natl Lib Med, Bethesda, MD 20894 USA. RP Wexler, P (reprint author), NIH, Natl Lib Med, Bethesda, MD 20894 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 9780-0-80-92003-0 PY 2009 BP XXXIII EP XXXIV DI 10.1016/B978-0-12-373593-5.00117-8 PG 2 WC Toxicology SC Toxicology GA BEI30 UT WOS:000316691900003 ER PT J AU Wexler, P AF Wexler, Philip BE Wexler, P TI Information Resources in Toxicology Fourth Edition Preface to the Second Edition SO INFORMATION RESOURCES IN TOXICOLOGY, 4TH EDITION LA English DT Editorial Material; Book Chapter C1 NIH, Natl Lib Med, Bethesda, MD 20894 USA. RP Wexler, P (reprint author), NIH, Natl Lib Med, Bethesda, MD 20894 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 9780-0-80-92003-0 PY 2009 BP XXXV EP XXXVI DI 10.1016/B978-0-12-373593-5.00118-X PG 2 WC Toxicology SC Toxicology GA BEI30 UT WOS:000316691900004 ER PT J AU Wexler, P AF Wexler, Philip BE Wexler, P TI Information Resources in Toxicology Fourth Edition Preface to the First Edition SO INFORMATION RESOURCES IN TOXICOLOGY, 4TH EDITION LA English DT Editorial Material; Book Chapter C1 NIH, Natl Lib Med, Bethesda, MD 20894 USA. RP Wexler, P (reprint author), NIH, Natl Lib Med, Bethesda, MD 20894 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 9780-0-80-92003-0 PY 2009 BP XXXVII EP XXXVIII DI 10.1016/B978-0-12-373593-5.00119-1 PG 2 WC Toxicology SC Toxicology GA BEI30 UT WOS:000316691900005 ER PT J AU Hakkinen, PJ AF Hakkinen, Pertti J. BE Wexler, P TI Chemicals: Cosmetics and Other Consumer Products SO INFORMATION RESOURCES IN TOXICOLOGY, 4TH EDITION LA English DT Article; Book Chapter C1 NIH, Natl Lib Med, Bethesda, MD 20892 USA. RP Hakkinen, PJ (reprint author), NIH, Natl Lib Med, 6707 Democracy Blvd,Suite 510, Bethesda, MD 20892 USA. RI Hakkinen, Pertti/G-4803-2016 OI Hakkinen, Pertti/0000-0002-8295-9738 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 9780-0-80-92003-0 PY 2009 BP 129 EP 131 DI 10.1016/B978-0-12-373593-5.00013-6 PG 3 WC Toxicology SC Toxicology GA BEI30 UT WOS:000316691900018 ER PT J AU Mohapatra, A Schwala, D Hakkinen, PJ AF Mohapatra, Asish Schwala, Dieter Hakkinen, Pertti J. BE Wexler, P TI Environmental Toxicology: Air SO INFORMATION RESOURCES IN TOXICOLOGY, 4TH EDITION LA English DT Article; Book Chapter C1 [Mohapatra, Asish] Hlth Canada Alberta Reg, Safe Environm Directorate, Calgary, AB, Canada. [Schwala, Dieter] Univ York, SEI, York YO10 5DD, N Yorkshire, England. [Hakkinen, Pertti J.] NIH, Natl Lib Med, Bethesda, MD 20892 USA. RP Mohapatra, A (reprint author), Hlth Canada Alberta Reg, Safe Environm Directorate, Calgary, AB, Canada. RI Hakkinen, Pertti/G-4803-2016 OI Hakkinen, Pertti/0000-0002-8295-9738 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 9780-0-80-92003-0 PY 2009 BP 217 EP 237 DI 10.1016/B978-0-12-373593-5.00024-0 PG 21 WC Toxicology SC Toxicology GA BEI30 UT WOS:000316691900029 ER PT J AU Mohapatra, A Hakkinen, PJ AF Mohapatra, Asish Hakkinen, Pertti J. BE Wexler, P TI Everyday Exposures SO INFORMATION RESOURCES IN TOXICOLOGY, 4TH EDITION LA English DT Article; Book Chapter C1 [Mohapatra, Asish] Hlth Canada Alberta Reg, Safe Environm Directorate, Calgary, AB, Canada. [Hakkinen, Pertti J.] NIH, Natl Lib Med, Bethesda, MD 20892 USA. RP Mohapatra, A (reprint author), Hlth Canada Alberta Reg, Safe Environm Directorate, Calgary, AB, Canada. RI Hakkinen, Pertti/G-4803-2016 OI Hakkinen, Pertti/0000-0002-8295-9738 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 9780-0-80-92003-0 PY 2009 BP 269 EP 279 DI 10.1016/B978-0-12-373593-5.00030-6 PG 11 WC Toxicology SC Toxicology GA BEI30 UT WOS:000316691900035 ER PT J AU Gilbert, SG van Leeuwen, K Hakkinen, PJ AF Gilbert, Steven G. van Leeuwen, Kees Hakkinen, Pertti J. BE Wexler, P TI Precautionary Principle SO INFORMATION RESOURCES IN TOXICOLOGY, 4TH EDITION LA English DT Article; Book Chapter C1 [Gilbert, Steven G.] Inst Neurotoxicol & Neurol Disorders, Seattle, WA 98115 USA. [van Leeuwen, Kees] Commiss European Communities, Joint Res Ctr, Inst Hlth & Consumer Protect, I-21020 Ispra, Italy. [Hakkinen, Pertti J.] NIH, Natl Lib Med, Bethesda, MD 20892 USA. RP Gilbert, SG (reprint author), Inst Neurotoxicol & Neurol Disorders, 8232 14th Ave NE, Seattle, WA 98115 USA. RI Hakkinen, Pertti/G-4803-2016 OI Hakkinen, Pertti/0000-0002-8295-9738 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 9780-0-80-92003-0 PY 2009 BP 387 EP 393 DI 10.1016/B978-0-12-373593-5.00043-4 PG 7 WC Toxicology SC Toxicology GA BEI30 UT WOS:000316691900048 ER PT J AU de Bruin, YB Eskes, C Langezaal, I Coecke, S Kinsner-Ovaskainen, A Hakkinen, PJ AF de Bruin, Yuri Bruinen Eskes, Chantra Langezaal, Ingrid Coecke, Sandra Kinsner-Ovaskainen, Agnieszka Hakkinen, Pertti J. BE Wexler, P TI Testing Methods and Toxicity Assessment (Including Alternatives) SO INFORMATION RESOURCES IN TOXICOLOGY, 4TH EDITION LA English DT Article; Book Chapter C1 [de Bruin, Yuri Bruinen] RIVM SEC Expertise Ctr Subst, NL-3720 BA Bilthoven, Netherlands. [Eskes, Chantra; Langezaal, Ingrid; Coecke, Sandra; Kinsner-Ovaskainen, Agnieszka] Commiss European Communities, Joint Res Ctr, Inst Hlth & Consumer Protect, I-21027 Ispra, VA, Italy. [Hakkinen, Pertti J.] NIH, Natl Lib Med, Bethesda, MD 20892 USA. RP de Bruin, YB (reprint author), RIVM SEC Expertise Ctr Subst, POB 1, NL-3720 BA Bilthoven, Netherlands. RI Hakkinen, Pertti/G-4803-2016 OI Hakkinen, Pertti/0000-0002-8295-9738 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 9780-0-80-92003-0 PY 2009 BP 497 EP 513 PG 17 WC Toxicology SC Toxicology GA BEI30 UT WOS:000316691900065 ER PT J AU Wexler, P Hakkinen, PJ Mohapatra, A Gilbert, SG AF Wexler, Philip Hakkinen, Pertti J. Mohapatra, Asish Gilbert, Steven G. BE Wexler, P TI Organizations SO INFORMATION RESOURCES IN TOXICOLOGY, 4TH EDITION LA English DT Article; Book Chapter C1 [Wexler, Philip] NIH, Natl Lib Med, Bethesda, MD 20894 USA. [Hakkinen, Pertti J.] NIH, Natl Lib Med, Bethesda, MD 20892 USA. [Mohapatra, Asish] Hlth Canada Alberta Reg, Safe Environm Directorate, Calgary, AB, Canada. [Gilbert, Steven G.] Inst Neurotoxicol & Neurol Disorders, Seattle, WA 98115 USA. RP Wexler, P (reprint author), NIH, Natl Lib Med, Bethesda, MD 20894 USA. RI Hakkinen, Pertti/G-4803-2016 OI Hakkinen, Pertti/0000-0002-8295-9738 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 9780-0-80-92003-0 PY 2009 BP 525 EP 555 PG 31 WC Toxicology SC Toxicology GA BEI30 UT WOS:000316691900067 ER PT J AU Stoss, FW Gilbert, SG Wexler, P AF Stoss, Frederick W. Gilbert, Steven G. Wexler, Philip BE Wexler, P TI Audiovisual and Non-Print Resources SO INFORMATION RESOURCES IN TOXICOLOGY, 4TH EDITION LA English DT Article; Book Chapter C1 [Stoss, Frederick W.] SUNY Buffalo, Sci & Engn Lib 5131, Buffalo, NY 14260 USA. [Gilbert, Steven G.] Inst Neurotoxicol & Neurol Disorders, Seattle, WA 98115 USA. [Wexler, Philip] NIH, Natl Lib Med, Bethesda, MD 20894 USA. RP Stoss, FW (reprint author), SUNY Buffalo, Sci & Engn Lib 5131, Caspen Hall, Buffalo, NY 14260 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 9780-0-80-92003-0 PY 2009 BP 607 EP 610 DI 10.1016/B978-0-12-373593-5.00066-5 PG 4 WC Toxicology SC Toxicology GA BEI30 UT WOS:000316691900071 ER PT J AU Gilbert, SG Mohapatra, A Hakkinen, PJ Wexler, P AF Gilbert, Steven G. Mohapatra, Asish Hakkinen, Pertti J. Wexler, Philip BE Wexler, P TI The Internet: Recent Trends SO INFORMATION RESOURCES IN TOXICOLOGY, 4TH EDITION LA English DT Article; Book Chapter C1 [Gilbert, Steven G.] Inst Neurotoxicol & Neurol Disorders, Seattle, WA 98115 USA. [Mohapatra, Asish] Hlth Canada Alberta Reg, Safe Environm Directorate, Calgary, AB, Canada. [Hakkinen, Pertti J.] NIH, Natl Lib Med, Bethesda, MD 20892 USA. [Wexler, Philip] NIH, Natl Lib Med, Bethesda, MD 20894 USA. RP Gilbert, SG (reprint author), Inst Neurotoxicol & Neurol Disorders, 8232 14th Ave NE, Seattle, WA 98115 USA. RI Hakkinen, Pertti/G-4803-2016 OI Hakkinen, Pertti/0000-0002-8295-9738 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 9780-0-80-92003-0 PY 2009 BP 613 EP 617 PG 5 WC Toxicology SC Toxicology GA BEI30 UT WOS:000316691900072 ER PT J AU Mohapatra, A Wexler, P AF Mohapatra, Asish Wexler, Philip BE Wexler, P TI Web-Based Databases SO INFORMATION RESOURCES IN TOXICOLOGY, 4TH EDITION LA English DT Article; Book Chapter C1 [Mohapatra, Asish] Hlth Canada Alberta Reg, Safe Environm Directorate, Calgary, AB, Canada. [Wexler, Philip] NIH, Natl Lib Med, Bethesda, MD 20894 USA. RP Mohapatra, A (reprint author), Hlth Canada Alberta Reg, Safe Environm Directorate, Calgary, AB, Canada. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 9780-0-80-92003-0 PY 2009 BP 619 EP 630 DI 10.1016/B978-0-12-373593-5.00068-9 PG 12 WC Toxicology SC Toxicology GA BEI30 UT WOS:000316691900073 ER PT J AU Hakkinen, PJ AF Hakkinen, Pertti J. BE Wexler, P TI European Union SO INFORMATION RESOURCES IN TOXICOLOGY, 4TH EDITION LA English DT Article; Book Chapter C1 NIH, Natl Lib Med, Bethesda, MD 20892 USA. RP Hakkinen, PJ (reprint author), NIH, Natl Lib Med, 6707 Democracy Blvd,Suite 510, Bethesda, MD 20892 USA. RI Hakkinen, Pertti/G-4803-2016 OI Hakkinen, Pertti/0000-0002-8295-9738 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 9780-0-80-92003-0 PY 2009 BP 739 EP 741 DI 10.1016/B978-0-12-373593-5.00079-3 PG 3 WC Toxicology SC Toxicology GA BEI30 UT WOS:000316691900084 ER PT J AU Wexler, P AF Wexler, Philip BE Wexler, P TI TOXICOLOGICAL QUOTATIONS: FAMOUS, INFAMOUS, OBSCURE SO INFORMATION RESOURCES IN TOXICOLOGY, 4TH EDITION LA English DT Article; Book Chapter C1 NIH, Natl Lib Med, Bethesda, MD 20894 USA. RP Wexler, P (reprint author), NIH, Natl Lib Med, Bethesda, MD 20894 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 9780-0-80-92003-0 PY 2009 BP 1343 EP 1347 PG 5 WC Toxicology SC Toxicology GA BEI30 UT WOS:000316691900116 ER PT B AU Herr, BW Talley, EM Burns, GAPC Newman, D LaRowe, G AF Herr, Bruce W., II Talley, Edmund M. Burns, Gully A. P. C. Newman, David LaRowe, Gavin BE Banissi, E Stuart, L Wyeld, TG Jern, M Andrienko, G Memon, N Alhajj, R Burkhard, RA Grinstein, G Groth, D Ursyn, A Johansson, J Forsell, C Cvek, U Trutschl, M Marchese, FT Maple, C Cowell, AJ Moere, AV TI The NIH Visual Browser: An Interactive Visualization of Biomedical Research SO INFORMATION VISUALIZATION, IV 2009, PROCEEDINGS LA English DT Proceedings Paper CT 4th Information Visualization Conference CY JUL 15-17, 2009 CL Barcelona, SPAIN SP IEEE DE information visualization; scientific funding; topic modeling; information navigation ID KNOWLEDGE; NETWORKS; SCIENCE AB This paper presents a technical description of the methods used to generate an interactive, two-dimensional visualization of 60,568 grants funded by the National Institutes of Health in 2007. The visualization is made intelligible by providing inlet-active features for assessing the data in a web-based visual browser, see http://www.nihmaps.org. The key features include deep zooming, selection, full-text querying, overlays, colors-coding schemes, and multi-level labeling. Major insights, broader applicability, and future directions are discussed. C1 [Herr, Bruce W., II; Talley, Edmund M.; Burns, Gully A. P. C.; Newman, David; LaRowe, Gavin] Univ Calif Irvine, ChalkLabs, Natl Inst Neurol Disorders & Stroke, Inst Informat Sci,NICTA Australia, Irvine, CA 92717 USA. RP Herr, BW (reprint author), Univ Calif Irvine, ChalkLabs, Natl Inst Neurol Disorders & Stroke, Inst Informat Sci,NICTA Australia, Irvine, CA 92717 USA. EM bh2@chalklabs.net; talleye@ninds.nih.gov; gully@usc.edu; newman@uci.edu; gl@chalklabs.net OI Burns, Gully/0000-0003-1493-865X NR 21 TC 5 Z9 5 U1 0 U2 5 PU IEEE COMPUTER SOC PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, PO BOX 3014, LOS ALAMITOS, CA 90720-1264 USA BN 978-0-7695-3733-7 PY 2009 BP 505 EP 509 DI 10.1109/IV.2009.105 PG 5 WC Computer Science, Information Systems; Computer Science, Software Engineering SC Computer Science GA BMM35 UT WOS:000272794200072 ER PT B AU Iantorno, M Muniyappa, R Quon, MJ AF Iantorno, Micaela Muniyappa, Ranganath Quon, Michael J. BE Yao, EB TI Insulin Resistance and Endothelial Dysfunction: An Unhappy Union SO INSULIN RESISTANCE: NEW RESEARCH LA English DT Article; Book Chapter ID NITRIC-OXIDE SYNTHASE; PROTEIN-KINASE-C; TYPE-2 DIABETES-MELLITUS; DEPENDENT PLATELET-AGGREGATION; CARDIOVASCULAR RISK-FACTORS; CORONARY-ARTERY-DISEASE; LIFE-STYLE MODIFICATION; GLYCATION END-PRODUCTS; SKELETAL-MUSCLE CELLS; FATTY-ACID OXIDATION AB Metabolic actions of insulin promoting glucose disposal are augmented by vascular actions of insulin in endothelium stimulating production of the vasodilator nitric oxide (NO). NO-dependent increases in blood flow to skeletal muscle account for similar to 25% of the increase in glucose uptake in response to insulin stimulation. Phosphatidylinositol 3-kinase (PI3K)-dependent insulin signaling pathways regulating endothelial NO production share parallels with metabolic insulin signaling pathways in skeletal muscle. Distinct MAPK-dependent insulin-signaling pathways (largely unrelated to metabolic actions) regulate secretion of the vasoconstrictor endothelin-1 from endothelium. These and other cardiovascular actions of insulin help couple metabolic and hemodynamic homeostasis under healthy conditions. Cardiovascular diseases are leading causes of morbidity and mortality in insulin-resistant individuals. Insulin resistance is typically defined as decreased sensitivity and/or responsiveness to metabolic actions of insulin. This cardinal feature of diabetes, obesity, and dyslipidemia is also a prominent component of hypertension, coronary heart disease, and atherosclerosis that are all characterized by endothelial dysfunction. Conversely, endothelial dysfunction is often present in metabolic diseases. Insulin resistance is characterized by selective impairment in PI3K-dependent (but not MAPK-dependent) insulin signaling that underlies reciprocal relationships between insulin resistance and endothelial dysfunction. Pharmacological and non-pharmacological (e.g., diet and exercise) interventions that rebalance signaling in PI3K- and MAPK-dependent branches of insulin signaling networks simultaneously improves metabolic and vascular function. Molecular, cellular, physiological, and human clinical investigations demonstrate reciprocal relationships between endothelial dysfunction and insulin resistance that help link cardiovascular and metabolic diseases. In the present review, we discuss pathophysiological mechanisms coupling endothelial dysfunction with insulin resistance to emphasize important therapeutic implications. C1 [Iantorno, Micaela; Muniyappa, Ranganath; Quon, Michael J.] NIH, Diabet Unit, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA. RP Quon, MJ (reprint author), NIH, Diabet Unit, Natl Ctr Complementary & Alternat Med, 9 Mem Dr Bldg 9,Room 1N-105 MSC 0920, Bethesda, MD 20892 USA. EM quonm@nih.gov NR 133 TC 0 Z9 0 U1 0 U2 1 PU NOVA SCIENCE PUBLISHERS, INC PI HAUPPAUGE PA 400 OSER AVE, STE 1600, HAUPPAUGE, NY 11788-3635 USA BN 978-1-60692-332-0 PY 2009 BP 117 EP 135 PG 19 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA BLV89 UT WOS:000271192200004 ER PT J AU George, AA Schiltz, RL Hager, GL AF George, Anuja A. Schiltz, R. Louis Hager, Gordon L. TI Dynamic access of the glucocorticoid receptor to response elements in chromatin SO INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY LA English DT Review DE Glucocorticoid receptor; Hormone response elements; Chromatin; Dynamics; Nuclear hormone receptor ID TUMOR VIRUS PROMOTER; NUCLEAR HORMONE RECEPTORS; LIGAND-SPECIFIC DYNAMICS; LONG TERMINAL REPEAT; DNA-BINDING DOMAIN; LIVING CELLS; ESTROGEN-RECEPTOR; TRANSCRIPTION FACTORS; IN-VIVO; REMODELING COMPLEX AB Transcriptional activation as a rate-limiting step of gene expression is often triggered by all environmental stimulus that is transmitted through a signaling cascade to specific transcription factors. Transcription factors must then find appropriate target genes in the context of chromatin. Sub-sequent modulation of local chromatin domains is now recognized as a major mechanism of gene regulation. The interactions of transcription factors with chromatin structures have recently been observed to be highly dynamic, with residence times measured in seconds. Thus. the concept of static, multi-protein complexes forming at regulatory elements in the genome has been replaced by a new paradigm that envisages rapid and continuous exchange events with the template. These highly dynamic interactions are a property of both DNA-protein and protein-protein interactions and are inherent to every stage of the transcriptional response. In this review we discuss the dynamics of a nuclear receptor, and its transcriptional response in the chromatin context. Published by Elsevier Ltd. C1 [George, Anuja A.; Schiltz, R. Louis; Hager, Gordon L.] NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA. RP Hager, GL (reprint author), NCI, Lab Receptor Biol & Gene Express, NIH, Bldg 41,B602,41 Lib Dr, Bethesda, MD 20892 USA. EM hagerg@exchange.nih.gov RI George, Anuja/C-5963-2017 OI George, Anuja/0000-0003-2643-6307 FU Intramural NIH HHS [Z01 BC005450-24] NR 128 TC 33 Z9 35 U1 1 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 1357-2725 J9 INT J BIOCHEM CELL B JI Int. J. Biochem. Cell Biol. PD JAN PY 2009 VL 41 IS 1 BP 214 EP 224 DI 10.1016/j.biocel.2008.09.019 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 396VX UT WOS:000262620400026 PM 18930837 ER PT J AU Xu, ZL Wang, W Deng, CX Man, YG AF Xu, Zheli Wang, Wan Deng, Chu-Xia Man, Yan-gao TI Aberrant p63 and WT-1 expression in myoepithelial cells of pregnancy-associated breast cancer: implications for tumor aggressiveness and invasiveness SO INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES LA English DT Article DE Pregnancy-associated breast cancer; myoepithelial cells; p63; WT-1; tumor stem cells ID WILMS-TUMOR; LAYER DISRUPTIONS; EPITHELIAL-CELLS; DNA PHENOTYPE; IN-VITRO; INVASION; CLUSTERS; GENE; WT1; PROLIFERATION AB Our recent studies revealed that focal alterations in breast myoepithelial cell layers significantly impact the biological presentation of associated epithelial cells. As pregnancy-associated breast cancer (PABC) has a significantly more aggressive clinical course and mortality rate than other forms of breast malignancies, our current study compared tumor suppressor expression in myoepithelial cells of PABC and non-PABC, to determine whether myoepithelial cells of PABC may have aberrant expression of tumor suppressors. Tissue sections from 20 cases of PABC and 20 cases of stage, grade, and age matched non-PABC were subjected to immunohistochemistry, and the expression of tumor suppressor maspin, p63, and Wilms' tumor 1 (WT-1) in calponin positive myoepithelial cells were statistically compared. The expression profiles of maspin, p63, and WT-1 in myoepithelial cells of all ducts encountered were similar between PABC and non-PABC. PABC, however, displayed several unique alterations in terminal duct and lobular units (TDLU), acini, and associated tumor tissues that were not seen in those of non-PABC, which included the absence of p63 and WT-1 expression in a vast majority of the myoepithelial cells, cytoplasmic localization of p63 in the entire epithelial cell population of some lobules, and substantially increasing WT-1 expression in vascular structures of the invasive cancer component. All or nearly all epithelial cells with aberrant p63 and WT-1 expression lacked the expression of estrogen receptor and progesterone receptor, whereas they had a substantially higher proliferation index than their counterparts with p63 and WT-1 expression. Hyperplastic cells with cytoplasmic p63 expression often adjacent to, and share a similar immunohistochemical and cytological profile with, invasive cancer cells. To our best knowledge, our main finings have not been previously reported. Our findings suggest that the functional status of myoepithelial cells may be significantly associated with tumor aggressiveness and invasiveness. C1 [Man, Yan-gao] Armed Forces Inst Pathol, Dept Gynecol & Breast Pathol, Gynecol & Breast Res Lab, Washington, DC 20306 USA. [Man, Yan-gao] Armed Forces Inst Pathol, Dept Infect & Parasit Dis Pathol, Amer Registry Pathol, Washington, DC 20306 USA. [Deng, Chu-Xia] NIDDK, Mammalian Genet Sect, GDDB, NIH, Bethesda, MD USA. [Xu, Zheli; Wang, Wan] Jilin Univ, China Japan Union Hosp, Dept Thyroid & Breast Surg, Changchun 130023, Jilin, Peoples R China. RP Man, YG (reprint author), Armed Forces Inst Pathol, Dept Gynecol & Breast Pathol, Gynecol & Breast Res Lab, 6825 16th St NW, Washington, DC 20306 USA. EM man@afip.osd.mil RI deng, chuxia/N-6713-2016 FU Ministry of Chinese Science and Technology Department [2006CB910505]; The National Natural Science Foundation of China [30801176]; Congressionally Directed Medical Research Programs [DAMD17-01-1-0129, DAMD17-01-1-0130, PC051308]; The Susan G. Komen Breast Cancer Foundation [BCTR0706983] FX The opinions and assertions contained herein represent the personal views of the authors and arenot to be construed as official or as representing the views of the Department of the Army or the Department of Defense. NR 53 TC 11 Z9 13 U1 0 U2 3 PU IVYSPRING INT PUBL PI LAKE HAVEN PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA SN 1449-2288 J9 INT J BIOL SCI JI Int. J. Biol. Sci. PY 2009 VL 5 IS 1 BP 82 EP 96 PG 15 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 439AZ UT WOS:000265600300010 PM 19173015 ER PT J AU Deng, CX AF Deng, Chu-Xia TI SIRT1, Is It a Tumor Promoter or Tumor Suppressor? SO INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES LA English DT Review DE SIRT1; tumor promoter; tumor suppressor; DNA damage repair ID SMALL-MOLECULE ACTIVATORS; DNA-DAMAGE RESPONSE; CALORIC RESTRICTION; CELL-SURVIVAL; DEACETYLASE SIRT1; PROSTATE-CANCER; REGULATES SIRT1; BREAST-CANCER; LIFE-SPAN; MICE AB SIRT1 has been considered as a tumor promoter because of its increased expression in some types of cancers and its role in inactivating proteins that are involved in tumor suppression and DNA damage repair. However, recent studies demonstrated that SIRT1 levels are reduced in some other types of cancers, and that SIRT1 deficiency results in genetic instability and tumorigenesis, while overexpression of SIRT1 attenuates cancer formation in mice heterozygous for tumor suppressor p53 or APC. Here, I review these recent findings and discuss the possibility that activation of SIRT1 both extends lifespan and inhibits cancer formation. C1 NIDDKD, Genet Dev & Dis Branch, NIH, Bethesda, MD 20892 USA. RP Deng, CX (reprint author), NIDDKD, Genet Dev & Dis Branch, NIH, 10-9N105, Bethesda, MD 20892 USA. EM chuxiad@bdg10.niddk.nih.gov RI deng, chuxia/N-6713-2016 FU Intramural Research Program of the National Institute of Diabetes; Digestive and Kidney Diseases; National Institutes of Health, USA FX I thank members of Dr. Deng lab for their critical discussion of this work. This work was supported by the Intramural Research Program of the National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, USA. NR 54 TC 165 Z9 178 U1 0 U2 2 PU IVYSPRING INT PUBL PI LAKE HAVEN PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA SN 1449-2288 J9 INT J BIOL SCI JI Int. J. Biol. Sci. PY 2009 VL 5 IS 2 BP 147 EP 152 PG 6 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 439BA UT WOS:000265600400005 PM 19173036 ER PT J AU Liu, AJ Wei, LX Gardner, WA Deng, CX Man, YG AF Liu, Aijun Wei, Lixin Gardner, William A. Deng, Chu-Xia Man, Yan-Gao TI Correlated alterations in prostate basal cell layer and basement membrane SO INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES LA English DT Article DE focal basal cell layer disruption; prostate tumors; basement membrane ID INTRAEPITHELIAL NEOPLASIA PIN; CANCER DNA PHENOTYPE; MASPIN EXPRESSION; TUMOR INVASION; CARCINOMA; METASTASIS; PROLIFERATION; GROWTH; CARCINOGENESIS; PROGRESSION AB Our recent studies revealed that focal basal cell layer disruption (FBCLD) induced auto-immunoreactions represented a contributing factor for human prostate tumor progression and invasion. As the basement membrane surrounds and attaches to the basal cell layer, our current study assessed whether FBCLD would impact the physical integrity of the associated basement membrane. Paraffin sections from 25-human prostate tumors were subjected to double immunohistochemistry to simultaneously elucidate the basal cell layer and the basement membrane with corresponding biomarkers. The physical integrity of the basement membrane overlying FBCLD was examined to determine the extent of correlated alterations. Of a total of 89 FBCLD encountered, 76 (85%) showed correlated alterations in the overlying basement membrane, which included distinct focal disruptions or fragmentations. In the remaining 13 (15%) FBCLD, the overlying basement membrane showed significant attenuation or reduction of the immunostaining intensity. The basement membrane in all or nearly all ducts or acini with p63 positive basal cells was substantially thicker and more uniform than that in ducts or acini without p63 positive basal cells, and also, a vast majority of the focal disruptions occurred near basal cells that lack p63 expression. These findings suggest that focal disruptions in the basal cell layer and alterations in the basement membrane are correlated events and that the physical and functional status of the basal cells could significantly impact the physical integrity of the overlying basement membrane. As the degradation of both the basal cell layer and the basement membrane is a pre-requisite for prostate tumor invasion or progression, ducts or acini with focally disrupted basal cell layer and basement membrane are likely at greater risk to develop invasive lesions. Thus, further elucidation of the specific molecules and mechanism associated with these events may lead to the development of a more effective alternative for repeat biopsy to monitor tumor progression and invasion. C1 [Man, Yan-Gao] Armed Forces Inst Pathol, Gynecol & Breast Res Lab, Washington, DC 20306 USA. [Man, Yan-Gao] Amer Registry Pathol, Washington, DC USA. [Liu, Aijun; Wei, Lixin] Chinese Peoples Liberat Army Gen Hosp, Dept Pathol, Beijing, Peoples R China. [Gardner, William A.; Deng, Chu-Xia] NIDDK, Mammalian Genet Sect, GDDB, NIH, Bethesda, MD USA. RP Man, YG (reprint author), Armed Forces Inst Pathol, Gynecol & Breast Res Lab, Washington, DC 20306 USA. EM man@afip.osd.mil RI deng, chuxia/N-6713-2016 FU Ministry of Chinese Science and Technology Department [2006CB910505]; US Congressionally Directed Medical Research Programs [DAMD17-01-1-0129, DAMD17-01-1-0130, PC051308]; The Susan G. Komen Breast Cancer Foundation [BCTR0706983]; AFIP/ARP [05AA] FX This study was supported in part by grant 2006CB910505 from the Ministry of Chinese Science and Technology Department to Drs. Xichen Zhang and Yan-gao Man, and also by grants DAMD17-01-1-0129, DAMD17-01-1-0130, and PC051308 from the US Congressionally Directed Medical Research Programs, grant BCTR0706983 from The Susan G. Komen Breast Cancer Foundation, and grant 05AA from the AFIP/ARP joint research initiative project to Dr. Yan-gao Man. NR 55 TC 14 Z9 14 U1 0 U2 6 PU IVYSPRING INT PUBL PI LAKE HAVEN PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA SN 1449-2288 J9 INT J BIOL SCI JI Int. J. Biol. Sci. PY 2009 VL 5 IS 3 BP 276 EP 285 PG 10 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 439BB UT WOS:000265600600007 PM 19343113 ER PT J AU Dey-Guha, I Mukhopadhyay, M Phillips, M Westphal, H AF Dey-Guha, Ipsita Mukhopadhyay, Mahua Phillips, Matthew Westphal, Heiner TI Role of Ldb1 in Adult Intestinal Homeostasis SO INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES LA English DT Article DE Ldb1; small intestine; tissue homeostasis; stem cell niche; tamoxifen ID STEM-CELLS; EXPRESSION PATTERN; MOUSE INTESTINE; WNT SIGNALS; IN-VIVO; EPITHELIUM; GENE; DIFFERENTIATION; PROLIFERATION; LOCALIZATION AB Ldb1 is an essential co-regulator of transcription in embryonic development. It acts in conjunction with nuclear LIM-homeodomain and LIM-only proteins to control key events of organogenesis as precursor cells enter lineage specification. Here we ask whether Ldb1 exerts control over stem cell activation and differentiation throughout the life of the organism as required for tissue homeostasis. To help answer this question, we have generated conditional Ldb1 mouse mutants with an Ldb1 floxed/floxed;ROSA26CreER genotype. Tamoxifen treatment of 60 day-old mutant animals results in near-ubiquitous Cre-mediated Ldb1 inactivation. As a consequence, the stem cell microenvironment of intestinal crypts is drastically affected. Cells that normally express Ldb1 together with markers that identify them as lineage progenitors cease to retain bromodeoxyuridine and are gradually lost. Ldb1 inactivation in intestinal crypts and/or in neighboring mesenchymal cells also triggers activation of Wnt signaling in the stem cell niches of the small intestine. Cell proliferation is markedly increased in the epithelia of the small intestine, and Lgr5-expressing stem cells disappear from the base of the crypts. This perturbation of the normal process of tissue homeostasis causes apoptosis, and the animals do not survive. We conclude that Ldb1-mediated transcriptional regulation plays a major role in adult intestinal homeostasis. C1 [Dey-Guha, Ipsita; Mukhopadhyay, Mahua; Phillips, Matthew; Westphal, Heiner] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Lab Mammalian Genes & Dev, NIH, HHS, Bethesda, MD 20892 USA. RP Westphal, H (reprint author), NICHD, Lab Mammalian Genes & Dev, NIH, Bethesda, MD 20892 USA. EM hw@mail.nih.gov FU Eunice Kennedy Shriver National Institute of Child Health and Human Development FX We thank Dr. H. Clevers for the in situ hybridization protocol, Drs. Li Qi Li and Paul Love for the Ldb1 antibody, Ms. Rui Lin for genotyping and Dr. Sohyun Ahn for helpful discussions. This research was supported by the Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development. NR 30 TC 8 Z9 8 U1 0 U2 0 PU IVYSPRING INT PUBL PI LAKE HAVEN PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA SN 1449-2288 J9 INT J BIOL SCI JI Int. J. Biol. Sci. PY 2009 VL 5 IS 7 BP 686 EP 694 PG 9 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 526FE UT WOS:000272272300006 PM 19918297 ER PT J AU Rubinstein, DB Karmely, M Pichinuk, E Ziv, R Benhar, I Feng, NP Smorodinsky, NI Wreschner, DH AF Rubinstein, Daniel B. Karmely, Maya Pichinuk, Edward Ziv, Ravit Benhar, Itai Feng, Ningping Smorodinsky, Nechama I. Wreschner, Daniel H. TI The MUC1 oncoprotein as a functional target: Immunotoxin binding to alpha/beta junction mediates cell killing SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article DE MUC1; alpha/beta; junction; oncogene; cancer cell killing; target-specific therapy ID HUMAN BREAST-CANCER; TYROSINE PHOSPHORYLATION; EPITHELIAL MUCIN; OVARIAN-CANCER; BETA-CATENIN; SEA MODULE; IN-VIVO; PROTEIN; RECEPTOR; EXPRESSION AB MUC1, a heavily glycosylated mucin, has generated considerable interest as a target for tumor killing because of its overexpression in malignancies. Full-length MUC1 (MUC1/TM) is proteolytically cleaved after synthesis generating alpha and beta subunits, which specifically bind in a noncovalent interaction. Although the beta chain remains on the cell surface, the a chain binds in an on-and-off interaction. Most anti-MUC1 antibodies (Abs) described to date recognize epitopes within the highly immunogenic a-chain tandem repeat. Because the a-chain is shed, such Abs are sequestered and fail to reach MUC1-expressing cells. Immunizing with cDNA encoding MUC1/TM and the spliced MUC1/X isoform from which the tandem repeat has been deleted yielded antibodies to the MUC1 alpha/beta junction. Pseudomonas toxin PE38 linked to polyclonal anti-MUC1 alpha/beta junction Abs both bound and killed MUC1-positive malignant cells. Monoclonal DMC209 binds the MUC1 alpha/beta junction in both MUC1/X and MUC1/TM. When injected into SCID mice xenotransplanted with human breast cancer MDA-MB-231, monoclonal DMC209 showed significant in vivo tumor-suppressive activity. The MUC1/X alpha/beta junction presents a biologically-significant target in MUC1-expressing malignancies because (i) antibodies directed against cell-bound alpha/beta junction epitopes reach the intended cellular target, (ii) antibodies to junction epitope are internalized into cells, (iii) anti alpha/beta junction antibodies can effectively kill high MUC1-expressing cancer cells as antibody-toxin conjugates and (iv) antibodies targeting the MUC1 cell-bound alpha/beta junction results in tumor suppression in vivo. Our results indicate that cell-bound MUC1 alpha/beta junction, unlike shed alpha chain, represents a highly effective moiety for targeting and killing MUC1-expressing malignancies. (C) 2008 Wiley-Liss, Inc. C1 [Karmely, Maya; Pichinuk, Edward; Ziv, Ravit; Smorodinsky, Nechama I.; Wreschner, Daniel H.] Tel Aviv Univ, Dept Cell Res & Immunol, Ramat Aviv, Israel. [Rubinstein, Daniel B.] NCI, NIH, Bethesda, MD 20892 USA. [Feng, Ningping] Arius Res, Toronto, ON, Canada. [Smorodinsky, Nechama I.] Tel Aviv Univ, Alec & Myra Marmot Hybridoma Lab, Ramat Aviv, Israel. [Wreschner, Daniel H.] Biomodifying Inc, San Diego, CA USA. RP Wreschner, DH (reprint author), Tel Aviv Univ, Dept Cell Res & Immunol, Ramat Aviv, Israel. EM danielhw@post.tau.ac.il NR 46 TC 8 Z9 9 U1 0 U2 6 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 JAN 1 PY 2009 VL 124 IS 1 BP 46 EP 54 DI 10.1002/ijc.23910 PG 9 WC Oncology SC Oncology GA 383HL UT WOS:000261664600007 PM 18821582 ER PT J AU Nistico, P Capone, I Palermo, B Del Bello, D Ferraresi, V Moschella, F Arico, E Valentini, M Bracci, L Cognetti, F Ciccarese, M Vercillo, G Roselli, M Fossile, E Tosti, ME Wang, E Marincola, F Imberti, L Catricala, C Natali, PG Belardeli, F Proietti, E AF Nistico, Paola Capone, Imerio Palermo, Belinda Del Bello, Duilia Ferraresi, Virginia Moschella, Federica Arico, Eleonora Valentini, Mara Bracci, Laura Cognetti, Francesco Ciccarese, Mariangela Vercillo, Giuseppe Roselli, Mario Fossile, Emanuela Tosti, Maria Elena Wang, Ena Marincola, Francesco Imberti, Luisa Catricala, Caterina Natali, Pier Giorgio Belardeli, Filippo Proietti, Enrico TI Chemotherapy enhances vaccine-induced antitumor immunity in melanoma patients SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article DE chemoimmunotherapy; dacarbazine; human melanoma; peptide vaccination ID REGULATORY T-CELLS; ADOPTIVE IMMUNOTHERAPY; CANCER-IMMUNOTHERAPY; EXPRESSION PATTERNS; MALIGNANT-MELANOMA; DENDRITIC CELLS; CYCLOPHOSPHAMIDE; INTERLEUKIN-15; ACTIVATION; MELAN-A/MART-1 AB Combination of chemotherapy with cancer vaccines is currently regarded as a potentially valuable therapeutic approach for the treatment of some metastatic tumors, but optimal modalities remain unknown. We designed a phase I/II pilot study for evaluating the effects of dacarbazine (DTIC) on the immune response in HLA-A2(+) disease-free melanoma patients who received anticancer vaccination 1 day following chemotherapy (800 mg/mq i.v.). The vaccine, consisting of a combination of HLA-A2 restricted melanoma antigen A (Melan-A/MART-1) and gp100 analog peptides (250 mu g each, i.d.), was administered in combination or not with DTIC to 2 patient groups. The combined treatment is nontoxic. The comparative immune monitoring demonstrates that patients receiving DTIC 1 day before the vaccination have a significantly improved long-lasting memory CD8(+) T cell response. Of relevance, these CD8(+) T cells recognize and lyse HLA-A2(+)/Melan-A(+) tumor cell lines. Global transcriptional analysis of peripheral blood mononuclear cells (PBMC) revealed a DTIC-induced activation of genes involved in cytokine production, leukocyte activation, immune response and cell motility that can favorably condition tumor antigen-specific CD8(+) T cell responses. This study represents a proof in humans of a chemotherapy-induced enhancement of CD8(+) memory T cell response to cancer vaccines, which opens new opportunities to design novel effective combined therapies improving cancer vaccination effectiveness. (C) 2008 Wiley-Liss, Inc. C1 [Nistico, Paola] Regina Elena Inst Canc Res, Immunol Lab, Dept Expt Oncol, I-00158 Rome, Italy. [Capone, Imerio; Moschella, Federica; Arico, Eleonora; Valentini, Mara; Bracci, Laura; Belardeli, Filippo; Proietti, Enrico] Ist Super Sanita, Dept Cell Biol & Neurosci, I-00161 Rome, Italy. [Ferraresi, Virginia; Cognetti, Francesco; Ciccarese, Mariangela] Regina Elena Inst Canc Res, Dept Med Oncol, I-00158 Rome, Italy. [Vercillo, Giuseppe] Regina Elena Inst Canc Res, Dept Pathol, I-00158 Rome, Italy. [Roselli, Mario; Fossile, Emanuela] Univ Roma Tor Vergata, Rome, Italy. [Tosti, Maria Elena] Ist Super Sanita, Natl Ctr Epidemiol Surveillance & Hlth Promot, I-00161 Rome, Italy. [Wang, Ena; Marincola, Francesco] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA. [Imberti, Luisa] Spedali Civil Brescia, Diagnost Dept, I-25125 Brescia, Italy. [Catricala, Caterina] S Gallicano Dermatol Inst, Dept Dermatol Oncol, Rome, Italy. RP Nistico, P (reprint author), Regina Elena Inst Canc Res, Immunol Lab, Dept Expt Oncol, Via Messi Oro 156, I-00158 Rome, Italy. EM nistico@ifo.it; proietti@iss.it RI BRACCI, LAURA/J-8777-2016; Moschella, Federica/K-8168-2016; OI BRACCI, LAURA/0000-0002-2535-4353; Moschella, Federica/0000-0001-9023-2072; Tosti, Maria Elena/0000-0003-1392-9874; Moschella, Federica/0000-0002-1965-6523; Nistico', Paola/0000-0003-4409-2261 FU ISS-NIH; collaboration program 2004-6; Italian Ministry of Health Ricerca Finalizzata 2002 [Fasc.3AO/F]; Italian Association for Cancer Research (AIRC) FX Grant sponsors: ISS-NIH, collaboration program 2004-6, Italian Ministry of Health Ricerca Finalizzata 2002 Fasc.3AO/F. L.B. is a recipient of a fellowship from the Italian Association for Cancer Research (AIRC). NR 39 TC 50 Z9 52 U1 0 U2 5 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 JAN 1 PY 2009 VL 124 IS 1 BP 130 EP 139 DI 10.1002/ijc.23886 PG 10 WC Oncology SC Oncology GA 383HL UT WOS:000261664600017 PM 18839429 ER PT J AU Nemesure, B Wu, SY Hambleton, IR Leske, MC Hennis, AJ AF Nemesure, Barbara Wu, Suh-Yuh Hambleton, Ian R. Leske, M. Cristina Hennis, Anselm J. CA Barbados Natl Canc Study Grp TI Risk factors for breast cancer in a black population-The Barbados National Cancer Study SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article DE breast cancer; risk factors; African-origin population ID AFRICAN-AMERICAN WOMEN; REPRODUCTIVE FACTORS; ORIGIN POPULATION; NIGERIAN WOMEN; WHITE WOMEN; DISEASE; INCREASE; OBESITY; RACE AB The Barbados National Cancer Study (BNCS) is a nationwide case-control study investigating environmental and genetic factors for breast cancer (BC) in a predominantly African-origin population with similar ancestry as African-Americans. This report evaluates associations of incident BC in the BNCS to various factors, including demographic, anthropometric, reproductive and family history variables, not investigated previously in this population. The BNCS included 241 incident BC cases and 481. age-matched female controls, with mean ages of 57 and 56 years, respectively. In addition to a reported family history of BC in a close relative [odds ratios (OR) = 3.74, 95% CI (1.41, 9.90) in a parent; OR = 3.26 (1.47, 7.21) in a sibling], other factors associated with BC were older age at first full-term pregnancy [OR = 1..04 (1.00, 1.07)] and having a history of benign breast disease [OR = 1.88 (1.19, 2.99)]. Increased parity reduced the risk of BC [OR = 0.34 (0.15, 0.77) among those with >= 3 children]. The reproductive patterns of African-Barbadian (AB) women tended to differ from those of African-American (AA) women (later age of menarche, earlier age at first pregnancy, higher frequency of lactation and infrequent use of exogenous hormones) and could help to explain their considerably lower postmenopausal incidence of BC. The relationship between reported family history and BC, combined with the associations noted for several reproductive and other variables, supports the genetic and environmental contributions to BC, which may vary in populations across the African diaspora. Further investigations of other populations may clarify these issues. (C) 2008 Wiley-Liss, Inc. C1 [Nemesure, Barbara; Wu, Suh-Yuh; Leske, M. Cristina; Hennis, Anselm J.] SUNY Stony Brook, Dept Prevent Med, Stony Brook, NY 11794 USA. [Hambleton, Ian R.; Hennis, Anselm J.] Univ W Indies, Chron Dis Res Ctr, Bridgetown, Barbados. [Hennis, Anselm J.] Minist Hlth, Bridgetown, Barbados. Univ W Indies, Fac Chem & Biol Sci, Bridgetown, Barbados. Translat Genom Res Inst, Phoenix, AZ USA. [Barbados Natl Canc Study Grp] NHGRI, Bethesda, MD 20892 USA. RP Nemesure, B (reprint author), SUNY Stony Brook, Dept Prevent Med, L3 HSC Room 086, Stony Brook, NY 11794 USA. EM bnemesure@notes.cc.sunysb.edu RI Brinton, Louise/G-7486-2015 OI Brinton, Louise/0000-0003-3853-8562 FU NCI NIH HHS [R01 CA114379, R01 CA114379-01A2, R01 CA114379-02, R01 CA114379-03] NR 41 TC 15 Z9 15 U1 2 U2 3 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0020-7136 EI 1097-0215 J9 INT J CANCER JI Int. J. Cancer PD JAN 1 PY 2009 VL 124 IS 1 BP 174 EP 179 DI 10.1002/ijc.23827 PG 6 WC Oncology SC Oncology GA 383HL UT WOS:000261664600022 PM 18814239 ER PT J AU Shea, L Raben, N AF Shea, L. Raben, N. TI Autophagy in skeletal muscle: implications for Pompe disease SO INTERNATIONAL JOURNAL OF CLINICAL PHARMACOLOGY AND THERAPEUTICS LA English DT Article; Proceedings Paper CT 8th International Symposium on Lysosomal Storage Diseases CY APR, 2008 CL Paris, FRANCE DE autophagy; enzyme replacement therapy; glycogen; Pompe disease; skeletal muscle ID ACID ALPHA-GLUCOSIDASE; ENZYME REPLACEMENT THERAPY; STORAGE-DISEASE; RECOMBINANT; RECEPTORS; PATHWAYS; GLYCOGEN; FIBERS; MILK AB Pompe disease is caused by an inherited deficiency of acid a-glucosidase (GAA), a lysosomal enzyme that catalyzes the breakdown of glycogen to glucose. In the absence of GAA, enlarged, glycogen-laden lysosomes accumulate in multiple tissues, although the major clinical manifestations are seen in cardiac and skeletal muscle. For many years, it was believed that the rupture of glycogen-filled lysosomes was the major cause of the profound muscle damage observed in patients with Pompe disease. Here, we present evidence that a failure of productive autophagy in muscle tissue contributes strongly to disease pathology in both patients with Pompe disease and GAA-knockout mice. In the GAA-knockout mouse model, progressive accumulation of autophagic vesicles is restricted to Type II-rich muscle fibers. Not only does this build-up of autophagosomes disrupt the contractile apparatus in the muscle fibers, it also interferes with enzyme replacement therapy by acting as a sink for the recombinant enzyme and preventing its efficient delivery to the lysosomes. Our data indicate that a re-examination of the presumed pathological mechanism in Pompe disease is necessary, and suggest that Successful treatment of patients with Pompe disease will require consideration of the dramatic failure of autophagy that occurs in this disease. C1 [Shea, L.; Raben, N.] NIAMSD, Arthrit & Rheumatism Branch, NIH, Bethesda, MD 20892 USA. RP Raben, N (reprint author), NIAMS, NIH, 50 South Dr,9000 Rockville Pike,Bld 50,Room 1345, Bethesda, MD 20892 USA. EM rabenn@arb.niams.nih.gov FU Intramural NIH HHS [Z99 AR999999] NR 24 TC 33 Z9 33 U1 1 U2 5 PU DUSTRI-VERLAG DR KARL FEISTLE PI DEISENHOFEN-MUENCHEN PA BAHNHOFSTRASSE 9 POSTFACH 49, D-82032 DEISENHOFEN-MUENCHEN, GERMANY SN 0946-1965 J9 INT J CLIN PHARM TH JI Int. J. Clin. Pharmacol. Ther. PY 2009 VL 47 BP S42 EP S47 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 537GV UT WOS:000273102100007 PM 20040311 ER PT J AU Zeng, XQ Li, GZ Wu, GF Yang, JY Yang, MQ AF Zeng, Xue-Qiang Li, Guo-Zheng Wu, Geng-Feng Yang, Jack Y. Yang, Mary Qu TI Irrelevant gene elimination for Partial Least Squares based Dimension Reduction by using feature probes SO INTERNATIONAL JOURNAL OF DATA MINING AND BIOINFORMATICS LA English DT Article CT 22nd ACM Symposium on Applied Computing CY MAR 11-15, 2007 CL Seoul, SOUTH KOREA SP ACM DE PLS; partial least squares; dimension reduction; gene selection; microarray analysis; data mining; bioinformatics ID EXPRESSION MICROARRAY DATA; TUMOR CLASSIFICATION; CANCER; PREDICTION; REGRESSION; PATTERNS AB It is hard to analyse gene expression data which has only a few observations but with thousands of measured genes. Partial Least Squares based Dimension Reduction (PLSDR) is superior for handling such high dimensional problems, but irrelevant features will introduce errors into the dimension reduction process. Here, feature selection is applied to filter the data and an algorithm named PLSDR(g) is described by integrating PLSDR with gene elimination, which is performed by the indication of t-statistic scores on standardised probes. Experimental results on six microarray data sets show that PLSDR(g) is effective and reliable to improve generalisation performance of classifiers. C1 [Li, Guo-Zheng] Tongji Univ, Dept Control Sci & Engn, Shanghai 201804, Peoples R China. [Zeng, Xue-Qiang; Wu, Geng-Feng] Shanghai Univ, Sch Comp Engn & Sci, Shanghai 200072, Peoples R China. [Yang, Jack Y.] Harvard Univ, Sch Med, Boston, MA 02114 USA. [Yang, Jack Y.] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA. [Yang, Mary Qu] NHGRI, NIH, US Dept Hlth & Human Serv, Bethesda, MD 20852 USA. [Yang, Mary Qu] US DOE, Oak Ridge, TN USA. RP Li, GZ (reprint author), Tongji Univ, Dept Control Sci & Engn, Shanghai 201804, Peoples R China. EM stamina_zeng@shu.edu.cn; drgzli@gmail.com; gfwu@shu.edu.cn; yang@hadron.mgh.Harvard.edu; yangma@mail.NIH.GOV RI Li, Guo-Zheng /D-5744-2011 OI Li, Guo-Zheng /0000-0001-5568-0347 NR 27 TC 8 Z9 9 U1 0 U2 2 PU INDERSCIENCE ENTERPRISES LTD PI GENEVA PA WORLD TRADE CENTER BLDG, 29 ROUTE DE PRE-BOIS, CASE POSTALE 896, CH-1215 GENEVA, SWITZERLAND SN 1748-5673 J9 INT J DATA MIN BIOIN JI Int. J. Data Min. Bioinform. PY 2009 VL 3 IS 1 BP 85 EP 103 PG 19 WC Mathematical & Computational Biology SC Mathematical & Computational Biology GA 438FN UT WOS:000265541400007 PM 19432378 ER PT J AU Escalante-Alcalde, D Morales, SL Stewart, CL AF Escalante-Alcalde, Diana Morales, Sara L. Stewart, Colin L. TI Generation of a reporter-null allele of Ppap2b/Lpp3 and its expression during embryogenesis SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL BIOLOGY LA English DT Article DE Ppap2b; Lpp3; reporter allele; expression ID LIPID PHOSPHATE PHOSPHATASES; PROGENITOR-CELL IDENTITY; EMBRYONIC MAMMARY-GLAND; MIGRATING GERM-CELLS; LYSOPHOSPHATIDIC ACID; NEURITE RETRACTION; EPITHELIAL-CELLS; PLASMA-MEMBRANE; PHOSPHOLIPASE-D; NEURONAL FATE AB Our knowledge of how bioactive lipids participate during development has been limited principally due to the difficulties of working with lipids. The availability of some of these lipids is regulated by the Lipid phosphate phosphatases (LPPs). The targeted inactivation of Ppap2b, which codes for the isoenzyme Lpp3, has profound developmental defects. Lpp3 deficient embryos die around E9.5 due to extraembryonic vascular defects, making difficult to analyze its participation in later stages of mouse development. To gain some predictive information regarding the possible participation of Lpp3 in later stages of development, we generated a Ppap2b null reporter allele and it was used to establish its expression pattern in E8.5-13.5 embryos. We found that Ppap2b expression during these stages was highly dynamic with significant expression in structures where multiple inductive interactions occur such as the limb buds, mammary gland primordia, heart cushions and valves among others. These observations suggest that Lpp3 expression may play a key role in modulating/integrating multiple signaling pathways during development. C1 [Escalante-Alcalde, Diana; Morales, Sara L.] Univ Nacl Autonoma Mexico, Inst Fisiol Celular, Dept Neurociencias, Mexico City 04510, DF, Mexico. [Escalante-Alcalde, Diana; Stewart, Colin L.] NCI, Canc & Dev Biol Lab, Frederick, MD 21701 USA. RP Escalante-Alcalde, D (reprint author), Univ Nacl Autonoma Mexico, Inst Fisiol Celular, Dept Neurociencias, Circuito Exterior S-N Ciudad Univ, Mexico City 04510, DF, Mexico. EM descalante@ifc.unam.mx FU CONACyT [39995]; PAPIIT [IN215605] FX We are grateful to T. Rosenbaum and I. Velasco for comments and carefully reading of the manuscript. This work was partially supported by CONACyT 39995 and PAPIIT IN215605. NR 50 TC 11 Z9 11 U1 0 U2 1 PU U B C PRESS PI BILBAO PA UNIV BASQUE COUNTRY, EDITORIAL SERVICES, PO BOX 1397, E-48080 BILBAO, SPAIN SN 0214-6282 J9 INT J DEV BIOL JI Int. J. Dev. Biol. PY 2009 VL 53 IS 1 BP 139 EP 147 DI 10.1387/ijdb.082745de PG 9 WC Developmental Biology SC Developmental Biology GA 417PQ UT WOS:000264089000015 PM 19123136 ER PT J AU Ruzickova, J Piatigorsky, J Kozmik, Z AF Ruzickova, Jana Piatigorsky, Joram Kozmik, Zbynek TI Eye-specific expression of an ancestral jellyfish PaxB gene interferes with Pax6 function despite its conserved Pax6/Pax2 characteristics SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL BIOLOGY LA English DT Article DE Pax; eye; lens; retina ID HOMEOBOX-CONTAINING GENE; RETINAL GANGLION-CELLS; TRANSCRIPTION FACTORS; LENS MORPHOGENESIS; ANTERIOR SEGMENT; PROX1 FUNCTION; PAIRED DOMAIN; OPTIC VESICLE; MOUSE RETINA; EYELESS GENE AB Pax transcription factors are evolutionarily conserved regulators of eye development and can be distinguished on the basis of three functional domains: two DNA-binding domains (the paired domain and the paired-type homeodomain), and the octapeptide motif. PaxB of the eyed cubozoan jellyfish, Tripedalia cystophora, is characterized by a Pax2-like paired domain and octapeptide, and a Pax6-like homeodomain. In mice, functionally distinct Pax6 and Pax2 proteins have unique as well as redundant roles in eye morphogenesis. Here, we show that expression of the jellyfish PaxB gene in mouse embryonic eye tissues impairs normal development of lens and retina. Our data show that PaxB misexpression leads to a downregulation of endogenous Pax6 protein in the prospective lens and in subsets of cells within the inner nuclear layer of transgenic retina. In addition to Pax6 downregulation, the expression of PaxB leads to an almost complete loss of amacrine cells in the adult transgenic retina, a phenotype that differs from a loss-of-function of the Pax6 gene. The present data suggest that PaxB, due to its Pax2-like paired domain and Pax-6 like homeodomain, disturbs the transcriptional network regulated by Pax6 in the developing lens and retina. Taken together, our data suggest that molecular properties of individual mouse Pax2 and Pax6 proteins are essential determinants of mouse eye development and cannot be substituted for by jellyfish PaxB which possesses elements of vertebrate Pax2 and Pax6. C1 [Ruzickova, Jana; Kozmik, Zbynek] Acad Sci Czech Republic, Inst Mol Genet, CR-14220 Prague 4, Czech Republic. [Piatigorsky, Joram] NEI, NIH, Bethesda, MD 20892 USA. RP Kozmik, Z (reprint author), Acad Sci Czech Republic, Inst Mol Genet, Videnska 1083, CR-14220 Prague 4, Czech Republic. EM kozmik@img.cas.cz RI Kozmik, Zbynek/G-3581-2014; Kozmik, Zbynek/I-8807-2014 FU Academy of Sciences of the Czech Republic [AV0Z50520514, IAA500520908]; Ministry of Education, Youths and Sports of the Czech Republic [1M6837805002]; Grant Agency of Czech Republic [20410811618] FX This work was supported in part by grants no. AV0Z50520514 and IAA500520908 from the Academy of Sciences of the Czech Republic, by Center for Applied Genomics grant no. 1M6837805002 awarded by Ministry of Education, Youths and Sports of the Czech Republic and grant no. 20410811618 from the Grant Agency of Czech Republic. NR 83 TC 1 Z9 1 U1 0 U2 3 PU U B C PRESS PI BILBAO PA UNIV BASQUE COUNTRY, EDITORIAL SERVICES, PO BOX 1397, E-48080 BILBAO, SPAIN SN 0214-6282 J9 INT J DEV BIOL JI Int. J. Dev. Biol. PY 2009 VL 53 IS 4 BP 469 EP 482 DI 10.1387/ijdb.082793jr PG 14 WC Developmental Biology SC Developmental Biology GA 476UY UT WOS:000268472800003 PM 19378250 ER PT J AU Kondo, S Iwashita, M Yamaguchi, M AF Kondo, Shigeru Iwashita, Motoko Yamaguchi, Motoomi TI How animals get their skin patterns: fish pigment pattern as a live Turing wave SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL BIOLOGY LA English DT Article DE pattern formation; reaction-diffusion system; zebrafish; pigment cell; Turing ID K+ CHANNEL KIR7.1; REACTION-DIFFUSION SYSTEM; LEFT-RIGHT ASYMMETRY; NEURAL-CREST; DANIO-RERIO; PERMEATION PROPERTIES; POSITIONAL INFORMATION; LATERAL-INHIBITION; ZEBRAFISH; MECHANISM AB It is more than fifty years since Alan Turing first presented the reaction-diffusion (RD) model, to account for the mechanism of biological pattern formation. In the paper entitled "The chemical basis of morphogenesis", Turing concluded that spatial patterns autonomously made in the embryo are generated as the stationary wave of the chemical (cellular) reactions. Although this novel idea was paid little attention by experimental biologists, recent experimental data are suggesting that the RD mechanism really functions in some of the course of animal development. Among the phenomena in which involvement of the RD mechanism is suspected, the striped pigment pattern of zebrafish has been highlighted as an ideal model system for the following reasons: the stationary wave made by the RD mechanism stays alive and can be observed only in the fish skin; and in zebrafish, we can utilize genomic information and molecular genetic techniques to clarify the molecular basis of pattern formation. In this review, we summarize recent progresses in the study of zebrafish pigment pattern formation that is uncovering how the RD wave is made and maintained in the skin. C1 [Kondo, Shigeru] Osaka Univ, Grad Sch Frontier Biosci, Suita, Osaka 5650871, Japan. [Iwashita, Motoko] NIMH, Unit Neural Circuits & Adapt Behav, Genes Cognit & Psychosis Program, NIH, Bethesda, MD USA. [Yamaguchi, Motoomi] RIKEN, Ctr Dev Biol, Chuo Ku, Wako, Saitama, Japan. RP Kondo, S (reprint author), Osaka Univ, Grad Sch Frontier Biosci, 1-3 Yamadaoka, Suita, Osaka 5650871, Japan. EM shigerukondo@gmail.com NR 63 TC 31 Z9 31 U1 1 U2 27 PU UNIV BASQUE COUNTRY UPV-EHU PRESS PI BILBAO PA PO BOX 1397, BILBAO, BIZKAIA E-48080, SPAIN SN 0214-6282 EI 1696-3547 J9 INT J DEV BIOL JI Int. J. Dev. Biol. PY 2009 VL 53 IS 5-6 SI SI BP 851 EP 856 DI 10.1387/ijdb.072502sk PG 6 WC Developmental Biology SC Developmental Biology GA 483FW UT WOS:000268949100021 PM 19557690 ER PT J AU Tanofsky-Kraff, M Yanovski, SZ Schvey, NA Olsen, CH Gustafson, J Yanovski, JA AF Tanofsky-Kraff, Marian Yanovski, Susan Z. Schvey, Natasha A. Olsen, Cara H. Gustafson, Jennifer Yanovski, Jack A. TI A Prospective Study of Loss of Control Eating for Body Weight Gain in Children at High Risk for Adult Obesity SO INTERNATIONAL JOURNAL OF EATING DISORDERS LA English DT Article DE middle childhood; loss of control eating; disordered eating; weight gain; high risk ID BMI Z-SCORE; ADOLESCENT GIRLS; ONSET; DISORDER; OVERWEIGHT; BEHAVIORS; ADIPOSITY; GROWTH; FAT AB Objective: Limited data suggest that disordered-eating may predispose children to excessive weight gain. We investigated the relationship between baseline responses to the Eating Disorder Examination adapted for Children (ChEDE) and change in BMI (kg/m(2)) in children at high risk for adult obesity. Method: Children (6-12 years) were administered the ChEDE to assess loss of control (LOC) eating, dietary restraint, and eating, shape, and weight concern. Height and weight were measured at baseline and annually. Results: Between July, 1999, and August, 2007, 772 measurements were obtained from 143 children over 4.5 +/- 1.9 years. LOC eating predicted an increased rate of BMI growth over time (p =.02). Compared with children without LOC, those reporting LOC gained an additional mean 2.4 kg of weight per year. Conclusion: LOC is a salient predictor of weight gain during middle childhood. Interventions that decrease LOC eating should be evaluated for their ability to prevent excessive pediatric weight gain. (C) 2008 by Wiley Periodicals, Inc. C1 [Tanofsky-Kraff, Marian; Schvey, Natasha A.] USUHS, Dept Med & Clin Psychol, Bethesda, MD 20814 USA. [Tanofsky-Kraff, Marian; Yanovski, Susan Z.; Schvey, Natasha A.; Gustafson, Jennifer; Yanovski, Jack A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Unit Growth & Obes, Program Dev Endocrinol & Genet, NIH,DHHS, Bethesda, MD 20892 USA. [Yanovski, Susan Z.] NIDDK, Div Digest Dis & Nutr, NIH, DHHS, Bethesda, MD USA. [Olsen, Cara H.] USUHS, Dept Prevent Med & Biometr, Bethesda, MD USA. RP Tanofsky-Kraff, M (reprint author), USUHS, Dept Med & Clin Psychol, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA. EM mtanofsky@usuhs.edu OI Yanovski, Jack/0000-0001-8542-1637 FU National Institute of Child Health and Human Development [Z01-HD-00641] FX Supported by Z01-HD-00641 (to JAY) from the National Institute of Child Health and Human Development. NR 26 TC 86 Z9 88 U1 0 U2 3 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0276-3478 J9 INT J EAT DISORDER JI Int. J. Eating Disord. PD JAN PY 2009 VL 42 IS 1 BP 26 EP 30 DI 10.1002/eat.20580 PG 5 WC Psychology, Clinical; Nutrition & Dietetics; Psychiatry; Psychology SC Psychology; Nutrition & Dietetics; Psychiatry GA 389VR UT WOS:000262123100004 PM 18720473 ER PT J AU Jason, LA Pokorny, SB Adams, ML Topliff, A Harris, CC Hunt, Y AF Jason, Leonard A. Pokorny, Steven B. Adams, Monica L. Topliff, Annie Harris, Courtney C. Hunt, Yvonne TI Effects of Youth Tobacco Access and Possession Policy Interventions on Heavy Adolescent Smokers SO INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH LA English DT Article DE PUP laws; minors' access to tobacco ID SMOKING; LAWS; PURCHASE; IMPACT AB This study evaluated the effects of tobacco PUP (Purchase, Use and Possession) laws on tobacco use patterns among students in twenty-four towns, which were randomly assigned into an experimental and a control group. The experimental group involved both PUP law enforcement and reducing minors' access to commercial sources of tobacco, and the condition for the control group involved only efforts to reduce minors' access to commercial sources of tobacco. The present study found that adolescents in the control group had a significantly greater increase in the percentage of youth who smoked 20 or more cigarettes per day when compared to the experimental group. C1 [Jason, Leonard A.; Adams, Monica L.; Topliff, Annie; Harris, Courtney C.] Depaul Univ, Ctr Community Res, Chicago, IL 60614 USA. [Pokorny, Steven B.] Univ Florida, Dept Hlth Educ & Behav, Gainesville, FL 32611 USA. [Hunt, Yvonne] NCI, Bethesda, MD 20892 USA. RP Jason, LA (reprint author), Depaul Univ, Ctr Community Res, 990 Fullerton Ave,Suite 3100, Chicago, IL 60614 USA. EM ljason@depaul.edu; spokorny@hhp.ufl.edu; madams8@depaul.edu; atopliff@gmail.com; charri30@depaul.edu; yvonnehunt@gmail.com FU National Cancer Institute [CA80288] FX The authors appreciate the funding provided by the National Cancer Institute (grant number CA80288). We also appreciate the help provided by Michael Schoeny in setting up the data set and data cleaning, as well as Jonathan Cook in statistical consultation during data analysis. NR 23 TC 1 Z9 1 U1 1 U2 5 PU MOLECULAR DIVERSITY PRESERVATION INTERNATIONAL-MDPI PI BASEL PA KANDERERSTRASSE 25, CH-4057 BASEL, SWITZERLAND SN 1660-4601 J9 INT J ENV RES PUB HE JI Int. J. Environ. Res. Public Health PD JAN PY 2009 VL 6 IS 1 BP 1 EP 9 DI 10.3390/ijerph6010001 PG 9 WC Environmental Sciences; Public, Environmental & Occupational Health SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health GA 449GK UT WOS:000266318600001 PM 19440265 ER PT J AU Kitchener, HC Trimble, EL AF Kitchener, Henry C. Trimble, Edward L. CA Endometrial Canc Working Grp Gynec TI Endometrial Cancer State of the Science Meeting SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER LA English DT Article DE Endometrial cancer; Clinical trials; Translational research ID GYNECOLOGIC-ONCOLOGY-GROUP; PHASE-III TRIAL; MEDROXYPROGESTERONE ACETATE; POSTOPERATIVE IRRADIATION; RANDOMIZED-TRIAL; UTERINE-CANCER; CARCINOMA; ADJUVANT; CHEMOTHERAPY; RECURRENT AB There is a pressing need to improve our understanding of endometrial cancer (EC) and uterine carcinosarcoma and to develop new treatment strategies to improve outcomes. In recognition of this, a State of the Science meeting on EC was held last November 28 and 29, 2006, in Manchester, United Kingdom. The meeting was cosponsored by the National Cancer Research Institute (UK), the National Cancer Institute (US), and the Gynecological Cancer Intergroup. The objectives of the meeting were as follows: 1. To review current knowledge and understanding of EC and its treatments. 2. To identify key issues for translational research and clinical trials. 3. To identify the most important trials for women with endometrial carcinoma and uterine carcinosarcoma, both those already underway C1 [Trimble, Edward L.] NCI, CIB, CTEP, DCTD,NIH, Bethesda, MD 20892 USA. [Kitchener, Henry C.] UK Natl Canc Res Inst, Manchester, Lancs, England. [Kitchener, Henry C.] Univ Manchester, Manchester, Lancs, England. RP Trimble, EL (reprint author), NCI, CIB, CTEP, DCTD,NIH, 610 Execut Blvd,Suite 7025, Bethesda, MD 20892 USA. EM tt6m@nih.gov RI Miller, David/H-4604-2011; salvesen, Helga/C-1187-2017 OI Miller, David/0000-0002-8215-5887; salvesen, Helga/0000-0002-4438-8831 NR 33 TC 44 Z9 46 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1048-891X J9 INT J GYNECOL CANCER JI Int. J. Gynecol. Cancer PD JAN PY 2009 VL 19 IS 1 BP 134 EP 140 DI 10.1111/IGC.0b013e3181995f90 PG 7 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA 457ZB UT WOS:000266976100024 PM 19258955 ER PT J AU Gaffney, DK Du Bois, A Narayan, K Reed, N Toita, T Pignata, S Blake, P Portelance, L Sadoyze, A Potter, R Colombo, A Randall, M Mirza, MR Trimble, EL AF Gaffney, David K. Du Bois, Andreas Narayan, Kailash Reed, Nick Toita, Takafumi Pignata, Sandro Blake, Peter Portelance, Lorraine Sadoyze, Azmat Potter, Richard Colombo, Alessandro Randall, Marcus Mirza, Mansoor R. Trimble, Edward L. TI Patterns of Care for Radiotherapy in Vulvar Cancer: A Gynecologic Cancer Intergroup Study SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER LA English DT Article DE Vulva; Chemoradiation; Cooperative group ID SQUAMOUS-CELL CARCINOMA; RISK CERVICAL-CANCER; CONCURRENT CHEMOTHERAPY; ONCOLOGY-GROUP; RADIATION-THERAPY; UTERINE CERVIX; PELVIC RADIATION; CISPLATIN; RECURRENCE; SURVIVAL AB Background: This study aimed to describe radiotherapeutic practice in the treatment of vulvar cancer in member study groups of the Gynecologic Cancer Intergroup (GCIG). Methods: A Survey was developed and distributed to representatives of the member Study groups of the GCIG, targeting the use of radiotherapy (RT) in vulvar cancer. Results: Thirty-two surveys were returned from 12 different cooperative groups. The most common indications for neoadjuvant RT include unresectable disease or International Federation of Gynecology and Obstetrics stage >= III. For the neoadjuvant treatment of vulvar cancer, pelvic doses were 48.2 +/- 5.0 Gy (mean +/- SD). Tire tipper border of the pelvic field was L4/5 in 4, L5/S1 in 12, and not specified in 4. Of 21 groups that perform neoadjuvant RT, 17 use concomitant chemotherapy and 4 individualize treatment, Weekly cisplatin was the most commonly used chemotherapy. For the neoadjuvant RT treatment of the inguinal region, doses were 49.9 +/- 5.5 Gy (mean SD). Sixteen of 18 groups used Computed tomographic Simulation for planning. After initial surgery, the most common indications for RT included positive lymph nodes or positive margins. Chemotherapy was not routinely used after surgery. Conclusions: Doses of RT among GCIG members are similar; however, the indications for treatment, treatment fields, and use of chemotherapy differ somewhat between groups. This is likely due to the rarity of the disease. The lack of randomized trials may contribute to the absence of a broadly accepted standard. This underscores the importance of international cooperation as in GCIG to gather more reliable data for uncommon tumors in gynecologic oncology. C1 [Trimble, Edward L.] NCI, Bethesda, MD 20892 USA. RP Gaffney, DK (reprint author), Huntsman Canc Hosp, Dept Radiat Oncol, 1950 Circle Hope,Rm 1570, Salt Lake City, UT 84112 USA. EM david.gaffney@hci.utah.edu NR 32 TC 10 Z9 11 U1 0 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1048-891X J9 INT J GYNECOL CANCER JI Int. J. Gynecol. Cancer PD JAN PY 2009 VL 19 IS 1 BP 163 EP 167 DI 10.1111/IGC.0b013e3181996ac3 PG 5 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA 457ZB UT WOS:000266976100029 PM 19258960 ER PT J AU Philippon, S Broutin, H de Magny, GC Toure, K Diakite, CH Fourquet, N Courel, MF Sultan, B Guegan, JF AF Philippon, Solenne Broutin, Helene de Magny, Guillaume Constantin Toure, Kandioura Diakite, Cheick Hamala Fourquet, Nicole Courel, Marie-Francoise Sultan, Benjamin Guegan, Jean-Francois TI Meningococcal meningitis in Mali: a long-term study of persistence and spread SO INTERNATIONAL JOURNAL OF INFECTIOUS DISEASES LA English DT Article DE Meningococcal meningitis; Mali; Epidemiology; Persistence; Spread ID NEISSERIA-MENINGITIDIS; EPIDEMIC MENINGITIS; SEROGROUP W135; BURKINA-FASO; VACCINATION; DISEASE; DYNAMICS; AFRICA; BELT; GHANA AB Objectives: Meningococcal meningitis (MM) is still a huge threat in the African meningitis belt. To fight against epidemics, a strengthened health information system, based upon weekly collected data, was set up in Mali. We aimed to study the spatio-temporal dynamics of MM in this country between 1992 and 2003. Methods: We were first interested in the impact of population size on the disease persistence. We then used cross-correlation analysis to study the spread of the disease on three different spatial scales, i.e., inter-region (global) and inter-district and intra-district (local) levels. Results: We found no persistence of MM at district level in Mali during the whole of the study period. However, we found persistence on a nationwide scale after the 1997 big epidemics, as opposed to the 1992-1996 time periods. In terms of spread, two main regions seem to lead MM dynamics in Mali, even if on a local scale the 'cities-villages' diffusion pattern was not systematically observed. Conclusions: This study improves knowledge on the spread and persistence of MM in Mali in recent years. It constitutes a first spatial study describing persistence and spread of MM in an African meningitis belt country. The next step should be the integration of vaccination and genetic variability data to clarify the route of spread of the disease in the human population. (C) 2008 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved. C1 [Philippon, Solenne; Fourquet, Nicole; Courel, Marie-Francoise] Univ Paris 07, Univ Paris 06, Univ Paris 01, CNRS,PRODIG,UMR 8586,EPHE, Paris, France. [Broutin, Helene; Guegan, Jean-Francois] IRD, Equipe Dynam Syst & Malad Infect, CNRS, GEMI,UMR 2724, F-34394 Montpellier 5, France. [de Magny, Guillaume Constantin] Univ Maryland, Inst Adv Comp Studies, College Pk, MD 20742 USA. [Toure, Kandioura] Minist Sante, DNS DE, Bamako, Mali. [Sultan, Benjamin] Univ Paris 06, CNRS, IRD, UR LOCEAN 86,UMR 7617, Paris, France. RP Broutin, H (reprint author), NIH, Fogarty Int Ctr, Bldg 10, Bethesda, MD 20892 USA. EM broutinh@mail.nih.gov RI Sultan, Benjamin/C-8957-2012 FU Paris I Pantheon-Sorbonne University; French Ministry of National Education, Research and Technology; French Institute of Research for Development (IRD); Fogarty International Center at the National Institutes of Health; NOAA; IRD; National Center for Scientific Research (CNRS) FX SP was supported by the Paris I Pantheon-Sorbonne University and received a research grant from the French Ministry of National Education, Research and Technology. HB was supported by the French Institute of Research for Development (IRD) and is now funded by the Fogarty International Center at the National Institutes of Health. GCDM is funded by NOAA. JFG is supported by both the IRD and the National Center for Scientific Research (CNRS). NR 28 TC 2 Z9 2 U1 1 U2 6 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 1201-9712 J9 INT J INFECT DIS JI Int. J. Infect. Dis. PD JAN PY 2009 VL 13 IS 1 BP 103 EP 109 DI 10.1016/j.ijid.2008.05.1223 PG 7 WC Infectious Diseases SC Infectious Diseases GA 398CY UT WOS:000262711400015 PM 18674942 ER PT J AU Lustig, A Carter, A Bertak, D Enika, D Vandanmagsar, B Wood, W Becker, KG Weeraratna, AT Taub, DD AF Lustig, Ana Carter, Arnell Bertak, Dorothy Enika, Divya Vandanmagsar, Bolormaa Wood, William Becker, Kevin G. Weeraratna, Ashani T. Taub, Dennis D. TI Transcriptome analysis of murine thymocytes reveals age-associated changes in thymic gene expression SO INTERNATIONAL JOURNAL OF MEDICAL SCIENCES LA English DT Article DE thymus; involution; aging; microarray; AGEMAP; thymocytes; caloric restriction ID B-CELLS; OXIDATIVE-PHOSPHORYLATION; MITOCHONDRIAL DYSFUNCTION; INDUCED APOPTOSIS; YOUNG-ADULT; MICE; IMMUNOSENESCENCE; INVOLUTION; RECEPTOR; SURVIVAL AB The decline in adaptive immunity, naive T-cell output and a contraction in the peripheral T cell receptor (TCR) repertoire with age are largely attributable to thymic involution and the loss of critical cytokines and hormones within the thymic microenvironment. To assess the molecular changes associated with this loss of thymic function, we used cDNA microarray analyses to examine the transcriptomes of thymocytes from mice of various ages ranging from very young (1 month) to very old (24 months). Genes associated with various biological and molecular processes including oxidative phosphorylation, T- and B-cell receptor signaling and antigen presentation were observed to significantly change with thymocyte age. These include several immunoglobulin chains, chemokine and ribosomal proteins, annexin A2, vav 1 and several S100 signaling proteins. The increased expression of immunoglobulin genes in aged thymocytes could be attributed to the thymic B cells which were found to be actively producing IgG and IgM antibodies. Upon further examination, we found that purified thymic T cells derived from aged but not young thymi also exhibited IgM on their cell surface suggesting the possible presence of auto-antibodies on the surface thymocytes with advancing age. These studies provide valuable insight into the cellular and molecular mechanisms associated with thymic aging. C1 [Lustig, Ana; Carter, Arnell; Bertak, Dorothy; Enika, Divya; Vandanmagsar, Bolormaa; Weeraratna, Ashani T.; Taub, Dennis D.] NIA, Immunol Lab, Intramural Res Program, NIH, Baltimore, MD 21224 USA. [Wood, William; Becker, Kevin G.] NIA, Res Resources Branch, Intramural Res Program, NIH, Baltimore, MD 21224 USA. RP Taub, DD (reprint author), NIA, Immunol Lab, Intramural Res Program, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. EM taubd@grc.nia.nih.gov OI Becker, Kevin/0000-0002-6794-6656 FU National Institute on Aging, National Institutes of Health FX We would like to thank Dr. Dan Longo for his thoughtful review of this manuscript. This research was entirely supported by the Intramural Research Program of the National Institute on Aging, National Institutes of Health. NR 64 TC 17 Z9 17 U1 0 U2 2 PU IVYSPRING INT PUBL PI LAKE HAVEN PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA J9 INT J MED SCI JI Int. J. Med. Sci. PY 2009 VL 6 IS 1 BP 51 EP 64 PG 14 WC Medicine, General & Internal SC General & Internal Medicine GA 540XT UT WOS:000273375100007 PM 19214242 ER PT J AU French, AD Fiori, JL Camilli, TC Leotlela, PD O'Connell, MP Frank, BP Subaran, S Indig, FE Taub, DD Weeraratna, AT AF French, Amanda D. Fiori, Jennifer L. Camilli, Tura C. Leotlela, Poloko D. O'Connell, Michael P. Frank, Brittany P. Subaran, Sarah Indig, Fred E. Taub, Dennis D. Weeraratna, Ashani T. TI PKC and PKA Phosphorylation Affect the Subcellular Localization of Claudin-1 in Melanoma Cells SO INTERNATIONAL JOURNAL OF MEDICAL SCIENCES LA English DT Article DE Claudin; melanoma; metastasis; PKC; PKA ID PROTEIN-KINASE-C; JUNCTION BARRIER FUNCTION; TIGHT JUNCTIONS; OVARIAN-CANCER; EXPRESSION; MOTILITY; INVASION; CONTRIBUTES; PATHWAY; GENE AB Cytoplasmic expression of claudin-1 in metastatic melanoma cells correlates to increased migration, and increased secretion of MMP-2 in a PKC dependent manner, whereas claudin-1 nuclear expression is found in benign nevi. Melanoma cells were transfected with a vector expressing CLDN-1 fused to a nuclear localization signal (NLS). Despite significant nuclear localization of claudin-1, there was still transport of claudin-1 to the cytoplasm. Phorbol ester treatment of cells transfected with NLS-claudin-1 resulted in an exclusion of claudin-1 from the nucleus, despite the NLS. To ascertain whether PKC or PKA were involved in this translocation, we mutated the putative phosphorylation sites within the protein. We found that mutating the PKC phosphorylation sites to mimic a non-phosphorylated state did not cause a shift of claudin-1 to the nucleus of the cells, but mutating the PKA sites did. Mutations of either site to mimic constitutive phosphorylation resulted in cytoplasmic claudin-1 expression. Stable claudin-1 transfectants containing non-phosphorylatable PKA sites exhibited decreased motility. These data imply that subcellular localization of claudin-1 can be controlled by phosphorylation, dicating effects on metastatic capacity. C1 [Weeraratna, Ashani T.] NIA, Immunol Lab, NIH, Biomed Res Ctr, Baltimore, MD 21224 USA. [Frank, Brittany P.; Subaran, Sarah; Indig, Fred E.] NIA, Res Resources Branch, Baltimore, MD 21224 USA. RP Weeraratna, AT (reprint author), NIA, Immunol Lab, NIH, Biomed Res Ctr, 251 Bayview Blvd,RM 08C226, Baltimore, MD 21224 USA. EM weerarat@grc.nia.nih.gov FU National Institute on Aging FX This work was supported by the Intramural Research Program of the National Institute on Aging. We thank Dr. Pat J. Morin for helpful comments on the manuscript. NR 21 TC 41 Z9 44 U1 0 U2 2 PU IVYSPRING INT PUBL PI LAKE HAVEN PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA J9 INT J MED SCI JI Int. J. Med. Sci. PY 2009 VL 6 IS 2 BP 93 EP 101 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA 540XV UT WOS:000273375300005 PM 19305641 ER PT J AU Loh, YP Lee, T Murthy, SRK Cawley, NX Hewitt, S Ng, I Poon, R AF Loh, Y. Peng Lee, Terence Murthy, Saravana R. K. Cawley, Niamh X. Hewitt, Stephen Ng, Irene Poon, Ronnie TI A carboxypeptidase E isoform controls and predicts metastatic potential of human cancers SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE LA English DT Meeting Abstract C1 [Loh, Y. Peng; Murthy, Saravana R. K.; Cawley, Niamh X.] NICHD, Cellular Neurobiol Sect, NIH, Bethesda, MD USA. [Lee, Terence; Ng, Irene; Poon, Ronnie] Univ Hong Kong, Dept Pathol, Pokfulam, Hong Kong, Peoples R China. [Hewitt, Stephen] NCI, Tissue Array Res Program, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPANDIDOS PUBL LTD PI ATHENS PA POB 18179, ATHENS, 116 10, GREECE SN 1107-3756 J9 INT J MOL MED JI Int. J. Mol. Med. PY 2009 VL 24 MA 237 BP S39 EP S39 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 502YQ UT WOS:000270497500138 ER PT J AU Popescu, NC AF Popescu, Nicholas C. TI Deleted in liver cancer (DLC1) as a metastasis suppressor gene SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE LA English DT Meeting Abstract C1 [Popescu, Nicholas C.] NCI, Expt Carcinogenesis Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPANDIDOS PUBL LTD PI ATHENS PA POB 18179, ATHENS, 116 10, GREECE SN 1107-3756 J9 INT J MOL MED JI Int. J. Mol. Med. PY 2009 VL 24 MA 138 BP S14 EP S14 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 502YQ UT WOS:000270497500039 ER PT J AU Wang, H Patel, V Miyazaki, H Gutkind, JS Yeudall, WA AF Wang, H. Patel, V. Miyazaki, H. Gutkind, J. S. Yeudall, W. A. TI EPS8 in oncogenesis SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE LA English DT Meeting Abstract C1 [Wang, H.; Miyazaki, H.; Yeudall, W. A.] Virginia Commonwealth Univ, Philips Inst Oral & Craniofacial Mol Biol, Richmond, VA 23298 USA. [Miyazaki, H.; Yeudall, W. A.] Virginia Commonwealth Univ, Dept Biochem & Mol Biol, Richmond, VA 23298 USA. [Yeudall, W. A.] Virginia Commonwealth Univ, Massey Canc Ctr, Richmond, VA 23298 USA. [Patel, V.; Gutkind, J. S.] Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPANDIDOS PUBL LTD PI ATHENS PA POB 18179, ATHENS, 116 10, GREECE SN 1107-3756 J9 INT J MOL MED JI Int. J. Mol. Med. PY 2009 VL 24 MA 338 BP S64 EP S64 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 502YQ UT WOS:000270497500239 ER PT J AU Williams, JL Ji, P Kopelovich, L Rigas, B AF Williams, Jennie L. Ji, Ping Kopelovich, Levy Rigas, Basil TI Nitric oxide-donating aspirin S-nitrosylates signaling proteins in colon cancer cells: Implications for its mecanhism of action SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE LA English DT Meeting Abstract C1 [Williams, Jennie L.; Ji, Ping; Rigas, Basil] SUNY Stony Brook, Canc Prevent Div, Stony Brook, NY 11794 USA. [Kopelovich, Levy] NCI, Canc Prevent Div, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SPANDIDOS PUBL LTD PI ATHENS PA POB 18179, ATHENS, 116 10, GREECE SN 1107-3756 J9 INT J MOL MED JI Int. J. Mol. Med. PY 2009 VL 24 MA 266 BP S46 EP S46 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 502YQ UT WOS:000270497500167 ER PT J AU Picchioni, D Killgore, WDS Balkin, TJ Braun, AR AF Picchioni, Dante Killgore, William D. S. Balkin, Thomas J. Braun, Allen R. TI POSITRON EMISSION TOMOGRAPHY CORRELATES OF VISUALLY-SCORED ELECTROENCEPHALOGRAPHIC WAVEFORMS DURING NON-RAPID EYE MOVEMENT SLEEP SO INTERNATIONAL JOURNAL OF NEUROSCIENCE LA English DT Article DE delta waves/slow waves; electroencephalography; K-complexes; positron emission tomography; sleep; sleep spindles ID DECLARATIVE MEMORY CONSOLIDATION; CEREBRAL-BLOOD-FLOW; SPONTANEOUS K-COMPLEX; STAGE-2 SLEEP; DELTA-WAVES; MOTOR MEMORY; HUMAN BRAIN; SPINDLES; PLASTICITY; NEURONS AB Visually-scored, non-Rapid Eye Movement (REM) sleep electroencephalographic (EEG) waveform activity for each 30-s sleep scored epoch-including the number of sleep spindles, the number of K-complexes, and the percentage of delta waves occupying the epoch-was correlated with H(2)(15)O positron emission tomography. Sleep spindle correlations included positive correlations in the thalamus and right hippocampus. K-complex correlations included positive correlations in the frontomedian prefrontal cortex and cerebellum. Delta wave correlations included negative correlations in the thalamus, frontomedian prefrontal cortex, dorsal pons, and primary visual cortex. Each pattern of correlations may suggest a functional significance for these waveforms that relates to a waking outcome. C1 [Picchioni, Dante; Balkin, Thomas J.] Walter Reed Army Inst Res, Div Psychiat & Neurosci, Silver Spring, MD 20910 USA. [Killgore, William D. S.] McLean Hosp, Cognit Neuroimaging Lab, Belmont, MA 02178 USA. [Braun, Allen R.] Natl Inst Deafness & Other Commun Disorders, NIH, Bethesda, MD USA. RP Picchioni, D (reprint author), Walter Reed Army Inst Res, Div Psychiat & Neurosci, 503 Robert Grant Ave, Silver Spring, MD 20910 USA. EM dante.picchioni@amedd.army.mil OI Killgore, William/0000-0002-5328-0208 NR 59 TC 5 Z9 5 U1 1 U2 2 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 0020-7454 J9 INT J NEUROSCI JI Int. J. Neurosci. PY 2009 VL 119 IS 11 BP 2074 EP 2099 DI 10.1080/00207450903139770 PG 26 WC Neurosciences SC Neurosciences & Neurology GA 512UF UT WOS:000271275600006 PM 19863262 ER PT J AU Wardle, J Llewellyn, C Sanderson, S Plomin, R AF Wardle, J. Llewellyn, C. Sanderson, S. Plomin, R. TI The FTO gene and measured food intake in children SO INTERNATIONAL JOURNAL OF OBESITY LA English DT Article DE FTO; diet; children; appetite; eating behaviour ID BODY-MASS INDEX; ENERGY-EXPENDITURE; CHILDHOOD OBESITY; PHYSICAL-ACTIVITY; ADULT OBESITY; FAT MASS; ADIPOSITY; VARIANTS; ABSENCE; WEIGHT AB Objective: Polymorphisms in the obesity-associated gene, FTO, have been linked with sensitivity to satiety in children, indicating FTO may be influencing one of the regulatory drivers underlying food intake. In this study, we tested the hypothesis that food intake in a standard eating behaviour paradigm in which palatable food is offered under conditions of satiety would be associated with FTO genotype status, after controlling for differences in body mass index (BMI). Methods: Participants were 131 children aged 4-5 years, taking part in a behavioural study of food intake for whom DNA was available for genotyping. The phenotypic indicator of intake was the child's consumption of palatable food presented after having eaten a meal. We also assessed physical activity using parental reports of the child's enjoyment of active games, their level of activity relative to other children and a standard measure of fidgetiness. Associations between polymorphisms of the intronic FTO single nucleotide polymorphism (rs9939609) and behaviour ( food intake and activity) were assessed by analysis of variance controlling for sex, age and BMI s.d. scores. Results: The distribution of AA (homogenous for A allele), AT (heterogeneous T and A alleles) and TT (homogenous for T allele) genotypes was 18, 50 and 32%, respectively. As predicted, TT homozygotes ate significantly less than heterozygotes (P = 0.03) or AA homozygotes (P = 0.02). The effect was not diminished by controlling for BMI s.d. scores. There were no significant associations between FTO genotype and any marker of physical activity. Conclusions: We showed that children with two copies of the lower-risk FTO alleles ate less than those with one or two higher-risk alleles. We conclude that the T allele is protective against overeating by promoting responsiveness to internal signals of satiety. C1 [Wardle, J.; Llewellyn, C.] UCL, Hlth Behav Res Ctr, Dept Epidemiol & Publ Hlth, London WC1E 6BT, England. [Sanderson, S.] NHGRI, Social & Behav Res Branch, Natl Inst Hlth, Bethesda, MD 20892 USA. [Plomin, R.] Kings Coll London, Inst Psychiat, Social Genet & Dev Psychiat Ctr, London WC2R 2LS, England. RP Wardle, J (reprint author), UCL, Hlth Behav Res Ctr, Dept Epidemiol & Publ Hlth, Gower St,2-16 Torrington Pl, London WC1E 6BT, England. EM j.wardle@ucl.ac.uk RI Plomin, Robert/B-8911-2008; OI Llewellyn, Clare/0000-0002-0066-2827; Plomin, Robert/0000-0002-0756-3629 FU Biotechnology and Biological Sciences Research Council [D19086] FX We are very grateful to all the families who made this research possible. The research was funded by a grant from the Biotechnology and Biological Sciences Research Council (D19086). NR 21 TC 140 Z9 145 U1 2 U2 22 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0307-0565 J9 INT J OBESITY JI Int. J. Obes. PD JAN PY 2009 VL 33 IS 1 BP 42 EP 45 DI 10.1038/ijo.2008.174 PG 4 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA 393ML UT WOS:000262377300008 PM 18838977 ER PT J AU Roberts, C Freeman, J Samdal, O Schnohr, CW de Looze, ME Gabhainn, SN Iannotti, R Rasmussen, M AF Roberts, C. Freeman, J. Samdal, O. Schnohr, C. W. de Looze, M. E. Gabhainn, S. Nic Iannotti, R. Rasmussen, M. CA Int HBSC Study Grp TI The Health Behaviour in School-aged Children (HBSC) study: methodological developments and current tensions SO INTERNATIONAL JOURNAL OF PUBLIC HEALTH LA English DT Article DE Survey development; Large-scale surveys; Scientific versus policy concerns; Cross-national data management ID POLICY; VALIDITY; RELIABILITY; ADOLESCENTS; VALIDATION; COMPLAINTS; SCALE AB Objectives: To describe the methodological development of the HBSC survey since its inception and explore methodological tensions that need to be addressed in the ongoing work on this and other large-scale cross-national surveys. Methods: Using archival data and conversations with members of the network, we collaboratively analysed our joint understandings of the survey's methodology. Results: We identified four tensions that are likely to be present in upcoming survey cycles: (1) maintaining quality standards against a background of rapid growth, (2) continuous improvement with limited financial resources, (3) accommodating analysis of trends with the need to improve and adapt questionnaire content, and (4) meeting the differing requirements of scientific and policy audiences. Conclusions: While these challenges are not trivial, the structure of the HBSC network and its long-term experience in working through such challenges renders it likely that HBSC can provide a model of other similar studies facing these tensions. C1 [Roberts, C.] Welsh Assembly Govt, Publ Hlth & Hlth Profess Dept, Res & Evaluat Branch, Publ Hlth Strategy Div, Cardiff CF10 3NQ, S Glam, Wales. [Freeman, J.] Queens Univ, Fac Educ, Kingston, ON, Canada. [Samdal, O.] Univ Bergen, Fac Psychol, Res Ctr Hlth Promot, N-5020 Bergen, Norway. [Schnohr, C. W.; Rasmussen, M.] Univ Copenhagen, Dept Publ Hlth, DK-1168 Copenhagen, Denmark. [de Looze, M. E.] Univ Utrecht, Fac Social & Behav Sci, NL-3508 TC Utrecht, Netherlands. [Gabhainn, S. Nic] Natl Univ Ireland, Hlth Promot Res Ctr, Galway, Ireland. [Iannotti, R.] NICHHD, Bethesda, MD 20892 USA. RP Roberts, C (reprint author), Welsh Assembly Govt, Publ Hlth & Hlth Profess Dept, Res & Evaluat Branch, Publ Hlth Strategy Div, Cathays Pk, Cardiff CF10 3NQ, S Glam, Wales. EM Chris.Roberts@wales.gsi.gov.uk RI Gaspar de Matos, Margarida/H-3824-2012; OI Gaspar de Matos, Margarida/0000-0003-2114-2350; Csemy, Ladislav/0000-0002-5397-5253 FU Intramural NIH HHS [Z99 HD999999] NR 31 TC 195 Z9 195 U1 1 U2 31 PU BIRKHAUSER VERLAG AG PI BASEL PA VIADUKSTRASSE 40-44, PO BOX 133, CH-4010 BASEL, SWITZERLAND SN 1661-8556 J9 INT J PUBLIC HEALTH JI Int. J. Public Health PY 2009 VL 54 BP 140 EP 150 DI 10.1007/s00038-009-5405-9 PG 11 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 511KK UT WOS:000271162900006 PM 19639259 ER PT J AU Iannotti, RJ Janssen, I Haug, E Kololo, H Annaheim, B Borraccino, A AF Iannotti, Ronald J. Janssen, Ian Haug, Ellen Kololo, Hanna Annaheim, Beatrice Borraccino, Alberto CA HBSC Phys Activity Focus Grp TI Interrelationships of adolescent physical activity, screen-based sedentary behaviour, and social and psychological health SO INTERNATIONAL JOURNAL OF PUBLIC HEALTH LA English DT Article DE Physical activity; Sedentary behaviour; Life satisfaction; Social relationships; Health complaints; Substance use ID MIDDLE-SCHOOL-CHILDREN; AGGRESSIVE-BEHAVIOR; SPORT; YOUTH; PATTERNS; RISK; QUESTIONNAIRE; ASSOCIATIONS; RELIABILITY; TELEVISION AB Objectives: To examine how adolescent physical activity (PA) and screen-based media sedentary behaviours (SBM) relate to psychological and social health and identify cross-national differences in these relationships. Methods: Associations were examined in five regions using two Health Behaviour in School-Aged Children (HBSC) countries from each. Results: Self-reported psychological and social health indices such as self-image, perceived health status, and Life Satisfaction were positively related to PA in all five regions but, with a few exceptions, negatively related to SBM. Negative health indices such as health complaints and tobacco use were negatively related to PA but, with exceptions, positively related to SBM. Significant regional differences were present. Conclusions: Regional differences in correlates of PA and SBM suggest cultural differences in potential effects of PA and SBM and the need to tailor school and public health efforts to the different meanings of PA and SBM for positive and negative health consequences. C1 [Iannotti, Ronald J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Prevent Res Branch, Div Epidemiol Stat & Prevent Res, NIH,DHHS, Bethesda, MD 20892 USA. [Janssen, Ian] Queens Univ, Dept Epidemiol & Community Hlth, Kingston, ON, Canada. [Janssen, Ian] Queens Univ, Sch Phys & Hlth, Kingston, ON, Canada. [Haug, Ellen] Univ Bergen, Res Ctr Hlth Promot, Bergen, Norway. [Kololo, Hanna] Inst Mother & Child NRIMC, Dept Child & Adolescent Hlth, Warsaw, Poland. [Annaheim, Beatrice] Swiss Inst Prevent Alcohol & Drug Problems, Lausanne, Switzerland. [Borraccino, Alberto] Univ Turin, Dept Publ Hlth, I-10124 Turin, Italy. RP Iannotti, RJ (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Prevent Res Branch, Div Epidemiol Stat & Prevent Res, NIH,DHHS, 6100 Execut Blvd,7B05, Bethesda, MD 20892 USA. EM iannottr@mail.nih.gov RI Calmeiro, Luis/G-6284-2010; Borraccino, Alberto/C-9013-2012; Calmeiro, Luis/G-5451-2014; Janssen, Ian/B-7700-2009; Gaspar de Matos, Margarida/H-3824-2012 OI Borraccino, Alberto/0000-0001-8235-8775; Calmeiro, Luis/0000-0002-7551-6445; Gaspar de Matos, Margarida/0000-0003-2114-2350 FU Eunice Kennedy Shriver National Institute of Child Health and Human Development FX Work on this manuscript was supported by the Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development. NR 41 TC 62 Z9 62 U1 4 U2 27 PU SPRINGER BASEL AG PI BASEL PA PICASSOPLATZ 4, BASEL, 4052, SWITZERLAND SN 1661-8556 EI 1661-8564 J9 INT J PUBLIC HEALTH JI Int. J. Public Health PY 2009 VL 54 SU 2 BP 191 EP 198 DI 10.1007/s00038-009-5410-z PG 8 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 511KK UT WOS:000271162900011 PM 19639256 ER PT J AU Simons-Morton, BG Farhat, T ter Bogt, TFM Hublet, A Kuntsche, E Gabhainn, SN Godeau, E Kokkevi, A AF Simons-Morton, Bruce G. Farhat, Tilda ter Bogt, Tom F. M. Hublet, Anne Kuntsche, Emmanuel Gabhainn, Saoirse Nic Godeau, Emmanuelle Kokkevi, Anna CA HBSC Risk Behav Focus Grp TI Gender specific trends in alcohol use: cross-cultural comparisons from 1998 to 2006 in 24 countries and regions SO INTERNATIONAL JOURNAL OF PUBLIC HEALTH LA English DT Article DE Alcohol; Drunkenness; Adolescents; Trends; Cross-national; Gender ID EUROPEAN COUNTRIES; ADOLESCENTS; PERSPECTIVE; DEPENDENCE; ABUSE AB Objective: To examine trends in the prevalence of monthly alcohol use and lifetime drunkenness among 15 year olds in 20 European countries, the Russian Federation, Israel, the United States of America, and Canada. Methods: Alcohol use prevalence and drunkenness were assessed in the Health Behavior in School-aged Children Survey conducted in each country in 1998, 2002, and 2006. Trends were determined using the Cochran-Mantel-Haenszel test for trends. Results: Average monthly alcohol use across all countries declined from 45.3 % to 43.6 % and drunkenness declined from 37.2% to 34.8. There was substantial variability across countries, with decreases in some countries and increases or no change in use or drunkenness in others. The overall decline was greater among boys, from 41.2 % to 36.7 % than among girls, 33.3 % to 31.9 %. In most of the countries where drinking or drunkenness increased, it was due mainly to increases among girls. Conclusions: Trends in alcohol use and drunkenness varied by country. Drinking and drunkenness remained higher among boys than girls, but the gap between boys and girls declined and girls appear to be catching up with boys in some countries. C1 [Simons-Morton, Bruce G.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Prevent Res Branch, Div Epidemiol Stat & Prevent Res, NIH, Bethesda, MD 20892 USA. [ter Bogt, Tom F. M.] Univ Utrecht, Netherlands Inst Mental Heath & Addict, NL-3508 TC Utrecht, Netherlands. [Hublet, Anne] Univ Ghent, Dept Publ Hlth, Ghent, Belgium. [Kuntsche, Emmanuel] Swiss Inst Prevent Alcohol & Drug Problems, Res Dept, Lausanne, Switzerland. [Gabhainn, Saoirse Nic] Natl Univ Ireland, Dept Hlth Promot, Ctr Hlth Promot Studies, Dublin, Ireland. [Godeau, Emmanuelle] Univ Toulouse 3, INSERM, UMR, U558,Serv Med Rectorat Toulouse, F-31062 Toulouse, France. [Kokkevi, Anna] Univ Athens, Sch Med, Univ Mental Hlth Res Inst, GR-11527 Athens, Greece. [Kokkevi, Anna] Univ Athens, Sch Med, Dept Psychiat, GR-11527 Athens, Greece. RP Simons-Morton, BG (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Prevent Res Branch, Div Epidemiol Stat & Prevent Res, NIH, 6100 Execut Blvd,7B13M, Bethesda, MD 20892 USA. EM mortonb@exchange.nih.gov RI Simoes, Celeste/I-6444-2012; Zezula, Ivan/B-8791-2017; Jimenez-Iglesias, Antonia/L-4562-2014; OI Simons-Morton, Bruce/0000-0003-1099-6617; Simoes, Celeste/0000-0003-0229-1422; Zezula, Ivan/0000-0001-9091-3935; Jimenez-Iglesias, Antonia/0000-0001-6262-4001; Csemy, Ladislav/0000-0002-5397-5253; Fotiou, Anastasios/0000-0001-7905-3241; Kolarcik, Peter/0000-0003-4504-5256 FU Eunice Kennedy Shriver National Institute of Child Health and Human Development [N01-HD5-3401] FX This research was supported in part by the intramural research program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (Contract # N01-HD5-3401). NR 26 TC 50 Z9 50 U1 3 U2 18 PU BIRKHAUSER VERLAG AG PI BASEL PA VIADUKSTRASSE 40-44, PO BOX 133, CH-4010 BASEL, SWITZERLAND SN 1661-8556 J9 INT J PUBLIC HEALTH JI Int. J. Public Health PY 2009 VL 54 BP 199 EP 208 DI 10.1007/s00038-009-5411-y PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 511KK UT WOS:000271162900012 PM 19618110 ER PT J AU Kuntsche, E Simons-Morton, B ter Bogt, T Sanchez-Queija, I Tinoco, VM de Matos, MG Santinello, M Lenzi, M AF Kuntsche, Emmanuel Simons-Morton, Bruce ter Bogt, Tom Sanchez-Queija, Inmaculada Munoz Tinoco, Victoria de Matos, Margarida Gaspar Santinello, Massimo Lenzi, Michela CA HBSC Peer Culture Focus Grp TI Electronic media communication with friends from 2002 to 2006 and links to face-to-face contacts in adolescence: an HBSC study in 31 European and North American countries and regions SO INTERNATIONAL JOURNAL OF PUBLIC HEALTH LA English DT Article DE Electronic media use; Face-to-face; Peer groups; Adolescents; Trend study; Cross-cultural research ID INTERNET PARADOX; PEER AB Objective: Because the potential for electronic media communication (EMC) has increased greatly, it is of interest to describe trends in EMC between adolescents and their friends and to investigate whether EMC facilitate or supersede face-to-face contacts among peers. Methods: Answers of 275,571 adolescents concerning contacting friends by means of the phone, text messages, and the internet (i.e. EMC), the number of close friends, and the number of afternoons and evenings per week spent out with friends were analysed by means of chi(2)-tests; and multiple regression. Results: In 2006, between more than one third (11-year olds) and nearly two thirds (15-year olds) communicated electronically with their friends daily or nearly daily. From 2002 to 2006, EMC increased in almost all participating countries. Particularly high increases were found in Eastern Europe. Across countries, the higher the frequency of EMC the higher the number of afternoons and evenings spent with friends. Conclusion: The results are surprisingly consistent across the 31 countries and suggest that EMC among adolescents facilitate rather than supersede face-to-face peer contacts. C1 [Kuntsche, Emmanuel] Swiss Inst Prevent Alcohol & Drug Problems, Res Dept, CH-1001 Lausanne, Switzerland. [Simons-Morton, Bruce] NICHHD, Prevent Res Branch, NIH, Bethesda, MD 20892 USA. [ter Bogt, Tom] Univ Utrecht, Netherlands Inst Mental Hlth & Addict, NL-3508 TC Utrecht, Netherlands. [Sanchez-Queija, Inmaculada] Natl Distance Univ Spain, Dept Dev & Educ Psychol, Madrid, Spain. [Munoz Tinoco, Victoria] Univ Seville, Dept Dev & Educ Psychol, Seville, Spain. [de Matos, Margarida Gaspar] Univ Tecn Lisboa, Fac Human Kinet, P-1100 Lisbon, Portugal. [Santinello, Massimo; Lenzi, Michela] Univ Padua, Dept Dev & Social Psychol, I-35100 Padua, Italy. RP Kuntsche, E (reprint author), Swiss Inst Prevent Alcohol & Drug Problems, Res Dept, POB 870, CH-1001 Lausanne, Switzerland. EM EKuntsche@sfa-ispa.ch RI Sanchez-Queija, Inmaculada/E-9927-2011; Loureiro, Nuno/I-6400-2012; Tome, Gina/I-7128-2012; Gaspar de Matos, Margarida/H-3824-2012; Perez-Moreno, Pedro/I-2512-2015; OI Lenzi, Michela/0000-0001-7721-2448; Sanchez-Queija, Inmaculada/0000-0002-4688-4206; Loureiro, Nuno/0000-0002-1166-3219; Tome, Gina/0000-0002-4440-6868; Gaspar de Matos, Margarida/0000-0003-2114-2350; Perez-Moreno, Pedro/0000-0002-6074-9385; Camacho, Ines/0000-0002-0454-4107; Simons-Morton, Bruce/0000-0003-1099-6617 FU SIPA; Swiss Federal Office of Public Health [04.001776/2.24.02.-64] FX The principal author was supported by SIPA and the Swiss Federal Office of Public Health (Grant No. 04.001776/2.24.02.-64). NR 28 TC 18 Z9 18 U1 3 U2 16 PU SPRINGER BASEL AG PI BASEL PA PICASSOPLATZ 4, BASEL, 4052, SWITZERLAND SN 1661-8556 J9 INT J PUBLIC HEALTH JI Int. J. Public Health PY 2009 VL 54 SU 2 BP 243 EP 250 DI 10.1007/s00038-009-5416-6 PG 8 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 511KK UT WOS:000271162900017 PM 19623474 ER PT J AU Gilbert, ES AF Gilbert, Ethel S. TI Ionising radiation and cancer risks: What have we learned from epidemiology? SO INTERNATIONAL JOURNAL OF RADIATION BIOLOGY LA English DT Review DE Epidemiology; ionising radiation; cancer risks; dose-response ID ATOMIC-BOMB SURVIVORS; US RADIOLOGIC TECHNOLOGISTS; CONTRALATERAL BREAST-CANCER; TECHA RIVER COHORT; X-RAY TREATMENT; LUNG-CANCER; THYROID-CANCER; CHILDHOOD-CANCER; ANKYLOSING-SPONDYLITIS; HODGKINS-DISEASE AB Purpose: Epidemiologic studies of persons exposed to ionising radiation offer a wealth of information on cancer risks in humans. The Life Span Study cohort of Japanese A-bomb survivors, a large cohort that includes all ages and both sexes with a wide range of well-characterised doses, is the primary resource for estimating carcinogenic risks from low linear energy transfer external exposure. Extensive data on persons exposed for therapeutic or diagnostic medical reasons offer the opportunity to study fractionated exposure, risks at high therapeutic doses, and risks of site-specific cancers in non-Japanese populations. Studies of persons exposed for occupational and environmental reasons allow a direct evaluation of exposure at low doses and dose rates, and also provide information on different types of radiation such as radon and iodine-131. This article summarises the findings from these studies with emphasis on studies with well-characterised doses. Conclusions: Epidemiologic studies provide the necessary data for quantifying cancer risks as a function of dose and for setting radiation protection standards. Leukaemia and most solid cancers have been linked with radiation. Most solid cancer data are reasonably well described by linear-dose response functions although there may be a downturn in risks at very high doses. Persons exposed early in life have especially high relative risks for many cancers, and radiation-related risk of solid cancers appears to persist throughout life. C1 NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Gilbert, ES (reprint author), NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd, Bethesda, MD 20892 USA. EM gilberte@mail.nih.gov FU Intramural NIH HHS [Z99 CA999999] NR 101 TC 42 Z9 43 U1 2 U2 14 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 0955-3002 J9 INT J RADIAT BIOL JI Int. J. Radiat. Biol. PY 2009 VL 85 IS 6 BP 467 EP 482 AR PII 910782193 DI 10.1080/09553000902883836 PG 16 WC Biology; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA 448SH UT WOS:000266281800001 PM 19401906 ER PT J AU Batra, S Matsumoto, S Hyodo, F Mitchell, J Krishna, MC AF Batra, S. Matsumoto, S. Hyodo, F. Mitchell, J. Krishna, M. C. TI MRI Assessment of Angiogenesis Inhibitor Sunitinib's Influence on Tumor Oxygenation to Identify an Optimal Chemoradiotherapeutic Window SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract CT 51st Annual Meeting of the American-Society-for-Radiation-Oncology CY NOV 01-05, 2009 CL Chicago, IL SP Amer Soc Radiat Oncol C1 [Batra, S.] Stanford Univ, Palo Alto, CA 94304 USA. [Batra, S.; Matsumoto, S.; Hyodo, F.; Mitchell, J.; Krishna, M. C.] NIH, Bethesda, MD 20892 USA. NR 0 TC 3 Z9 3 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 2009 VL 75 IS 3 BP S43 EP S43 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 503WW UT WOS:000270573600092 ER PT J AU Buchanan, IM Burgan, WE Burgess, TL Camphausen, K AF Buchanan, I. M. Burgan, W. E. Burgess, T. L. Camphausen, K. TI Radiosensitization of Glioblastoma Multiforme by Modulation of Met Signaling with the Hepatocyte Growth Factor Neutralizing Antibody, AMG102 SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract CT 51st Annual Meeting of the American-Society-for-Radiation-Oncology CY NOV 01-05, 2009 CL Chicago, IL SP Amer Soc Radiat Oncol C1 [Buchanan, I. M.; Camphausen, K.] NCI, Radiat Oncol Branch, Bethesda, MD 20892 USA. [Buchanan, I. M.] Howard Hughes Med Inst, Chevy Chase, MD USA. [Burgan, W. E.] NCI, Mol Radiat Therapeut Branch, Frederick, MD 21701 USA. [Burgan, W. E.] NCI, Sci Applicat Int Corp Frederick, Frederick, MD 21701 USA. [Burgess, T. L.] Amgen Inc, Thousand Oaks, CA 91320 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 2009 VL 75 IS 3 BP S69 EP S69 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 503WW UT WOS:000270573600146 ER PT J AU Caballero, JA Gameiro, S Higgins, J Boehm, A Franzusoff, A Schlom, J Hodge, J AF Caballero, J. A. Gameiro, S. Higgins, J. Boehm, A. Franzusoff, A. Schlom, J. Hodge, J. TI Chemotherapy can Enhance the Therapeutic Potential of Vaccine-mediated Immunotherapy SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract CT 51st Annual Meeting of the American-Society-for-Radiation-Oncology CY NOV 01-05, 2009 CL Chicago, IL SP Amer Soc Radiat Oncol C1 [Caballero, J. A.; Gameiro, S.; Higgins, J.; Boehm, A.; Schlom, J.; Hodge, J.] NCI, Tumor Immunol & Biol Lab, Canc Res Ctr, NIH, Bethesda, MD 20892 USA. [Franzusoff, A.] Globelmmune Inc, Louisville, CO USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 2009 VL 75 IS 3 BP S570 EP S570 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 503WW UT WOS:000270573602177 ER PT J AU Chung, E Urick, M Kurshan, N Shield, W Riley, H Citrin, D AF Chung, E. Urick, M. Kurshan, N. Shield, W. Riley, H. Citrin, D. TI The Mitogen-activated Protein Kinase (MAPK)/Extracellular Signal-regulated Kinase (ERK) 1/2 Kinase Inhibitor, AZD6244 (ARRY-142886) Enhances Radiosensitivity by Interfering with Radiation-induced TGF-alpha Signaling SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract CT 51st Annual Meeting of the American-Society-for-Radiation-Oncology CY NOV 01-05, 2009 CL Chicago, IL SP Amer Soc Radiat Oncol C1 [Chung, E.; Urick, M.; Kurshan, N.; Shield, W.; Riley, H.; Citrin, D.] NCI, NIH, Bethesda, MD 20892 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 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 2009 VL 75 IS 3 BP S564 EP S564 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 503WW UT WOS:000270573602163 ER PT J AU Housri, N Ondos, J Choyke, PL Barbara, A Ning, H Citrin, D Singh, AK Kaushal, A AF Housri, N. Ondos, J. Choyke, P. L. Barbara, A. Ning, H. Citrin, D. Singh, A. K. Kaushal, A. TI Tumor Nodule Location Predicts the Feasibility of Intraprostatic High-dose Irradiation in Men with Localized Prostate Cancer SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract CT 51st Annual Meeting of the American-Society-for-Radiation-Oncology CY NOV 01-05, 2009 CL Chicago, IL SP Amer Soc Radiat Oncol C1 [Housri, N.; Ondos, J.; Barbara, A.; Ning, H.; Citrin, D.; Kaushal, A.] NCI, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA. [Choyke, P. L.] NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. [Singh, A. K.] Roswell Pk Canc Inst, Dept Radiat Med, Buffalo, NY 14263 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 2009 VL 75 IS 3 BP S143 EP S144 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 503WW UT WOS:000270573600307 ER PT J AU Hsu, S Tseng, Y Liu, J Shih, S Ou, C Chang, L Chen, Y Hong, K Melillo, G Yang, L AF Hsu, S. Tseng, Y. Liu, J. Shih, S. Ou, C. Chang, L. Chen, Y. Hong, K. Melillo, G. Yang, L. TI TLC388, a Novel Topotecan Derivative, as a Chemoradiosensitizer SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract CT 51st Annual Meeting of the American-Society-for-Radiation-Oncology CY NOV 01-05, 2009 CL Chicago, IL SP Amer Soc Radiat Oncol C1 [Hsu, S.; Hong, K.] TLC Biopharmaceut Inc, San Francisco, CA USA. [Tseng, Y.; Liu, J.; Shih, S.; Ou, C.; Chang, L.; Chen, Y.] Taiwan Liposome Co, Taipei, Taiwan. [Melillo, G.] NCI, Sci Applicat Int Corp Frederick Inc, Frederick, MD 21701 USA. [Yang, L.] Calif Pacific Med Ctr, Res Inst, Radiobiol Lab, San Francisco, CA USA. NR 0 TC 0 Z9 0 U1 1 U2 4 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 2009 VL 75 IS 3 BP S560 EP S560 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 503WW UT WOS:000270573602153 ER PT J AU Jung, E Eisner, M Martinez, SR Chen, SL Do, LV Chen, AM AF Jung, E. Eisner, M. Martinez, S. R. Chen, S. L. Do, L. V. Chen, A. M. TI Racial Disparities in the Use of Radiation Therapy in Women with Early-stage Breast Cancer after Lumpectomy SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract CT 51st Annual Meeting of the American-Society-for-Radiation-Oncology CY NOV 01-05, 2009 CL Chicago, IL SP Amer Soc Radiat Oncol C1 [Jung, E.; Martinez, S. R.; Chen, S. L.; Do, L. V.; Chen, A. M.] UC Davis, Sacramento, CA USA. [Eisner, M.] NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 2009 VL 75 IS 3 BP S199 EP S200 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 503WW UT WOS:000270573600426 ER PT J AU Kil, W Camphausen, K AF Kil, W. Camphausen, K. TI Enhanced Radiation Response in Human Carcinoma Cell Lines by the Cardiovascular Drug Hydralazine SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract CT 51st Annual Meeting of the American-Society-for-Radiation-Oncology CY NOV 01-05, 2009 CL Chicago, IL SP Amer Soc Radiat Oncol C1 [Kil, W.; Camphausen, K.] NCI, Bethesda, MD 20892 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 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 2009 VL 75 IS 3 BP S549 EP S549 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 503WW UT WOS:000270573602128 ER PT J AU Li, G Xie, H Miller, DA Zhuge, Y Klein, EE Low, D Ning, H Citrin, D Camphausen, K Miller, RW AF Li, G. Xie, H. Miller, D. A. Zhuge, Y. Klein, E. E. Low, D. Ning, H. Citrin, D. Camphausen, K. Miller, R. W. TI Investigation of using Optical Surface Imaging for Volumetric Prediction of Respiratory Organ Motion SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract CT 51st Annual Meeting of the American-Society-for-Radiation-Oncology CY NOV 01-05, 2009 CL Chicago, IL SP Amer Soc Radiat Oncol C1 [Li, G.; Xie, H.; Zhuge, Y.; Ning, H.; Citrin, D.; Camphausen, K.; Miller, R. W.] NCI, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA. [Miller, D. A.; Klein, E. E.; Low, D.] Washington Univ, Sch Med, St Louis, MO USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 2009 VL 75 IS 3 BP S578 EP S578 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 503WW UT WOS:000270573602194 ER PT J AU Ly, D Savage, JE Shankavaram, UT Saleh, AD Mitchell, JB Soule, BP Simone, NL AF Ly, D. Savage, J. E. Shankavaram, U. T. Saleh, A. D. Mitchell, J. B. Soule, B. P. Simone, N. L. TI Interactions between mir-21 and its Targets in Radiation-induced Fibrosis SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract CT 51st Annual Meeting of the American-Society-for-Radiation-Oncology CY NOV 01-05, 2009 CL Chicago, IL SP Amer Soc Radiat Oncol C1 [Ly, D.; Savage, J. E.; Shankavaram, U. T.; Saleh, A. D.; Mitchell, J. B.; Soule, B. P.; Simone, N. L.] NCI, NIH, Bethesda, MD 20892 USA. [Ly, D.] Case Western Reserve Univ, Cleveland Clin, Lerner Coll Med, Cleveland, OH 44106 USA. NR 0 TC 0 Z9 0 U1 2 U2 3 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. PY 2009 VL 75 IS 3 BP S537 EP S538 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 503WW UT WOS:000270573602103 ER PT J AU Mitchell, JB Choudhuri, R Citrin, D Sowers, AL DeGraff, W Zabludoff, SD Cook, JA AF Mitchell, J. B. Choudhuri, R. Citrin, D. Sowers, A. L. DeGraff, W. Zabludoff, S. D. Cook, J. A. TI In Vitro and In Vivo Radiation Sensitization of Human Tumor Cells by a Novel Checkpoint Kinase Inhibitor SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract CT 51st Annual Meeting of the American-Society-for-Radiation-Oncology CY NOV 01-05, 2009 CL Chicago, IL SP Amer Soc Radiat Oncol C1 [Mitchell, J. B.; Choudhuri, R.; Citrin, D.; Sowers, A. L.; DeGraff, W.; Cook, J. A.] NCI, Bethesda, MD 20892 USA. [Zabludoff, S. D.] AstraZeneca R&D, Waltham, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 2009 VL 75 IS 3 BP S67 EP S67 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 503WW UT WOS:000270573600142 ER PT J AU Ray, GL Baidoo, KE Wong, KJ Williams, M Garmestani, KG Brechbiel, MW Milenic, DE AF Ray, G. L. Baidoo, K. E. Wong, K. J. Williams, M. Garmestani, K. G. Brechbiel, M. W. Milenic, D. E. TI Radioimmunoconjugates: Pre-clinical Evaluation of Monoclonal Antibodies Targeting the Epidermal Growth Factor (EGFR) for Radioimmunodiagnostic and Radioimmunotherapeutic Applications SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract CT 51st Annual Meeting of the American-Society-for-Radiation-Oncology CY NOV 01-05, 2009 CL Chicago, IL SP Amer Soc Radiat Oncol C1 [Ray, G. L.; Baidoo, K. E.; Garmestani, K. G.; Brechbiel, M. W.; Milenic, D. E.] NCI, Radioimmune & Inorgan Chem Sect, Radiat Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA. [Wong, K. J.; Williams, M.] NCI, Mol Imaging Program, CCR, NIH, Bethesda, MD 20892 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 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 2009 VL 75 IS 3 BP S568 EP S569 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 503WW UT WOS:000270573602173 ER PT J AU Shapiro, LQ Karimi, S Gutin, PH Iwamoto, FM Zhang, Z Lassman, AB Abrey, LE Beal, K AF Shapiro, L. Q. Karimi, S. Gutin, P. H. Iwamoto, F. M. Zhang, Z. Lassman, A. B. Abrey, L. E. Beal, K. TI Patterns of Failure Following Concurrent Bevacizumab and Hypofractionated Stereotactic Radiotherapy for Recurrent High-grade Glioma SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract CT 51st Annual Meeting of the American-Society-for-Radiation-Oncology CY NOV 01-05, 2009 CL Chicago, IL SP Amer Soc Radiat Oncol C1 [Shapiro, L. Q.; Karimi, S.; Gutin, P. H.; Zhang, Z.; Lassman, A. B.; Abrey, L. E.; Beal, K.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. [Iwamoto, F. M.] NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 2009 VL 75 IS 3 BP S125 EP S125 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 503WW UT WOS:000270573600268 ER PT J AU Simone, CB Ly, D Soule, BP Savage, JE Mitchell, JB Simone, NL AF Simone, C. B. Ly, D. Soule, B. P. Savage, J. E. Mitchell, J. B. Simone, N. L. TI Alterations in Acute and Late Cytokine Expression Correlate with Radiation-induced Fibrosis SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract CT 51st Annual Meeting of the American-Society-for-Radiation-Oncology CY NOV 01-05, 2009 CL Chicago, IL SP Amer Soc Radiat Oncol C1 [Simone, C. B.; Ly, D.; Soule, B. P.; Savage, J. E.; Mitchell, J. B.; Simone, N. L.] NCI, Bethesda, MD 20892 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 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 2009 VL 75 IS 3 BP S541 EP S542 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 503WW UT WOS:000270573602112 ER PT J AU Ulrich, CM James, J Grady, C Byron, C Hanlon, A Watkins-Bruner, D Curran, W AF Ulrich, C. M. James, J. Grady, C. Byron, C. Hanlon, A. Watkins-Bruner, D. Curran, W. TI Factors Associated with Attrition in RTOG Clinical Trials SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract CT 51st Annual Meeting of the American-Society-for-Radiation-Oncology CY NOV 01-05, 2009 CL Chicago, IL SP Amer Soc Radiat Oncol C1 [Ulrich, C. M.; Byron, C.; Hanlon, A.; Watkins-Bruner, D.] Univ Penn, Philadelphia, PA 19104 USA. [James, J.] RTOG, Philadelphia, PA USA. [Grady, C.] NIH, Bethesda, MD 20892 USA. [Curran, W.] Emory, Atlanta, GA 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 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 2009 VL 75 IS 3 BP S89 EP S90 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 503WW UT WOS:000270573600191 ER PT J AU Zhuge, Y Xie, H Cheng, J Miller, RW AF Zhuge, Y. Xie, H. Cheng, J. Miller, R. W. TI GPU Accelerated Monte Carlo Simulation for Radiotherapy Dose Calculation SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Meeting Abstract CT 51st Annual Meeting of the American-Society-for-Radiation-Oncology CY NOV 01-05, 2009 CL Chicago, IL SP Amer Soc Radiat Oncol C1 [Zhuge, Y.; Xie, H.; Cheng, J.; Miller, R. W.] NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 2009 VL 75 IS 3 BP S702 EP S702 PG 1 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 503WW UT WOS:000270573602467 ER PT J AU Stanford, J Tongngam, S AF Stanford, Jeffrey Tongngam, Sutep TI Approximation algorithm for maximum lifetime in wireless sensor networks with data aggregation SO INTERNATIONAL JOURNAL OF SENSOR NETWORKS LA English DT Article; Proceedings Paper CT 1st International Conference on New Materials for Extreme Environments CY JUN 02-04, 2008 CL San Sebastian, SPAIN SP ExtreMat Project, INASMET Tecnal, Max Planck Inst Plasma Phys, European Comm DE lifetime; aggregation; approximation; optimum ID EFFICIENT ALGORITHMS; OPTIMUM BRANCHINGS AB We consider the problem of maximising the lifetime of sensor networks with data aggregation, which was previously investigated by Kalpakis et al. (2003). They propose an exact polynomial-time algorithm, which is however very slow, and faster heuristics, where an approximation ratio is not guaranteed. In this paper, we demonstrate an alternative approach based on the Garg and Konemann (1998) algorithm for packing linear programs, combined with the exact computation of minimum cost arborescence. For any epsilon > 0, our approach obtains a solution achieving at least 1 c times the optimum lifetime with significantly faster running time than that of the exact algorithm. The simulation result also shows that our algorithm achieves a solution that is within 0.02% of optimum and is not slower than the heuristics previously proposed by Kalpakis et al. (2003). C1 [Tongngam, Sutep] NIDA, Sch Appl Stat, Dept Comp Sci, Bangkok, Thailand. [Stanford, Jeffrey] IIT, Dept Comp Sci, Chicago, IL 60616 USA. RP Tongngam, S (reprint author), NIDA, Sch Appl Stat, Dept Comp Sci, Bangkok, Thailand. EM stanjefl@gmail.com; sutep@as.nida.ac.th NR 17 TC 6 Z9 6 U1 0 U2 1 PU INDERSCIENCE ENTERPRISES LTD PI GENEVA PA WORLD TRADE CENTER BLDG, 29 ROUTE DE PRE-BOIS, CASE POSTALE 896, CH-1215 GENEVA, SWITZERLAND SN 1748-1279 J9 INT J SENS NETW JI Int. J. Sens. Netw. PY 2009 VL 6 IS 1 SI SI BP 44 EP 50 PG 7 WC Computer Science, Information Systems; Telecommunications SC Computer Science; Telecommunications GA 628GZ UT WOS:000280104300005 ER PT J AU Robenack, K Goel, P AF Roebenack, Klaus Goel, Pranay TI A combined observer and filter based approach for the determination of unknown parameters SO INTERNATIONAL JOURNAL OF SYSTEMS SCIENCE LA English DT Article DE parameter-dependent systems; non-linear observer; filter ID NONLINEAR-SYSTEMS; ADAPTIVE OBSERVERS; EXPONENTIAL RATE; IDENTIFICATION; MODELS; CONVERGENCE AB We consider the simultaneous reconstruction of the state vector and unknown parameters for a special class of non-linear parameter-dependent systems. The approach suggested here consists of two stages. First, the state is reconstructed by a reduced order unknown input observer. Second, this observer is augmented by a filter to obtain the desired parameter. The design procedure is straightforward and may be used for an online estimation of the unknown parameter. In contrast to previous work on adaptive systems, we do not require a persistence of excitation. The approach is illustrated on two non-linear cell models. C1 [Roebenack, Klaus] Tech Univ Dresden, Inst Regelungs & Steurungstheorie, Fak Elektrotech & Informat Tech, Dresden, Germany. [Goel, Pranay] NIDDK, Lab Biol Modeling, NIH, Bethesda, MD USA. RP Robenack, K (reprint author), Tech Univ Dresden, Inst Regelungs & Steurungstheorie, Fak Elektrotech & Informat Tech, Dresden, Germany. EM klaus@roebenack.de RI Goel, Pranay/D-1081-2013; OI Goel, Pranay/0000-0002-2249-0288 FU Deutsche Forschungsgemeinschaft [RO 2427/1]; National Science Foundation [0112050] FX The work of the first author was supported by Deutsche Forschungsgemeinschaft under research grant RO 2427/1. The contribution of the second author is based upon work supported by the National Science Foundation under Agreement No. 0112050. NR 54 TC 1 Z9 1 U1 0 U2 4 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 0020-7721 J9 INT J SYST SCI JI Int. J. Syst. Sci. PY 2009 VL 40 IS 3 BP 213 EP 221 AR PII 905047658 DI 10.1080/00207720802298715 PG 9 WC Automation & Control Systems; Computer Science, Theory & Methods; Operations Research & Management Science SC Automation & Control Systems; Computer Science; Operations Research & Management Science GA 413VH UT WOS:000263820100002 ER PT J AU Gruebbel, MM Singh, BP AF Gruebbel, Margarita M. Singh, Bhanu P. TI Histopathology of Nonneoplastic Eye Lesions in Rats and Mice SO INTERNATIONAL JOURNAL OF TOXICOLOGY LA English DT Meeting Abstract CT 29th Annual Meeting of the American-College-of-Toxicology CY NOV 09-12, 2008 CL Tucson, AZ SP Amer Coll Toxicol DE Rats and mice; Eye; Nonneoplastic lesions C1 [Gruebbel, Margarita M.] Expt Pathol Labs, Res Triangle Pk, NC USA. [Singh, Bhanu P.] NIEHS, Cellular & Mol Pathol Branch, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 1091-5818 J9 INT J TOXICOL JI Int. J. Toxicol. PD JAN-FEB PY 2009 VL 28 IS 1 MA P24 BP 52 EP 52 PG 1 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA 463IH UT WOS:000267425000028 ER PT J AU Smith, PC Schofield, P Merrick, J AF Smith, Paula C. Schofield, Patricia Merrick, Joav TI The challenge of palliative care in the 21st century SO INTERNATIONAL JOURNAL ON DISABILITY AND HUMAN DEVELOPMENT LA English DT Editorial Material C1 [Smith, Paula C.] Univ Bath, Dept Psychol, Bath BA2 7AY, Avon, England. [Schofield, Patricia] Univ Aberdeen, Ctr Adv Studies Nursing, Dept Gen Practice & Primary Care, Aberdeen AB9 1FX, Scotland. [Merrick, Joav] Univ Kentucky, NICHHD, Jerusalem & Kentucky Childrens Hosp, Lexington, KY USA. [Merrick, Joav] Univ Kentucky, Minist Social Affairs, Jerusalem & Kentucky Childrens Hosp, Lexington, KY USA. RP Smith, PC (reprint author), Univ Bath, Dept Psychol, Bath BA2 7AY, Avon, England. EM pcs21@bath.ac.uk; p.a.schofield@abdn.ac.uk; jmerrick@zahav.net.il NR 5 TC 0 Z9 0 U1 0 U2 0 PU FREUND PUBLISHING HOUSE LTD PI TEL AVIV PA PO BOX 35010, TEL AVIV 61350, ISRAEL SN 1565-012X J9 INT J DISABIL HUM DE JI Int. J. Disabil. Hum. Dev. PD JAN-MAR PY 2009 VL 8 IS 1 SI SI BP 1 EP 2 DI 10.1515/IJDHD.2009.8.1.1 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 443HO UT WOS:000265901000001 ER PT J AU Demberg, T Robert-Guroff, M AF Demberg, Thorsten Robert-Guroff, Marjorie TI Mucosal Immunity and Protection Against HIV/SIV Infection: Strategies and Challenges for Vaccine Design SO INTERNATIONAL REVIEWS OF IMMUNOLOGY LA English DT Review DE HIV vaccine; mucosal immunity; mucosal immunization; cellular and humoral responses ID HUMAN-IMMUNODEFICIENCY-VIRUS; ESCHERICHIA-COLI ENTEROTOXIN; INACTIVATED INFLUENZA VACCINE; CELL-MEDIATED-IMMUNITY; DENDRITIC CELLS; RHESUS MACAQUES; T-CELLS; EPITHELIAL-CELLS; HIV-1 INFECTION; GENITAL-TRACT AB To date, most HIV vaccine strategies have focused on parenteral immunization and systemic immunity. These approaches have not yielded the efficacious HIV vaccine urgently needed to control the AIDS pandemic. As HIV is primarily mucosally transmitted, efforts are being re-focused on mucosal vaccine strategies, in spite of complexities of immune response induction and evaluation. Here, we outline issues in mucosal vaccine design and illustrate strategies with examples from the recent literature. Development of a successful HIV vaccine will require in-depth understanding of the mucosal immune system, knowledge that ultimately will benefit vaccine design for all mucosally transmitted infectious agents. C1 [Demberg, Thorsten; Robert-Guroff, Marjorie] NCI, NIH, Vaccine Branch, Bethesda, MD 20892 USA. RP Robert-Guroff, M (reprint author), NCI, NIH, Vaccine Branch, 41 Medlars Dr,Bldg 41,Rm D804, Bethesda, MD 20892 USA. EM guroffm@mail.nih.gov FU Intramural Research Program of the National Institutes of Health, National Cancer Institute FX This research was supported by the Intramural Research Program of the National Institutes of Health, National Cancer Institute. NR 158 TC 38 Z9 39 U1 0 U2 3 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0883-0185 J9 INT REV IMMUNOL JI Int. Rev. Immunol. PY 2009 VL 28 IS 1-2 BP 20 EP 48 AR PII 909038009 DI 10.1080/08830180802684331 PG 29 WC Immunology SC Immunology GA 412HL UT WOS:000263715800004 PM 19241252 ER PT S AU Martin, B Dotson, CD Shin, YK Ji, SG Drucker, DJ Maudsley, S Munger, SD AF Martin, Bronwen Dotson, Cedrick D. Shin, Yu-Kyong Ji, Sunggoan Drucker, Daniel J. Maudsley, Stuart Munger, Steven D. BE Finger, TE TI Modulation of Taste Sensitivity by GLP-1 Signaling in Taste Buds SO INTERNATIONAL SYMPOSIUM ON OLFACTION AND TASTE SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 15th International Symposium on Olfaction and Taste CY JUL 21-26, 2008 CL San Francisco, CA DE glucagon-like peptide-1; hormone; sweet; umami; glutamate ID GASTROINTESTINAL-TRACT; MAMMALIAN GUT; RECEPTORS; GUSTDUCIN; CELLS; EXPRESSION AB Modulation of sensory function can help animals adjust to a changing external and internal environment. Even so, mechanisms for modulating taste sensitivity are poorly understood. Using immunohistochemical, biochemical, and behavioral approaches, we found that the peptide hormone glucagon-like peptide-1 (GLP-1) and its receptor (GLP-1R) are expressed in mammalian taste buds. Furthermore, we found that GLP-1 signaling plays an important role in the modulation of taste sensitivity: GLP-1R knockout mice exhibit a dramatic reduction in sweet taste sensitivity as well as an enhanced sensitivity to umami-tasting stimuli. Together, these findings suggest a novel paracrine mechanism for the hormonal modulation of taste function in mammals. C1 [Dotson, Cedrick D.; Munger, Steven D.] Univ Maryland, Sch Med, Dept Anat & Neurobiol, Baltimore, MD 21201 USA. [Martin, Bronwen; Shin, Yu-Kyong; Ji, Sunggoan; Maudsley, Stuart] NIA, NIH, Baltimore, MD 21224 USA. [Drucker, Daniel J.] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Dept Med, Toronto, ON M5G 1X5, Canada. [Drucker, Daniel J.] Univ Toronto, Banting & Best Diabet Ctr, Toronto, ON M5G 1L5, Canada. RP Munger, SD (reprint author), Univ Maryland, Sch Med, Dept Anat & Neurobiol, 20 Penn St,Room S251, Baltimore, MD 21201 USA. EM smung001@umaryland.edu RI Drucker, Daniel/A-4092-2010 FU National Institute on Aging Intramural Program; National Institute on Deafness and Other Communication Disorders [DC005786, DC008301]; National Institute on Dental and Craniofacial Research [DE007309] FX This work was supported by the National Institute on Aging Intramural Program and by grants from the National Institute on Deafness and Other Communication Disorders (S.D.M.: DC005786, DC008301). C.D.D. is supported by a training grant from the National Institute on Dental and Craniofacial Research (DE007309). NR 14 TC 48 Z9 49 U1 2 U2 11 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXEN, ENGLAND SN 0077-8923 BN 978-1-57331-738-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2009 VL 1170 BP 98 EP 101 DI 10.1111/j.1749-6632.2009.03920.x PG 4 WC Behavioral Sciences; Cell Biology; Multidisciplinary Sciences; Neurosciences; Physiology SC Behavioral Sciences; Cell Biology; Science & Technology - Other Topics; Neurosciences & Neurology; Physiology GA BLL92 UT WOS:000270495700022 PM 19686117 ER PT S AU Hoffman, HJ Davis, B Cruickshanks, KJ AF Hoffman, Howard J. Davis, Barry Cruickshanks, Karen J. BE Finger, TE TI Symposium Overview Epidemiological Studies of Taste and Smell SO INTERNATIONAL SYMPOSIUM ON OLFACTION AND TASTE SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Editorial Material CT 15th International Symposium on Olfaction and Taste CY JUL 21-26, 2008 CL San Francisco, CA C1 [Hoffman, Howard J.] NIDCD, Div Sci Program, Epidemiol & Stat Program, NIH, Bethesda, MD 20892 USA. [Davis, Barry] NIDCD, Taste & Smell Program, Div Sci Program, NIH, Bethesda, MD 20892 USA. [Cruickshanks, Karen J.] Univ Wisconsin, Sch Med & Publ Hlth, Dept Ophthalmol & Visual Sci & Populat Hlth Sci, Madison, WI USA. RP Hoffman, HJ (reprint author), NIDCD, Div Sci Program, Epidemiol & Stat Program, NIH, Execut Pl S Bldg,Suite 400A,6120 Execut Blvd,MSC, Bethesda, MD 20892 USA. EM hoffmanh@nidcd.nih.gov FU NEI NIH HHS [R01 EY013279]; NIA NIH HHS [R01 AG021917, R01 AG011099, R37 AG011099] NR 0 TC 2 Z9 2 U1 0 U2 2 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXEN, ENGLAND SN 0077-8923 BN 978-1-57331-738-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2009 VL 1170 BP 511 EP 513 DI 10.1111/j.1749-6632.2009.04598.x PG 3 WC Behavioral Sciences; Cell Biology; Multidisciplinary Sciences; Neurosciences; Physiology SC Behavioral Sciences; Cell Biology; Science & Technology - Other Topics; Neurosciences & Neurology; Physiology GA BLL92 UT WOS:000270495700092 PM 19686187 ER PT S AU Hofman, HJ Cruickshanks, KJ Davis, B AF Hofman, Howard J. Cruickshanks, Karen J. Davis, Barry BE Finger, TE TI Perspectives on Population-based Epidemiological Studies of Olfactory and Taste Impairment SO INTERNATIONAL SYMPOSIUM ON OLFACTION AND TASTE SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT 15th International Symposium on Olfaction and Taste CY JUL 21-26, 2008 CL San Francisco, CA DE epidemiology; population studies; olfactory impairment; taste impairment; methodological challenges; risk factors ID REPORTED HEARING-LOSS; GUSTATORY FUNCTION; NUTRITIONAL-STATUS; PROP BITTERNESS; ORAL SENSATION; HEAD TRAUMA; DYSFUNCTION; PERCEPTION; PREVALENCE; SMELL AB Epidemiological studies of the senses of olfaction (smell) and gustation (taste) are needed since impairments in these senses have important implications for health. Only a few attempts have been made to measure the prevalence of olfactory and gustatory or taste dysfunction, and many methodological challenges remain to be addressed. These challenges differ from those faced in studies based in the clinic or research laboratory. Epidemiological studies of smell and taste represent translational research, because they can be used to understand how findings from laboratory or clinical studies apply to the general population. This paper briefly reviews existing methods for "how" to measure smell and taste dysfunction and then illustrates findings based on prior epidemiological studies to indicate "why" we wish to measure smell and taste functioning in population-based samples. Self-reported information collected on smell and taste loss in a national sample, the 1994-1995 Disability Sample (phase I screening) of the National Health Interview Survey, is contrasted with results provided by an exam-based measure of olfactory impairment in an epidemiological study conducted in Beaver Dam, WI. The comparison of self-reported and exam-based measures of smell or taste loss leads to the question of how to best define smell or taste impairment in population samples, since unlike other sensory domains (namely, vision and hearing), there are no internationally accepted standards of impairment for the chemosenses. In addition to highlighting existing epidemiological studies, the current development of an NIH Tool-box of brief exam measures is described. Through this symposium, we hope to advance the nascent field of olfactory and taste epidemiology. C1 [Hofman, Howard J.] NIDCD, Div Sci Program, Epidemiol & Stat Program, NIH, Bethesda, MD 20892 USA. [Cruickshanks, Karen J.] NIDCD, Taste & Smell Program, Div Sci Program, NIH, Bethesda, MD 20892 USA. [Davis, Barry] Univ Wisconsin, Sch Med & Publ Hlth, Dept Ophthalmol & Visual Sci & Populat Hlth Sci, Madison, WI USA. RP Hofman, HJ (reprint author), NIDCD, Div Sci Program, Epidemiol & Stat Program, NIH, Execut Pl S Bldg,Suite 400A,6120 Execut Blvd,MSC, Bethesda, MD 20892 USA. EM hoffmanh@nidcd.nih.gov NR 82 TC 0 Z9 0 U1 2 U2 6 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN STREET, MALDEN 02148, MA USA SN 0077-8923 BN 978-1-57331-738-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2009 VL 1170 BP 514 EP 530 DI 10.1111/j.1749-6632.2009.04597.x PG 17 WC Behavioral Sciences; Cell Biology; Multidisciplinary Sciences; Neurosciences; Physiology SC Behavioral Sciences; Cell Biology; Science & Technology - Other Topics; Neurosciences & Neurology; Physiology GA BLL92 UT WOS:000270495700093 ER PT S AU Chen, WG AF Chen, Wen G. BE Finger, TE TI Symposium Overview A Systems Approach to Studying Chemical Senses and Aging: Moving from Populations to Mechanisms SO INTERNATIONAL SYMPOSIUM ON OLFACTION AND TASTE SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Editorial Material CT 15th International Symposium on Olfaction and Taste CY JUL 21-26, 2008 CL San Francisco, CA ID MILD COGNITIVE IMPAIRMENT; ALZHEIMERS-DISEASE; OLDER-ADULTS; APOLIPOPROTEIN-E; PREVALENCE; OLFACTION; IDENTIFICATION; DEFICITS; BRAIN; AGE C1 NIA, Div Neurosci, NIH,DHHS,Sensory & Motor Disorders Aging Sect, Behav & Syst Neurosci Branch, Bethesda, MD 20892 USA. RP Chen, WG (reprint author), NIA, Div Neurosci, NIH,DHHS,Sensory & Motor Disorders Aging Sect, Behav & Syst Neurosci Branch, 7201 Wisconsin Ave,Suite 350, Bethesda, MD 20892 USA. EM chenw@nia.nih.gov NR 29 TC 0 Z9 0 U1 2 U2 3 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXEN, ENGLAND SN 0077-8923 BN 978-1-57331-738-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2009 VL 1170 BP 702 EP 707 DI 10.1111/j.1749-6632.2009.04596.x PG 6 WC Behavioral Sciences; Cell Biology; Multidisciplinary Sciences; Neurosciences; Physiology SC Behavioral Sciences; Cell Biology; Science & Technology - Other Topics; Neurosciences & Neurology; Physiology GA BLL92 UT WOS:000270495700121 PM 19686216 ER PT J AU Iuliano, AD Feingold, E Wahed, AS Kleiner, DE Belle, SH Conjeevaram, HS Zmuda, J Liang, TJ Yee, LJ AF Iuliano, A. Danielle Feingold, Eleanor Wahed, Abdus S. Kleiner, David E. Belle, Steven H. Conjeevaram, Hari S. Zmuda, Joseph Liang, T. Jake Yee, Leland J. CA Virahep-C Study TI Host Genetics, Steatosis and Insulin Resistance among African Americans and Caucasian Americans with Hepatitis C Virus Genotype-1 Infection SO INTERVIROLOGY LA English DT Article DE Steatosis; Insulin resistance; Hepatitis C virus; Host genetics ID HOMEOSTASIS MODEL ASSESSMENT; IMPACT; POLYMORPHISM; PROGRESSION; LIVER; PEGINTERFERON; ASSOCIATION; RIBAVIRIN; FIBROSIS; PROMOTER AB Hepatic steatosis is the accumulation of fat in liver cells. Insulin resistance (IR) occurs when normal amounts of insulin do not stimulate insulin activity in cells. Both conditions have been described in hepatitis C virus (HCV) infection and are thought to be biologically related. This study examined the association of genetic variants with steatosis and IR among 167 African Americans and 184 Caucasian Americans with HCV genotype-1. Steatosis was defined as at least 5% of fat in cells on liver biopsy. IR was quantified as a score greater than 2 from the Homeostasis Model Assessment, version 2.2 (HOMA2-IR). Associations were investigated by estimating odds ratios separately by race. Statistically significant associations (p < 0.05) were observed for variants in interleukin-10 (IL10), leptin receptor (LEPR), interleukin-6 (IL6) and transforming growth factor beta-1 (TGF-beta 1) for both outcomes. Some significant interactions were observed between IL10, LEPR and TGF-beta 1 polymorphisms and HOMA2-IR scores when examining steatosis. The interaction of HOMA2-IR and IL10 was consistent in both races whereas for LEPR and TGF-beta 1 the interactions were statistically significant in only one of the racial groups. These results could imply that some IL10, LEPR and TGF-beta 1 polymorphisms may modify an association between steatosis and IR. Copyright (C) 2009 S. Karger AG, Basel C1 [Iuliano, A. Danielle; Belle, Steven H.; Zmuda, Joseph; Yee, Leland J.] Univ Pittsburgh, Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15260 USA. [Feingold, Eleanor; Belle, Steven H.; Zmuda, Joseph] Univ Pittsburgh, Sch Publ Hlth, Dept Human Genet, Pittsburgh, PA 15260 USA. [Feingold, Eleanor; Wahed, Abdus S.] Univ Pittsburgh, Sch Publ Hlth, Dept Biostat, Pittsburgh, PA 15260 USA. [Yee, Leland J.] Univ Pittsburgh, Sch Med, Dept Med, Div Infect Dis, Pittsburgh, PA USA. [Conjeevaram, Hari S.] Univ Michigan, Ann Arbor, MI 48109 USA. [Kleiner, David E.] Natl Canc Inst, Bethesda, MD USA. [Liang, T. Jake] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA. RP Yee, LJ (reprint author), A511 Crabtree Hall,130 DeSoto St, Pittsburgh, PA 15261 USA. EM yeel@edc.pitt.edu OI Wahed, Abdus/0000-0001-6911-7221; Feingold, Eleanor/0000-0003-2898-6484; Kleiner, David/0000-0003-3442-4453 FU Intramural NIH HHS [Z01 DK054511-01, Z01 DK054511-02, Z99 DK999999, ZIA DK054511-03]; NCRR NIH HHS [M01 RR000042, 1KL2 RR024154-01, KL2 RR024154, M01 RR000046, M01 RR000079, M01 RR000645, M01 RR016500]; NIDDK NIH HHS [U01 DK060309, U01 DK060324, U01 DK060327, U01 DK060329, U01 DK060329-01, U01 DK060335, U01 DK060340, U01 DK060341, U01 DK060342, U01 DK060344, U01 DK060345, U01 DK060346, U01 DK060349, U01 DK060352, U01 DK60309, U01 DK60324, U01 DK60327, U01 DK60329, U01 DK60335, U01 DK60340, U01 DK60341, U01 DK60342, U01 DK60344, U01 DK60345, U01 DK60346, U01 DK60349, U01 DK60352] NR 28 TC 6 Z9 6 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0300-5526 J9 INTERVIROLOGY JI Intervirology PY 2009 VL 52 IS 1 BP 49 EP 56 DI 10.1159/000214380 PG 8 WC Virology SC Virology GA 439KY UT WOS:000265627200008 PM 19401628 ER PT J AU Umeki, K Hisada, M Maloney, EM Hanchard, B Okayama, A AF Umeki, Kazumi Hisada, Michie Maloney, Elizabeth M. Hanchard, Barrie Okayama, Akihiko TI Proviral Loads and Clonal Expansion of HTLV-1-Infected Cells following Vertical Transmission: A 10-Year Follow-Up of Children in Jamaica SO INTERVIROLOGY LA English DT Article DE HTLV-1 infection; Clonal expansion, infected cells; Transmission, vertical ID VIRUS TYPE-I; TROPICAL SPASTIC PARAPARESIS; INFECTIVE DERMATITIS; LEUKEMIA-VIRUS; LEUKEMIA/LYMPHOMA; MYELOPATHY; HTLV-1; SEROCONVERTERS; INTEGRATION; CARRIERS AB Objective: Few studies have specifically examined proviral load (PVL) and clonal evolution of human T-lymphotropic virus type 1 (HTLV-1)-infected cells in vertically infected children. Methods: Sequential samples (from ages 1 to 16 years) from 3 HTLV-1-infected children (cases A, B and C) in the Jamaica Mother Infant Cohort Study were analyzed for their PVL and clonal expansion of HTLV-1- infected cells in peripheral blood mononuclear cells (PBMCs) by inverse-long PCR. Results: The baseline PVL (per 100,000 PBMCs) of case A was 260 (at 1 year of age) and of case B it was 1,867 (at 3 years of age), and they remained constant for more than 10 years. Stochastic patterns of clonal expansion of HTLV-1-infected cells were predominately detected. In contrast, case C, who had lymphadenopathy, seborrheic dermatitis and hyperreflexia, showed an increase in PVL from 2,819 at 1.9 years to 13,358 at 13 years of age, and expansion of 2 dominant clones. Conclusion: The clonal expansion of HTLV-1-infected cells is induced in early childhood after infection acquired from their mothers. Youths with high PVL and any signs and symptoms associated with HTLV-1 infection should be closely monitored. Copyright (C) 2009 S. Karger AG, Basel C1 [Okayama, Akihiko] Miyazaki Univ, Dept Rheumatol Infect Dis & Lab Med, Fac Med, Miyazaki 8891692, Japan. [Hisada, Michie] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA. [Maloney, Elizabeth M.] Ctr Dis Control & Prevent, Atlanta, GA USA. [Hanchard, Barrie] Univ W Indies, Dept Pathol, Mona, Jamaica. RP Okayama, A (reprint author), Miyazaki Univ, Dept Rheumatol Infect Dis & Lab Med, Fac Med, 5200 Kihara, Miyazaki 8891692, Japan. EM okayama@med.miyazaki-u.ac.jp FU Japanese Ministry of Education, Science, Sports and Culture; Miyazaki Prefecture Collaboration of Regional Entities for the Advancement of Technological Excellence (JST); Jamaica Mother Infant Cohort Study; Intramural Research Program of the NIH; National Cancer Institute; Division of Cancer Epidemiology and Genetics FX W e thank Mrs. Beverley Granston for her contribution to the study conduct. This study was supported in part by a grant- in- aid from the Japanese Ministry of Education, Science, Sports and Culture, and the Miyazaki Prefecture Collaboration of Regional Entities for the Advancement of Technological Excellence (JST). The Jamaica Mother Infant Cohort Study was supported by the Intramural Research Program of the NIH, National Cancer Institute, Division of Cancer Epidemiology and Genetics. NR 29 TC 10 Z9 10 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0300-5526 J9 INTERVIROLOGY JI Intervirology PY 2009 VL 52 IS 3 BP 115 EP 122 DI 10.1159/000219384 PG 8 WC Virology SC Virology GA 456WT UT WOS:000266883600001 PM 19468234 ER PT J AU Cunningham, MA Austin, BA Li, ZQ Liu, BY Yeh, S Chan, CC Anglade, E Velagaleti, P Nussenblatt, RB AF Cunningham, Matthew A. Austin, Bobbie Ann Li, Zhuqing Liu, Baoying Yeh, Steven Chan, Chi-Chao Anglade, Eddy Velagaleti, Poonam Nussenblatt, Robert B. TI LX211 (Voclosporin) Suppresses Experimental Uveitis and Inhibits Human T Cells SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article ID EXPERIMENTAL AUTOIMMUNE UVEORETINITIS; SIGHT-THREATENING UVEITIS; RETINOID-BINDING PROTEIN; CYCLOSPORINE-A; CALCINEURIN INHIBITOR; IMMUNOSUPPRESSIVE DRUGS; TACROLIMUS FK506; ISA(TX)247; RATS; DISEASE AB PURPOSE. To test the therapeutic effectiveness of voclosporin against experimental autoimmune uveoretinitis (EAU) in rats and to evaluate its effect on human T cells. METHODS. EAU was induced by immunization with a uveitogenic protein. Voclosporin administration, by subcutaneous injection, began on day (d) 0 or d7 after immunization. Treatment effectiveness was evaluated in vivo using clinical EAU scoring (d7-d13) and histopathologic evaluation of enucleated eyes after experimental termination. Rodent lymphocytes were harvested from lymph nodes on d14 for antigen-specific proliferation assays. The effect of voclosporin on human T-cell proliferation and cytokine secretion was examined in vitro. RESULTS. Voclosporin prevented EAU development in rats receiving medium and high preventive doses, whereas high-dose voclosporin administration effectively treated EAU. Lymphocytes from animals treated with voclosporin had decreased antigen-specific proliferation in vitro compared with lymphocytes from untreated animals. No evidence of abnormal ocular histopathology was found in the eyes from animals that received high doses of therapeutic voclosporin. Using human T cells, voclosporin inhibited human T-cell proliferation up to 100-fold. Furthermore, voclosporin treatment of human T cells significantly reduced pan T-cell effector responses. CONCLUSIONS. Voclosporin effectively suppressed uveoretinitis in an animal model that imitates the human inflammatory ocular disease by inhibiting lymphocyte proliferation. In addition, voclosporin effectively inhibited human T-cell proliferation and function in vitro. The authors report the first evidence supporting the application of voclosporin to treat intraocular inflammation. (Invest Ophthalmol Vis Sci. 2009; 50: 249-255) DOI: 10.1167/iovs.08-1891 C1 [Cunningham, Matthew A.; Austin, Bobbie Ann; Li, Zhuqing; Liu, Baoying; Yeh, Steven; Chan, Chi-Chao; Nussenblatt, Robert B.] NEI, NIH, Bethesda, MD 20892 USA. [Anglade, Eddy; Velagaleti, Poonam] Lux Biosci, Jersey City, NJ USA. RP Nussenblatt, RB (reprint author), NEI, NIH, 10 Ctr Dr,Bldg 10-10N112, Bethesda, MD 20892 USA. EM drbob@nei.nih.gov FU National Institutes of Health Lux Biosciences FX Supported by National Institutes of Health Intramural Research and by Lux Biosciences. NR 37 TC 12 Z9 12 U1 0 U2 1 PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC PI ROCKVILLE PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD JAN PY 2009 VL 50 IS 1 BP 249 EP 255 DI 10.1167/iovs.08-1891 PG 7 WC Ophthalmology SC Ophthalmology GA 390YP UT WOS:000262199900033 PM 18708627 ER PT S AU Klein, HG Bryant, BJ AF Klein, H. G. Bryant, B. J. GP ISBT TI Pathogen-reduction methods: advantages and limits SO ISBT SCIENCE SERIES, VOL 4, NO 1, STATE OF THE ART PRESENTATIONS SE ISBT Science Series LA English DT Proceedings Paper CT 19th Regional Congress of the International-Society-of-Blood-Transfusion CY MAR 21-25, 2009 CL Cairo, EGYPT SP Int Soc Blood Transfus DE Blood safety; pathogen inactivation; pathogen reduction; transfusion; transfusion safety ID FRESH-FROZEN PLASMA; PHOTOCHEMICAL INACTIVATION; THERAPEUTIC-EFFICACY; BLOOD-TRANSFUSION; METHYLENE-BLUE; AMOTOSALEN HCL; SPRINT TRIAL; SAFETY; VIRUSES; LIGHT AB Pathogen-reduction (inactivation) provides a proactive approach to reducing transfusion-transmitted infection. Pathogen-reduction technologies have been successfully implemented by plasma fractionators resulting in no transmission of human immunodeficiency, hepatitis C, or hepatitis B viruses by US-licensed plasma derivatives since 1987. Fractionation technologies cannot be used to treat cellular blood components. Although blood donor screening, deferral and disease testing have drastically reduced the incidence of transfusion-transmitted diseases, the threat of new or re-emerging pathogens remains. Of particular concern is the silent emergence of a new agent with a prolonged latent period in which asymptomatic infected carriers would donate and spread infection. The ultimate goal of pathogen-inactivation is to reduce transmission of potential pathogens without significantly compromising the therapeutic efficacy of the cellular and protein constituents of blood. The acceptable technology must not introduce toxicities into the blood supply nor result in neoantigen formation and subsequent antibody production. Several promising pathogen-inactivation technologies are being developed and tested, and others are currently in use, but all of them have limits. Pathogen-reduction promises an additional 'layer of protection' from infectious agents and has the potential to impact the safety of blood transfusions worldwide. C1 [Klein, H. G.] NIH, Dept Transfus Med, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA. [Bryant, B. J.] Univ Texas Galveston, Dept Pathol, Blood Bank Div, Galveston, TX USA. RP Klein, HG (reprint author), NIH, Dept Transfus Med, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA. EM hklein@cc.nih.gov NR 30 TC 8 Z9 8 U1 0 U2 1 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN STREET, MALDEN 02148, MA USA SN 1751-2816 J9 ISBT SCI SER PY 2009 VL 4 IS 1 BP 154 EP + PG 3 WC Hematology SC Hematology GA BJD60 UT WOS:000265020700028 ER PT J AU Bonichini, S Axia, G Bornstein, MH AF Bonichini, Sabrina Axia, Giovanna Bornstein, Marc H. TI Validation of the Parent Health Locus of Control Scales in an Italian sample SO ITALIAN JOURNAL OF PEDIATRICS LA English DT Article ID CONTROL BELIEFS; BEHAVIOR; MOTHERS AB Aim: This study examined the psychometric properties and the replicability of De Vellis's (1993) Parent Health Locus of Control (PHLOC) scales in an Italian sample. Method: The Italian version of PHLOC was administered to 470 mothers of birth to 3-year-old children. Results: Varimax rotated confirmatory factor analysis identified the six original subscales, namely Child, Divine, Fate, Media, Parental, and Professional influences over child health. Internal consistency of the subscales was good (alpha > .70), and test-retest correlations were adequate (r > .80). More highly educated mothers rated media influence as most important. No differences were found considering children's age, gender, and birth order. Conclusion: The results offer good evidence of the cross-cultural validity of the PHLOC scales, an instrument that can be useful in interventions with families by the health care practitioners to prevent neglectful childrearing practices. C1 [Bonichini, Sabrina; Axia, Giovanna] Univ Padua, Dept Dev Psychol & Socializat, I-35131 Padua, Italy. [Bornstein, Marc H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD 20814 USA. RP Bonichini, S (reprint author), Univ Padua, Dept Dev Psychol & Socializat, I-35131 Padua, Italy. EM s.bonichini@unipd.it; s.bonichini@unipd.it; bornstem@cfr.nichd.nih.gov FU NIH, NICHD FX This research was supported by the Intramural Research Program of the NIH, NICHD. NR 16 TC 1 Z9 1 U1 2 U2 3 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1720-8424 J9 ITAL J PEDIATR JI Ital. J. Pediatr. PY 2009 VL 35 AR 13 DI 10.1186/1824-7288-35-13 PG 5 WC Pediatrics SC Pediatrics GA V18OT UT WOS:000208014800012 PM 19490604 ER PT J AU Shishehbor, MH Madhwal, S Rajagopal, V Hsu, A Kelly, P Gurm, HS Kapadia, SR Lauer, MS Topol, EJ AF Shishehbor, Mehdi H. Madhwal, Surabhi Rajagopal, Vivek Hsu, Amy Kelly, Peter Gurm, Hitinder S. Kapadia, Samir R. Lauer, Michael S. Topol, Eric J. TI Impact of Blood Transfusion on Short- and Long-Term Mortality in Patients With ST-Segment Elevation Myocardial Infarction SO JACC-CARDIOVASCULAR INTERVENTIONS LA English DT Article DE blood transfusion; ST-segment elevation myocardial infarction; long-term outcome; propensity analysis ID ACUTE CORONARY SYNDROMES; CLINICAL-OUTCOMES; HEMOGLOBIN LEVELS; CRITICALLY-ILL; STORED BLOOD; CARDIAC-SURGERY; OXYGEN DELIVERY; UNSTABLE ANGINA; ANEMIA; ACTIVATION AB Objectives We sought to examine the short- and long-term outcomes of blood transfusion in patients presenting with ST-segment elevation myocardial infarction (STEMI). Background The short- and long-term consequences of blood transfusion in anemic patients with recent STEMI remain controversial. Methods We evaluated 30-day, 6-month, and 1-year all-cause mortality among 4,131 STEMI patients enrolled in the GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) IIb trial. Patients were categorized according to whether they received a blood transfusion during hospitalization. Cox proportional hazards survival models with transfusion as a time-dependent covariate were conducted for the whole and for the propensity-matched groups. Additionally, a series of sensitivity analyses assessed the magnitude of hidden bias that would need to be present to explain the associations actually observed. Results Death at 30 days (13.7% vs. 5.5%), 6 months (19.7% vs. 6.9%), and 1 year (21.8% vs. 8.7%) was significantly higher for transfused patients than for nontransfused patients, respectively. After adjusting for over 25 baseline characteristics, nadir hemoglobin, and propensity score for transfusion, and using transfusion as a time-dependent covariate, transfusion remained significantly associated with increased risk of mortality at 30 days (hazard ratio [HR]: 3.89, 95% confidence interval [Cl]: 2.66 to 5.68, p < 0.001), 6 months (HR: 3.63, 95% Cl: 2.67 to 4.95, p < 0.001), and 1 year (HR: 3.03, 95% Cl: 2.25 to 4.08, p < 0.001). Similar results were observed in the propensity-matched patients. Conclusions Blood transfusion is associated with increased short- and long-term mortality in the setting of STEMI. (J Am Coll Cardiol Intv 2009;2:46-53) (C) 2009 by the American College of Cardiology Foundation C1 [Shishehbor, Mehdi H.; Kelly, Peter; Kapadia, Samir R.] Cleveland Clin, Dept Cardiovasc Med, Cleveland, OH 44195 USA. [Madhwal, Surabhi] Cleveland Clin, Dept Internal Med, Cleveland, OH 44195 USA. [Hsu, Amy] Cleveland Clin, Dept Quantitat Hlth Sci, Cleveland, OH 44195 USA. [Rajagopal, Vivek] Piedmont Heart Inst, Dept Cardiol, Atlanta, GA USA. [Gurm, Hitinder S.] Univ Michigan, Dept Cardiovasc Med, Ann Arbor, MI 48109 USA. [Lauer, Michael S.] NHLBI, Div Prevent & Populat Sci, NIH, Bethesda, MD 20892 USA. [Topol, Eric J.] Scripps Clin, Div Cardiovasc Dis, La Jolla, CA 92037 USA. [Topol, Eric J.] Scripps Res Inst, La Jolla, CA 92037 USA. RP Shishehbor, MH (reprint author), Cleveland Clin, Dept Cardiovasc Med, 9500 Euclid Ave,JJ40, Cleveland, OH 44195 USA. EM shishem@gmail.com RI Lauer, Michael/L-9656-2013; OI Lauer, Michael/0000-0002-9217-8177; Gurm, Hitinder/0000-0002-1646-0218; Topol, Eric/0000-0002-1478-4729 FU National Institutes of Health, National Institute of Child Health and Human Development [K12 (HD049091)] FX Division of Cardiovascular Diseases, Scripps Clinic and The Scripps Research Institute, La Jolla, California. Dr. Shishehbor is supported in part by the National Institutes of Health, National Institute of Child Health and Human Development, Multidisciplinary Clinical Research Career Development Programs Grant K12 (HD049091). NR 44 TC 37 Z9 38 U1 2 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 1936-8798 J9 JACC-CARDIOVASC INTE JI JACC-Cardiovasc. Interv. PD JAN PY 2009 VL 2 IS 1 BP 46 EP 53 DI 10.1016/j.jcin.2008.09.011 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 613HO UT WOS:000278970200007 PM 19463397 ER PT J AU Wilson, N Cadet, JL AF Wilson, Natascha Cadet, Jean Lud TI Comorbid Mood, Psychosis, and Marijuana Abuse Disorders: A Theoretical Review SO JOURNAL OF ADDICTIVE DISEASES LA English DT Review DE Addiction; cannabis; neuropsychiatry; depression; schizophrenia ID SUBSTANCE USE DISORDERS; CEREBRAL-BLOOD-FLOW; BIPOLAR-I DISORDER; ENDOCANNABINOID SIGNALING SYSTEM; TRANSCRANIAL DOPPLER SONOGRAPHY; ENDOGENOUS CANNABINOID SYSTEM; POSITRON EMISSION TOMOGRAPHY; CARD SORTING TEST; SCHIZOPHRENIC-PATIENTS; PREFRONTAL CORTEX AB There is a need to bridge the gap between the fields of addiction psychiatry and general psychiatry to effectively treat co-morbid substance abuse and psychiatric disorders. This alarming epidemic transcends communities and severely impacts healthcare worldwide, yielding poor treatment outcomes and prognoses for afflicted patients. Because substance abuse can exacerbate or trigger psychosis and mood disorders, it is important to keep these issues in the forefront when evaluating patients. To address some of the complications stemming from not enough interactions between various groups of practitioners, this review addresses the neurobehavioral effects of cannabis use and their impact on patients who suffer from psychotic or affective disorders. The hope is that this article will serve as a spring board for further discussions among practitioners who treat these patients. Greater interactions between caretakers are bound to impact the care of our patients in a very positive way. C1 [Wilson, Natascha; Cadet, Jean Lud] NIDA, Mol Neuropsychiat Res Branch, DHHS, NIH,Intramural Res Program, Baltimore, MD 21224 USA. RP Cadet, JL (reprint author), NIDA, Mol Neuropsychiat Res Branch, DHHS, NIH,Intramural Res Program, 251 Bayview Blvd, Baltimore, MD 21224 USA. EM jcadet@intra.nida.nih.gov FU Intramural NIH HHS [Z01 DA000497-01] NR 150 TC 13 Z9 14 U1 5 U2 17 PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 1055-0887 EI 1545-0848 J9 J ADDICT DIS JI J. Addict. Dis. PY 2009 VL 28 IS 4 BP 309 EP 319 DI 10.1080/10550880903182960 PG 11 WC Substance Abuse SC Substance Abuse GA 518RE UT WOS:000271710000003 PM 20155601 ER PT J AU Blair, A Freeman, LB AF Blair, Aaron Freeman, Laura Beane TI Epidemiologic Studies in Agricultural Populations: Observations and Future Directions SO JOURNAL OF AGROMEDICINE LA English DT Article DE Agriculture; cancer; epidemiology AB This paper reviews epidemiologic studies of cancer among agricultural populations to identify possible associations and to provide a focus for future investigations. Meta-analyses of mortality surveys of farmers find excesses of several cancers, including connective tissue, non-Hodgkin's lymphoma, Hodgkin's disease, multiple myeloma and cancers of the skin, stomach, and brain, and deficits for total mortality, heart disease, total cancer, and cancers of the esophagus, colon, lung, and bladder. Meta-analyses of studies of individual cancers also support these findings, indicating a need to identify exposures and lifestyle factors that might account for this mortality pattern. Although cancer studies of other occupations that might have pesticide exposures in common with farmers show some similarities with observations among farmers, the overall patterns are quite different. This suggests that pesticides are not likely to fully explain the cancer and other disease patterns observed among farmers. Because exposures vary by type of farm operation, exposures for individual farmers can differ considerably. Studies in the future need to focus on the full range of exposures to fully understand the cancer pattern in farmers. C1 [Blair, Aaron; Freeman, Laura Beane] NCI, Div Canc Epidemiol & Genet, Occupat & Environm Epidemiol Branch, Bethesda, MD 20892 USA. RP Blair, A (reprint author), NCI, Div Canc Epidemiol & Genet, Occupat & Environm Epidemiol Branch, Execut Plaza S,Room 8008, Bethesda, MD 20892 USA. EM blaira@mail.nih.gov RI Beane Freeman, Laura/C-4468-2015 OI Beane Freeman, Laura/0000-0003-1294-4124 FU NIH (Division of Cancer Epidemiology and Genetics, National Cancer Institute) FX This research was supported by the Intramural Research Program of the NIH (Division of Cancer Epidemiology and Genetics, National Cancer Institute). NR 22 TC 57 Z9 59 U1 1 U2 7 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1059-924X J9 J AGROMEDICINE JI J. Agromedicine PY 2009 VL 14 IS 2 SI SI BP 125 EP 131 DI 10.1080/10599240902779436 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA V21QP UT WOS:000208222400008 PM 19437268 ER PT J AU Chiu, BCH Blair, A AF Chiu, Brian C-H. Blair, Aaron TI Pesticides, Chromosomal Aberrations, and Non-Hodgkin's Lymphoma SO JOURNAL OF AGROMEDICINE LA English DT Article DE Chromosomal abnormalities; epidemiology; lymphoma; pesticides; t(14;18) AB An excessive incidence of non-Hodgkin's lymphoma (NHL) has been reported among farmers and other occupational groups working with pesticides. Some pesticides exhibit immunotoxic and genotoxic activities. Individuals exposed to pesticides have also been found to have an increased prevalence of chromosomal abnormalities including the t(14;18)(q32;q21), one of the most common chromosomal abnormalities in NHL. Two recent epidemiologic studies reported that the association between pesticide exposures and risk of NHL was largely limited to NHL cases with the chromosomal translocation t(14;18). This review summarizes the findings from these epidemiologic studies, speculates on implications, and suggests the research needed to clarify the role of pesticides in NHL. C1 [Chiu, Brian C-H.] Northwestern Univ, Dept Prevent Med, Feinberg Sch Med, Chicago, IL 60611 USA. [Blair, Aaron] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP Chiu, BCH (reprint author), Northwestern Univ, Dept Prevent Med, Feinberg Sch Med, 680 N Lake Shore Dr,Suite 1102, Chicago, IL 60611 USA. EM bchiu@northwestern.edu FU U.S. National Cancer Institute, National Institutes of Health [R03CA94770, R03CA132153, R01CA100555] FX This research was supported by grants R03CA94770, R03CA132153, and R01CA100555 from the U.S. National Cancer Institute, National Institutes of Health. NR 20 TC 15 Z9 18 U1 0 U2 3 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1059-924X J9 J AGROMEDICINE JI J. Agromedicine PY 2009 VL 14 IS 2 SI SI BP 250 EP 255 DI 10.1080/10599240902773140 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA V21QP UT WOS:000208222400025 PM 19437285 ER PT J AU Cohen, SG AF Cohen, Sheldon G. TI Asthma and obesity: An archival addendum SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Letter C1 [Cohen, Sheldon G.] NIAID, Bethesda, MD 20892 USA. [Cohen, Sheldon G.] Natl Lib Med, Hist Med Div, NIH, Bethesda, MD USA. RP Cohen, SG (reprint author), NIAID, 9000 Rockville Pike, Bethesda, MD 20892 USA. EM scohen@niaid.nih.gov NR 4 TC 1 Z9 1 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 2009 VL 123 IS 1 BP 265 EP 266 DI 10.1016/j.jaci.2008.07.038 PG 2 WC Allergy; Immunology SC Allergy; Immunology GA 399IP UT WOS:000262793900043 PM 19130940 ER PT J AU Feinberg, LS Stephan, RB Fogarty, KP Voortman, L Tiller, WA Cassiani-Ingoni, R AF Feinberg, Leslie S. Stephan, Robert B. Fogarty, Kathleen P. Voortman, Lynn Tiller, William A. Cassiani-Ingoni, Riccardo TI Resolution of Cavitational Osteonecrosis Through NeuroModulation Technique, a Novel Form of Intention-Based Therapy: A Clinical Case Study SO JOURNAL OF ALTERNATIVE AND COMPLEMENTARY MEDICINE LA English DT Article ID ALVEOLAR OSTEONECROSIS; HYPOFIBRINOLYSIS; THROMBOPHILIA; JAWS; PAIN; FEATURES; DISEASE AB Objectives: This study evaluated the possibility of using NeuroModulation Technique (NMT), a form of intention-based medicine, to induce osteogenesis and healing of cavitational osteonecrosis, a common progressive form of ischemic disease of the alveolar arch. Design: Eleven (11) adult patients were enrolled based on the presence of lesions in the jawbone. Ten (10) subjects underwent NMT therapy for up to 10 months, while 1 subject received no treatment. Outcome measures: A sensitive analysis of bone density in the alveolar processes of maxilla and mandible was performed before and after therapy using the U. S. Food and Drug Administration-approved Cavitat system of through-transmission ultrasonography and computer imaging. Results: All subjects presented between one and six cavitational lesions at the first scan, most of which (92%) were associated with sites of previous tooth extraction. NMT-treated patients demonstrated significant improvement in bone density in 27 of the 34 lesions analyzed (79%). The median number of lesions per patient was 4 pretreatment and 0 post-treatment (p < 0.01). One NMT-treated patient, 1 surgically treated patient, and the control subject were also imaged at later time points, showing a durable healing of the lesions through NMT comparable to that of surgery, as opposed to disease persistence in the untreated control. Conclusions: NMT therapy provides a safe and potentially effective treatment for jawbone osteonecrosis. Preclinical placebo-controlled trials are encouraged to investigate in depth the potential of NMT for treating inflammatory and degenerative pathologies. C1 [Feinberg, Leslie S.] Columbia Chiropract Clin, Hermiston, OR USA. [Stephan, Robert B.] Holist Dent Ctr, Spokane, WA USA. [Fogarty, Kathleen P.] Fogarty Naturopath Off, Bellevue, WA USA. [Voortman, Lynn] Pathways Naturopath Clin, Oakville, ON, Canada. [Tiller, William A.] William A Tiller Fdn New Sci, Payson, AZ USA. [Cassiani-Ingoni, Riccardo] NINDS, NIH, Bethesda, MD 20892 USA. [Cassiani-Ingoni, Riccardo] Univ Roma La Sapienza, Dept Human Physiol & Pharmacol, Rome, Italy. RP Cassiani-Ingoni, R (reprint author), POB 527,633 E Main St, Hermiston, OR 97838 USA. EM cassianiingoni@gmail.com RI Rastelli, Marcio/B-8034-2011 NR 31 TC 1 Z9 2 U1 0 U2 1 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1075-5535 J9 J ALTERN COMPLEM MED JI J. Altern. Complement Med. PD JAN PY 2009 VL 15 IS 1 BP 25 EP 33 DI 10.1089/acm.2008.0095 PG 9 WC Integrative & Complementary Medicine SC Integrative & Complementary Medicine GA 399XM UT WOS:000262832600006 PM 19769473 ER PT J AU Pilotto, A Sancarlo, D Panza, F Paris, F D'Onofrio, G Cascavilla, L Addante, F Seripa, D Solfrizzi, V Dallapiccola, B Franceschi, M Ferrucci, L AF Pilotto, Alberto Sancarlo, Daniele Panza, Francesco Paris, Francesco D'Onofrio, Grazia Cascavilla, Leandro Addante, Filomena Seripa, Davide Solfrizzi, Vincenzo Dallapiccola, Bruno Franceschi, Marilisa Ferrucci, Luigi TI The Multidimensional Prognostic Index (MPI), Based on a Comprehensive Geriatric Assessment, Predicts Short- and Long-Term Mortality in Hospitalized Older Patients with Dementia SO JOURNAL OF ALZHEIMERS DISEASE LA English DT Article DE Comprehensive Geriatric Assessment (CGA); dementia; mortality; Multidimensional Prognostic Index (MPI); prognosis; survival ID FOLLOW-UP; ALZHEIMERS-DISEASE; ELDERLY-PATIENTS; VASCULAR DEMENTIA; 1-YEAR MORTALITY; VALIDATION; DIAGNOSIS; DISCHARGE; SURVIVAL; CRITERIA AB Aim of this study was to evaluate the usefulness of a Multidimensional Prognostic Index (MPI) based on a Comprehensive Geriatric Assessment (CGA) for predicting mortality risk in older patients with dementia. The present was a retrospective study with a year of follow-up that included 262 patients aged 65 years and older with a diagnosis of dementia. A standardized CGA that included information on clinical, cognitive, functional, and nutritional aspects, as well as comorbidity, medications, and social support network, was used to calculate MPI. The predictive value of the MPI for all-cause mortality over 1 month, 6 months, and 12 months of follow-up was evaluated. Higher MPI values were significantly associated with higher mortality at 1 month (MPI-1, low risk = 0%, MPI-2, moderate risk = 5.2%, MPI-3, severe risk = 13.7%; p < 0.002), 6-months (MPI-1 = 2.7%, MPI-2 = 11.2%, MPI-3 = 28.8%; p < 0.001), and 12-months (MPI-1 = 2.7%, MPI-2 = 18.2%, MPI-3 = 35.6%; p < 0.001) of follow-up. The discrimination of the MPI was also good, with areas under the ROC curves of 0.77 (sensitivity = 82.9%, specificity = 66.0%, with a cut off value > 0.16) at 12-months of follow up. In conclusion, the MPI, calculated from information collected in a standardized CGA, accurately stratified hospitalized elderly patients with dementia into groups at varying risk of short- and long-term mortality. C1 [Pilotto, Alberto; Sancarlo, Daniele; Paris, Francesco; D'Onofrio, Grazia; Cascavilla, Leandro; Addante, Filomena; Seripa, Davide; Franceschi, Marilisa] IRCCS Casa Sollievo Sofferenza, Geriatr Unit, I-71013 San Giovanni Rotondo, FG, Italy. [Pilotto, Alberto; Sancarlo, Daniele; Paris, Francesco; D'Onofrio, Grazia; Cascavilla, Leandro; Addante, Filomena; Seripa, Davide; Franceschi, Marilisa] IRCCS Casa Sollievo Sofferenza, Dept Med Sci, Gerontol Geriatr Res Lab, I-71013 San Giovanni Rotondo, FG, Italy. [Panza, Francesco; Solfrizzi, Vincenzo] Univ Bari, Ctr Aging Brain, Memory Unit, Dept Geriatr, Bari, Italy. [Dallapiccola, Bruno] Univ Roma La Sapienza, Dept Expt Med & Pathol, Rome, Italy. [Dallapiccola, Bruno] Casa Sollievo Sofferenza Mendel Inst, Rome, Italy. [Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Harbor Hosp Ctr, Baltimore, MD 21224 USA. RP Pilotto, A (reprint author), IRCCS Casa Sollievo Sofferenza, Geriatr Unit, Viale Cappuccini 1, I-71013 San Giovanni Rotondo, FG, Italy. EM alberto.pilotto@operapadrepio.it RI D'Onofrio, Grazia/K-9740-2016; Sancarlo, Daniele/C-1056-2017; Dallapiccola, Bruno/K-8692-2016; OI D'Onofrio, Grazia/0000-0002-5905-6063; Sancarlo, Daniele/0000-0001-9541-6364; Dallapiccola, Bruno/0000-0002-5031-1013; Panza, Francesco/0000-0002-7220-0656 FU Ministero della Salute, IRCCS Research Program FX This work was fully supported by grants from Ministero della Salute, IRCCS Research Program 2006-2008, Line 2: "Malattie di rilevanza sociale". NR 36 TC 38 Z9 38 U1 0 U2 3 PU IOS PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 1387-2877 J9 J ALZHEIMERS DIS JI J. Alzheimers Dis. PY 2009 VL 18 IS 1 BP 191 EP 199 DI 10.3233/JAD-2009-1139 PG 9 WC Neurosciences SC Neurosciences & Neurology GA 492BQ UT WOS:000269629500019 PM 19584441 ER PT J AU Mueller, C Magaki, S Schrag, M Ghosh, MC Kirsch, WM AF Mueller, Claudius Magaki, Shino Schrag, Matthew Ghosh, Manik C. Kirsch, Wolff M. TI Iron Regulatory Protein 2 is Involved in Brain Copper Homeostasis SO JOURNAL OF ALZHEIMERS DISEASE LA English DT Article DE Alzheimer's disease; amyloid-beta; amyloid-beta protein precursor (A beta PP); iron regulatory protein 2 (IRP2) ID AMYLOID PRECURSOR PROTEIN; ALZHEIMERS-DISEASE; OXIDATIVE STRESS; SUPEROXIDE-DISMUTASE; RESPONSIVE ELEMENT; TRANSGENIC MICE; CEREBRAL-CORTEX; BETA; ZINC; BINDING AB Trace metal homeostasis is tightly controlled in the brain, as even a slight dysregulation may severely impact normal brain function. This is especially apparent in Alzheimer's disease, where brain homeostasis of trace metals such as copper and iron is dysregulated. As it is known that iron and copper metabolism are linked, we wanted to investigate if a common mechanism could explain the increase in iron and decrease in copper seen in Alzheimer's disease brain. Amyloid-beta protein precursor (A beta PP) has been implicated in copper efflux from the brain. Furthermore, it was shown that iron regulatory proteins (IRP), which regulate iron homeostasis, can block A beta PP mRNA translation. In a correlative study we have therefore compared brain regional copper levels and A beta PP expression in mice with a targeted deletion of IRP2-/-. Compared with controls, six week old IRP2-/- mice had significantly less brain copper in the parietal cortex, hippocampus, ventral striatum, thalamus, hypothalamus, and whole brain, while A beta PP was significantly upregulated in the hippocampus (p < 0.05) and showed a trend toward upregulation in the thalamus (p < 0.1). This is the first study to demonstrate that iron regulatory proteins affect brain copper levels, which has significant implications for neurodegenerative diseases. C1 [Mueller, Claudius; Magaki, Shino; Schrag, Matthew; Kirsch, Wolff M.] Loma Linda Univ, Sch Med, Neurosurg Ctr Res Training & Educ, Loma Linda, CA 92354 USA. [Ghosh, Manik C.] NICHHD, Cell Biol & Metab Branch, US Natl Inst Hlth, Bethesda, MD USA. RP Kirsch, WM (reprint author), Loma Linda Univ, Sch Med, Neurosurg Ctr Res Training & Educ, Loma Linda, CA 92354 USA. EM wkirsch@llu.edu RI Mueller, Claudius/A-4459-2012 OI Mueller, Claudius/0000-0003-4499-4724 FU National Institute on Aging, NIH [AG20948] FX We want to thank Dr. RL Levine and Dr. JR Prohaska for suggestions on the manuscript as well as Waheed Baqai for suggestions on the statistical evaluation of results. This work was supported by the National Institute on Aging, NIH, AG20948. NR 57 TC 5 Z9 5 U1 0 U2 1 PU IOS PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 1387-2877 J9 J ALZHEIMERS DIS JI J. Alzheimers Dis. PY 2009 VL 18 IS 1 BP 201 EP 210 DI 10.3233/JAD-2009-1136 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 492BQ UT WOS:000269629500020 PM 19584448 ER PT J AU Dosunmu, R Wu, JF Adwan, L Maloney, B Basha, MR McPherson, CA Harry, GJ Rice, DC Zawia, NH Lahiri, DK AF Dosunmu, Remi Wu, Jinfang Adwan, Lina Maloney, Bryan Basha, Md Riyaz McPherson, Christopher A. Harry, G. Jean Rice, Deborah C. Zawia, Nasser H. Lahiri, Debomoy K. TI Lifespan Profiles of Alzheimer's Disease-Associated Genes and Products in Monkeys and Mice SO JOURNAL OF ALZHEIMERS DISEASE LA English DT Article DE Amyloid-beta protein precursor (A beta PP); amyloidogenesis; BACE1; development; primates; rodents; specificity protein 1 (SP1); transcription ID AMYLOID PRECURSOR PROTEIN; AGE-RELATED-CHANGES; E ALLELE EPSILON-4; A-BETA PEPTIDES; TRANSGENIC MICE; MESSENGER-RNAS; TRANSLATIONAL REGULATION; DIFFERENTIAL EXPRESSION; NEUROLOGICAL DISORDERS; DEVELOPMENTAL ORIGIN AB Alzheimer's disease (AD) is characterized by plaques of amyloid-beta (A beta) peptide, cleaved from amyloid-beta protein precursor (A beta PP). Our hypothesis is that lifespan profiles of AD-associated mRNA and protein levels in monkeys would differ from mice and that differential lifespan expression profiles would be useful to understand human AD pathogenesis. We compared profiles of A beta PP mRNA, A beta PP protein, and A beta levels in rodents and primates. We also tracked a transcriptional regulator of the A beta PP gene, specificity protein 1 (SP1), and the beta amyloid precursor cleaving enzyme (BACE1). In mice, A beta PP and SP1 mRNA and their protein products were elevated late in life; A beta levels declined in old age. In monkeys, SP1, A beta PP, and BACE1 mRNA declined in old age, while protein products and A beta levels rose. Proteolytic processing in both species did not match production of A beta. In primates, A beta PP and SP1 mRNA levels coordinate, but an inverse relationship exists with corresponding protein products as well as A beta levels. Comparison of human DNA and mRNA sequences to monkey and mouse counterparts revealed structural features that may explain differences in transcriptional and translational processing. These findings are important for selecting appropriate models for AD and other age-related diseases. C1 [Dosunmu, Remi; Wu, Jinfang; Adwan, Lina; Basha, Md Riyaz; Zawia, Nasser H.] Univ Rhode Isl, Dept Biomed & Pharmaceut Sci, Kingston, RI 02881 USA. [McPherson, Christopher A.; Harry, G. Jean] NIH, Res Triangle Pk, NC USA. [Rice, Deborah C.] Maine Dept Hlth & Human Serv, Augusta, ME USA. [Maloney, Bryan; Lahiri, Debomoy K.] Indiana Univ, Sch Med, Dept Psychiat & Med & Mol Genet, Inst Psychiat Res, Indianapolis, IN 46202 USA. RP Lahiri, DK (reprint author), Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA. EM nzawia@uri.edu; dlahiri@iupui.edu RI Maloney, Bryan/C-4924-2011; OI Maloney, Bryan/0000-0003-2364-9649; Adwan, Lina/0000-0003-4134-9586 FU Intramural Research Program of the National Institutes of Health (NIH), National Institute of Environmental Health Sciences (NIEHS) [ES013022, AG027246]; National Center for Research Resources (NCRR) [P20RR016457]; Alzheimer's Association and National Institute on Aging, NIH [AG18379, AG18884] FX This research was supported by the Intramural Research Program of the National Institutes of Health (NIH), National Institute of Environmental Health Sciences (NIEHS) and by grants (ES013022 and AG027246) from the NIH awarded to NHZ. The research core facility was funded (P20RR016457) by the National Center for Research Resources (NCRR), a component of NIH. Work at DKL's laboratory was funded by grants from the Alzheimer's Association and National Institute on Aging, NIH (AG18379 and AG18884). NR 81 TC 16 Z9 16 U1 0 U2 1 PU IOS PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 1387-2877 J9 J ALZHEIMERS DIS JI J. Alzheimers Dis. PY 2009 VL 18 IS 1 BP 211 EP 230 DI 10.3233/JAD-2009-1138 PG 20 WC Neurosciences SC Neurosciences & Neurology GA 492BQ UT WOS:000269629500021 PM 19584442 ER PT J AU O'Brien, RJ Resnick, SM Zonderman, AB Ferrucci, L Crain, BJ Pletnikova, O Rudow, G Iacono, D Riudavets, MA Driscoll, I Price, DL Martin, LJ Troncoso, JC AF O'Brien, Richard J. Resnick, Susan M. Zonderman, Alan B. Ferrucci, Luigi Crain, Barbara J. Pletnikova, Olga Rudow, Gay Iacono, Diego Riudavets, Miguel A. Driscoll, Ira Price, Donald L. Martin, Lee J. Troncoso, Juan C. TI Neuropathologic Studies of the Baltimore Longitudinal Study of Aging (BLSA) SO JOURNAL OF ALZHEIMERS DISEASE LA English DT Article DE alpha-synuclein; Alzheimer's disease; asymptomatic Alzheimer's disease; amyloid-beta; dementia; Parkinson's disease; stereology; successful aging; tau ID MILD COGNITIVE IMPAIRMENT; ALZHEIMERS-DISEASE; PARKINSONS-DISEASE; SENILE PLAQUES; LEWY BODIES; DEMENTIA; PATHOLOGY; HYPERTROPHY; MULTICENTER; RELIABILITY AB The Baltimore Longitudinal Study of Aging (BLSA) was established in 1958 and is one the oldest prospective studies of aging in the USA and the world. The BLSA is supported by the National Institute of Aging (NIA) and its mission is to learn what happens to people as they get old and how to sort out changes due to aging from those due to disease or other causes. In 1986, an autopsy program combined with comprehensive neurologic and cognitive evaluations was established in collaboration with the Johns Hopkins University Alzheimer's Disease Research Center (ADRC). Since then, 211 subjects have undergone autopsy. Here we review the key clinical neuropathological correlations from this autopsy series. The focus is on the morphological and biochemical changes that occur in normal aging, and the early neuropathological changes of neurodegenerative diseases, especially Alzheimer's disease (AD). We highlight the combined clinical, pathologic, morphometric, and biochemical evidence of asymptomatic AD, a state characterized by normal clinical evaluations in subjects with abundant AD pathology. We conclude that in some individuals, successful cognitive aging results from compensatory mechanisms that occur at the neuronal level (i.e., neuronal hypertrophy and synaptic plasticity) whereas a failure of compensation may culminate in disease. C1 [Troncoso, Juan C.] Johns Hopkins Univ, Sch Med, Dept Pathol, Div Neuropathol, Baltimore, MD 21224 USA. [O'Brien, Richard J.; Troncoso, Juan C.] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21224 USA. [Resnick, Susan M.; Zonderman, Alan B.; Driscoll, Ira] NIA, Lab Personal & Cognit, Intramural Res Program, NIH, Baltimore, MD 21224 USA. [Ferrucci, Luigi] NIA, Clin Res Branch, Intramural Res Program, NIH, Baltimore, MD 21224 USA. [Riudavets, Miguel A.] FLENI, Dept Pathol, Buenos Aires, DF, Argentina. RP Troncoso, JC (reprint author), Johns Hopkins Univ, Sch Med, Dept Pathol, Div Neuropathol, Baltimore, MD 21224 USA. EM troncoso@jhmi.edu OI Zonderman, Alan B/0000-0002-6523-4778 FU Johns Hopkins University Alzheimer's Disease Research Center (National Institutes of Health) [AG05146]; Burroughs Wellcome Fund for Translational Research; National Institute of Aging FX This work was supported by the Johns Hopkins University Alzheimer's Disease Research Center (National Institutes of Health, AG05146), the Burroughs Wellcome Fund for Translational Research, and the Intramural Research Program of the National Institute of Aging and National Institutes of Health. NR 47 TC 42 Z9 43 U1 1 U2 4 PU IOS PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 1387-2877 J9 J ALZHEIMERS DIS JI J. Alzheimers Dis. PY 2009 VL 18 IS 3 BP 665 EP 675 DI 10.3233/JAD-2009-1179 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 533XS UT WOS:000272860100018 PM 19661626 ER PT J AU Basselin, M Nguyen, HN Chang, L Bell, JM Rapoport, SI AF Basselin, Mireille Nguyen, Henry N. Chang, Lisa Bell, Jane M. Rapoport, Stanley I. TI Acute but not Chronic Donepezil Increases Muscarinic Receptor-Mediated Signaling via Arachidonic Acid in Unanesthetized Rats SO JOURNAL OF ALZHEIMERS DISEASE LA English DT Article DE Acetylcholine; acetylcholinesterase; Alzheimer's disease; anticholinesterase; arachidonic acid; brain; desensitization; donepezil; imaging; muscarinic receptors; phospholipase A(2) ID CYTOSOLIC PHOSPHOLIPASE A(2); HUMAN NEUROBLASTOMA-CELLS; PROTEIN-KINASE-C; ALZHEIMERS-DISEASE; BRAIN PHOSPHOLIPIDS; CHOLINERGIC RECEPTORS; AWAKE RATS; STIMULATES PHOSPHOLIPASE-A2; CHOLINESTERASE-INHIBITORS; ACETYLCHOLINE-RECEPTORS AB Donepezil, an acetylcholinesterase (AChE) inhibitor used for treating Alzheimer's disease patients, is thought to act by increasing brain extracellular acetylcholine (ACh), and ACh binding to cholinergic receptors. Muscarinic receptors are coupled to cytosolic phospholipase A(2) (cPLA(2)) activation and arachidonic acid (AA) release from synaptic membrane phospholipid. This activation can be imaged in rodents as an AA incorporation coefficient k*, using quantitative autoradiography. Acute and chronic effects of donepezil on the AA signal, k* for AA, were measured in 81 brain regions of unanesthetized rats. Twenty min after a single oral dose (3.0 mg/kg) of donepezil, k* was increased significantly in 37 brain regions, whereas k* did not differ from control 7 h afterwards or following chronic (21 days) of donepezil. Pretreatment with atropine prevented the 20-min increments in k* following donepezil. Donepezil also increased the brain ACh concentration and reduced brain AChE activity, but did not change cPLA(2) activity, regardless of administration regimen. These results show that donepezil acutely increases the brain AA signal that is mediated by ACh acting at muscarinic receptors, but that this signal is rapidly desensitized despite continued elevated brain ACh concentration. In contrast, the AA signal in response to arecoline was not altered following donepezil. C1 [Basselin, Mireille; Nguyen, Henry N.; Chang, Lisa; Bell, Jane M.; Rapoport, Stanley I.] NIA, Brain Physiol & Metab Sect, NIH, Bethesda, MD 20892 USA. RP Basselin, M (reprint author), NIA, Brain Physiol & Metab Sect, NIH, Bldg 9,Room 1S126, Bethesda, MD 20892 USA. EM mirvasln@mail.nih.gov FU Intramural Research Program of the NIH; National Institute on Aging FX This work was supported entirely by the Intramural Research Program of the NIH, National Institute on Aging. None of the authors has a financial or other conflict of interest related to this work. We thank Mrs. Kathy Benjamin for proofreading this paper. NR 79 TC 5 Z9 5 U1 1 U2 1 PU IOS PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 1387-2877 J9 J ALZHEIMERS DIS JI J. Alzheimers Dis. PY 2009 VL 17 IS 2 BP 369 EP 382 DI 10.3233/JAD-2009-1058 PG 14 WC Neurosciences SC Neurosciences & Neurology GA 461RV UT WOS:000267289500015 PM 19363262 ER PT J AU Nagababu, E Usatyuk, PV Enika, D Natarajan, V Rifkind, JM AF Nagababu, Enika Usatyuk, Peter V. Enika, Divya Natarajan, Viswanathan Rifkind, Joseph M. TI Vascular Endothelial Barrier Dysfunction Mediated by Amyloid-beta Proteins SO JOURNAL OF ALZHEIMERS DISEASE LA English DT Article DE Alzheimer's disease; amyloid-beta; endothelial cells; permeability ID BLOOD-BRAIN-BARRIER; RADICAL OXIDATIVE STRESS; FOCAL ADHESION KINASE; ALZHEIMERS-DISEASE; TYROSINE PHOSPHORYLATION; HYDROGEN-PEROXIDE; INDUCED MIGRATION; IN-VITRO; CELL; PEPTIDE AB Neuronal inflammation is very common in Alzheimer's disease (AD). This inflammation can be caused by infiltration of neutrophils across the blood brain barrier. Endothelial permeability changes are required for the infiltration of high molecular weight components to the brain. Deposition of toxic amyloid-beta (A beta) fibrils in the cerebral vasculature, as well as in brain neurons, has been implicated in the development of AD. This study investigates the effect of A beta fibrils on the permeability of the endothelium and the mechanism for the observed permeability changes. A beta(1-40) and A beta(1-42) fibrils, but not monomers, were found to increase permeability of bovine pulmonary arterial endothelial cells in a dose- and time dependent manner as detected by transendothelial electrical resistance. This increase in permeability is only partially (25%) inhibited by catalase and is not associated with an increase in cytosolic Ca(+2) or tyrosine phosphorylation. These results indicate that hydrogen peroxide is not the primary mediator for the permeability changes. Treatment of cells with both amyloid fibrils resulted in stress fiber formation, disruption and aggregation of actin filaments, and cellular gap formation. The results of this study reveal that A beta increases the permeability of endothelium by inducing change in the cytoskeleton network. C1 [Nagababu, Enika; Rifkind, Joseph M.] NIA, Mol Dynam Sect, NIH, Baltimore, MD 21224 USA. [Usatyuk, Peter V.; Enika, Divya; Natarajan, Viswanathan] Univ Chicago, Dept Med, Pulm & Crit Care Sect, Chicago, IL 60637 USA. RP Rifkind, JM (reprint author), NIA, Mol Dynam Sect, NIH, 251 Bayview Blvd, Baltimore, MD 21224 USA. EM rifkindj@grc.nia.nih.gov FU National Institutes of Health; National Institute on Aging FX This research was supported by Intramural Research Program of the National Institutes of Health, National Institute on Aging. NR 51 TC 17 Z9 17 U1 0 U2 2 PU IOS PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 1387-2877 J9 J ALZHEIMERS DIS JI J. Alzheimers Dis. PY 2009 VL 17 IS 4 BP 845 EP 854 DI 10.3233/JAD-2009-1104 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 492BP UT WOS:000269629400012 PM 19542618 ER PT J AU Tinoco-Gracia, L Quiroz-Romero, H Quintero-Martinez, MT Renteria-Evangelista, TB Barreras-Serrano, A Hori-Oshima, S Lopez-Valencia, G Tamayo-Sosa, AR Medina-Basulto, G Haro-Alvarez, P Moro, M Vinasco, J AF Tinoco-Gracia, Luis Quiroz-Romero, Hetor Teresa Quintero-Martinez, Maria Renteria-Evangelista, Tomas Benjamin Barreras-Serrano, Alberto Hori-Oshima, Sawako Lopez-Valencia, Gilberto Rossana Tamayo-Sosa, Alma Medina-Basulto, Gerardo Haro-Alvarez, Paulina Moro, Manuel Vinasco, Javier TI Prevalence and Risk Factors for Borrelia burgdorferi Infection in Dogs of Animal Control Centers from Mexicali, Baja California: A Mexico-US Border City SO JOURNAL OF ANIMAL AND VETERINARY ADVANCES LA English DT Article DE Borrelia burgdorferi; tick; lyme disease; borreliosis ID LYME-DISEASE; TICKS; REGION AB Lyme borreliosis, a worldwide zoonotic disease and characterized by polisystemic disorders, is caused by the spirochete B. burgdorferi, which is transmitted by a tick bite, primarily from Ixodes scapularis and L pacificus. In Mexico, native Lyme disease has been recently reported in humans, while canine B. burgdorferi infection has been also reported in several areas of the country. In Monterrey, Mexico, a seroprevalence of 16% was observed in dogs (160/850) and molecular evidence was found in canine synovial fluid. Moreover, a preliminar study performed in 2003 in Mexicali, Mexico showed a prevalence of 7.4% (7/94) in dogs infested only by the tick Rhipicephalus sanguineus. The aim of this study was to estimate the seroprevalence of B. burgdorferi in dogs captured by personnel from the animal control centers in the city of Mexicali. Blood samples from 384 dogs were randomly selected from February 2005 to December 2006 and their sera were analized by the semiquantitative kit Borrelia burgdorferi ELISA (R) Helica Biosystems, Inc., with 96% sensitivity and 95% specificity. An adjusted prevalence of 12% (95% IC 7.5-14.3%) was obtained using the Rogan-Gladcn estimator. The seroprevalence obtained in this study was lower compared to those in Monterrey (16%) where the principal vector was Ixodes scapularis and in Sao Paulo, Brazil (15.6%) where the main vector was Amblyomma cajennense. No risk factors were associated with B. burgdorfieri seropositivity. This study confirms the existence of B. burgdorferi past/present infection in dogs in an area where the only identified tick is R. sanguineus. C1 [Tinoco-Gracia, Luis; Renteria-Evangelista, Tomas Benjamin; Barreras-Serrano, Alberto; Hori-Oshima, Sawako; Lopez-Valencia, Gilberto; Rossana Tamayo-Sosa, Alma; Medina-Basulto, Gerardo; Haro-Alvarez, Paulina] Univ Autonoma Baja California, Inst Invest Ciencias Vet, Mexicali 21100, Baja California, Mexico. [Quiroz-Romero, Hetor; Teresa Quintero-Martinez, Maria] Univ Nacl Autonoma Mexico, Fac Med Vet & Zootecnia, Mexico City 04510, DF, Mexico. [Moro, Manuel] NIH, Div Comparat Med, Natl Ctr Res Resources, Bethesda, MD 20892 USA. [Vinasco, Javier] Kansas State Univ, Coll Vet Med, Manhattan, KS 66506 USA. RP Tinoco-Gracia, L (reprint author), Av Michoacan 2101, Mexicali 21130, Baja California, Mexico. NR 19 TC 2 Z9 2 U1 1 U2 6 PU MEDWELL ONLINE PI FAISALABAD PA ANSINET BUILDING, 308-LASANI TOWN, SARGODHA RD, FAISALABAD, 38090, PAKISTAN SN 1680-5593 J9 J ANIM VET ADV JI J. Anim. Vet. Adv. PY 2009 VL 8 IS 2 BP 251 EP 254 PG 4 WC Veterinary Sciences SC Veterinary Sciences GA 417UT UT WOS:000264104700010 ER PT J AU Berglund, C Ito, T Ma, XX Ikeda, M Watanabe, S Soderquist, B Hiramatsu, K AF Berglund, Carolina Ito, Teruyo Ma, Xiao Xue Ikeda, Megumi Watanabe, Shinya Soderquist, Bo Hiramatsu, Keiichi TI Genetic diversity of methicillin-resistant Staphylococcus aureus carrying type IV SCCmec in Orebro County and the western region of Sweden SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY LA English DT Article ID CASSETTE CHROMOSOME MEC; PANTON-VALENTINE LEUKOCIDIN; MULTIPLEX PCRS; CLONES; COMMUNITY; STRAINS; EMERGENCE; EVOLUTION; VARIANTS; MRSA AB Recent studies have shown a predominance of type IV SCCmec among the methicillin-resistant Staphylococcus aureus (MRSA) isolated in the low endemic areas of Orebro County and the western region of Sweden. However, many of these isolates were not possible to classify as existing subtypes IVa, IVb, IVc or IVd. We analysed 16 such MRSA isolates by multilocus sequence typing, spa typing, staphylocoagulase (SC) typing and detection of type IVg and IVh SCCmec. MRSA that remained as unknown type IV SCCmec were investigated by long-range PCR covering the J1 region; however, only two isolates were possible to amplify by PCR. The nucleotide sequences of the entire SCCmec of these two MRSA were determined. In addition, isolates that had unknown SC types were investigated by nucleotide sequencing of the coa genes. Five of 16 isolates were classified as type IVg SCCmec, and four isolates had type IVh SCCmec. Two subtypes of type IV SCCmec shared J1 regions previously identified in other types of SCCmec, types I.2 and II.2. The novel elements were designated as type IVi and IVj SCCmec. In addition, the genetic backgrounds of these Swedish MRSA were diverse and constituted at least nine sequence types and eight SC types, including four new types of SC. Type IV SCCmec is occurring in heterogeneous clones of MRSA in Sweden, and the majority of the type IV SCCmec were identified in community-acquired MRSA. We describe two novel subtypes of type IV SCCmec with common J1 regions shared by other types of SCCmec, which indicate that J1 regions occurred as primordial SCC. C1 [Berglund, Carolina; Soderquist, Bo] Orebro Univ Hosp, Dept Clin Microbiol, Orebro, Sweden. [Berglund, Carolina; Ito, Teruyo; Ikeda, Megumi; Watanabe, Shinya; Hiramatsu, Keiichi] Juntendo Univ, Dept Infect Control Sci, Postgrad Sch, Tokyo, Japan. [Ito, Teruyo; Ma, Xiao Xue; Ikeda, Megumi; Hiramatsu, Keiichi] Juntendo Univ, Sch Med, Dept Bacteriol, Tokyo 113, Japan. [Ma, Xiao Xue] China Med Univ, Dept Med Microbiol & Parasitol, Shenyang, Peoples R China. [Watanabe, Shinya] NIAID, TB Res Sect, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA. [Soderquist, Bo] Orebro Univ Hosp, Dept Infect Dis, Orebro, Sweden. RP Berglund, C (reprint author), Aleris MEDILAB, Dept Microbiol, SE-18315 Taby, Sweden. EM carolina.berglund@aleris.se RI Watanabe, Shinya/B-7008-2009 OI Watanabe, Shinya/0000-0001-6542-6502 FU Sweden - Japan Foundation; Swedish Society for Medical Research; Swedish Institute of Biomedical Laboratory Science; Orebro County Council Research Committee, Sweden; 21st Century COE Research; Ministry of Education and Science, Japan FX This study was supported by grants from the Sweden - Japan Foundation, the Swedish Society for Medical Research, the Swedish Institute of Biomedical Laboratory Science, the Orebro County Council Research Committee, Sweden, and a Grant-in-Aid for 21st Century COE Research, Ministry of Education and Science, Japan. NR 35 TC 24 Z9 27 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0305-7453 J9 J ANTIMICROB CHEMOTH JI J. Antimicrob. Chemother. PD JAN PY 2009 VL 63 IS 1 BP 32 EP 41 DI 10.1093/jac/dkn435 PG 10 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA 383NT UT WOS:000261681000007 PM 19001453 ER PT J AU Such, EA Benson, BE Luckenbaugh, DA Geraci, M Post, RM McCann, U AF Such, Elizabeth A. Benson, Brenda E. Luckenbaugh, David A. Geraci, Marilla Post, Robert M. McCann, Una TI Repetitive TMS combined with exposure therapy for PTSD: A preliminary study SO JOURNAL OF ANXIETY DISORDERS LA English DT Article DE Post-traumatic stress disorder (PTSD); Transcranial magnetic stimulation (TMS); Psychological desensitization; Psychological therapies; Extinction ID TRANSCRANIAL MAGNETIC STIMULATION; POSTTRAUMATIC-STRESS-DISORDER; DORSOLATERAL PREFRONTAL CORTEX; MAJOR DEPRESSION; ANXIETY DISORDERS; DORSAL PREMOTOR; MOTOR CORTEX; DOUBLE-BLIND; EXTINCTION; TRIAL AB Treatment for anxiety and post-traumatic stress disorder (PTSD) includes exposure therapy and medications, but some patients are refractory. Few studies of repetitive transcranial magnetic stimulation (rTMS) for anxiety or PTSD exist. In this preliminary report, rTMS was combined with exposure therapy for PTSD. Nine subjects with chronic, treatment-refractory PTSD were studied in a placebo-controlled, crossover design of imaginal exposure therapy with rTMS (1 Hz) versus sham. PTSD symptoms, serum and 24 h urine were obtained and analyzed. Effect sizes for PTSD symptoms were determined using Cohen's d. Active rTMS showed a larger effect size of improvement for hyperarousal symptoms compared to sham; 24-h urinary norepinephrine and serum T4 increased: serum prolactin decreased. Active rTMS with exposure may have symptomatic and physiological effects. Larger studies are needed to confirm these preliminary findings and verify whether rTMS plus exposure therapy has a role in the treatment of PTSD. (C) 2008 Elsevier Ltd. All rights reserved. C1 [Such, Elizabeth A.; Benson, Brenda E.; Luckenbaugh, David A.; Post, Robert M.; McCann, Una] NIMH, Biol Psychiat Branch, NIH, Bethesda, MA USA. [Geraci, Marilla] NIH, Clin Ctr Nursing Dept, Bethesda, MA USA. RP Such, EA (reprint author), Univ Western Ontario, Dept Psychiat, 339 Windermere Rd, London, ON N6A 4G5, Canada. EM Elizabeth.osuch@lhsc.on.ca NR 42 TC 1 Z9 2 U1 2 U2 10 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0887-6185 J9 J ANXIETY DISORD JI J. Anxiety Disord. PD JAN PY 2009 VL 23 IS 1 BP 54 EP 59 DI 10.1016/j.janxdis.2008.03.015 PG 6 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 398VU UT WOS:000262760400007 ER PT J AU Soja, AJ Al-Saadi, J Giglio, L Randall, D Kittaka, C Pouliot, G Kordzi, JJ Raffuse, S Pace, TG Pierce, TE Moore, T Roy, B Pierce, RB Szykman, JJ AF Soja, Amber J. Al-Saadi, Jassim Giglio, Louis Randall, Dave Kittaka, Chieko Pouliot, George Kordzi, Joseph J. Raffuse, Sean Pace, Thompson G. Pierce, Thomas E. Moore, Tom Roy, Biswadev Pierce, R. Bradley Szykman, James J. TI Assessing satellite-based fire data for use in the National Emissions Inventory SO JOURNAL OF APPLIED REMOTE SENSING LA English DT Article DE biomass burning; remote sensing; area burned; Environmental Protection Agency; climate change; Arizona and Oregon ID CARBON AB Biomass burning is significant to emission estimates because: (1) it can be a major contributor of particulate matter and other pollutants; (2) it is one of the most poorly documented of all sources; (3) it can adversely affect human health; and (4) it has been identified as a significant contributor to climate change through feedbacks with the radiation budget. Additionally, biomass burning can be a significant contributor to a regions inability to achieve the National Ambient Air Quality Standards for PM 2.5 and ozone, particularly on the top 20% worst air quality days. The United States does not have a standard methodology to track fire occurrence or area burned, which are essential components to estimating fire emissions. Satellite imagery is available almost instantaneously and has great potential to enhance emission estimates and their timeliness. This investigation compares satellite-derived fire data to ground-based data to assign statistical error and helps provide confidence in these data. The largest fires are identified by all satellites and their spatial domain is accurately sensed. MODIS provides enhanced spatial and temporal information, and GOES ABBA data are able to capture more small agricultural fires. A methodology is presented that combines these satellite data in Near-Real-Time to produce a product that captures 81 to 92% of the total area burned by wildfire, prescribed, agricultural and rangeland burning. Each satellite possesses distinct temporal and spatial capabilities that permit the detection of unique fires that could be omitted if using data from only one satellite. C1 [Soja, Amber J.] NIA, NASA, Langley Res Ctr, Hampton, VA 23681 USA. [Giglio, Louis] Sci Syst & Applicat Inc, Lanham, MD 20706 USA. [Randall, Dave] Air Sci Inc, Golden, CO 80401 USA. [Kittaka, Chieko] NASA, Sci Syst & Applicat Inc, Langley Res Ctr, Hampton, VA 23681 USA. [Pouliot, George; Pierce, Thomas E.] US EPA, ORD, Res Triangle Pk, NC 27711 USA. [Kordzi, Joseph J.; Roy, Biswadev] USEPA Reg 6, Dallas, TX 75202 USA. [Raffuse, Sean] STI, Petaluma, CA 94954 USA. [Pace, Thompson G.] US EPA, OAQPS, Div Environm Sci, Res Triangle Pk, NC 27711 USA. [Moore, Tom] Colorado State Univ, WRAP, Ft Collins, CO 80523 USA. [Pierce, R. Bradley] NOAA, Natl Environm Satellite Data & Informat Serv, Madison, WI 53706 USA. [Szykman, James J.] NASA, US EPA, Langley Res Ctr, Hampton, VA 23681 USA. RP Soja, AJ (reprint author), NIA, NASA, Langley Res Ctr, 21 Langley Blvd,MS 420, Hampton, VA 23681 USA. EM Amber.J.Soja@nasa.gov; j.a.al-saadi@nasa.gov; louis_giglio@ssaihq.com; drandall@airsci.com; Chieko.Kittaka-1@nasa.gov; Pouliot.George@epamail.epa.gov; Kordzi.Joe@epamail.epa.gov; sraffuse@sonomatech.com; Pace.Tom@epamail.epa.gov; pierce.tom@epa.gov; MooreT@cira.colostate.edu; Roy.Dev@epamail.epa.gov; brad.pierce@noaa.gov; james.j.szykman@nasa.gov RI Pierce, Robert Bradley/F-5609-2010 OI Pierce, Robert Bradley/0000-0002-2767-1643 NR 12 TC 9 Z9 9 U1 1 U2 8 PU SPIE-SOC PHOTO-OPTICAL INSTRUMENTATION ENGINEERS PI BELLINGHAM PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98225 USA SN 1931-3195 J9 J APPL REMOTE SENS JI J. Appl. Remote Sens. PY 2009 VL 3 SI SI AR 031504 DI 10.1117/1.3148859 PN 2 PG 29 WC Environmental Sciences; Remote Sensing; Imaging Science & Photographic Technology SC Environmental Sciences & Ecology; Remote Sensing; Imaging Science & Photographic Technology GA 520VY UT WOS:000271878800005 ER EF